Atherosclerosis: A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.Arteriosclerosis: Thickening and loss of elasticity of the walls of ARTERIES of all sizes. There are many forms classified by the types of lesions and arteries involved, such as ATHEROSCLEROSIS with fatty lesions in the ARTERIAL INTIMA of medium and large muscular arteries.Apolipoproteins E: A class of protein components which can be found in several lipoproteins including HIGH-DENSITY LIPOPROTEINS; VERY-LOW-DENSITY LIPOPROTEINS; and CHYLOMICRONS. Synthesized in most organs, Apo E is important in the global transport of lipids and cholesterol throughout the body. Apo E is also a ligand for LDL receptors (RECEPTORS, LDL) that mediates the binding, internalization, and catabolism of lipoprotein particles in cells. There are several allelic isoforms (such as E2, E3, and E4). Deficiency or defects in Apo E are causes of HYPERLIPOPROTEINEMIA TYPE III.Carotid Artery Diseases: Pathological conditions involving the CAROTID ARTERIES, including the common, internal, and external carotid arteries. ATHEROSCLEROSIS and TRAUMA are relatively frequent causes of carotid artery pathology.Diet, Atherogenic: A diet that contributes to the development and acceleration of ATHEROGENESIS.Aortic Diseases: Pathological processes involving any part of the AORTA.Aorta: The main trunk of the systemic arteries.Coronary Artery Disease: Pathological processes of CORONARY ARTERIES that may derive from a congenital abnormality, atherosclerotic, or non-atherosclerotic cause.Carotid Arteries: Either of the two principal arteries on both sides of the neck that supply blood to the head and neck; each divides into two branches, the internal carotid artery and the external carotid artery.Tunica Intima: The innermost layer of an artery or vein, made up of one layer of endothelial cells and supported by an internal elastic lamina.Tunica Media: The middle layer of blood vessel walls, composed principally of thin, cylindrical, smooth muscle cells and elastic tissue. It accounts for the bulk of the wall of most arteries. The smooth muscle cells are arranged in circular layers around the vessel, and the thickness of the coat varies with the size of the vessel.Cholesterol: The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.Plaque, Atherosclerotic: Lesions formed within the walls of ARTERIES.Risk Factors: An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.Lipoproteins, LDL: A class of lipoproteins of small size (18-25 nm) and light (1.019-1.063 g/ml) particles with a core composed mainly of CHOLESTEROL ESTERS and smaller amounts of TRIGLYCERIDES. The surface monolayer consists mostly of PHOSPHOLIPIDS, a single copy of APOLIPOPROTEIN B-100, and free cholesterol molecules. The main LDL function is to transport cholesterol and cholesterol esters to extrahepatic tissues.Intracranial Arteriosclerosis: Vascular diseases characterized by thickening and hardening of the walls of ARTERIES inside the SKULL. There are three subtypes: (1) atherosclerosis with fatty deposits in the ARTERIAL INTIMA; (2) Monckeberg's sclerosis with calcium deposits in the media and (3) arteriolosclerosis involving the small caliber arteries. Clinical signs include HEADACHE; CONFUSION; transient blindness (AMAUROSIS FUGAX); speech impairment; and HEMIPARESIS.Receptors, LDL: Receptors on the plasma membrane of nonhepatic cells that specifically bind LDL. The receptors are localized in specialized regions called coated pits. Hypercholesteremia is caused by an allelic genetic defect of three types: 1, receptors do not bind to LDL; 2, there is reduced binding of LDL; and 3, there is normal binding but no internalization of LDL. In consequence, entry of cholesterol esters into the cell is impaired and the intracellular feedback by cholesterol on 3-hydroxy-3-methylglutaryl CoA reductase is lacking.Mice, Knockout: Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.Lipids: A generic term for fats and lipoids, the alcohol-ether-soluble constituents of protoplasm, which are insoluble in water. They comprise the fats, fatty oils, essential oils, waxes, phospholipids, glycolipids, sulfolipids, aminolipids, chromolipids (lipochromes), and fatty acids. (Grant & Hackh's Chemical Dictionary, 5th ed)Carotid Intima-Media Thickness: A measurement of the thickness of the carotid artery walls. It is measured by B-mode ULTRASONOGRAPHY and is used as a surrogate marker for ATHEROSCLEROSIS.Hypercholesterolemia: A condition with abnormally high levels of CHOLESTEROL in the blood. It is defined as a cholesterol value exceeding the 95th percentile for the population.Cholesterol, Dietary: Cholesterol present in food, especially in animal products.Foam Cells: Lipid-laden macrophages originating from monocytes or from smooth muscle cells.Carotid Artery, Common: The two principal arteries supplying the structures of the head and neck. They ascend in the neck, one on each side, and at the level of the upper border of the thyroid cartilage, each divides into two branches, the external (CAROTID ARTERY, EXTERNAL) and internal (CAROTID ARTERY, INTERNAL) carotid arteries.Macrophages: The relatively long-lived phagocytic cell of mammalian tissues that are derived from blood MONOCYTES. Main types are PERITONEAL MACROPHAGES; ALVEOLAR MACROPHAGES; HISTIOCYTES; KUPFFER CELLS of the liver; and OSTEOCLASTS. They may further differentiate within chronic inflammatory lesions to EPITHELIOID CELLS or may fuse to form FOREIGN BODY GIANT CELLS or LANGHANS GIANT CELLS. (from The Dictionary of Cell Biology, Lackie and Dow, 3rd ed.)Endothelium, Vascular: Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.Calcinosis: Pathologic deposition of calcium salts in tissues.Mice, Inbred C57BLInflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.Lipoproteins: Lipid-protein complexes involved in the transportation and metabolism of lipids in the body. They are spherical particles consisting of a hydrophobic core of TRIGLYCERIDES and CHOLESTEROL ESTERS surrounded by a layer of hydrophilic free CHOLESTEROL; PHOSPHOLIPIDS; and APOLIPOPROTEINS. Lipoproteins are classified by their varying buoyant density and sizes.Coronary Vessels: The veins and arteries of the HEART.Hyperlipidemias: Conditions with excess LIPIDS in the blood.Disease Models, Animal: Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.Disease Progression: The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis.Aorta, Thoracic: The portion of the descending aorta proceeding from the arch of the aorta and extending to the DIAPHRAGM, eventually connecting to the ABDOMINAL AORTA.Biological Markers: Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.Chlamydophila pneumoniae: A species of CHLAMYDOPHILA that causes acute respiratory infection, especially atypical pneumonia, in humans, horses, and koalas.Cholesterol, HDL: Cholesterol which is contained in or bound to high-density lipoproteins (HDL), including CHOLESTEROL ESTERS and free cholesterol.Czechoslovakia: Created as a republic in 1918 by Czechs and Slovaks from territories formerly part of the Austro-Hungarian Empire. The country split into the Czech Republic and Slovakia 1 January 1993.Cholesterol, LDL: Cholesterol which is contained in or bound to low density lipoproteins (LDL), including CHOLESTEROL ESTERS and free cholesterol.Muscle, Smooth, Vascular: The nonstriated involuntary muscle tissue of blood vessels.TriglyceridesAorta, Abdominal: The aorta from the DIAPHRAGM to the bifurcation into the right and left common iliac arteries.Arteries: The vessels carrying blood away from the heart.C-Reactive Protein: A plasma protein that circulates in increased amounts during inflammation and after tissue damage.Rabbits: The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.Cells, Cultured: Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.Cardiovascular Diseases: Pathological conditions involving the CARDIOVASCULAR SYSTEM including the HEART; the BLOOD VESSELS; or the PERICARDIUM.Vascular Cell Adhesion Molecule-1: Cytokine-induced cell adhesion molecule present on activated endothelial cells, tissue macrophages, dendritic cells, bone marrow fibroblasts, myoblasts, and myotubes. It is important for the recruitment of leukocytes to sites of inflammation. (From Pigott & Power, The Adhesion Molecule FactsBook, 1993, p154)Lipid Metabolism: Physiological processes in biosynthesis (anabolism) and degradation (catabolism) of LIPIDS.Coronary Disease: An imbalance between myocardial functional requirements and the capacity of the CORONARY VESSELS to supply sufficient blood flow. It is a form of MYOCARDIAL ISCHEMIA (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels.Prospective Studies: Observation of a population for a sufficient number of persons over a sufficient number of years to generate incidence or mortality rates subsequent to the selection of the study group.Probucol: A drug used to lower LDL and HDL cholesterol yet has little effect on serum-triglyceride or VLDL cholesterol. (From Martindale, The Extra Pharmacopoeia, 30th ed, p993).Monocytes: Large, phagocytic mononuclear leukocytes produced in the vertebrate BONE MARROW and released into the BLOOD; contain a large, oval or somewhat indented nucleus surrounded by voluminous cytoplasm and numerous organelles.Endothelial Cells: Highly specialized EPITHELIAL CELLS that line the HEART; BLOOD VESSELS; and lymph vessels, forming the ENDOTHELIUM. They are polygonal in shape and joined together by TIGHT JUNCTIONS. The tight junctions allow for variable permeability to specific macromolecules that are transported across the endothelial layer.Apolipoprotein A-I: The most abundant protein component of HIGH DENSITY LIPOPROTEINS or HDL. This protein serves as an acceptor for CHOLESTEROL released from cells thus promoting efflux of cholesterol to HDL then to the LIVER for excretion from the body (reverse cholesterol transport). It also acts as a cofactor for LECITHIN CHOLESTEROL ACYLTRANSFERASE that forms CHOLESTEROL ESTERS on the HDL particles. Mutations of this gene APOA1 cause HDL deficiency, such as in FAMILIAL ALPHA LIPOPROTEIN DEFICIENCY DISEASE and in some patients with TANGIER DISEASE.Carotid Stenosis: Narrowing or stricture of any part of the CAROTID ARTERIES, most often due to atherosclerotic plaque formation. Ulcerations may form in atherosclerotic plaques and induce THROMBUS formation. Platelet or cholesterol emboli may arise from stenotic carotid lesions and induce a TRANSIENT ISCHEMIC ATTACK; CEREBROVASCULAR ACCIDENT; or temporary blindness (AMAUROSIS FUGAX). (From Adams et al., Principles of Neurology, 6th ed, pp 822-3)Coronary Angiography: Radiography of the vascular system of the heart muscle after injection of a contrast medium.Myocytes, Smooth Muscle: Non-striated, elongated, spindle-shaped cells found lining the digestive tract, uterus, and blood vessels. They are derived from specialized myoblasts (MYOBLASTS, SMOOTH MUSCLE).Aryldialkylphosphatase: An enzyme which catalyzes the hydrolysis of an aryl-dialkyl phosphate to form dialkyl phosphate and an aryl alcohol. It can hydrolyze a broad spectrum of organophosphate substrates and a number of aromatic carboxylic acid esters. It may also mediate an enzymatic protection of LOW DENSITY LIPOPROTEINS against oxidative modification and the consequent series of events leading to ATHEROMA formation. The enzyme was previously regarded to be identical with Arylesterase (EC 3.1.1.2).Vasculitis: Inflammation of any one of the blood vessels, including the ARTERIES; VEINS; and rest of the vasculature system in the body.Lipoproteins, HDL: A class of lipoproteins of small size (4-13 nm) and dense (greater than 1.063 g/ml) particles. HDL lipoproteins, synthesized in the liver without a lipid core, accumulate cholesterol esters from peripheral tissues and transport them to the liver for re-utilization or elimination from the body (the reverse cholesterol transport). Their major protein component is APOLIPOPROTEIN A-I. HDL also shuttle APOLIPOPROTEINS C and APOLIPOPROTEINS E to and from triglyceride-rich lipoproteins during their catabolism. HDL plasma level has been inversely correlated with the risk of cardiovascular diseases.Chemokine CCL2: A chemokine that is a chemoattractant for MONOCYTES and may also cause cellular activation of specific functions related to host defense. It is produced by LEUKOCYTES of both monocyte and lymphocyte lineage and by FIBROBLASTS during tissue injury. It has specificity for CCR2 RECEPTORS.Anticholesteremic Agents: Substances used to lower plasma CHOLESTEROL levels.Oxidative Stress: A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).Time Factors: Elements of limited time intervals, contributing to particular results or situations.Vascular Calcification: Deposition of calcium into the blood vessel structures. Excessive calcification of the vessels are associated with ATHEROSCLEROTIC PLAQUES formation particularly after MYOCARDIAL INFARCTION (see MONCKEBERG MEDIAL CALCIFIC SCLEROSIS) and chronic kidney diseases which in turn increase VASCULAR STIFFNESS.Inflammation Mediators: The endogenous compounds that mediate inflammation (AUTACOIDS) and related exogenous compounds including the synthetic prostaglandins (PROSTAGLANDINS, SYNTHETIC).Hypertension: Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.Diabetic Angiopathies: VASCULAR DISEASES that are associated with DIABETES MELLITUS.Cohort Studies: Studies in which subsets of a defined population are identified. These groups may or may not be exposed to factors hypothesized to influence the probability of the occurrence of a particular disease or other outcome. Cohorts are defined populations which, as a whole, are followed in an attempt to determine distinguishing subgroup characteristics.Hydroxymethylglutaryl-CoA Reductase Inhibitors: Compounds that inhibit HMG-CoA reductases. They have been shown to directly lower cholesterol synthesis.Arteritis: INFLAMMATION of any ARTERIES.Lipoprotein(a): A lipoprotein that resembles the LOW-DENSITY LIPOPROTEINS but with an extra protein moiety, APOPROTEIN (A) also known as APOLIPOPROTEIN (A), linked to APOLIPOPROTEIN B-100 on the LDL by one or two disulfide bonds. High plasma level of lipoprotein (a) is associated with increased risk of atherosclerotic cardiovascular disease.Dietary Fats: Fats present in food, especially in animal products such as meat, meat products, butter, ghee. They are present in lower amounts in nuts, seeds, and avocados.Femoral Artery: The main artery of the thigh, a continuation of the external iliac artery.Risk Assessment: The qualitative or quantitative estimation of the likelihood of adverse effects that may result from exposure to specified health hazards or from the absence of beneficial influences. (Last, Dictionary of Epidemiology, 1988)USSRApolipoproteins B: Major structural proteins of triacylglycerol-rich LIPOPROTEINS. There are two forms, apolipoprotein B-100 and apolipoprotein B-48, both derived from a single gene. ApoB-100 expressed in the liver is found in low-density lipoproteins (LIPOPROTEINS, LDL; LIPOPROTEINS, VLDL). ApoB-48 expressed in the intestine is found in CHYLOMICRONS. They are important in the biosynthesis, transport, and metabolism of triacylglycerol-rich lipoproteins. Plasma Apo-B levels are high in atherosclerotic patients but non-detectable in ABETALIPOPROTEINEMIA.Cholesterol, VLDL: Cholesterol which is contained in or bound to very low density lipoproteins (VLDL). High circulating levels of VLDL cholesterol are found in HYPERLIPOPROTEINEMIA TYPE IIB. The cholesterol on the VLDL is eventually delivered by LOW-DENSITY LIPOPROTEINS to the tissues after the catabolism of VLDL to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LDL.European Continental Ancestry Group: Individuals whose ancestral origins are in the continent of Europe.Chlamydophila Infections: Infections with bacteria of the genus CHLAMYDOPHILA.Hyperlipoproteinemia Type II: A group of familial disorders characterized by elevated circulating cholesterol contained in either LOW-DENSITY LIPOPROTEINS alone or also in VERY-LOW-DENSITY LIPOPROTEINS (pre-beta lipoproteins).Brachiocephalic Trunk: The first and largest artery branching from the aortic arch. It distributes blood to the right side of the head and neck and to the right arm.Predictive Value of Tests: In screening and diagnostic tests, the probability that a person with a positive test is a true positive (i.e., has the disease), is referred to as the predictive value of a positive test; whereas, the predictive value of a negative test is the probability that the person with a negative test does not have the disease. Predictive value is related to the sensitivity and specificity of the test.Brachial Artery: The continuation of the axillary artery; it branches into the radial and ulnar arteries.Sinus of Valsalva: The dilatation of the aortic wall behind each of the cusps of the aortic valve.Blood Pressure: PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.Antioxidants: Naturally occurring or synthetic substances that inhibit or retard the oxidation of a substance to which it is added. They counteract the harmful and damaging effects of oxidation in animal tissues.Vasa Vasorum: Nutrient blood vessels which supply the walls of large arteries or veins.ATP Binding Cassette Transporter 1: A superfamily of large integral ATP-binding cassette membrane proteins whose expression pattern is consistent with a role in lipid (cholesterol) efflux. It is implicated in TANGIER DISEASE characterized by accumulation of cholesteryl ester in various tissues.Antigens, CD36: Leukocyte differentiation antigens and major platelet membrane glycoproteins present on MONOCYTES; ENDOTHELIAL CELLS; PLATELETS; and mammary EPITHELIAL CELLS. They play major roles in CELL ADHESION; SIGNAL TRANSDUCTION; and regulation of angiogenesis. CD36 is a receptor for THROMBOSPONDINS and can act as a scavenger receptor that recognizes and transports oxidized LIPOPROTEINS and FATTY ACIDS.Severity of Illness Index: Levels within a diagnostic group which are established by various measurement criteria applied to the seriousness of a patient's disorder.Cross-Sectional Studies: Studies in which the presence or absence of disease or other health-related variables are determined in each member of the study population or in a representative sample at one particular time. This contrasts with LONGITUDINAL STUDIES which are followed over a period of time.Linear Models: Statistical models in which the value of a parameter for a given value of a factor is assumed to be equal to a + bx, where a and b are constants. The models predict a linear regression.Vascular Diseases: Pathological processes involving any of the BLOOD VESSELS in the cardiac or peripheral circulation. They include diseases of ARTERIES; VEINS; and rest of the vasculature system in the body.Prevalence: The total number of cases of a given disease in a specified population at a designated time. It is differentiated from INCIDENCE, which refers to the number of new cases in the population at a given time.Case-Control Studies: Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group.Homocysteine: A thiol-containing amino acid formed by a demethylation of METHIONINE.Macaca fascicularis: A species of the genus MACACA which typically lives near the coast in tidal creeks and mangrove swamps primarily on the islands of the Malay peninsula.RNA, Messenger: RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.Vasodilation: The physiological widening of BLOOD VESSELS by relaxing the underlying VASCULAR SMOOTH MUSCLE.Oxidation-Reduction: A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471).Mice, Transgenic: Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.Cholesterol Esters: Fatty acid esters of cholesterol which constitute about two-thirds of the cholesterol in the plasma. The accumulation of cholesterol esters in the arterial intima is a characteristic feature of atherosclerosis.Apolipoprotein E3: A 34-kDa glycosylated protein. A major and most common isoform of apolipoprotein E. Therefore, it is also known as apolipoprotein E (ApoE). In human, Apo E3 is a 299-amino acid protein with a cysteine at the 112 and an arginine at the 158 position. It is involved with the transport of TRIGLYCERIDES; PHOSPHOLIPIDS; CHOLESTEROL; and CHOLESTERYL ESTERS in and out of the cells.Insulin Resistance: Diminished effectiveness of INSULIN in lowering blood sugar levels: requiring the use of 200 units or more of insulin per day to prevent HYPERGLYCEMIA or KETOSIS.Diabetes Mellitus, Type 2: A subclass of DIABETES MELLITUS that is not INSULIN-responsive or dependent (NIDDM). It is characterized initially by INSULIN RESISTANCE and HYPERINSULINEMIA; and eventually by GLUCOSE INTOLERANCE; HYPERGLYCEMIA; and overt diabetes. Type II diabetes mellitus is no longer considered a disease exclusively found in adults. Patients seldom develop KETOSIS but often exhibit OBESITY.Macrophages, Peritoneal: Mononuclear phagocytes derived from bone marrow precursors but resident in the peritoneum.Ultrasonography, Interventional: The use of ultrasound to guide minimally invasive surgical procedures such as needle ASPIRATION BIOPSY; DRAINAGE; etc. Its widest application is intravascular ultrasound imaging but it is useful also in urology and intra-abdominal conditions.Hypolipidemic Agents: Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS.Follow-Up Studies: Studies in which individuals or populations are followed to assess the outcome of exposures, procedures, or effects of a characteristic, e.g., occurrence of disease.Autopsy: Postmortem examination of the body.Apolipoprotein B-100: A 513-kDa protein synthesized in the LIVER. It serves as the major structural protein of low-density lipoproteins (LIPOPROTEINS, LDL; LIPOPROTEINS, VLDL). It is the ligand for the LDL receptor (RECEPTORS, LDL) that promotes cellular binding and internalization of LDL particles.Gene Expression Regulation: Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.Age Factors: Age as a constituent element or influence contributing to the production of a result. It may be applicable to the cause or the effect of a circumstance. It is used with human or animal concepts but should be differentiated from AGING, a physiological process, and TIME FACTORS which refers only to the passage of time.Tomography, X-Ray Computed: Tomography using x-ray transmission and a computer algorithm to reconstruct the image.Metabolic Syndrome X: A cluster of metabolic risk factors for CARDIOVASCULAR DISEASES and TYPE 2 DIABETES MELLITUS. The major components of metabolic syndrome X include excess ABDOMINAL FAT; atherogenic DYSLIPIDEMIA; HYPERTENSION; HYPERGLYCEMIA; INSULIN RESISTANCE; a proinflammatory state; and a prothrombotic (THROMBOSIS) state. (from AHA/NHLBI/ADA Conference Proceedings, Circulation 2004; 109:551-556)Regression Analysis: Procedures for finding the mathematical function which best describes the relationship between a dependent variable and one or more independent variables. In linear regression (see LINEAR MODELS) the relationship is constrained to be a straight line and LEAST-SQUARES ANALYSIS is used to determine the best fit. In logistic regression (see LOGISTIC MODELS) the dependent variable is qualitative rather than continuously variable and LIKELIHOOD FUNCTIONS are used to find the best relationship. In multiple regression, the dependent variable is considered to depend on more than a single independent variable.Receptors, Scavenger: A large group of structurally diverse cell surface receptors that mediate endocytic uptake of modified LIPOPROTEINS. Scavenger receptors are expressed by MYELOID CELLS and some ENDOTHELIAL CELLS, and were originally characterized based on their ability to bind acetylated LOW-DENSITY LIPOPROTEINS. They can also bind a variety of other polyanionic ligand. Certain scavenger receptors can internalize micro-organisms as well as apoptotic cells.Multivariate Analysis: A set of techniques used when variation in several variables has to be studied simultaneously. In statistics, multivariate analysis is interpreted as any analytic method that allows simultaneous study of two or more dependent variables.Blood Vessels: Any of the tubular vessels conveying the blood (arteries, arterioles, capillaries, venules, and veins).Scavenger Receptors, Class A: A family of scavenger receptors that mediate the influx of LIPIDS into MACROPHAGES and are involved in FOAM CELL formation.Ethnic Groups: A group of people with a common cultural heritage that sets them apart from others in a variety of social relationships.Peripheral Vascular Diseases: Pathological processes involving any one of the BLOOD VESSELS in the vasculature outside the HEART.Genotype: The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.Signal Transduction: The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.Sex Factors: Maleness or femaleness as a constituent element or influence contributing to the production of a result. It may be applicable to the cause or effect of a circumstance. It is used with human or animal concepts but should be differentiated from SEX CHARACTERISTICS, anatomical or physiological manifestations of sex, and from SEX DISTRIBUTION, the number of males and females in given circumstances.Lipid Peroxidation: Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor.Dyslipidemias: Abnormalities in the serum levels of LIPIDS, including overproduction or deficiency. Abnormal serum lipid profiles may include high total CHOLESTEROL, high TRIGLYCERIDES, low HIGH DENSITY LIPOPROTEIN CHOLESTEROL, and elevated LOW DENSITY LIPOPROTEIN CHOLESTEROL.Genetic Predisposition to Disease: A latent susceptibility to disease at the genetic level, which may be activated under certain conditions.Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents.Smoking: Inhaling and exhaling the smoke of burning TOBACCO.Intercellular Adhesion Molecule-1: A cell-surface ligand involved in leukocyte adhesion and inflammation. Its production is induced by gamma-interferon and it is required for neutrophil migration into inflamed tissue.Apolipoproteins: Protein components on the surface of LIPOPROTEINS. They form a layer surrounding the hydrophobic lipid core. There are several classes of apolipoproteins with each playing a different role in lipid transport and LIPID METABOLISM. These proteins are synthesized mainly in the LIVER and the INTESTINES.United StatesAsymptomatic Diseases: Diseases that do not exhibit symptoms.Diabetes Complications: Conditions or pathological processes associated with the disease of diabetes mellitus. Due to the impaired control of BLOOD GLUCOSE level in diabetic patients, pathological processes develop in numerous tissues and organs including the EYE, the KIDNEY, the BLOOD VESSELS, and the NERVE TISSUE.Phenotype: The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.Ankle Brachial Index: Comparison of the BLOOD PRESSURE between the BRACHIAL ARTERY and the POSTERIOR TIBIAL ARTERY. It is a predictor of PERIPHERAL ARTERIAL DISEASE.Diet: Regular course of eating and drinking adopted by a person or animal.Scavenger Receptors, Class E: A class of oxidized LDL receptors that contain LECTIN-like extracellular domains.Odds Ratio: The ratio of two odds. The exposure-odds ratio for case control data is the ratio of the odds in favor of exposure among cases to the odds in favor of exposure among noncases. The disease-odds ratio for a cohort or cross section is the ratio of the odds in favor of disease among the exposed to the odds in favor of disease among the unexposed. The prevalence-odds ratio refers to an odds ratio derived cross-sectionally from studies of prevalent cases.Mice, Mutant Strains: Mice bearing mutant genes which are phenotypically expressed in the animals.Stroke: A group of pathological conditions characterized by sudden, non-convulsive loss of neurological function due to BRAIN ISCHEMIA or INTRACRANIAL HEMORRHAGES. Stroke is classified by the type of tissue NECROSIS, such as the anatomic location, vasculature involved, etiology, age of the affected individual, and hemorrhagic vs. non-hemorrhagic nature. (From Adams et al., Principles of Neurology, 6th ed, pp777-810)Diet, High-Fat: Consumption of excessive DIETARY FATS.Vitamin E: A generic descriptor for all TOCOPHEROLS and TOCOTRIENOLS that exhibit ALPHA-TOCOPHEROL activity. By virtue of the phenolic hydrogen on the 2H-1-benzopyran-6-ol nucleus, these compounds exhibit varying degree of antioxidant activity, depending on the site and number of methyl groups and the type of ISOPRENOIDS.Polymorphism, Genetic: The regular and simultaneous occurrence in a single interbreeding population of two or more discontinuous genotypes. The concept includes differences in genotypes ranging in size from a single nucleotide site (POLYMORPHISM, SINGLE NUCLEOTIDE) to large nucleotide sequences visible at a chromosomal level.Fibrinogen: Plasma glycoprotein clotted by thrombin, composed of a dimer of three non-identical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products.Diabetes Mellitus: A heterogeneous group of disorders characterized by HYPERGLYCEMIA and GLUCOSE INTOLERANCE.1-Alkyl-2-acetylglycerophosphocholine Esterase: A lipoprotein-associated PHOSPHOLIPASE A2 which modulates the action of PLATELET ACTIVATING FACTOR by hydrolyzing the SN-2 ester bond to yield the biologically inactive lyso-platelet-activating factor. It has specificity for phospholipid substrates with short-chain residues at the SN-2 position, but inactive against long-chain phospholipids. Deficiency in this enzyme is associated with many diseases including ASTHMA, and HYPERCHOLESTEROLEMIA.Incidence: The number of new cases of a given disease during a given period in a specified population. It also is used for the rate at which new events occur in a defined population. It is differentiated from PREVALENCE, which refers to all cases, new or old, in the population at a given time.Liver: A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.ATP-Binding Cassette Transporters: A family of MEMBRANE TRANSPORT PROTEINS that require ATP hydrolysis for the transport of substrates across membranes. The protein family derives its name from the ATP-binding domain found on the protein.Blood Glucose: Glucose in blood.African Continental Ancestry Group: Individuals whose ancestral origins are in the continent of Africa.Orphan Nuclear Receptors: A broad category of receptor-like proteins that may play a role in transcriptional-regulation in the CELL NUCLEUS. Many of these proteins are similar in structure to known NUCLEAR RECEPTORS but appear to lack a functional ligand-binding domain, while in other cases the specific ligands have yet to be identified.Cytokines: Non-antibody proteins secreted by inflammatory leukocytes and some non-leukocytic cells, that act as intercellular mediators. They differ from classical hormones in that they are produced by a number of tissue or cell types rather than by specialized glands. They generally act locally in a paracrine or autocrine rather than endocrine manner.Iliac Artery: Either of two large arteries originating from the abdominal aorta; they supply blood to the pelvis, abdominal wall and legs.Interleukin-6: A cytokine that stimulates the growth and differentiation of B-LYMPHOCYTES and is also a growth factor for HYBRIDOMAS and plasmacytomas. It is produced by many different cells including T-LYMPHOCYTES; MONOCYTES; and FIBROBLASTS.Xanthomatosis: A condition marked by the development of widespread xanthomas, yellow tumor-like structures filled with lipid deposits. Xanthomas can be found in a variety of tissues including the SKIN; TENDONS; joints of KNEES and ELBOWS. Xanthomatosis is associated with disturbance of LIPID METABOLISM and formation of FOAM CELLS.Leukocytes: White blood cells. These include granular leukocytes (BASOPHILS; EOSINOPHILS; and NEUTROPHILS) as well as non-granular leukocytes (LYMPHOCYTES and MONOCYTES).Heptanoic Acids: 7-carbon saturated monocarboxylic acids.Hispanic Americans: Persons living in the United States of Mexican (MEXICAN AMERICANS), Puerto Rican, Cuban, Central or South American, or other Spanish culture or origin. The concept does not include Brazilian Americans or Portuguese Americans.Myocardial Infarction: NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).Thrombosis: Formation and development of a thrombus or blood clot in the blood vessel.Scavenger Receptors, Class B: A family of scavenger receptors that are predominately localized to CAVEOLAE of the PLASMA MEMBRANE and bind HIGH DENSITY LIPOPROTEINS.Nitric Oxide Synthase Type III: A CALCIUM-dependent, constitutively-expressed form of nitric oxide synthase found primarily in ENDOTHELIAL CELLS.African Americans: Persons living in the United States having origins in any of the black groups of Africa.Nitric Oxide: A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.Logistic Models: Statistical models which describe the relationship between a qualitative dependent variable (that is, one which can take only certain discrete values, such as the presence or absence of a disease) and an independent variable. A common application is in epidemiology for estimating an individual's risk (probability of a disease) as a function of a given risk factor.Hyperhomocysteinemia: Condition in which the plasma levels of homocysteine and related metabolites are elevated (>13.9 µmol/l). Hyperhomocysteinemia can be familial or acquired. Development of the acquired hyperhomocysteinemia is mostly associated with vitamins B and/or folate deficiency (e.g., PERNICIOUS ANEMIA, vitamin malabsorption). Familial hyperhomocysteinemia often results in a more severe elevation of total homocysteine and excretion into the urine, resulting in HOMOCYSTINURIA. Hyperhomocysteinemia is a risk factor for cardiovascular and neurodegenerative diseases, osteoporotic fractures and complications during pregnancy.Lipoproteins, VLDL: A class of lipoproteins of very light (0.93-1.006 g/ml) large size (30-80 nm) particles with a core composed mainly of TRIGLYCERIDES and a surface monolayer of PHOSPHOLIPIDS and CHOLESTEROL into which are imbedded the apolipoproteins B, E, and C. VLDL facilitates the transport of endogenously made triglycerides to extrahepatic tissues. As triglycerides and Apo C are removed, VLDL is converted to INTERMEDIATE-DENSITY LIPOPROTEINS, then to LOW-DENSITY LIPOPROTEINS from which cholesterol is delivered to the extrahepatic tissues.MississippiObesity: A status with BODY WEIGHT that is grossly above the acceptable or desirable weight, usually due to accumulation of excess FATS in the body. The standards may vary with age, sex, genetic or cultural background. In the BODY MASS INDEX, a BMI greater than 30.0 kg/m2 is considered obese, and a BMI greater than 40.0 kg/m2 is considered morbidly obese (MORBID OBESITY).Adiponectin: A 30-kDa COMPLEMENT C1Q-related protein, the most abundant gene product secreted by FAT CELLS of the white ADIPOSE TISSUE. Adiponectin modulates several physiological processes, such as metabolism of GLUCOSE and FATTY ACIDS, and immune responses. Decreased plasma adiponectin levels are associated with INSULIN RESISTANCE; TYPE 2 DIABETES MELLITUS; OBESITY; and ATHEROSCLEROSIS.Pravastatin: An antilipemic fungal metabolite isolated from cultures of Nocardia autotrophica. It acts as a competitive inhibitor of HMG CoA reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES).Gene Expression: The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.Up-Regulation: A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.Aging: The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.Reactive Oxygen Species: Molecules or ions formed by the incomplete one-electron reduction of oxygen. These reactive oxygen intermediates include SINGLET OXYGEN; SUPEROXIDES; PEROXIDES; HYDROXYL RADICAL; and HYPOCHLOROUS ACID. They contribute to the microbicidal activity of PHAGOCYTES, regulation of signal transduction and gene expression, and the oxidative damage to NUCLEIC ACIDS; PROTEINS; and LIPIDS.Aortitis: Inflammation of the wall of the AORTA.Reference Values: The range or frequency distribution of a measurement in a population (of organisms, organs or things) that has not been selected for the presence of disease or abnormality.Ankle: The region of the lower limb between the FOOT and the LEG.Bone Marrow Transplantation: The transference of BONE MARROW from one human or animal to another for a variety of purposes including HEMATOPOIETIC STEM CELL TRANSPLANTATION or MESENCHYMAL STEM CELL TRANSPLANTATION.Asian Americans: Persons living in the United States having origins in any of the original peoples of the Far East, Southeast Asia, or the Indian subcontinent.Carotid Artery, Internal: Branch of the common carotid artery which supplies the anterior part of the brain, the eye and its appendages, the forehead and nose.Disease Susceptibility: A constitution or condition of the body which makes the tissues react in special ways to certain extrinsic stimuli and thus tends to make the individual more than usually susceptible to certain diseases.Cell Movement: The movement of cells from one location to another. Distinguish from CYTOKINESIS which is the process of dividing the CYTOPLASM of a cell.E-Selectin: Cell adhesion molecule and CD antigen that mediates neutrophil, monocyte, and memory T-cell adhesion to cytokine-activated endothelial cells. E-selectin recognizes sialylated carbohydrate groups related to the Lewis X or Lewis A family.Comorbidity: The presence of co-existing or additional diseases with reference to an initial diagnosis or with reference to the index condition that is the subject of study. Comorbidity may affect the ability of affected individuals to function and also their survival; it may be used as a prognostic indicator for length of hospital stay, cost factors, and outcome or survival.JapanChaperonin 60: A group I chaperonin protein that forms the barrel-like structure of the chaperonin complex. It is an oligomeric protein with a distinctive structure of fourteen subunits, arranged in two rings of seven subunits each. The protein was originally studied in BACTERIA where it is commonly referred to as GroEL protein.Magnetic Resonance Angiography: Non-invasive method of vascular imaging and determination of internal anatomy without injection of contrast media or radiation exposure. The technique is used especially in CEREBRAL ANGIOGRAPHY as well as for studies of other vascular structures.Body Mass Index: An indicator of body density as determined by the relationship of BODY WEIGHT to BODY HEIGHT. BMI=weight (kg)/height squared (m2). BMI correlates with body fat (ADIPOSE TISSUE). Their relationship varies with age and gender. For adults, BMI falls into these categories: below 18.5 (underweight); 18.5-24.9 (normal); 25.0-29.9 (overweight); 30.0 and above (obese). (National Center for Health Statistics, Centers for Disease Control and Prevention)NF-kappa B: Ubiquitous, inducible, nuclear transcriptional activator that binds to enhancer elements in many different cell types and is activated by pathogenic stimuli. The NF-kappa B complex is a heterodimer composed of two DNA-binding subunits: NF-kappa B1 and relA.Apolipoproteins A: Structural proteins of the alpha-lipoproteins (HIGH DENSITY LIPOPROTEINS), including APOLIPOPROTEIN A-I and APOLIPOPROTEIN A-II. They can modulate the activity of LECITHIN CHOLESTEROL ACYLTRANSFERASE. These apolipoproteins are low in atherosclerotic patients. They are either absent or present in extremely low plasma concentration in TANGIER DISEASE.Polymorphism, Single Nucleotide: A single nucleotide variation in a genetic sequence that occurs at appreciable frequency in the population.FluorobenzenesRisk: The probability that an event will occur. It encompasses a variety of measures of the probability of a generally unfavorable outcome.Peripheral Arterial Disease: Lack of perfusion in the EXTREMITIES resulting from atherosclerosis. It is characterized by INTERMITTENT CLAUDICATION, and an ANKLE BRACHIAL INDEX of 0.9 or less.

Recombinant human interleukin-10 inhibits proliferation of vascular smooth muscle cells stimulated by advanced glycation end products and neointima hyperplasia after carotid injury in the rat. (1/6610)

The purposes of this study was to determine the effects of recombinant human interleukin-10 (rhIL-10) on proliferation of vascular smooth muscle cells (VSMCs) stimulated by advanced glycation end products (AGE) and neointima hyperplasia after rat carotid arterial injury. Rat aortic VSMCs were cultured and treated with rhIL-10 or AGE respectively, and then co-treated with rhIL-10 and AGE. Proliferation of VSMCs was quantified by colormetric assay. Cell cycle analysis was performed by flow cytomertry. Sprague-Dawley rats were treated with recombinant human IL-10 (rhIL-10) for 3 d after carotid arteries injury. The ratio of neointima to media area at the site of arterial injury was measured 28 d after balloon injury. The p44/42 MAPK activity was evaluated by the immunoblotting technique using anti-p44/42 phospho-MAPK antibody. Compared to control, AGE stimulated VSMCs proliferation. rhIL-10 alone had no effect on VSMCs growth. With AGE stimulation, rhIL-10, at dose as low as 10 ng/ml, inhibited VSMCs growth (P<0.05). The cell number in G(0)/G(1) phase of AGE and rhIL-10 co-treatment group was higher than that of AGE treatment alone (P<0.01) by flow cytometry analysis. Compared with the control group of neointima hyperplasia in rats, the ratio of neointima to media area of recombinant human IL-10 group was reduced by 45% (P<0.01). The p44/42 MAPK activity was significantly enhanced by AGE. The AGE effects were opposed by rhIL-10. The anti-inflammatory cytokine rhIL-10 inhibits AGE-induced VSMCs proliferation. Recombinant human IL-10 also inhibited neointima hyperplasia after carotid artery injury in rats. The results suggest the possibility that recombinant human IL-10, as a potential therapeutic approach, prevents neointimal hyperplasia.  (+info)

Adiponectin concentrations as a criterion of metabolic control in persons with type 2 diabetes mellitus? (2/6610)

Adiponectin (ADP) is an adipocytokin with many antiatherogenic properties; its decreased level is associated with numerous atherogenic diseases and syndromes (e.g. diabetes mellitus (DM), dyslipidemia, endothelial dysfunction, hypertension, and obesity). Decreased ADP values in blood may be an independent risk factor of atherosclerotic (ATS) complications. AIM OF THE STUDY: 1) Do persons with type 2 diabetes have lower ADP values than individuals without DM but with a high risk of ATS complications? 2) Do ADP values differ between persons with well controlled and persons with uncontrolled type 2 diabetes? We examined 109 patients of the Metabolic Center of Hospital Sternberk. Out of them, 58 had type 2 diabetes, others were individuals with variously expressed risk factors of early atherosclerosis (obesity, hypertension, age, family history, smoking, dyslipidemia, etc.). In all persons under this study the following parameters were determined in peripheral venous blood: adiponectin, resistin, leptin, ObRe, cholesterol, HDL-cholesterol, triacylglycerols, glucose, HbA1c, creatinine, urea, ALT, AST, CRP, homocysteine, thrombocyte aggregation after CPG induction. The whole group was divided according to the presence of type 2DM into two subgroups; persons with diabetes were divided into the well controlled and uncontrolled subgroups. All data obtained were processed statistically using the software SPSS for Windows and Medcalc. The adiponectin/BMI index correlated negatively with HbA1c value (correlation coefficient -0.37, p = 0.00053), triacylglycerols (-0.4, p = 0.000001), P-glucose (-0.3, p = 0.0017), uricemia (-0.35, p = 0.0007) and positively with HDL-cholesterol value (0.6, p=0.00001). Women had higher adiponectin values than men. Persons with hypertension and with diabetes mellitus, individuals with atherogenic lipotype or persons with inflammation signs had lower values than individuals without these diseases and syndromes. Persons with wellcontrolled diabetes mellitus had higher values than persons with uncontrolled diabetes (medians of the adiponectin/BMI index 9.7 vs. 6.7, p < 0.01). Persons with type 2 diabetes mellitus have lower ADP values than persons with a high ATS risk without diabetes mellitus. Persons with wellcontrolled diabetes mellitus (DM) and with satisfactory compensation have significantly higher ADP levels (independently of other metabolic parameters of DM control). ADP may be a new marker of metabolic control in persons with a high risk of atherosclerotic complications.  (+info)

The importance of indicators of the initial phase of atherosclerosis in patients with microvascular angina. (3/6610)

Endothelial dysfunction (ED) is generally considered to be the initial step in the progression to atherosclerosis but there is still much uncertainty about the role of the microvascular form of angina in patients with a normal coronary angiogram with regard to ED. The authors investigated the extent of endothelial perturbation and thereby whether the microvascular form of angina precedens macroscopic atherosclerosis by means of non-invasive ultrasound measurement of the intima-media thickening (IMT) in common carotid artery and flow mediated dilatation (FMD) in the brachial artery. 28 patients with stable angina with positive exercise test and ST segment depression (22 females, 6 males, average age 54 years) were compared with a control group consisting of 28 patients with no clinical signs of coronary artery disease (18 females, 10 males, average age 53 years). No significant difference in FMD% (7.3 vs. 10.8, p = 0.07) was found between the groups, though specific measurements (average dilatation of the brachial artery induced by ischemic insult, peak blood flow and peak hyperemic flow) differed considerably. Also IMT did not vary significantly between the groups (0.74 vs. 0.65, p = 0.08). In patients with IMT > 0.8 mm (6 patients in each group) a significant decrease of FMD was found as compared with patients with normal IMT (p < 0.05). It was concluded that in patients with increased IMT an inverse relationship between FMD and IMT exists both in patients with microvascular angina and in the healthy control subjects whereas in the group of patients with normal IMT no ED was demonstrated. This supports the hypothesis that the microvascular form of angina is the early stage of coronary artery atherosclerosis and this escapes angiographic recognition.  (+info)

Loss of collagen XVIII enhances neovascularization and vascular permeability in atherosclerosis. (4/6610)

BACKGROUND: Plaque neovascularization is thought to promote atherosclerosis; however, the mechanisms of its regulation are not understood. Collagen XVIII and its proteolytically released endostatin fragment are abundant proteoglycans in vascular basement membranes and the walls of major blood vessels. We hypothesized that collagen XVIII in the aortic wall inhibits the proliferation and intimal extension of vasa vasorum. METHODS AND RESULTS: To test our hypothesis, we bred collagen XVIII-knockout (Col18a1(-/-)) mice into the atherosclerosis-prone apolipoprotein E-deficient (ApoE(-/-)) strain. After 6 months on a cholesterol diet, aortas from ApoE(-/-);Col18a1(-/-) and ApoE(-/-);Col18a1(+/-) heterozygote mice showed increased atheroma coverage and enhanced lipid accumulation compared with wild-type littermates. We observed more extensive vasa vasorum and intimal neovascularization in knockout but not heterozygote aortas. Endothelial cells sprouting from Col18a1(-/-) aortas were increased compared with heterozygote and wild-type aortas. In contrast, vascular permeability of large and small blood vessels was enhanced with even heterozygous loss of collagen XVIII but was not suppressed by increasing serum endostatin to wild-type levels. CONCLUSIONS: Our results identify a previously unrecognized function for collagen XVIII that maintains vascular permeability. Loss of this basement membrane proteoglycan enhances angiogenesis and vascular permeability during atherosclerosis by distinct gene-dose-dependent mechanisms.  (+info)

Protective effect of propylthiouracil independent of its hypothyroid effect on atherogenesis in cholesterol-fed rabbits: PTEN induction and inhibition of vascular smooth muscle cell proliferation and migration. (5/6610)

BACKGROUND: Propylthiouracil (PTU) is used to treat hyperthyroid patients by its hypothyroid effect. PTU also is found to have potent antioxidant and immunosuppressive effects. These findings suggest that PTU may play a role in the prevention of atherosclerosis. METHODS AND RESULTS: This study evaluates the effect of PTU on atherosclerotic change in rabbits fed a high-cholesterol diet. The pronounced atherosclerotic lesions in the aortas of rabbits fed a 2% cholesterol diet for 12 weeks were significantly attenuated by the concurrent addition of 0.1% PTU to the drinking water. However, exogenous supplementation of thyroid hormone in hypothyroid PTU-treated rabbits did not abrogate the protective effect of PTU on atherogenesis. Immunohistochemical analysis showed that PTU administration apparently reduced the intimal smooth muscle cell/macrophage ratio in the atherosclerotic plaques of rabbits fed a 2% cholesterol diet. In vitro, the addition of PTU to the medium of cultured rat vascular smooth muscle cells led to a dose-dependent inhibition of cell proliferation and migration. Furthermore, this study confirmed that PTU dose-dependently increased expression of PTEN, a tumor suppressor gene known to be involved in the coordinate inhibition of VSMC proliferation and migration. CONCLUSIONS: This study demonstrated that PTU inhibited the development of atherosclerosis through a thyroid-independent mechanism that may be explained, at least in part, by the ability of PTU to inhibit vascular smooth muscle cell proliferation and migration. Furthermore, PTEN induction, via disruption of the phosphatidylinsitol 3-kinase-mediated pathway, plays a crucial role in mediating the inhibitory action on vascular smooth muscle cell proliferation and migration.  (+info)

Association of mitral annulus calcification, aortic valve calcification with carotid intima media thickness. (6/6610)

BACKGROUND: Mitral annular calcification (MAC) and aortic annular calcification (AVC) may represent a manifestation of generalized atherosclerosis in the elderly. Alterations in vascular structure, as indexed by the intima media thickness (IMT), are also recognized as independent predictors of adverse cardiovascular outcomes. AIM: To examine the relationship between the degree of calcification at mitral and/or aortic valve annulus and large artery structure (thickness). METHODS: We evaluated 102 consecutive patients who underwent transthoracic echocardiography and carotid artery echoDoppler for various indications; variables measured were: systemic blood pressure (BP), pulse pressure (PP=SBP-DBP), body mass index (BMI), fasting glucose, total, HDL, LDL chlolesterol, triglycerides, cIMT. The patients were divided according to a grading of valvular/annular lesions independent scores based on acoustic densitometry: 1 = annular/valvular sclerosis/calcification absence; 2 = annular/valvular sclerosis; 3 = annular calcification; 4 = annular-valvular calcification; 5 = valvular calcification with no recognition of the leaflets. RESULTS: Patient score was the highest observed for either valvular/annulus. Mean cIMT increased linearly with increasing valvular calcification score, ranging from 3.9 +/- 0.48 mm in controls to 12.9 +/- 1.8 mm in those subjects scored 5 (p < 0.0001). In the first to fourth quartile of cIMT values the respective maximal percentual of score were: score 1: 76.1%, score 2: 70.1%, score 4: 54.3% and score 5: 69.5% (p > 0.0001). CONCLUSION: MAC and AVC score can identify subgroups of patients with different cIMT values which indicate different incidence and prevalence of systemic artery diseases. This data may confirm MAC-AVC as a useful important diagnostic parameter of systemic atherosclerotic disease.  (+info)

Adiponectin, an adipocyte-derived protein. (7/6610)

Adipose tissue is a hormonally active tissue, producing adipocytokines which may influence activity of other tissues. Adiponectin, abundantly present in the plasma increases insulin sensitivity by stimulating fatty acid oxidation, decreases plasma triglycerides and improves glucose metabolism. Adiponectin levels are inversely related to the degree of adiposity. Anorexia nervosa and type 1 diabetes are associated with increased plasma adiponectin levels and higher insulin sensitivity. Decreased plasma adiponectin levels were reported in insulin-resistant states, such as obesity and type 2 diabetes and in patients with coronary artery disease. Activity of adiponectin is associated with leptin, resistin and with steroid and thyroid hormones, glucocorticoids, NO and others. Adiponectin suppresses expression of extracellular matrix adhesive proteins in endothelial cells and atherosclerosis potentiating cytokines. Anti-atherogenic and anti-inflammatory properties of adiponectin and the ability to stimulate insulin sensitivity have made adiponectin an important object for physiological and pathophysiological studies with the aim of potential therapeutic applications.  (+info)

Carotid plaque pathology: thrombosis, ulceration, and stroke pathogenesis. (8/6610)

BACKGROUND AND PURPOSE: To determine the relationship between ulceration, thrombus, and calcification of carotid artery atherosclerotic plaques and symptoms of ipsilateral or contralateral stroke. METHODS: We compared microscopic plaque morphology from patients with and without stroke symptoms ipsilateral or contralateral to the plaque. Plaques were characterized for ulceration, thrombus, and calcification. We analyzed plaques from 241 subjects: 170 patients enrolled in the Asymptomatic Carotid Atherosclerosis Study (ACAS) and 71 patients enrolled in the North American Symptomatic Carotid Endarterectomy Trial (NASCET); 128 subjects had no history of stroke symptoms, 80 subjects had ipsilateral symptoms, and 33 had contralateral symptoms. RESULTS: Plaque ulceration was more common in plaques taken from symptomatic patients than those without symptoms (36% versus 14%; P<0.001); frequency of ulceration was similar for plaques associated with ipsilateral (34%) and contralateral (42%) symptoms. Thrombus was most common in plaques taken from patients with both ipsilateral symptoms and ulceration. The extent of calcification was unassociated with stroke symptoms. CONCLUSIONS: Carotid plaque ulceration and thrombosis are more prevalent in symptomatic patients. Ulceration is more common in symptomatic patients regardless of side of carotid symptoms, whereas thrombus is associated with ipsilateral symptoms and plaque ulceration. Preoperative identification of carotid ulceration and thrombus should lead to greater efficacy of stroke prevention by carotid endarterectomy.  (+info)

*Atherosclerosis

... is the number one cause of death and disability in the developed world. Atherosclerosis was first described in ... "What Is Atherosclerosis? - NHLBI, NIH". www.nhlbi.nih.gov. 22 June 2016. Retrieved 6 November 2017. "How Is Atherosclerosis ... Atherosclerosis. Harvard Health Publications Harvard Health Publications. Health Topics A - Z, (2011) Atherosclerosis. National ... The magic and mystery of microRNA-27 in atherosclerosis. Atherosclerosis 2012;222:314e23. Sacco J, Adeli K. MicroRNAs: emerging ...

*Atherosclerosis (journal)

Atherosclerosis is a monthly peer-reviewed scientific journal established in 1970 and published by Elsevier. It is the official ... "The European Atherosclerosis Society (EAS)". Society description of journal. August 2010. Archived from the original on 22 ... The journal covers all aspects of atherosclerosis and related diseases. This journal is abstracted and indexed in: Chemical ... journal of the European Atherosclerosis Society and is affiliated with both the International Atherosclerosis Society and the ...

*Cerebral atherosclerosis

... is a type of atherosclerosis where build-up of plaque in the blood vessels of the brain occurs. Some ... Diseases cerebral atherosclerosis and associated diseases can cause are: Alzheimer's disease Alzheimer's disease is a form of ... The risk of cerebral atherosclerosis and its associated diseases appears to increase with increasing age; however there are ... Corti R, Fuster V (2011). "Imaging of atherosclerosis: magnetic resonance imaging". European Heart Journal (Review). 32 (14): ...

*Current Atherosclerosis Reports

... is a bimonthly peer-reviewed medical journal publishing review articles pertaining to ... "Current Atherosclerosis Reports". 2014 Journal Citation Reports. Web of Science (Science ed.). Thomson Reuters. 2015. Official ... atherosclerosis. It was established in 1999 and is published by Springer Science+Business Media. The editor-in-chief is Antonio ...

*Atherosclerosis Risk in Communities

"Atherosclerosis Risk in Communities Study Description , Atherosclerosis Risk in Communities". www2.cscc.unc.edu. Retrieved 2015 ... The Atherosclerosis Risk in Communities (ARIC) Study is a multi-site, prospective, biracial cohort study funded by the National ... "The Atherosclerosis Risk in Communities Study (ARIC), NHLBI Obesity Research - NHLBI, NIH". www.nhlbi.nih.gov. Retrieved 2015- ... "The Atherosclerosis Risk in Communities (ARIC) Study: design and objectives. The ARIC investigators". American Journal of ...

*Apolipoprotein C4

211 (2): 551-7. doi:10.1016/j.atherosclerosis.2010.04.001. PMID 20430392. Talmud PJ, Drenos F, Shah S, et al. (2009). "Gene- ... 2010). "No interaction between alcohol consumption and HDL-related genes on HDL cholesterol levels". Atherosclerosis. ... Atherosclerosis. 152 (1): 193-201. doi:10.1016/S0021-9150(99)00459-1. PMID 10996355. Klos KL, Sing CF, Boerwinkle E, et al. ( ...

*LDL receptor

doi:10.1016/j.atherosclerosis.2014.08.038. PMID 25222343. Goldstein JL, Brown MS (April 2009). "The LDL receptor". ... In humans, LDL is directly involved in the development of atherosclerosis,which is the process responsible for the majority of ... A vast number of studies have described the relevance of LDL receptors in the pathophysiology of atherosclerosis, metabolomics ... In addition, LDLR modulation is associated with early atherosclerosis-related lymphatic dysfunction. Synthesis of receptors in ...

*Collagen, type IV, alpha 2

Atherosclerosis. 60 (3): 251-62. doi:10.1016/0021-9150(86)90172-3. PMID 3089234. Soininen R, Huotari M, Hostikka SL, et al. ( ...

*ATP5S

Atherosclerosis. 191 (1): 63-72. doi:10.1016/j.atherosclerosis.2006.05.032. PMID 16806233. ...

*PHACTR1

Atherosclerosis. 250: 95-105. doi:10.1016/j.atherosclerosis.2016.04.025. ISSN 1879-1484. PMC 4917897 . PMID 27187934. Fils-Aimé ... Atherosclerosis. 228 (2): 400-405. doi:10.1016/j.atherosclerosis.2013.02.039. ISSN 1879-1484. PMID 23561647. Freilinger, Tobias ... "Genetic and environmental risk factors for atherosclerosis regulate transcription of phosphatase and actin regulating gene ...

*ACAT2

Atherosclerosis. 207 (1): 266-71. doi:10.1016/j.atherosclerosis.2009.04.010. PMC 2784173 . PMID 19467657. Pramfalk C, Angelin B ...

*ABCA1

Singaraja RR, Brunham LR, Visscher H, Kastelein JJ, Hayden MR (2004). "Efflux and atherosclerosis: the clinical and biochemical ... Atherosclerosis. 164 (2): 245-50. doi:10.1016/S0021-9150(02)00106-5. PMID 12204794. Kozak M (2003). "Emerging links between ... rare and common variants in ABCA1 and their impact on HDL cholesterol levels and atherosclerosis". Annual Review of Nutrition. ... "plays a central role in common age-associated diseases such as atherosclerosis, cancer, and macular degeneration" Knockout ...

*Squalene monooxygenase

Atherosclerosis. 191 (1): 63-72. doi:10.1016/j.atherosclerosis.2006.05.032. PMID 16806233. Laden BP, Tang Y, Porter TD (Feb ...

*Cathepsin F

Atherosclerosis. 192 (2): 323-7. doi:10.1016/j.atherosclerosis.2006.08.001. PMID 16963053. The MEROPS online database for ...

*Remnant cholesterol

Atherosclerosis. 202 (2): 405-414. doi:10.1016/j.atherosclerosis.2008.05.024. PMID 18582890. RLP (Remnant Lipoprotein). ... doi:10.1016/j.atherosclerosis.2008.05.024. PMID 10650304. Nakamura T, Kugiyama K (2006). "Triglycerides and remnant particles ... Fujioka Y, Ishikawa Y (2009). "Remnant lipoproteins as strong key particles to atherogenesis". JOURNAL OF ATHEROSCLEROSIS AND ... European Atherosclerosis Society Consensus Panel (2011). "Triglyceride-rich lipoproteins and high-density lipoprotein ...

*Flavan-3-ol

Atherosclerosis. 153 (1): 107-17. doi:10.1016/S0021-9150(00)00377-4. PMID 11058705. BBC News , Health , Chocolate 'has health ...

*Bone morphogenetic protein 6

Atherosclerosis. 113 (2): 153-6. doi:10.1016/0021-9150(94)05438-O. PMID 7605353. Gitelman SE, Kobrin MS, Ye JQ, et al. (1994 ...

*Elaidic acid

Atherosclerosis. 106 (1): 99-107. doi:10.1016/0021-9150(94)90086-8. PMID 8018112. ...

*Celacade

"Effects of VasoCare therapy on the initiation and progression of atherosclerosis". Atherosclerosis. 162 (1): 45-53. doi:10.1016 ... The results of ACCLAIM support the hypothesis that immune dysfunction plays a role in the pathogenesis of atherosclerosis and ...

*Kinesiology

Atherosclerosis. 216 (2): 489-95. doi:10.1016/j.atherosclerosis.2011.02.037. PMID 21402378. Borghouts, LB; Keizer, HA (January ...

*High-density lipoprotein

All these properties may contribute to the ability of HDL to protect from atherosclerosis, and it is not yet known which are ... In Arnold von Eckardstein (Ed.) Atherosclerosis: Diet and Drugs. Springer. pp. 171-172. ISBN 978-3-540-22569-0. Soudijn W, van ... Meyers CD, Kamanna VS, Kashyap ML (Dec 2004). "Niacin therapy in atherosclerosis". Current Opinion in Lipidology. 15 (6): 659- ... Sirtori, Cesare R. (October 2006). "HDL and the progression of atherosclerosis: new insights". European Heart Journal ...

*Long-term effects of alcohol consumption

Atherosclerosis. 210 (2): 531-535. doi:10.1016/j.atherosclerosis.2010.02.033. PMID 20226461. IARC Alcohol causes more than half ... American Medical Association press release, September 22, 1994 Ridker, P. (1996). "The Pathogenesis of Atherosclerosis and ...

*Oxidative stress

Atherosclerosis. 2003 Mar;167(1):111-20 Free Radic Biol Med. 2015 Feb;79:164-75. doi:10.1016/j.freeradbiomed.2014.12.004 Kyung- ... "Atherosclerosis and oxidative stress". Histol. Histopathol. 23: 381-90. PMID 18072094. Singh, N., Dhalla, A.K., Seneviratne, C ... biochemical implications in atherosclerosis and the problems of premature neonates". Essays Biochem. 29: 39-63. PMID 9189713. ... atherosclerosis, heart failure, myocardial infarction, fragile X syndrome, Sickle Cell Disease, lichen planus, vitiligo, autism ...

*Collagen, type VIII, alpha 1

Atherosclerosis. 166 (1): 1-11. doi:10.1016/S0021-9150(01)00766-3. PMID 12482545. Illidge C, Kielty C, Shuttleworth A (1998). " ...

*17β-Aminoestrogen

Atherosclerosis. 208 (1): 62-8. PMID 19615684. doi:10.1016/j.atherosclerosis.2009.06.017. Lemini C, Rubio-Póo C, Franco Y, ...
[Atherosclerosis-related aortic dissection].: Penetrating atherosclerotic aortic ulcers (PAU) can cause aortic dissection. Of 38 autopsy cases with aortic disse
Our studies demonstrate the possibility of inhibiting development of atherosclerosis by activation of atheroprotective immune responses against apoB-100 peptide sequences. The existence of atheroprotective immune response has previously been suggested by studies demonstrating that treatment with cyclosporin accelerates atherosclerosis in hypercholesterolemic rabbits26 and mice27 and by the observation of increased atherosclerosis in major histocompatability complex class I-deficient C57BL/6 mice fed a high-fat diet.28 B cell reconstitution inhibits development of atherosclerosis in splenectomized apoE-null mice,29,30⇓ as well as neointima formation after carotid injury in RAG-1 mice.31 The latter studies suggest that humoral immune responses are particularly important for atheroprotection, a notion that is further supported by studies demonstrating that repeated injections of immunoglobulins reduce atherosclerosis in apoE-null mice.32. High levels of IgG and IgM against both apoB-100 peptide ...
Background: Prior studies have shown an association between atherosclerotic burden and vascular events, as well as the relationship among severe carotid obstruction and stroke, in patients undergoing cardiac surgery. The association between carotid atherosclerosis burden and cerebrovascular events after postoperative cardiac surgery is unknown. Purposes. To assess the relationship between carotid atherosclerosis burden, as a possible marker of aortic atherosclerotic plaque, and the occurrence of stroke in patients undergoing isolated coronary bypass surgery(CABG) and/or aortic valve replacement(AVR).. Methods: 1974 consecutive patients(pts), undergoing CABG surgery and/or AVR were enrolled in a retrospective study from 01/2003 to 12/2009. Doppler ultrasound of the carotid arteries was performed within 30 days prior to surgery. Pts,50 year or with a previous carotid procedure were excluded. A multiple logistic regression model was developed to estimate the carotid atherosclerotic burden score ...
Atherosclerosis Diagnosis. Atherosclerosis, also known as arteriosclerotic vascular disease, is a medical condition in which arteries begin to narrow because of an excessive amount of plaque surrounding the artery wall. This accumulation can interrupt the bodys usual blood flow, leading to dangerous possibilities in an individuals cardiovascular system. Though atherosclerosis can affect a variety of arteries, the bigger high-pressure arteries are most often influenced by this vascular condition.. Due to sometimes similar definitions, atherosclerosis and arteriosclerosis are often used interchangeably. There is a subtle difference between the two terms. Arteriosclerosis refers to the artery walls becoming hardened while atherosclerosis is defined as the artery becoming narrow due to an accumulation of plaque. Those who have atherosclerosis also have arteriosclerosis, but those with arteriosclerosis do not always have atherosclerosis.. Possible Signs of Atherosclerosis. Initial signs of ...
ER stress occurs in macrophage-rich areas of advanced atherosclerotic lesions and contributes to macrophage apoptosis and subsequent plaque necrosis. Therefore, signaling pathways that alter ER stressinduced apoptosis may affect advanced atherosclerosis. Here we placed Apoe/ mice deficient in macrophage p38α MAPK on a Western diet and found that they had a marked increase in macrophage apoptosis and plaque necrosis. The macrophage p38αdeficient lesions also exhibited a significant reduction in collagen content and a marked thinning of the fibrous cap, which suggests that plaque progression was advanced in these mice. Consistent with our in vivo data, we found that ER stressinduced apoptosis in cultured primary mouse macrophages was markedly accelerated under conditions of p38 inhibition. Pharmacological inhibition or genetic ablation of p38 suppressed activation of Akt in cultured macrophages and in atherosclerotic lesions. In addition, inhibition of Akt enhanced ER stressinduced macrophage ...
A critical review of the relationship between post-transplant atherosclerotic events and cytomegalovirus exposure in kidney transplant recipients. Expert Rev Anti Infect Ther. 2019 Dec 18;: Authors: Rodríguez-Goncer I, Fernández-Ruiz M, Aguado JM Abstract Introduction: Cytomegalovirus (CMV) infection after kidney transplantation (KT) has been implicated in the so...
February 26, 2015 - Nanometer-sized "drones" could become a new way to prevent heart attacks caused by atherosclerosis, according to a study in pre-clinical models by scientists at Brigham and Womens Hospital (BWH) and Columbia University Medical Center. The drones could be used to deliver a special type of healing molecule to fat deposits in arteries, according to findings published in the February 18th online issue of Science Translational Medicine.. Although current treatments have reduced the number of deaths from atherosclerosis-related disease, atherosclerosis remains a dangerous health problem: Atherosclerosis of the coronary arteries is the No. 1 killer of women and men in the United States, resulting in one out of every four deaths.. In the study, targeted biodegradable nano drones that delivered a special type of drug that promotes healing (resolution) successfully restructured atherosclerotic plaques in mice to make them more stable. This remodeling of the plaque environment ...
XVIIIIth International Symposium on Atherosclerosis (ISA 2018) to be held in Toronto, Canada from June 9-12, 2018.. Since 1966, the International Atherosclerosis Society (IAS) has held triennial meetings to bring together leading atherosclerosis researchers from across the globe. In its current form, the International Symposium on Atherosclerosis brings together scientists from over 65 constituent societies with over 17,000 active members. It remains today the premier meeting for international atherosclerosis research.. In keeping with the time-honored tradition of this worldclass symposium, ISA 2018 will bring together top clinicians, researchers, and health practitioners from around the world. In addition to delivering a comprehensive and high quality scientific program, this meeting will also provide an opportunity for its attendees to participate in public health awareness and innovation forums focused on cardiovascular health.. The ISA 2018 Symposium will be focused on cutting-edge research ...
The present data on human CEA atherosclerotic plaques and on murine vulnerable lesions suggest that HO-1 expression is strongly associated with vulnerable plaque morphology: HO-1 protein expression was specifically upregulated in human vulnerable atherosclerotic lesions with lipid and macrophage accumulation and low collagen and VSMC content. These lesions typically express high levels of the proteolytic factor MMP-9 and proatherogenic cytokines (IL-6, IL-8) and show increased plaque thrombogenicity. HO-1 expression levels correlated closely with the extent of these vulnerable plaque characteristics. Furthermore, in a murine vulnerable plaque model, induction of HO-1, either by CoPPIX injection or by adenovirus-mediated transgenesis, prevented vulnerable plaque formation and led to the development of lesions with a more stable phenotype: HO-1 induction diminished the necrotic core and increased fibrous cap thickness, without affecting lesion size, and HO-1 reduced lipid and increased VSMC ...
Rationale: Atherosclerosis and aneurysms are leading causes of mortality worldwide. MicroRNAs (miRs) are key determinants of gene and protein expression, and atypical miR expression has been associated with a number of cardiovascular diseases; although their contributory role to atherosclerotic plaque and abdominal aortic aneurysm (AAA) stability are poorly understood. Objective: To investigate whether miR-181b regulates TIMP-3 expression and affects atherosclerosis and aneurysms Methods and Results: Here, we demonstrate that miR-181b was over-expressed in symptomatic human atherosclerotic plaques and abdominal aortic aneurysms, and correlated with decreased expression of predicted miR-181b targets, TIMP-3 and elastin. Utilising the well characterised mouse atherosclerosis models of Apoe-/- and Ldlr-/-, we observed that in vivo ,administration of locked nucleic acid anti-miR-181b retarded both the development and progression of atherosclerotic plaques. Systemic delivery of anti-miR-181b in ...
Two low-dose menopausal hormone regimens improved some cardiovascular parameters in healthy women but did not affect atherosclerosis progression, even when started early and continued for up to 4...
To the Editor: When is atherosclerosis not atherosclerosis? In the last decade, there have been 2 revolutions in the study of atherosclerosis. On the one hand, a more sophisticated appreciation of the relationship between the morphology and fate of human atherosclerotic plaques and clinical outcomes has been developed. On the other hand, the blossoming of mouse genetics has allowed us the possibility of exploring prospectively the mechanisms that lead to various types of atherosclerotic lesions. These advances, in the view of the author, should compel us as experimentalists, mainly using murine models, to fashion a more nuanced view and description of experimental atherosclerosis.. The last issue of Arteriosclerosis, Thrombosis, and Vascular Biology contained a review on a comprehensive morphologic classification scheme for atherosclerotic lesions, which was derived by studies of lesions from autopsy examinations of sudden coronary deaths.1 There was also a commentary by Dr H. Stary2 updating ...
The simple assessment of atherosclerotic risk factors is not an accurate tool to predict the risk of cardiovascular disease (CVD) in adults without past history of atherosclerotic disease. Preclinical atherosclerotic increases the global cardiovascular risk and should be evaluated for a better risk stratification. Intima-media thickness (IMT), reduced ankle-brachial pressure index (ABI) and impaired flow mediated dilatation (FMD) are independent markers of multifocal but subclinical atherosclerosis and result associated with an increased rate of cardiovascular events. Multidetector computed tomography (MDCT) may be a useful non-invasive technique to detect silent coronary disease (CAD) in patients with peripheral preclinical atherosclerosis. This ebook outlines "preclinical athersclerosis" and its markers in clinical practice. The ebook gives simple but clear information for a better stratification of global cardiovascular risk. The text serves as an important guide for medical professionals ...
Atherosclerotic cardiovascular disease (ASCVD) is the leading cause of mortality and disability in most countries (1). Approximately 30% of first acute events are fatal, and survivors often experience sequelae and a shortened life expectancy (2,3). Primary prevention is thus the best approach to fighting this pandemic disease. Current algorithms for risk detection, which combine behavioral, clinical, and biochemical markers, are of limited accuracy, and better risk stratification methods are definitely needed (4,5).. Used in combination with traditional risk factors, data on subclinical atherosclerosis can provide additional information about the risk of myocardial infarction, stroke, and cardiovascular disease (CVD) mortality (6-8). Carotid wall intima-media thickness estimated from ultrasonographic images has been proposed as a surrogate measure of subclinical atherosclerosis (9). Whereas some prospective studies have shown that intima-media thickness adds predictive capacity to traditional ...
Researchers at Emory and Georgia Tech have discovered a new technique which combats atherosclerosis by targeting a micro-RNA molecule instrumental to its development.. It was discovered that a drug that blocks micro-RNA - a molecule left over from ribosome formation - slows down the process of atherosclerosis. In animal models, the process was blocked despite the presence of a high fat diet.. While it is well known that exercise reduces the likelihood of atherosclerosis, the latest research helps to explain why this is the case.. Atherosclerosis occurs when the walls lining the arteries thicken due to a build-up of white blood cells, lipids and cholesterol; this can bring on strokes and heart attacks. A constant flow of blood through the arteries prevents atherosclerosis, whereas an erratic flow of blood is known to contribute to the diseases development. The scientists developed an animal model of the disease, inducing atherosclerosis in mice by partially restricting the blood flow in the ...
BACKGROUND:. Currently, the predominant hypothesis regarding atherosclerosis is that it is in major part driven by two independent pathways: hyperlipidemia (the stimulation) and inflammation (the response). Although vascular cells mediate the influence of inflammation on atherosclerosis, very little is known about vascular cell epidemiology and the relationship of vascular cell phenotypes to atherosclerosis. The main hypothesis tested in this study is that variation in vascular cell biology is related to the population variation in atherosclerosis.. DESIGN NARRATIVE:. The cross-sectional study will be nested within a large cohort study, the Multiethnic Study of Atherosclerosis (MESA). A partial sample of 1,000 individuals who have undergone other special laboratory analyses will be identified and new measures collected as part of their upcoming site visit. A number of novel cellular phenotypes describing the innate immune response (monocyte activation, natural killer and T cell counts), the ...
TY - JOUR. T1 - Lack of interleukin-1ß decreases the severity of atherosclerosis in apoE-deficient mice. AU - Kirii, Hirokazu. AU - Niwa, Tamikazu. AU - Yamada, Yasuhiro. AU - Wada, Hisayasu. AU - Saito, Kuniaki. AU - Iwakura, Yoichiro. AU - Asano, Masahide. AU - Moriwaki, Hisataka. AU - Seishima, Mitsuru. PY - 2003/4/1. Y1 - 2003/4/1. N2 - Objective - Atherosclerosis is considered to be a chronic inflammatory disease and many cytokines participate in the development of atherosclerosis, We focused on the role of interleukin-1β (IL-1β, one of the proinflammatory cytokines secreted by monocytes/macrophages, in the progression of atherosclerosis. Methods and Results - We generated mice lacking both apoE and IL-1β. The sizes of atherosclerotic lesions at the aortic sinus in apoE-/-/IL-1β-/- mice at 12 and 24 weeks of age showed a significant decrease of approximately 30% compared with apoE-/-/IL-1β+/+ mice, and the percentage of the atherosclerotic area to total area of apoE-/-/IL-1β-/- at 24 ...
The deleterious effects of high low-density lipoprotein (LDL) cholesterol levels on atherosclerosis has been known for almost a century,1 yet plasma cholesterol continues to be a challenge for clinicians in the treatment and prevention of cardiovascular disease.2,3 Atherogenesis involves uptake of cholesterol in the vascular wall, followed by inflammatory activation and growth of vascular smooth muscle cells.4,5 Indeed, proinflammatory mediators such as interleukins and cytokines stimulate vascular cell growth and atherogenesis (reviewed in4), whereas inhibition of inflammatory pathways attenuates cell growth and atherosclerosis.6 Therefore, we now view atherosclerosis as a vascular inflammatory process7 as was already proposed by Virchow8 and later by Anitschkow who noticed an "infiltrative character" of atherosclerotic lesions of cholesterol-fed animals.9. Differentiation and growth of vascular smooth muscle cells, a prerequisite of atherosclerosis progression, depends on a fine-tuned balance ...
Women with lupus have a five- to ten-fold increased risk of coronary heart disease compared to the general population. Several decades ago, when women with lupus died shortly after developing the disease, their deaths were attributed to previously undiagnosed and untreated active lupus. But when they died years after their diagnosis of lupus, their deaths were attributed to complications of atherosclerosis (hardening of the arteries). Similar to lupus, atherosclerosis is considered an inflammatory disease. Inflammation plays a major role in atherosclerosis, which results when fatty deposits, cholesterol and other materials accumulate in the blood vessels.. The combination of atherosclerosis and lupus greatly increases the risk of cardiovascular disease among women. Research has identified many factors that contribute to the risk of atherosclerosis in people with lupus. These include high blood pressure and abnormal cholesterol levels, chronic inflammation, antibodies that attack proteins that ...
Atherosclerosis is a disease of chronic inflammation, characterized by a dysfunctional interplay between the immune apparatus and lipids. Immune cells, as well as nonimmune cells, drive plaque inflammation through a complex crosstalk of inflammatory mediators. The cells are activated by risk factor-induced triggers, which are present in the circulation and in the vessel wall, such as shear stress, oxidized lipoproteins and oxidative stress. Without relief from risk factors, the activation of inflammatory processes persists, resulting in a chronic nonresolving inflammation. Inflammation is associated with severity of disease, and complex lesions, which are prone to rupture and cause acute events, are characterized by extensive inflammation. Thus, inflammation is an active driver of atherosclerotic plaque development and a risk factor for atherosclerotic events. It is therefore of utmost importance to understand the mechanisms behind these inflammatory processes and to be able to develop new diagnostics
Editors Note: The U.S. Transhumanist Party features this article by our guest Steve Hill, originally published by the Life Extension Advocacy Foundation (LEAF) on April 13, 2018. In this article, Mr. Hill reviews a study published by the La Jolla Institute for Allergy and Immunology, in which the study authors successfully vaccinated atherosclerotic mice. In fact, this method supported Dr. Aubrey de Greys early insight - his claim that we must attack plaque altogether.. ~ Bobby Ridge, Assistant Editor, July 5, 2019. Scientists could be one step closer to a solution to atherosclerosis by preventing the buildup of plaques that clog the arteries and lead to strokes and heart attacks.. What is atherosclerosis?. Atherosclerosis is the accumulation of cholesterol-containing plaques in the walls of arteries; this causes them to narrow, leading to reduced blood flow, higher blood pressure, and an increased risk of a heart attack or stroke. Atherosclerosis is the number one cause of death globally, ...
Background: Recent studies have found low-normal potassium (K) to be associated with increased diabetes risk. We sought to verify these associations in a multi-ethnic US cohort; and to determine if these associations extend to US Hispanics and Asian-Americans. Methods: We analyzed data from Multi-Ethnic Study of Atherosclerosis (MESA) participants who were free-of-diabetes at baseline. We examined cross-sectional associations between measures of K-serum, dietary, and urine-with fasting glucose and HOMA-IR. We examined longitudinal associations between K and diabetes risk over 8 years. Findings: In multivariable models, compared to those with higher serum K (≥4.5mmol/L), those with lower serum K (,4.0mmol/L) had significantly higher fasting glucose [1.3 mg/dL (95%CI 0.2, 2.4), P-value = 0.03]. Incident diabetes developed in 1281 of 5415 at-risk participants. In minimally-adjusted models, we found inverse associations between serum and dietary K and diabetes risk. Compared to those with higher ...
Atherosclerotic vascular disease manifests as a progressive narrowing of the vessel wall, and underlies coronary artery disease (CAD) and cerebrovascular disease. With consequences such as myocardial infarction and stroke, atherosclerosis remains the most frequent cause of death in the western world. While a strong heritable component is undisputed, the molecular inflammatory and immune mechanisms in the evolution of the disease are still not fully understood. By using both animal models of disease (foremost genetically manipulated mice) as well as human tissue, and more recently by employing unbiased approaches to discover genetic loci predisposing to disease development, investigators have revealed a complex picture of multilayered cellular processes and molecular mechanisms. Here we highlight the current view on atherosclerosis and provide an updated account of the critical factors involved in disease development, as illustrated by various prototypic examples.. In brief, the ...
Atherosclerosis, sometimes called "hardening of the arteries," occurs when cholesterol, calcium, and other substances build up in the inner lining of the arteries, forming a material called plaque. Over time, plaque buildup may narrow the artery and limit blood flow through it.. Coronary artery disease is atherosclerosis in the heart (coronary) arteries. Peripheral arterial disease of the legs is atherosclerosis in the leg arteries. If atherosclerosis affects the brain arteries (carotid or cerebral arteries), a stroke can occur.. ...
The traditional view of atherosclerosis as a pathological lipid deposition within the artery wall has been redefined by a more complex theory in which the presence of a dysfunctional endothelium plays a pivotal role. The discovery of progenitor cells of myeloid origin, which are able to replace old or injured mature endothelial cells and are able to differentiate into healthy and functional endothelial cells, has offered the prospect of merging the traditional theories on the pathogenesis of atherosclerosis with the evolving concept of a role of these progenitor cells in the repair of the injured vessel wall and the neovascularization of ischemic tissues. This article summarizes current knowledge about the biology of atherosclerosis with emphasis on the balance between endothelial injury and repair and on the concept that the turnover and replacement of endothelial cells is a major determinant in the maintenance of vascular integrity. Keywords: endothelial progenitor cells; atherosclerosis; ...
Atherosclerosis is a chronic inflammatory disease characterized by the accumulation of lipids, smooth muscle cell proliferation, cell apoptosis, necrosis, fibrosis, and local inflammation. Immune and inflammatory responses have significant effects on every phase of atherosclerosis, and increasing evidence shows that immunity plays a more important role in atherosclerosis by tightly regulating its progression. Therefore, understanding the relationship between immune responses and the atherosclerotic microenvironment is extremely important. This article reviews existing knowledge regarding the pathogenesis of immune responses in the atherosclerotic microenvironment, and the immune mechanisms involved in atherosclerosis formation and activation.. ...
phdthesis{ea60fb21-e33b-4c39-86f1-dbb1154e5a95, abstract = {The cholesterol-lowering effect of oats is well established, but the crucial properties eliciting this effect need to be further investigated to optimize the use of oats as functional foods. Furthermore, there are almost no reports investigating the effect of oats on atherosclerosis development. This thesis describes our work with finding,br/,,br, suitable mouse models to study cholesterol-lowering and anti-atherogenic effects of oats, the mechanism behind, and how processing of oat foods might interfere with these beneficial effects.,br/,,br, We found that supplementation of oat bran to an atherogenic diet significantly reduced plasma cholesterol and LDL+VLDL concentrations in C57BL/6 mice. The responsiveness to oats did however differ between two substrain of mice. Oat intake resulted in reduced plasma cholesterol, increased faecal excretion of bile acids and cholesterol, and increased expression of the bile acid producing enzyme ...
Systemic loss of one IL-6 cytokine member exhibits mild or unexpected morphological vascular phenotypes (19), e.g., systemic deletion of IL-6 in a mouse model prone to atherosclerosis elicits detrimental effects on atherosclerotic plaque development, potentially via an IL-6−dependent down-regulation of its counteracting cytokine IL-10 (20). The complete systemic gp130 knockout, in contrast, shows profound defects in cardiac and hematopoetic development, resulting in premature death in utero or soon after birth. Thus, to delineate the role of the hepatic APR in atherosclerosis, we selectively deleted the gp130 receptor in hepatocytes using the Cre-loxP system. The genetic modification was confirmed by a PCR reaction demonstrating the gene inactivation exclusively in liver, but not in heart, aorta, or spleen, and by functional analysis of gp130-dependent, LIF-induced STAT3 phosphorylation and SAA release from hepatocytes from controls, but not from gp130− mice. Thus, the introduction of loxP ...
Get this from a library! Atherosclerosis, clinical evaluation and therapy ; proceedings of the Fourth International Meeting on Atherosclerosis held in Bologna, Italy, 23-25 November 1981. [S Lenzi; G C Descovich; Università di Bologna. Istituto di clinica medica generale e terapia medica II.;]
Online information about atherosclerosis disease at altiusdirectory.com. symptoms, prognosis of atherosclerosis, causes, diagnosis, treatment for atherosclerosis.
Atherosclerosis is a disorder which begins at the childhood stage. This disease matures slowly and may sometimes take decades to become evident or for us to notice its symptoms. Atherosclerosis can be described as a condition which causes the arteries to harden. As a result, such hardened arteries become a cause of a majority of cardiovascular diseases.. Our arteries are clean and flexible. Arteries are the tubes which carry blood and oxygen to heart and other body parts. Atherosclerosis causes plaque to build up on the walls of the arteries. This plaque can be made of substances like fat, cholesterol, calcium, or any other component of the blood. As the time passes, such plaque settles in the arteries and hardens and causes the arteries to become narrower.. As a result, the flow of oxygen rich blood to various parts of the body reduces. The reduced flow of blood can be potentially fatal and may cause problems like heart attack, stroke or death of a person. In order to remove these blockages, a ...
R. John Davenport http://sageke.sciencemag.org/cgi/content/abstract/sageke;2002/36/nw126 Key Words: NCX-4016 hypercholesterolemia malondialdehyde isoprostanes. Abstract: Modern twists on old favorites sometimes make them better. According to a new study, a redesigned aspirin molecule that delivers nitric oxide battles atherosclerosis, at least in rodents. The modified molecule keeps fatty plaques from accumulating in blood vessels and choking circulation. The study suggests that the compound, already being tested as a gut-sparing painkiller, might double as an effective plaque-buster.. The signaling molecule NO relaxes blood vessels and soothes inflammation. Previous work suggested that NO also protects blood vessels from fatty buildup: Atherosclerosis-prone mice accumulate more plaques when treated with compounds that block NO production. But whether adding NO could prevent atherosclerosis was unclear.. To further explore NOs plaque-preventing prowess, Napoli and colleagues used an old standby ...
Atherosclerosis is a condition in which fatty material collects along the walls of arteries, forming a plaque. The plaque thickens and hardens over time, eventually blocking blood flow. Once thought of as a lipid storage disease, atherosclerosis is now also recognized as a chronic inflammatory condition that increases risk of coronary and cerebrovascular disease. Atherosclerotic plaques include macrophages, which release inflammatory cytokines into the surrounding area. The inflammatory processes that mediate atherosclerosis occur in disease states such as obesity, insulin resistance, and type 2 diabetes. Typical complications from this progressive disease include plaque rupture, which can cause clot formation. If the blood vessel is fully blocked, the plaque rupture can cause a stroke or heart attack. Analyzing the expression, regulation, and sequence of atherosclerotic genes can help determine their relative importance to the biology of the cellular or disease processes under study and further ...
The Atherosclerosis Risk in Communities Study (ARIC) is a prospective epidemiologic study being conducted in four U.S. communities. ARIC is designed to investigate the etiology and natural history of atherosclerosis, the etiology of clinical atherosclerotic diseases, and variation in cardiovascular risk factors, medical care and disease by race, sex, place and time. It includes two parts: the Cohort Component and the Community Surveillance Component. In the cohort component, the ARIC field center in each community randomly selected and recruited a cohort of approximately 4,000 individuals aged 45-64 years of age (15,800 participants total). Recruited participants have an extensive examination, including medical, social and demographic data. These participants are re-examined every three years. In the community surveillance component, these four communities are investigated to determine the occurrence of hospitalized myocardial infarction and coronary heart disease death in men and women aged 35-74 years
Oxidation of LDL contributes to the development of atherosclerosis. Oxidized LDL is found in atherosclerotic plaques, and oxidation of LDL appears to enhance its uptake by macrophages. This posed the question of whether treatment with antioxidants might retard the development of atherosclerosis. This hypothesis became more compelling when treatment antioxidants was shown to inhibit atherosclerosis in animal models. Epidemiologic studies initially suggested that vitamin E (but not vitamin C) was beneficial in reducing the risk of coronary heart disease in humans. The first two articles cited below are large prospective cohort studies - one in men and the other in women.. Rimm EB, et al.: Vitamin E Consumption and the Risk of Coronary Heart Disease in Men. N Engl J Med 1993; 328:1450-1456. From the abstract:. In 1986, 39,910 U.S. male health professionals 40 to 75 years of age who were free of diagnosed coronary heart disease, diabetes, and hypercholesterolemia completed detailed dietary ...
The pivotal stage of atherogenesis is antigen presentation by macrophages to T lymphocytes. This antigen could be a fragment of oxidized LDL"digested" by macrophage, heat shock protein 60, β2 glycoprotein I, or fragments of bacterial antigens. During interaction between these cells, an immunological response of type T helper 1 (cellular) or T helper 2 (humoral) arises. Th1 response and its mediators: (IFN-γ, TNF-α, interleukin 1, interleukin 12, and interleukin 18) increase atherogenesis, whereas Th2 response and its mediators: (interleukin 4, interleukin 5, and interleukin 10) decrease the development of atherosclerosis. The concept of atherosclerosis as an inflammatory disease is quite fresh; however, it is already considered an undisputable achievement of science, bringing particular therapeutic consequences ...
Almost 78% of the participants were classed as being metabolically unhealthy and 52% were obese (had a BMI of 30 or higher). The metabolically unhealthy participants were less likely to meet the recommended guidelines for eating four to five servings of fruits and vegetables each day. Participants who were defined as being metabolically unhealthy and not obese were found to be more likely to be older males with a waist circumference of about 38 inches. This group were also found to have less education than other participants. The metabolically unhealthy who were not clinically obese showed similar level of atherosclerosis to those who were obese, which suggests that metabolic risk has a stronger association to atherosclerosis among Mexican-Americans than obesity. This is an interesting finding as some previous studies have found that waist circumference is predictive of atherosclerosis. "Our findings are particularly relevant to future public health planning as interventions to maintain ...
It is unknown exactly how atherosclerosis begins or what causes it. Atherosclerosis may start as early as childhood. However, the disease has the potential to progress rapidly. It is generally characterized by the accumulation of fatty deposits along the innermost layer of the arteries. If the disease process progresses, plaque formation may take place. This thickening narrows the arteries and can decrease blood flow or completely block the flow of blood to organs and other body tissues and structures.. The presence of atherosclerosis in any one of these areas is a strong indicator that there is also the presence of atherosclerosis in the arteries of other parts of the body. Just as atherosclerosis in the arteries of the heart can cause a heart attack, or atherosclerosis of the arteries to the brain can cause a stroke, so can atherosclerosis of the leg arteries cause a blockage. A blockage can obstruct blood flow, and potentially result in pain in the leg(s), ulcers or wounds that do not heal, ...
Atherosclerotic disease is responsible for nearly half of all deaths in the western world. During the past three decades, considerable efforts have been made towards detection and assessment of atherosclerosis plaques in various vascular beds using different imaging techniques. Recently, both noninvasive and invasive modalities have frequently been used to refine cardiovascular risk assessment in high-risk individuals, to evaluate the natural history of atheroma burden and to reveal the impact of anti-atherosclerotic medical therapies on disease progression. In this review, we provide an overview of the currently available imaging modalities. This article will underscore arterial wall imaging to assess the impact of medical therapies on atherosclerosis and to develop the effective therapeutic strategies, resulting in the prevention of cardiovascular complications.
Assessment of subclinical atherosclerosis and cardiovascular risk.: Conventional cardiac risk factors do not fully explain the incidence of coronary artery dise
Researchers show that IKKβ functions in smooth muscle cells to regulate vascular inflammatory responses and atherosclerosis development in mice. Surprisingly, the lack of IKKβ also protects the animals from diet-induced obesity. The use of IKKβ inhibitors may provide an innovative treatment for atherosclerosis, obesity, and metabolic disorders.
... is a disease affecting blood vessels called arteries. Fatty material called plaque builds up within the inner lining of arteries causing them to narrow and be less flexible. This reduces the amount of blood and oxygen that is delivered to vital organs. Atherosclerosis can occur anywhere in your body, but it is especially dangerous when it affects the arteries leading to your brain, heart, kidneys and legs.. ...
Atherosclerosis is a systemic disease that refers to the buildup of fatty, waxy plaque in the arteries. While most people associate this disease with the heart, atherosclerosis can occur anywhere in the body and result in reduced blood flow, blood clots and heart attacks. Learn about the risk...
Home / Conditions / MODY/LADA / Predicting Atherosclerosis Disease in Patients With Diabetes Predicting Atherosclerosis Disease in Patients With Diabetes Carotid ultrasound shows atherosclerotic disease is not just a concern for patients with type 1 and type 2 diabetes, but LADA as well. Approximately 4-14% of pat
If atherosclerosis leads to symptoms, some symptoms such as angina pectoris can be treated. Non-pharmaceutical means are usually the first method of treatment, such as cessation of smoking and practicing regular exercise. If these methods do not work, medicines are usually the next step in treating cardiovascular diseases, and, with improvements, have increasingly become the most effective method over the long term.. Statins. In general, the group of medications referred to as statins has been the most popular and are widely prescribed for treating atherosclerosis. They have relatively few short-term or longer-term undesirable side-effects, and several clinical trials comparing statin treatment with placebo have fairly consistently shown strong effects in reducing atherosclerotic disease events and generally ~25% comparative mortality reduction, although one study design, ALLHAT, was less strongly favorable.. The newest statin, rosuvastatin, was the first to demonstrate regression of ...
(2016) Maimaiti et al. Lipids in Health and Disease. Background: Recent discoveries of the atherosclerosis-related miRNAs shed new light on the treatment of cardiovascular diseases. Of note, miR-106b ∼ 25 cluster and miR-17 ∼ 92 cluster are paralogs. Up till now, plenty of researches have shown t...
Atherosclerosis is a type of arteriosclerosis caused by a build-up of plaque in the inner lining of an artery. (Arteriosclerosis is a general term for thickening or hardening of the arteries.) Plaque is made up of deposits of fatty substances, cholesterol, cellular waste products, calcium, and fibrin, and can develop in medium or large arteries. The artery wall becomes thickened and loses its elasticity.. Atherosclerosis is a slow, progressive disease that may start as early as childhood. However, the disease has the potential to progress rapidly.. ...
Depending on the location of the plaque and the extent of blockage, other complications may result. Plaque buildup in the coronary arteries, which deliver blood to the heart, can lead to coronary heart disease - the primary cause of deaths in the Untied States. Reduced or halted blood flow to the heart may cause a heart attack. Plaque in the carotid arteries (carotid artery disease), which deliver blood to the brain, can cause a stroke. A blockage in the major arteries (peripheral artery disease) causes pain and numbness in the limbs and pelvis, while blockage in the renal arteries (chronic kidney disease) affects kidney function. An aneurysm is a bulge in the artery wall that can be lethal if it bursts.. Atherosclerosis can be managed (and prevented) with lifestyle changes and medical intervention. Every year approximately 380,000 Americans die from coronary heart disease.. ...
Atherosclerosis, sometimes called hardening of the arteries, occurs when cholesterol, calcium, and other substances build up in the inner lining of the arteries, forming a material called plaque. Over time, plaque buildup may narrow the artery and limit blood flow through it. Coronary artery disease is atherosclerosis...
HealthTap: Doctor answers on Symptoms, Diagnosis, Treatment, and More: Dr. Hines on what sort of problem is atherosclerosis: Atherosclerosis is an inflammatory process which occurs in arteries. Advanced stages cause narrowing of the arteries involved. The narrowing can lead to complete blockage of blood flow or to what is termed "plaque rupture" (when pieces of the lining of diseased artery break free. Clot forms and floats downstream). In the heart this causes heart attacks, in the brain this causes strokes.
Question - anatomy and physiology relating to the coronary arteries and atherosclerosis. Ask a Doctor about diagnosis, treatment and medication for Atherosclerosis, Ask a Cardiologist
Atherosclerosis is plaque build up in the arteries. Risk factors of it are high and symptoms not easily recognized. Treatment for Atherosclerosis causes must be given before arteries become blocked.
What is atherosclerosis? Atherosclerosis, sometimes called "hardening of the arteries," occurs when fat (cholesterol) and calcium build up inside the lining of the artery wall, forming a substance called plaque. Over time, the fat and calcium buildup narrows the artery and blocks blood flow through it...
ORLANDO, Florida, November 7 /PRNewswire/ -- - Data Presented at AHA Scientific Sessions Adds to Body of Evidence Highlighting Unique Benefits of CRESTOR Across the Spectrum of Atherosclerosis Disease Progression New analysis of the METEOR (Measuring Effects on intima media Thickness: an Evaluation Of Rosuvastatin) trial presented today showed CRES
Magnetic resonance imaging (MRI) of aortic atherosclerosis can predict the risk of heart attacks and other cardiovascular events in otherwise healthy individuals, researchers at UT Southwestern Medical Center have found.
Atherosclerosis, chronic disease caused by the deposition of fats, cholesterol, calcium, and other substances in the innermost layer of endothelium of the large and medium-sized arteries. Atherosclerosis is the most common arterial abnormality characterized as arteriosclerosis, which is defined by
Brief Answer: You shouldnt worry, continue with healthy lifesty Detailed Answer: Hi and thank you for asking! I read your query and understood your concerns. This findings on ct is normal at your age and is due to atherosclerosis and calcification of aorta. Atherosclerosis is a biological...
Definícia pre hľadané cudzie slovo atherosclerosis - ateroskleróza, kôrnatenie tepien, hromadenie tukových a väzivových plátov v cievnej stene s následným zúžením priesvitu artérie... Definícia pre hľadané cudzie slovo atherosclerosis - pozri...
Atherosclerosis has an open access mirror journal Atherosclerosis: X, sharing the same aims and scope, editorial team, submission system and rigorous...
There is compelling evidence indicating that some members of the matrix metalloproteinase (MMP) family play important roles in the pathogenesis of atherosclerosis and related vascular and cardiac conditions such as atherosclerotic plaque rupture lead
Flavia de Oliveira, Laura B.M. Maifrino, Gustavo P.P. de Jesus, Juliana G. Carvalho, Cláudia Marchon and Daniel A. Ribeiro). Estrogen deprivation in postmenopausal women increases cardiovascular risk. Cardiovascular risk as a result of atherosclerosis is able to induce an inflammatory disease as far as cyclooxygenase-2 (COX-2) expression. The purpose of the study was to investigate the role of COX-2 on exercise training in female mice LDL-KO with or without ovariectomy. Results showed that ovariectomy induced a strong immunoexpression in atherosclerosis lesion of LDL-KO mice. Nevertheless, a down-regulation of COX-2 expression was detected in LDL-KO trained ovariectomized when compared to LDL-KO sedentary. Our results are consistent with the notion that exercise training is able to modulate COX-2 expression in LDL-KO mice as a result of COX-2 down-regulation.. ...
Metabolic syndrome is directly linked with atherosclerotic burden and cell-free nucleic acids (cf-NA) analysis has recently emerged as a novel research tool in atherosclerosis prac..
It is surprising, therefore, that Rott et al. (1)found that inhibition of COX-2 aggravated atherosclerosis in the apoE knockout mouse. The study was more complex, as the authors set out to examine the effect of COX-2 inhibition on infectivity of cytomegalovirus and coincidentally showed increased disease burden in animals treated with the COX-2 inhibitor, including those not infected with the virus. Although it would be reasonable to conclude that this reflected selective suppression of PGI2and an unopposed effect of TXA2, the authors suggest as an alternative hypothesis the suppression of anti-inflammatory PGs, such as PGJ2, and its metabolite 15-deoxy-delta12,14-PGJ2(15d-PGJ2) (35).. Although COX-2 is usually thought of as contributing to inflammation, some authors have suggested that COX-2 may also play an anti-inflammatory role. The hypothesis arises from observations with COX-2 inhibitors and in animals in which the COX-2 gene has been disrupted. Although inducing an anti-inflammatory ...
TY - JOUR. T1 - Immune activation resulting from NKG2D/ligand interaction promotes atherosclerosis. AU - Xia, Mingcan. AU - Guerra, Nadia. AU - Sukhova, Galina K.. AU - Yang, Kangkang. AU - Miller, Carla K.. AU - Shi, Guo Ping. AU - Raulet, David H.. AU - Xiong, Na. PY - 2011/12/20. Y1 - 2011/12/20. N2 - BACKGROUND-: The interplay between the immune system and abnormal metabolic conditions sustains and propagates a vicious feedback cycle of chronic inflammation and metabolic dysfunction that is critical for atherosclerotic progression. It is well established that abnormal metabolic conditions, such as dyslipidemia and hyperglycemia, cause various cellular stress responses that induce tissue inflammation and immune cell activation, which in turn exacerbate the metabolic dysfunction. However, molecular events linking these processes are not well understood. METHODS AND RESULTS-: Tissues and organs of humans and mice with hyperglycemia and hyperlipidemia were examined for expression of ligands for ...
Atherosclerosis can be devastating, causing strokes, heart attacks and death. The good news is that you can take steps to protect yourself from this disease.
Atherosclerosis can be devastating, causing strokes, heart attacks and death. The good news is that you can take steps to protect yourself from this disease.
Judith Sluimer defended her PhD thesis at Maastricht University in 2008, under supervision of professor Mat Daemen. She established the first proof of hypoxia in human and murine atherosclerosis and investigated the hypoxia-dependent formation and leaky phenotype of atherosclerotic plaque angiogenesis. After her PhD defence, she joined the lab of Prof. Ira Tabas (Columbia University, NYC, USA) in 2008 as a post-doctoral fellow to further her expertise in macrophage apoptosis, efferocytosis and autophagy (funded by the Netherlands Scientific Organisation (NWO, Rubicon), the international atherosclerosis society (IAS), and Maastricht University). Since 2010, Judith has established an independent research line focusing on the functional role and imaging potential of hypoxia, oxygen sensors and leaky angiogenesis in atherosclerosis and diet-induced obesity in the department of Pathology of Maastricht University Medical Centre. In 2010 she acquired the VENI grant from NWO to investigate ...
A number of potential mechanisms have been proposed to explain the relation between endothelial dysfunction and cardiovascular risk. For example, it is possible that endothelial dysfunction simply reflects the presence and extent of atherosclerosis, and it would not be surprising for patients with more extensive atherosclerosis to have a higher risk of cardiovascular events compared to patients with less or no atherosclerosis. The two published studies demonstrating a weakened correlation between endothelial dysfunction and cardiovascular events after adjustment for extent of disease10,15 support this potential mechanism. Similarly, it is possible that endothelial dysfunction represents the cumulative effects of traditional risk factors on the vasculature and that patients with a higher level of risk factors will be more likely to develop atherosclerosis and associated cardiovascular events. However, as discussed above, nearly all of the available studies suggest that endothelial dysfunction ...
Tomoya Mita, Naoto Katakami, Hidenori Yoshii, Tomio Onuma, Hideaki Kaneto, Takeshi Osonoi, Toshihiko Shiraiwa, Keisuke Kosugi, Yutaka Umayahara, Tsunehiko Yamamoto, Hiroki Yokoyama, Nobuichi Kuribayashi, Hideaki Jinnouchi, Masahiko Gosho, Iichiro Shimomura, Hirotaka Watada and on behalf of the Collaborators on the Study of Preventive Effects of Alogliptin on Diabetic Atherosclerosis (SPEAD-A) Trial, on behalf of the Collaborators on the Study of Preventive Effects of Alogliptin on Diabetic Atherosclerosis (SPEAD-A) Trial ...
We have demonstrated for the first time that MNA, the major metabolite of nicotinamide and NicA, displays pronounced vasoprotective, anti-inflammatory, and anti-atherosclerotic in ApoE/LDLR−/− mice, associated with an improvement in PGI2- and NO-dependent endothelial function, inhibition of platelet activation, inhibition of inflammatory burden in plaques, and diminished systemic inflammation. Despite substantially higher MNA availability after NicA treatment compared with an equivalent dose of MNA, the antiatherosclerotic effect of NicA was not stronger. We suggest that detrimental effects of NicA itself or its metabolites other than MNA may limit beneficial effects of NicA-derived MNA.. In this work, 4-month-old mice with advanced atherosclerosis were used to study the effects of MNA and NicA. In this model, endothelial dysfunction is present at the age of 2 months, in the absence of visible atherosclerotic plaques. The first lesions, composed mostly of fatty streaks and infiltrating ...
The broad research focus of Dr. Majors laboratory is to understand immunological mechanisms of cardiovascular disease, specifically atherosclerosis. Atherosclerosis is the number one cause of mortality in developed countries and it is known that both lipids and immunity play significant roles. Work performed in her laboratory has significantly impacted our understanding of how the immune system modulates atherosclerosis as well as how dyslipidema and the atherosclerotic environment influence normal immune function.. It is widely accepted that increased circulating cholesterol (especially LDL) and modifications of lipids are the main culprits in the development of atherosclerosis in the general population. However, over the past three decades, increased focus has been on the role of immune cells, such as B cells and particular subsets of T cells, in the atherogenic process. Dr. Majors laboratory is interested in understanding the relationship between normal and abnormal T and B cell biology and ...
There is a wealth of clinical data showing the relationship between diabetes mellitus and atherosclerosis and its clinical complications. To dissect this relationship, investigators have attempted, usually unsuccessfully, to create a small-animal model in which diabetes accelerates vascular lesion development. This effort has often been complicated by development of hyperlipidemia leading to difficulty in differentiating the effects of hyperglycemia from those of lipid abnormalities. A study in the current issue of the JCI provides data on a new mouse model in which atherosclerosis initiation is accelerated in diabetic mice and is reduced by insulin therapy. Moreover, these animals have greater intra-arterial hemorrhage, which might be due to less stable plaques .. ...
Now back to the lipoproteins. The major culprit of atherosclerosis is thought (I dont know if they indeed found LDL in atheromas) to be type B LDL (the smaller more dense one as opposed to type A LDL) because its always present, small enough, and by its job, travels from the liver to the tissues (to deliver cholesterol) so at one time it must try to pass the arterial wall to reach the target tissue. Now there are theories/studies/etc. which say that eating cholesterol combined with saturated fat can have post-prandial (post eating) effect of increasing the activity and the number of LDL particles, although the LDL could return to basal level later. Some others say that chyclomicrons (the biggest lipoprotein) can lodge into the arterial wall and also say that actually most atheromas are initiated by stuck chyclomicons. As you now chyclomicrons exist around the time when you eat (to transfer the fat and cholesterol from the intestines to other parts of the body) so again it accentuates the ...
This book provides a critical review of the oxidative theory of atherosclerosis as well as highlighting new trends in research from basic to clinical, academic to commercial. The contributions of diabetes, vascular dysfunction, blood coagulation, plaque rupture, oxidative stress, lymphocytes, macrophages, growth factors, cytokines, and oxysterols to atherogenesis are all discussed, as are the roles of smooth muscle and endothelial cells.
We use cookies to ensure that we give you the best experience on our website. If you click Continue well assume that you are happy to receive all cookies and you wont see this message again. Click Find out more for information on how to change your cookie settings ...
The central role of VCAM-1 in the evolution of inflammatory vascular lesions and its exposed accessible position on the endothelial surface render this adhesion molecule an attractive imaging target for atherosclerosis, MI, and transplant rejection. Here we show that PET-CT can image VCAM-1 and describe the design, synthesis, and validation of the novel PET imaging agent 18F-4V. The technique detects VCAM-1 expression in murine aortas, vessels with a diameter considerably smaller than epicardial human coronary arteries. We also show that targeting VCAM-1 is useful for imaging of other cardiovascular diseases.. The initial design of 3 candidate probes derived from peptides identified by phage display (9,10). Although all of these peptides did target VCAM-1, the modified imaging probes differed in their affinity, molecular weight, and pharmacokinetics. TLP, the lead peptide with the highest affinity and most favorable pharmacokinetics, had an arborizing, tetrameric design. The multivalency of TLP ...
Get this from a library! Lipids and atherosclerosis annual 2001. [Allan Gaw; J Shepherd] -- Given the continuing development of new statins and their increasing, beneficial use in clinical practice and given the importance of clinical research into the atherosclerotic plaque and its role in ...
Our mission is to identify genetic pathways in atherosclerosis, and provide better therapeutic options to eradicate heart disease. Our ultimate goal is to prevent heart attack and stroke.
Definition: Atherosclerosis is a disorder in which arteries become clogged or narrowed due to abnormal fat deposits. The fat is first deposited on the inside of the artery walls and then hardens and calcifies. This leads to complications with coronary artery disease and other cardiovascular problems. Examples: There
Infections by opportunistic bacteria have significant contributions to morbidity and mortalityin humans. Atherosclerosis is a chronic inflammatory disease characterized by the formation of plaques inside arteries, leading to stroke in humans. In this scen
Next wednesday 15th January, Professor Alberico Catapano, from Faculty of Pharmacy, University of Milano, going to talk about "HDL and Atherosclerosis: Is All About Cholesterol?". Session will be hold at 11:30h at Sala Polivalent of the Centre for Omic Sciences. More information here. ...
Arterioslerosis and Atherosclerosis involve the build-up of deposits on the inside of arterial walls that cause thickening and hardening of the arteries. So what treatments are available?
Reverse Atherosclerosis, Prevent Heart Attacks, Clear Your Arteries!. Have you had a heart attack?. Do you have a stent?. Do cholesterol medications make you tired or forgetful?. Heart disease is a MANUFACTURED problem. You CAN reverse it. ...
What if you could learn to reverse one of the most dreaded degenerative diseases we face today? Atherosclerosis (arteriosclerosis), the buildup of plaque in the arteries leading to heart disease is, according to Dr. Levy, easy to prevent when we understand how it starts: deficiency of vitamin C in the innermost lining of the arteries...…
Arterial disease, atherosclerosis In our last blog we looked at why matters of the Heart and Mind can affect lifestyle issues that can play a big role in cardiovascular (CV) issues. Here we are going to look more at what happens in the tubes. Arterial disease accounts for the vast majority of patients that ...
... is a type of thickening or hardening of the arteries caused by a buildup of plaque in the inner lining of an artery. It can increase your risk of heart attack, stroke, and other circulatory conditions.
... is a type of thickening or hardening of the arteries caused by a buildup of plaque in the inner lining of an artery. It can increase your risk of heart attack, stroke, and other circulatory conditions.
Amgens cholesterol-fighter Repatha rolled back atherosclerosis in a new clinical trial, showing that the drug doesnt just push LDL cholesterol down by impressive margins. But the results might not be enough to give the PCSK9 drug an immediate boost, analysts said.
misc{af1af361-4a46-4b8d-841f-6199c37368dd, author = {Hansson, G K and Nilsson, J}, issn = {1365-2796}, language = {eng}, number = {5}, pages = {462--463}, publisher = {Wiley-Blackwell Publishing Ltd}, series = {Journal of Internal Medicine1989-01-01+01:00}, title = {Introduction: Atherosclerosis as inflammation: a controversial concept becomes accepted}, url = {http://dx.doi.org/10.1111/j.1365-2796.2008.01959.x}, volume = {263}, year = {2008 ...
Atherosclerosis is the term used to describe hardening of the arteries. Plaque buildup narrows and stiffens arteries, making it harder for blood to flow through them.
Biomarkers and triggers of atherosclerosis. Anti-inflammatory cytokines, Predominately Pro-inflammatory cytokines, Interleukin 18 (IL-18).
In seeking to understand the mechanism of pathogenesis of atherosclerosis it is important to realise that the genesis of a lesion proceeds by a number of phases. The simplest general notion is that...
Detail záznamu - Proinflammatory Status, Genetics and Atherosclerosis - Detail záznamu - Knihovna Akademie věd České republiky
ICD-9 code 440.1 for Atherosclerosis of renal artery is a medical classification as listed by WHO under the range - DISEASES OF ARTERIES, ARTERIOLES,
... is a condition in which plaque buildup causes hardening and narrowing of major arteries. This eMedTV article offers an overview of this topic, including symptoms, diagnosis, and what can happen if the condition is left untreated.
The controversial diabetes drug Avandia appears to slow the progression of atherosclerosis in diabetic patients who have undergone cardiac bypass surgery, thus
TY - JOUR. T1 - VCAM-1 is critical in atherosclerosis. AU - Ley, Klaus. AU - Huo, Yuqing. PY - 2001/1/1. Y1 - 2001/1/1. UR - http://www.scopus.com/inward/record.url?scp=0035024867&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0035024867&partnerID=8YFLogxK. U2 - 10.1172/JCI13005. DO - 10.1172/JCI13005. M3 - Comment/debate. C2 - 11375406. AN - SCOPUS:0035024867. VL - 107. SP - 1209. EP - 1210. JO - Journal of Clinical Investigation. JF - Journal of Clinical Investigation. SN - 0021-9738. IS - 10. ER - ...
... , (ath-er-o-skler-O-sis) comes from the Greek words athero - meaning gruel or paste and sclerosis meaning hardness - and is a hardening of the arteries - it is the most common cause of heart disease.
Sirt3 is a mitochondrial NAD+-dependent deacetylase that governs mitochondrial metabolism and reactive oxygen species homeostasis. Sirt3 deficiency has been reported to accelerate the development of the metabolic syndrome. However, the role of Sirt3 in atherosclerosis remains enigmatic. We aimed to investigate whether Sirt3 deficiency affects atherosclerosis, plaque vulnerability, and metabolic homeostasis. Low-density lipoprotein receptor knockout (LDLR −/−) and LDLR/Sirt3 double-knockout (Sirt3 −/− LDLR −/−) mice were fed a high-cholesterol diet (1.25 % w/w) for 12 weeks. Atherosclerosis was assessed en face in thoraco-abdominal aortae and in cross sections of aortic roots. Sirt3 deletion led to hepatic mitochondrial protein hyperacetylation. Unexpectedly, though plasma malondialdehyde levels were elevated in Sirt3-deficient mice, Sirt3 deletion affected neither plaque burden nor features of plaque vulnerability (i.e., fibrous cap thickness and necrotic core diameter). Likewise, ...
In the current study we report for the first time that serum FGF21 levels are strikingly elevated in newly diagnosed type 2 diabetic patients with subclinical atherosclerosis compared to those without subclinical atherosclerosis. This observation remained true in both men and women when the results were analyzed independently. Moreover, we detected a strong association of FGF21 with carotid IMT in women as well as iliac IMT in men and women with type 2 diabetes.. Several risk factors have been proposed as potential markers for improved detection of subclinical atherosclerosis. In particular, physical measurements such as neck circumference [21] and abdominal adiposity [22]; inflammatory biomarkers such as C-reactive protein (CRP) [23]; lipid parameters such as oxidized LDL; adhesion molecules such as E-selectin; cytokines such as osteoprotegerin; and adipokines such as leptin [24], have all been associated with subclinical atherosclerosis in different ethnic groups. However, each of these ...
TY - JOUR. T1 - Differential effects of glyoxalase 1 overexpression on diabetic atherosclerosis and renal dysfunction in streptozotocin-treated, apolipoprotein E-deficient mice. AU - Geoffrion, Michèle. AU - Du, Xueliang. AU - Irshad, Zehra. AU - Vanderhyden, Barbara C.. AU - Courville, Kerri. AU - Sui, Guangzhi. AU - DAgati, Vivette D.. AU - Ott-Braschi, Sylvie. AU - Rabbani, Naila. AU - Thornalley, Paul J.. AU - Brownlee, Michael. AU - Milne, Ross W.. PY - 2014/1/1. Y1 - 2014/1/1. N2 - The reactive dicarbonyls, glyoxal and methylglyoxal (MG), increase in diabetes and may participate in the development of diabetic complications. Glyoxal and MG are detoxified by the sequential activities of glyoxalase 1 (GLO1) and glyoxalase 2. To determine the contribution of these dicarbonyls to the etiology of complications, we have genetically manipulated GLO1 levels in apolipoprotein E-null (Apoe−/−) mice. Male Apoe−/− mice, hemizygous for a human GLO1 transgene (GLO1TGApoe−/− mice) or male ...
During a 6 year period 60 patients with atherosclerotic renovascular disease were followed by a single renal unit. Angiotensin converting enzyme inhibitors were being taken by 22% of patients at the time of diagnosis of the atherosclerotic renovascular disease. Intervention to revascularize renal tissue by surgery or angioplasty was performed...
Background: Air pollution is associated with significant adverse health effects including increased cardiovascular morbidity and mortality. However research on the cardiovascular effect of "real-world" exposure to ambient particulate matter (PM) in susceptible animal model is very limited. In this study, we aimed to investigate the association between Beijing ambient particle exposure and the atherosclerosis development in the apolipoprotein E knockout mice (ApoE-/-mice).. Methods: Two parallel exposure chambers were used for whole body exposure among ApoE knockout mice. One of the chambers was supplied with untreated ambient air (PM group) and the other chamber was treated with ambient air filtered by high-efficiency particulate air (HEPA) filter (FA group). Twenty mice were divided into two groups and exposed to ambient PM (n = 10 for PM group) or filtered air(n = 10 for FA group) for two months from January 18th to March 18th, 2010. During the exposure, the mass concentrations of PM2.5 and ...
TY - JOUR. T1 - Association of pathobiologic determinants of atherosclerosis in youth risk score and carotid artery intima-media thickness in asymptomatic young heterozygous familial hypercholesterolemia patients. AU - Cheng, Hao Ming. AU - Ye, Zhong Xuan. AU - Charng, Min Ji. PY - 2011/9. Y1 - 2011/9. N2 - Background: Familial hypercholesterolemia (FH) is an inherited disorder characterized by extremely high cholesterol level, accelerated atherosclerosis and premature cardiovascular disease.We need an early risk stratification method for this population. Arisk score formula to estimate the probability of advanced atherosclerosis using coronary heart disease risk factors was developed for persons 15-34 years of age by the Pathobiological Determinants of Atherosclerosis in Youth (PDAY) study. This studys aim was to investigate the relation between PDAY risk score and carotid intima-media thickness (IMT) and inflammation markers in asymptomatic young FH subjects. Methods: We included 23 ...
Thank you for your interest in spreading the word on Stroke.. NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address. ...
TY - JOUR. T1 - Significance of a positive family history for coronary heart disease in patients with a zero coronary artery calcium score (from the multi-ethnic study of atherosclerosis). AU - Cohen, Randy. AU - Budoff, Matthew. AU - McClelland, Robyn L.. AU - Sillau, Stefan. AU - Burke, Gregory. AU - Blaha, Michael. AU - Szklo, Moyses. AU - Uretsky, Seth. AU - Rozanski, Alan. AU - Shea, Steven. PY - 2014/10/15. Y1 - 2014/10/15. N2 - Although a coronary artery calcium (CAC) score of 0 is associated with a very low 10-year risk for cardiac events, this risk is nonzero. Subjects with a family history of coronary heart disease (CHD) has been associated with more subclinical atherosclerosis than subjects without a family history of CHD. The purpose of this study was to assess the significance of a family history for CHD in subjects with a CAC score of 0. The Multi-Ethnic Study of Atherosclerosis cohort includes 6,814 participants free of clinical cardiovascular disease (CVD) at baseline. Positive ...

Atherosclerosis | definition of atherosclerosis by Medical dictionaryAtherosclerosis | definition of atherosclerosis by Medical dictionary

... atherosclerosis explanation free. What is atherosclerosis? Meaning of atherosclerosis medical term. What does atherosclerosis ... Looking for online definition of atherosclerosis in the Medical Dictionary? ... Atherosclerosis. Definition. Atherosclerosis is the build up of a waxy plaque on the inside of blood vessels. In Greek, athere ... Atherosclerosis is complex. Its exact cause is still unknown. It is thought that atherosclerosis is caused by a response to ...
more infohttp://medical-dictionary.thefreedictionary.com/atherosclerosis

Click to printClick to print

Rice Bran Extract Reduces the Risk of Atherosclerosis in Post-Menopausal Vietnamese Women. J Nutr Sci Vitaminol (Tokyo). 2016; ...
more infohttps://www.realnatural.org/rice-bran-reduces-body-fat-cholesterol/

AtherosclerosisAtherosclerosis

... , (ath-er-o-skler-O-sis) comes from the Greek words athero - meaning gruel or paste and sclerosis meaning ... Diseases Associated with Atherosclerosis. Atherosclerosis can affect any artery in the body, including arteries in the heart, ... Precisely what causes atherosclerosis remains unknown, but research suggests that atherosclerosis is a slow, complex disease ... Atherosclerosis, (ath-er-o-skler-O-sis) comes from the Greek words athero - meaning gruel or paste and sclerosis meaning ...
more infohttps://www.news-medical.net/health/Atherosclerosis.aspx

Atherosclerosis | HealthCentralAtherosclerosis | HealthCentral

Atherosclerosis also causes a great deal of serious illness by reducing the flow of blood in other major arteries, such as to ... Why does atherosclerosis occur in the coronary arteries of some people but not others? An interplay of many factors including ... Atherosclerosis is responsible for more deaths in the U.S. than any other condition. Atherosclerotic heart disease, involving ... Unfortunately, atherosclerosis produces no symptoms until the damage to the arteries is severe enough to restrict blood flow. ...
more infohttps://www.healthcentral.com/encyclopedia/atherosclerosis

AtherosclerosisAtherosclerosis

... of the extremities - Atherosclerosis can narrow the major arteries that supply blood to the legs, especially ... It is possible to have atherosclerosis for many years without having symptoms. If you experience symptoms of an atherosclerosis ... Atherosclerosis leads to the number one cause of death in the United States and many other countries for both men and women: ... Abdomen - When atherosclerosis narrows the arteries to the intestines, there may be dull or cramping pain in the middle of the ...
more infohttps://www.womenshealthmag.com/health/a19949244/atherosclerosis/

Atherosclerosis | The BMJAtherosclerosis | The BMJ

Atherosclerosis. Br Med J 1968; 1 doi: https://doi.org/10.1136/bmj.1.5585.168-c (Published 20 January 1968) Cite this as: Br ...
more infohttp://www.bmj.com/content/1/5585/168.4

Atherosclerosis - FoodAtherosclerosis - Food

By Tim Cutcliffe The International Plant Sterols and Stanols Association (IPSSA) is today launching an initiative to provide more information on the importance of LDL- cholesterol as a key modifiable risk factor for heart disease, and what people can do in general to... ...
more infohttps://www.nutraingredients.com/tag/keyword/Food/Atherosclerosis

Atherosclerosis | pathology | Britannica.comAtherosclerosis | pathology | Britannica.com

Atherosclerosis is the most common arterial abnormality characterized as arteriosclerosis, which is defined by ... Atherosclerosis, chronic disease caused by the deposition of fats, cholesterol, calcium, and other substances in the innermost ... are among the factors that contribute to an increased risk of developing atherosclerosis. Men develop atherosclerosis more ... Atherosclerosis, chronic disease caused by the deposition of fats, cholesterol, calcium, and other substances in the innermost ...
more infohttps://www.britannica.com/science/atherosclerosis

Biochemistry of Atherosclerosis - Google BooksBiochemistry of Atherosclerosis - Google Books

... atherosclerosis will be the major cause of death from disease by the year 2020. Atherosclerosis is an extremely complex, ... At its present rate of growth, atherosclerosis will be the major cause of death from disease by the year 2020. Atherosclerosis ... Biochemistry of Atherosclerosis. Volume 1 of Advances in Biochemistry in Health and Disease. Volume 1 of Advances in ... Atherosclerosis.html?id=C-FqAAAAMAAJ&utm_source=gb-gplus-shareBiochemistry of Atherosclerosis. ...
more infohttps://books.google.com/books?id=C-FqAAAAMAAJ&q=adhesion&dq=related:ISBN3764361549&source=gbs_word_cloud_r&hl=en

Atherosclerosis | HypertensionAtherosclerosis | Hypertension

Our mission is to build healthier lives, free of cardiovascular diseases and stroke. That single purpose drives all we do. The need for our work is beyond question. Find Out More about the American Heart Association. ...
more infohttp://hyper.ahajournals.org/collection/atherosclerosis-0

Atherosclerosis | Causes, Symptoms & TreatmentAtherosclerosis | Causes, Symptoms & Treatment

Atherosclerosis in arteries that carry blood to the arms, legs, and pelvis can cause pain while walking, numbness and, in men, ... Atherosclerosis is a hardening of the arteries that results from a buildup of plaque. Plaque is made up of cholesterol, fat, ... Atherosclerosis in arteries that carry blood to the heart may cause chest pain and pressure - also symptoms of a heart attack. ... Atherosclerosis may not produce symptoms until it is at an advanced stage, at which time medical attention is needed. Symptoms ...
more infohttps://www.innerbody.com/diseases-conditions/atherosclerosis

Atherosclerosis | American Heart AssociationAtherosclerosis | American Heart Association

The American Heart Association explains how atherosclerosis starts, how atherosclerosis is affected by high cholesterol levels ... What is atherosclerosis? Atherosclerosis is a type of arteriosclerosis. ... Atherosclerosis. Atherosclerosis and cholesterol. When plaque (fatty deposits) clogs your arteries, thats called ... Atherosclerosis is a slow, progressive disease that may start in childhood. In some people, atherosclerosis progresses rapidly ...
more infohttp://www.heart.org/en/health-topics/cholesterol/about-cholesterol/atherosclerosis

Is Reversing Atherosclerosis Possible?Is Reversing Atherosclerosis Possible?

Gradually, the amount of plaque that forms will narrow your arteries While reversing atherosclerosis isnt feasible, you can ... Atherosclerosis is serious and life-threatening. If you have high cholesterol, excess cholesterol builds in the arteries ... What is atherosclerosis?. The word "atherosclerosis" comes from the Greek words "athero"("paste") and "sclerosis" ("hardness ... Atherosclerosis overview. Atherosclerosis, more commonly known as heart disease, is a serious and life-threatening condition. ...
more infohttps://www.healthline.com/health/heart-disease/reversing-atherosclerosis

Atherosclerosis - Journal - ElsevierAtherosclerosis - Journal - Elsevier

Atherosclerosis has an open access mirror journal Atherosclerosis: X, sharing the same aims and scope, editorial team, ... Official Journal of the European Atherosclerosis Society.. Atherosclerosis has an open access mirror journal Atherosclerosis: X ... Atherosclerosis has an open access mirror journal Atherosclerosis: X, sharing the same aims and scope, editorial team, ... Atherosclerosis brings together, from all sources, papers concerned with investigation on atherosclerosis, its risk factors and ...
more infohttps://www.journals.elsevier.com/atherosclerosis/

Atherosclerosis: MedlinePlus Medical Encyclopedia ImageAtherosclerosis: MedlinePlus Medical Encyclopedia Image

Atherosclerosis is a disease of the arteries in which fatty material is deposited in the vessel wall, resulting in narrowing ... Atherosclerosis is a disease of the arteries in which fatty material is deposited in the vessel wall, resulting in narrowing ...
more infohttps://medlineplus.gov/ency/imagepages/18050.htm

Atherosclerosis (Arteriosclerosis) | UPMCAtherosclerosis (Arteriosclerosis) | UPMC

Atherosclerosis, or a hardening of the arteries, is a type of arteriosclerosis. Learn about the symptoms and the personalized ... What Is Atherosclerosis, or Hardening of the Arteries?. Learn More About Atherosclerosis Risks. From our Health Library at UPMC ... What Is Atherosclerosis?. Atherosclerosis, also referred to as arteriosclerosis, causes a hardening of the arteries due to ... Atherosclerosis risk factors. At the UPMC Heart and Vascular Institute, we can screen people for atherosclerosis risk factors ...
more infohttps://www.upmc.com/services/heart-vascular/conditions-treatments/atherosclerosis

Cannabinoids and atherosclerosis.  - PubMed - NCBICannabinoids and atherosclerosis. - PubMed - NCBI

Cannabinoids and atherosclerosis.. Fisar Z1.. Author information. 1. Charles University in Prague, First Faculty of Medicine, ... effects on atherosclerosis specially, is described at the close. ...
more infohttps://www.ncbi.nlm.nih.gov/pubmed/19591373

Antithrombin III and Atherosclerosis | SpringerLinkAntithrombin III and Atherosclerosis | SpringerLink

Since Duguids modification of Rokitanskys theory, atherosclerosis has been related to thrombogenesis. Several... ... The mechanisms leading to the initiation of atherosclerosis are very complex. ... J.L. Kadish, Fibrin and atherosclerosis. A hypothesis. Atherosclerosis 33:409-413 (1979).PubMedCrossRefGoogle Scholar ... J.R. OBrien, Antithrombin III and heparin clotting times in thrombosis and atherosclerosis. Thromb. Piathes. Haemorrh. 32:116- ...
more infohttps://link.springer.com/chapter/10.1007/978-1-4684-8616-2_6

Reversing atherosclerosis with one shotReversing atherosclerosis with one shot

... it might be possible to reverse atherosclerosis in humans with a simple injection. ... What to know about atherosclerosis Arteries carry blood from the heart to the rest of the body. Atherosclerosis occurs when ... For these reasons, atherosclerosis may lead to coronary heart disease, angina, peripheral artery disease, or chronic kidney ... Atherosclerosis: Skipping breakfast may double risk. Researchers find an additional reason as to why you shouldnt skip the ...
more infohttps://www.medicalnewstoday.com/articles/321788.php

Vascular Macrophages in AtherosclerosisVascular Macrophages in Atherosclerosis

... Hailin Xu,1 Jingxin Jiang,2 Wuzhen Chen,2,3 Wenlu Li,4 and Zhigang Chen2,3 ... Figure 1: Roles of macrophages in different stages of atherosclerosis progression. Atherosclerosis is initiated by the ... A. J. Lusis, "Atherosclerosis," Nature, vol. 407, no. 6801, pp. 233-241, 2000. View at Publisher · View at Google Scholar · ... thus motivating a number of researchers to study the pathophysiology of atherosclerosis over the past decades. Atherosclerosis ...
more infohttps://www.hindawi.com/journals/jir/2019/4354786/

atherosclerosis | Heartatherosclerosis | Heart

206 B Cell-Specific FC Gamma Receptor IIB Over-Expression Enhances Atherosclerosis by Inhibiting B1 Cells Andrew Sage, Deirdre ... 214 A Multiscale Haemorheological Computer-Based Model of Atherosclerosis: An In-depth Investigation of Erythrocytes-Driven ... The aorta can act as site of t cell priming and promotes a local cd4+ adaptive immune response in early stage atherosclerosis ... cardiopulmonary bypass and examining use of crp/oxidised low density lipoprotein complexes as a biomarker of atherosclerosis ...
more infohttps://heart.bmj.com/keyword/atherosclerosis?page=2

Atherosclerosis - ExRx.netAtherosclerosis - ExRx.net

The major culprit of atherosclerosis is thought (I dont know if they indeed found LDL in atheromas) to be type B LDL (the ... From what Ive gathered, the mechanism of atherosclerosis is apparently quite clear but there may be more than what have been ... associated with subclinical atherosclerosis independent of. each other, traditional lipids, and established risk factors, with ... no association between LDL size and atherosclerosis after. accounting for the concentrations of the two subclasses. ...
more infohttps://exrx.net/forum/viewtopic.php?p=80822

Atherosclerosis - ExRx.netAtherosclerosis - ExRx.net

The major culprit of atherosclerosis is thought (I dont know if they indeed found LDL in atheromas) to be type B LDL (the ... From what Ive gathered, the mechanism of atherosclerosis is apparently quite clear but there may be more than what have been ... associated with subclinical atherosclerosis independent of. each other, traditional lipids, and established risk factors, with ... no association between LDL size and atherosclerosis after. accounting for the concentrations of the two subclasses. ...
more infohttps://exrx.net/forum/viewtopic.php?p=80825

Atherosclerosis - iHerb.comAtherosclerosis - iHerb.com

Atherosclerosis indicates hardening of the blood vessels due to a buildup of plaque. Plaque consists of fatty deposits, ...
more infohttps://www.iherb.com/c/azelique/atherosclerosis

When Does Atherosclerosis Begin?When Does Atherosclerosis Begin?

For others, atherosclerosis can begin in a persons 20s or 30s, and even in children as young as 10. Read on to learn more ... Most people dont experience the life-threatening complications of atherosclerosis (hardening of the arteries) until middle age ... about the symptoms of atherosclerosis and when they begin. ...
more infohttps://www.healthline.com/health/heart-disease/atherosclerosis-when-it-starts
  • Cigarette/tobacco smoke-Smoking increases both the chance of developing atherosclerosis and the chance of dying from coronary heart disease. (thefreedictionary.com)
  • Inflammation due to injury or another underlying condition enhances the chance of developing atherosclerosis. (innerbody.com)
  • I'm trying to understand the correlation of diet, cholesterol, and fat with coronary heart disease (my father got an angina once) and apparently it boils down to atherosclerosis. (exrx.net)
  • Atherosclerosis can begin in the late teens, but it usually takes decades to cause symptoms. (thefreedictionary.com)
  • As a rule atherosclerosis does not cause symptoms until an artery becomes narrowed or blocked, once this happens symptoms may include angina and cramping leg pain when walking - when the flow of oxygen-rich blood to organs and other parts of the body is reduced. (news-medical.net)
  • However, some people with atherosclerosis have no signs or symptoms and may not be diagnosed until after a heart attack or stroke. (news-medical.net)
  • Atherosclerosis usually doesn't cause any symptoms until blood supply to an organ is reduced. (womenshealthmag.com)
  • Atherosclerosis may not produce symptoms until it is at an advanced stage, at which time medical attention is needed. (innerbody.com)
  • Atherosclerosis shows no symptoms until a complication occurs. (medlineplus.gov)
  • It is thought that atherosclerosis is caused by a response to damage to the endothelium from high cholesterol, high blood pressure, and cigarette smoking . (thefreedictionary.com)
  • A family history of cardiovascular disease , smoking, stress, obesity , and high blood cholesterol levels, particularly in association with LDLs, are among the factors that contribute to an increased risk of developing atherosclerosis. (britannica.com)
  • She also researches the regulation of genes involved in cholesterol metabolism by hormone factors, the molecular basis of diabetes-accelerated atherosclerosis, and the mechanisms of lipid abnormalities caused by protease inhibitors. (google.com)
  • Elevated levels of cholesterol, fat, sugar, and certain proteins are detectable in the blood and can be associated with atherosclerosis. (innerbody.com)
  • Healthy dietary changes and regular exercise are both very important parts of reducing high blood pressure and high cholesterol, two major contributors to atherosclerosis. (healthline.com)
  • Current therapies for atherosclerosis include the use of statins, which help to regulate cholesterol levels. (medicalnewstoday.com)
  • The major culprit of atherosclerosis is thought (I don't know if they indeed found LDL in atheromas) to be type B LDL (the smaller more dense one as opposed to type A LDL) because it's always present, small enough, and by its job, travels from the liver to the tissues (to deliver cholesterol) so at one time it must try to pass the arterial wall to reach the target tissue. (exrx.net)
  • The clearest picture of inflammation's role in the onset of atherosclerosis comes from investigations into low-density lipoprotein, a.k.a. bad cholesterol. (scientificamerican.com)
  • Scientists have long known that although the body needs LDL and cholesterol, excessive amounts promote atherosclerosis. (scientificamerican.com)
  • New research demonstrates that injecting synthetically designed nanofibers in mice helps to break up the arterial plaque that is a hallmark of atherosclerosis. (medicalnewstoday.com)
  • Currently, it has been well established that atherosclerosis is both a component associated with metabolic disorder and a chronic inflammatory process in the arterial wall, which is induced initially by the subendothelial deposition of apolipoprotein B-containing lipoproteins (apoB-LPs) [ 3 ]. (hindawi.com)
  • Once thought of as a lipid storage disease, atherosclerosis is now also recognized as a chronic inflammatory condition that increases risk of coronary and cerebrovascular disease. (qiagen.com)
  • Atherosclerosis , more commonly known as heart disease, is a serious and life-threatening condition. (healthline.com)
  • The mechanisms leading to the initiation of atherosclerosis are very complex. (springer.com)
  • Macrophages, the major immune cell population in atherosclerotic lesions, have been shown to play critical roles in all stages of atherosclerosis, including the initiation and progression of advanced atherosclerosis. (hindawi.com)
  • The term atherogenic is used for substances or processes that cause atherosclerosis. (wikipedia.org)
  • This revised conception suggests new ideas for detecting and treating atherosclerosis. (scientificamerican.com)
  • Certain drugs can reduce the risks associated with atherosclerosis. (britannica.com)
  • Atherosclerosis generally starts when a person is young and worsens with age. (wikipedia.org)
  • Some people experience rapidly progressing atherosclerosis during their thirties, others during their fifties or sixties. (thefreedictionary.com)
  • In some people, atherosclerosis progresses rapidly in their 30s. (heart.org)
  • Many people don't know they have atherosclerosis until it starts causing health problems. (cardiosmart.org)
  • Atherosclerosis can be managed (and prevented) with lifestyle changes and medical intervention. (innerbody.com)
  • A listing of Atherosclerosis medical research trials actively recruiting patient volunteers. (centerwatch.com)
  • The first step in diagnosing atherosclerosis is a physical exam. (innerbody.com)
  • The UPMC Heart and Vascular Institute's multidisciplinary team of cardiologists, radiologists, surgeons, rehabilitation specialists, physical therapists, and nutritionists provides a full range of advanced atherosclerosis treatments. (upmc.com)