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.
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).
The principal sterol of all higher animals, distributed in body tissues, especially the brain and spinal cord, and in animal fats and oils.
Substances used to lower plasma CHOLESTEROL levels.
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.
Cholesterol which is contained in or bound to low density lipoproteins (LDL), including CHOLESTEROL ESTERS and free cholesterol.
Cholesterol present in food, especially in animal products.
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.
Compounds that inhibit HMG-CoA reductases. They have been shown to directly lower cholesterol synthesis.
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.
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.
A chlorinated epoxy compound used as an industrial solvent. It is a strong skin irritant and carcinogen.
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.
A diet that contributes to the development and acceleration of ATHEROGENESIS.
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)
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.
A derivative of LOVASTATIN and potent competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It may also interfere with steroid hormone production. Due to the induction of hepatic LDL RECEPTORS, it increases breakdown of LDL CHOLESTEROL.
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.
An individual having different alleles at one or more loci regarding a specific character.
A fungal metabolite isolated from cultures of Aspergillus terreus. The compound is a potent anticholesteremic agent. It inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It also stimulates the production of low-density lipoprotein receptors in the liver.
An individual in which both alleles at a given locus are identical.
Cholesterol which is contained in or bound to high-density lipoproteins (HDL), including CHOLESTEROL ESTERS and free cholesterol.
7-carbon saturated monocarboxylic acids.
Conditions with excess LIPIDS in the blood.
Any procedure in which blood is withdrawn from a donor, a portion is separated and retained and the remainder is returned to the donor.
Proteolytic enzymes that are involved in the conversion of protein precursors such as peptide prohormones into PEPTIDE HORMONES. Some are ENDOPEPTIDASES, some are EXOPEPTIDASES.
An antilipemic fungal metabolite isolated from cultures of Nocardia autotrophica. It acts as a competitive inhibitor of HMG CoA reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES).
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).
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.
Azoles of one NITROGEN and two double bonds that have aromatic chemical properties.
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.
High-molecular-weight insoluble polymers that contain functional cationic groups capable of undergoing exchange reactions with anions.
Polymers of high molecular weight which at some stage are capable of being molded and then harden to form useful components.
A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.
Dried, ripe seeds of PLANTAGO PSYLLIUM; PLANTAGO INDICA; and PLANTAGO OVATA. Plantain seeds swell in water and are used as demulcents and bulk laxatives.
Single pavement layer of cells which line the luminal surface of the entire vascular system and regulate the transport of macromolecules and blood components.
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.
The main trunk of the systemic arteries.
Substances that lower the levels of certain LIPIDS in the BLOOD. They are used to treat HYPERLIPIDEMIAS.
A strongly basic anion exchange resin whose main constituent is polystyrene trimethylbenzylammonium Cl(-) anion.
A condition of elevated levels of TRIGLYCERIDES in the blood.
The record of descent or ancestry, particularly of a particular condition or trait, indicating individual family members, their relationships, and their status with respect to the trait or condition.
A mixture of very-low-density lipoproteins (VLDL), particularly the triglyceride-poor VLDL, with slow diffuse electrophoretic mobilities in the beta and alpha2 regions which are similar to that of beta-lipoproteins (LDL) or alpha-lipoproteins (HDL). They can be intermediate (remnant) lipoproteins in the de-lipidation process, or remnants of mutant CHYLOMICRONS and VERY-LOW-DENSITY LIPOPROTEINS which cannot be metabolized completely as seen in FAMILIAL DYSBETALIPOPROTEINEMIA.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
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.
Highly crosslinked and insoluble basic anion exchange resin used as anticholesteremic. It may also may reduce triglyceride levels.
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.
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.
Nutrient blood vessels which supply the walls of large arteries or veins.
A corneal disease in which there is a deposition of phospholipid and cholesterol in the corneal stroma and anterior sclera.
Enzymes that catalyze the reversible reduction of alpha-carboxyl group of 3-hydroxy-3-methylglutaryl-coenzyme A to yield MEVALONIC ACID.
The physiological widening of BLOOD VESSELS by relaxing the underlying VASCULAR SMOOTH MUSCLE.
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.
An abnormal lipoprotein present in large amounts in patients with obstructive liver diseases such as INTRAHEPATIC CHOLESTASIS. LP-X derives from the reflux of BILE lipoproteins into the bloodstream. LP-X is a low-density lipoprotein rich in free CHOLESTEROL and PHOSPHOLIPIDS but poor in TRIGLYCERIDES; CHOLESTEROL ESTERS; and protein.
Pathological conditions involving the CARDIOVASCULAR SYSTEM including the HEART; the BLOOD VESSELS; or the PERICARDIUM.
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.
A family of sterols commonly found in plants and plant oils. Alpha-, beta-, and gamma-isomers have been characterized.
A class of organic compounds known as STEROLS or STEROIDS derived from plants.
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.
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.
A membrane-bound cytochrome P450 enzyme that catalyzes the 7-alpha-hydroxylation of CHOLESTEROL in the presence of molecular oxygen and NADPH-FERRIHEMOPROTEIN REDUCTASE. This enzyme, encoded by CYP7, converts cholesterol to 7-alpha-hydroxycholesterol which is the first and rate-limiting step in the synthesis of BILE ACIDS.
A type of familial lipid metabolism disorder characterized by a variable pattern of elevated plasma CHOLESTEROL and/or TRIGLYCERIDES. Multiple genes on different chromosomes may be involved, such as the major late transcription factor (UPSTREAM STIMULATORY FACTORS) on CHROMOSOME 1.
A genus in the family ROSACEAE of shrubs and small trees native to the North Temperate Zone. It is best known for a traditional medication for the heart.
Physiological processes in biosynthesis (anabolism) and degradation (catabolism) of LIPIDS.
Any of various animals that constitute the family Suidae and comprise stout-bodied, short-legged omnivorous mammals with thick skin, usually covered with coarse bristles, a rather long mobile snout, and small tail. Included are the genera Babyrousa, Phacochoerus (wart hogs), and Sus, the latter containing the domestic pig (see SUS SCROFA).
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.
Pathological processes of CORONARY ARTERIES that may derive from a congenital abnormality, atherosclerotic, or non-atherosclerotic cause.
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.
The veins and arteries of the HEART.
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.
Genetically developed small pigs for use in biomedical research. There are several strains - Yucatan miniature, Sinclair miniature, and Minnesota miniature.
A powerful vasodilator used in emergencies to lower blood pressure or to improve cardiac function. It is also an indicator for free sulfhydryl groups in proteins.
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
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.
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.
Drugs used to cause dilation of the blood vessels.
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.
A method of studying a drug or procedure in which both the subjects and investigators are kept unaware of who is actually getting which specific treatment.
A heterogeneous group of disorders characterized by HYPERGLYCEMIA and GLUCOSE INTOLERANCE.
Elements of limited time intervals, contributing to particular results or situations.
The outward appearance of the individual. It is the product of interactions between genes, and between the GENOTYPE and the environment.
Any member of the group of ENDOPEPTIDASES containing at the active site a serine residue involved in catalysis.
Steroid acids and salts. The primary bile acids are derived from cholesterol in the liver and usually conjugated with glycine or taurine. The secondary bile acids are further modified by bacteria in the intestine. They play an important role in the digestion and absorption of fat. They have also been used pharmacologically, especially in the treatment of gallstones.
The innermost layer of an artery or vein, made up of one layer of endothelial cells and supported by an internal elastic lamina.
Cell surface proteins that bind lipoproteins with high affinity. Lipoprotein receptors in the liver and peripheral tissues mediate the regulation of plasma and cellular cholesterol metabolism and concentration. The receptors generally recognize the apolipoproteins of the lipoprotein complex, and binding is often a trigger for endocytosis.
Fatty acids which are unsaturated in only one position.
Steroids with a hydroxyl group at C-3 and most of the skeleton of cholestane. Additional carbon atoms may be present in the side chain. (IUPAC Steroid Nomenclature, 1987)
A neurotransmitter found at neuromuscular junctions, autonomic ganglia, parasympathetic effector junctions, a subset of sympathetic effector junctions, and at many sites in the central nervous system.
Conditions with abnormally elevated levels of LIPOPROTEINS in the blood. They may be inherited, acquired, primary, or secondary. Hyperlipoproteinemias are classified according to the pattern of lipoproteins on electrophoresis or ultracentrifugation.
The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.
Regular course of eating and drinking adopted by a person or animal.
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).
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.
The transmission of traits encoded in GENES from parent to offspring.
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.
Pathological processes involving any part of the AORTA.
The vessels carrying blood away from the heart.
A diet that contains limited amounts of fat with less than 30% of calories from all fats and less than 10% from saturated fat. Such a diet is used in control of HYPERLIPIDEMIAS. (From Bondy et al, Metabolic Control and Disease, 8th ed, pp468-70; Dorland, 27th ed)
Proteins that bind to and transfer CHOLESTEROL ESTERS between LIPOPROTEINS such as LOW-DENSITY LIPOPROTEINS and HIGH-DENSITY LIPOPROTEINS.
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.
A plant genus of the family ROSACEAE. The common names of chokeberry or chokecherry are also used for some species of PRUNUS.
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.
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.
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.
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).
An enzyme that catalyzes the formation of cholesterol esters by the direct transfer of the fatty acid group from a fatty acyl CoA derivative. This enzyme has been found in the adrenal gland, gonads, liver, intestinal mucosa, and aorta of many mammalian species. EC 2.3.1.26.
Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.
An autosomal recessive disorder of lipid metabolism. It is caused by mutation of the microsomal triglyceride transfer protein that catalyzes the transport of lipids (TRIGLYCERIDES; CHOLESTEROL ESTERS; PHOSPHOLIPIDS) and is required in the secretion of BETA-LIPOPROTEINS (low density lipoproteins or LDL). Features include defective intestinal lipid absorption, very low serum cholesterol level, and near absent LDL.
A fibrous cord that connects the muscles in the back of the calf to the HEEL BONE.
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.
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.
An island republic in the eastern Mediterranean Sea. Its capital is Nicosia. It was colonized by the Phoenicians and ancient Greeks and ruled successively by the Assyrian, Persian, Ptolemaic, Roman, and Byzantine Empires. It was under various countries from the 12th to the 20th century but became independent in 1960. The name comes from the Greek Kupros, probably representing the Sumerian kabar or gabar, copper, famous in historic times for its copper mines. The cypress tree is also named after the island. (From Webster's New Geographical Dictionary, 1988, p308 & Room, Brewer's Dictionary of Names, 1992, p134)
An essential amino acid that is physiologically active in the L-form.
Therapy with two or more separate preparations given for a combined effect.
The portion of the descending aorta proceeding from the arch of the aorta and extending to the DIAPHRAGM, eventually connecting to the ABDOMINAL AORTA.
Inhaling and exhaling the smoke of burning TOBACCO.
Non-nucleated disk-shaped cells formed in the megakaryocyte and found in the blood of all mammals. They are mainly involved in blood coagulation.
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.
Genes that influence the PHENOTYPE only in the homozygous state.
Generic term for diseases caused by an abnormal metabolic process. It can be congenital due to inherited enzyme abnormality (METABOLISM, INBORN ERRORS) or acquired due to disease of an endocrine organ or failure of a metabolically important organ such as the liver. (Stedman, 26th ed)
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.
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.
Lipid-laden macrophages originating from monocytes or from smooth muscle cells.
Proteins which are present in or isolated from vegetables or vegetable products used as food. The concept is distinguished from PLANT PROTEINS which refers to non-dietary proteins from plants.
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.
PRESSURE of the BLOOD on the ARTERIES and other BLOOD VESSELS.
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.
The minute vessels that collect blood from the capillary plexuses and join together to form veins.
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.
An NADPH-dependent enzyme that catalyzes the conversion of L-ARGININE and OXYGEN to produce CITRULLINE and NITRIC OXIDE.
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.
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.
A competitive inhibitor of nitric oxide synthetase.
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.
Cell adhesion molecule and CD antigen that mediates the adhesion of neutrophils and monocytes to activated platelets and endothelial cells.
Peroxidase catalyzed oxidation of lipids using hydrogen peroxide as an electron acceptor.
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.
A naturally occurring prostaglandin that has oxytocic, luteolytic, and abortifacient activities. Due to its vasocontractile properties, the compound has a variety of other biological actions.
An enzyme of the hydrolase class that catalyzes the reaction of triacylglycerol and water to yield diacylglycerol and a fatty acid anion. The enzyme hydrolyzes triacylglycerols in chylomicrons, very-low-density lipoproteins, low-density lipoproteins, and diacylglycerols. It occurs on capillary endothelial surfaces, especially in mammary, muscle, and adipose tissue. Genetic deficiency of the enzyme causes familial hyperlipoproteinemia Type I. (Dorland, 27th ed) EC 3.1.1.34.
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)
Part of the arm in humans and primates extending from the ELBOW to the WRIST.
A mutation caused by the substitution of one nucleotide for another. This results in the DNA molecule having a change in a single base pair.
Connective tissue cells which secrete an extracellular matrix rich in collagen and other macromolecules.
The relationship between the dose of an administered drug and the response of the organism to the drug.
Uptake of substances through the lining of the INTESTINES.
Variation in a population's DNA sequence that is detected by determining alterations in the conformation of denatured DNA fragments. Denatured DNA fragments are allowed to renature under conditions that prevent the formation of double-stranded DNA and allow secondary structure to form in single stranded fragments. These fragments are then run through polyacrylamide gels to detect variations in the secondary structure that is manifested as an alteration in migration through the gels.

Distinct and combined vascular effects of ACE blockade and HMG-CoA reductase inhibition in hypertensive subjects. (1/3532)

Hypercholesterolemia and hypertension are frequently associated with elevated sympathetic activity. Both are independent cardiovascular risk factors and both affect endothelium-mediated vasodilation. To identify the effects of cholesterol-lowering and antihypertensive treatments on vascular reactivity and vasodilative capacity, we studied 30 hypercholesterolemic hypertensive subjects. They received placebo for 4 weeks, either enalapril or simvastatin for 14 weeks, and, finally, both medications for an additional 14 weeks. Postischemic forearm blood flow (MFBF) and minimal vascular resistance (mFVR) were used as indices of vasodilative capacity and structural vascular damage, respectively. Total (resting-stress-recovery phases) cardiovascular (blood pressure [BP] and heart rate [HR]) and regional hemodynamic (FBF and FVR) reactivity to stressful stimuli were calculated as area-under-the-curve (auc) (valuextime). Compared with baseline levels, simvastatin reduced total (TOT-C) and LDL cholesterol (LDL-C) (1.27 mmol/L, P<0.001 and 1.33 mmol/L, P<0.001, respectively). Enalapril also reduced TOT-C and LDL-C (0.6 mmol/L, P<0.001 and 0.58 mmol/L, P<0.05, respectively). MFBF was increased substantially by both treatments (P<0.001). Enalapril had a greater effect (-1.7 arbitrary units (AU), P<0.001) than simvastatin (-0.6 AU, P<0.05) on mFVR. During stress, FBF increased more with enalapril (4.4 FBFxminutes, P<0.001) than with simvastatin (1.8 FBFxminutes, P<0.01). Conversely, FVR stress response was reduced more with enalapril (9.1 FVRxminutes, P<0.001) than with simvastatin (2.9 FVRxminutes, P<0.01). During combination treatment, a significant (0.001>P<0.05) additive effect on hypercholesterolemia, structural vascular damage, BP, and FVR was shown. The findings suggest that angiotensin-converting enzyme (ACE) inhibition induces a larger reduction than HMG-CoA reductase blockade in vascular reactivity and structural damage in hypercholesterolemic hypertensive subjects.  (+info)

Protective effect of dietary tomato against endothelial dysfunction in hypercholesterolemic mice. (2/3532)

The effects of dietary ingestion of tomato were studied in mice that had been made hypercholesterolemic by feeding atherogenic diets. Mice which had been fed on the atherogenic diet without tomato for 4 months had significantly increased plasma lipid peroxide, and the vaso-relaxing activity in the aorta induced by acetylcholine (ACh) was harmed when compared with mice fed on a common commercial diet. On the other hand, mice which had been fed on the atherogenic diet containing 20% (w/w) lyophilized powder of tomato showed less increase in the plasma lipid peroxide level, and ACh-induced vaso-relaxation was maintained at the same level as that in normal mice. These results indicate that tomato has a preventive effect on atherosclerosis by protecting plasma lipids from oxidation.  (+info)

Effects of docosahexaenoic and eicosapentaenoic acid on lipid metabolism, eicosanoid production, platelet aggregation and atherosclerosis in hypercholesterolemic rats. (3/3532)

Exogenously hypercholesterolemic (ExHC) rats were fed on an atherogenic diet supplemented with 1% each of either ethyl ester docosahexaenoic acid [EE-DHA, 22:6(n-3)], ethyl ester eicosapentaenoic acid [EE-EPA, 20:5(n-3)] or safflower oil (SO) for 6 months. The rats fed on the diets containing EE-EPA or EE-DHA, compared with those fed on SO, had lower serum cholesterol and triacylglycerol levels, less aggregation of platelets and slower progress of intimal thickening in the ascending aorta. Relative to the SO-fed rats, both of the (n-3) fatty acid-fed rats had a significantly reduced proportion of arachidonic acid in the platelet and aortic phospholipids, and lower production of thromboxane A2 by platelets and of prostacyclin by the aorta. These results suggest that EPA and DHA are similarly involved in preventing atherosclerosis development by reducing hypercholesterolemia and modifying the platelet functions.  (+info)

Comparative hypocholesterolemic effects of five animal oils in cholesterol-fed rats. (4/3532)

The hypocholesterolemic efficacy of various animal oils was compared in rats given a cholesterol-enriched diet. After acclimatization for one week, male F344 DuCrj rats (8 weeks of age) that had been fed with a conventional diet were assigned to diets containing 5% of oil from emu (Dromaius), Japanese Sika deer (Cervus nippon yesoensis, Heude), sardine, beef tallow, or lard with 0.5% cholesterol for 6 weeks. After this feeding period, the concentrations of serum total cholesterol and of very-low-density lipoprotein + intermediate-density lipoprotein + low-density lipoprotein-cholesterol in the sardine oil group were significantly lower than those in the other groups. The serum high-density lipoprotein-cholesterol concentration in the Japanese Sika deer oil group was significantly higher than that in the other groups. The atherosclerotic index and liver cholesterol concentration in the sardine oil and Japanese Sika deer oil groups were significantly lower than those in the other groups. The fecal cholesterol excretion by the Japanese Sika deer oil group was significantly higher than that of the other groups, except for the sardine oil group, and the fecal bile acid excretion by the sardine oil group was significantly higher than that of the other groups, except for the lard group. These results suggest that Japanese Sika deer oil reduced the atherosclerotic index and liver cholesterol concentration in the presence of excess cholesterol in the diet as well as sardine oil did by increasing the excretion of cholesterol from the intestines of rats.  (+info)

Comparison of synthetic saponin cholesterol absorption inhibitors in rabbits: evidence for a non-stoichiometric, intestinal mechanism of action. (5/3532)

The hypocholesterolemic activities of pamaqueside and tiqueside, two structurally similar saponins, were evaluated in cholesterol-fed rabbits. The pharmacological profiles of the saponins were virtually identical: both dose-dependently decreased the intestinal absorption of labeled cholesterol 25-75%, increased fecal neutral sterol excretion up to 2.5-fold, and decreased hepatic cholesterol content 10-55%. High doses of pamaqueside (>5 mg/kg) or tiqueside (>125 mg/kg) completely prevented hypercholesterolemia. Decreases in plasma and hepatic cholesterol levels were strongly correlated with increased neutral sterol excretion. Ratios of neutral sterol excreted to pamaqueside administered were greater than 1:1 at all doses, in opposition to the formation of a stoichiometric complex previously suggested for tiqueside and other saponins. Ratios in tiqueside-treated rabbits were less than unity, a reflection of its lower potency. Pamaqueside-treated rabbits exhibited a more rapid decline in plasma cholesterol concentrations than control animals fed a cholesterol-free diet, indicating that the compound also inhibited the absorption of biliary cholesterol. Intravenous administration of pamaqueside had no effect on plasma cholesterol levels despite plasma levels twice those observed in rabbits given pamaqueside orally. These data indicate that pamaqueside and tiqueside induce hypocholesterolemia by blocking lumenal cholesterol absorption via a mechanism that apparently differs from the stoichiometric complexation of cholesterol hypothesized for other saponins.  (+info)

Identification of a novel Arg-->Cys mutation in the LDL receptor that contributes to spontaneous hypercholesterolemia in pigs. (6/3532)

We previously carried out genetic and metabolic studies in a partially inbred herd of pigs carrying cholesterol-elevating mutations. Quantitative pedigree analysis indicated that apolipoprotein (apo)B and a second major gene were responsible for the hypercholesterolemia in these animals. In this study, we assessed LDL receptor function by three different methods: ligand blots of liver membranes using beta-very low density lipoprotein (VLDL) as a ligand; low density lipoprotein (LDL)-dependent proliferation of T-lymphocytes; and direct binding of 125I-labeled LDL to cultured skin fibroblasts. All three methods demonstrated that LDL receptor ligands bound with decreased affinity to the LDL receptor in these animals. In skin fibroblasts from the hypercholesterolemic pigs, the Kd of binding was about 4-fold higher than in cells from normal pigs. The cDNA of the pig LDL receptor from normal and hypercholesterolemic pigs was isolated and sequenced. We identified a missense mutation that results in an Arg'Cys substitution at the position corresponding to Arg94 of the human LDL receptor. The mutation is in the third repeat of the ligand binding domain of the receptor. By single-stranded conformational polymorphism (SSCP) analysis, we studied the relationship between LDL receptor genotype and plasma cholesterol phenotype. In contrast to humans, the hypercholesterolemia associated with the LDL receptor mutation in pigs was expressed as a recessive trait. The LDL receptor mutation made a far more significant contribution to hypercholesterolemia than did the apoB mutation, consistent with observations made in human subjects with apoB mutations. Within each genotypic group (mutated apoB or mutated receptor), there was a wide range in plasma cholesterol. As the animals were on a well-controlled low-fat diet, this suggests that there are additional genetic factors that influence the penetrance of cholesterol-elevating mutations.  (+info)

Macroscopic distribution of coronary atherosclerotic lesions in cholesterol-fed rabbits. (7/3532)

In the present study we macroscopically examined a change in the distribution of coronary atherosclerosis in cholesterol-fed rabbits. Rabbits were fed a cholesterol-enriched diet for 15 weeks, then replaced by a normal diet, and were sacrificed at 15, 24, 32 and 42 weeks after the start of the experiment. The coronary atherosclerosis in the cholesterol-fed rabbits was distributed more densely in the proximal portion than in the middle and distal portions, and the lesions were severe at 24 and 32 weeks after the start of the experiment. comparison of lesions in the three portions at these time points showed that the percentages of lesion areas in the proximal portion, the middle portion and the distal portion were approximately 51%, 21 to 25% and 0.2 to 3.7%, respectively. Macroscopic observation of the coronary atherosclerotic lesions showed that the lesions formed over the vessel lumen in the proximal portion within the range of approximately 5 mm from the orifice of the left coronary artery. In the middle portion, the lesions formed predominantly around the orifices of branches as small patchy lesions from 1 to 3 mm in diameter. These findings support previous histopathological reports that suggested that the incidence of stenosis in the proximal portion was high, and the incidence of lesion occurrence in the middle and the distal portions varied. The method, macroscopical investigation of the coronary artery, is useful for analyzing coronary atherosclerosis in the rabbit.  (+info)

Variability in meta-analytic results concerning the value of cholesterol reduction in coronary heart disease: a meta-meta-analysis. (8/3532)

Despite official support for the efficacy of cholesterol reduction, considerable controversy exists, and meta-analyses of this topic have produced conflicting results. The authors assessed the variability of meta-analyses, evaluating the cardiovascular value of cholesterol reduction while attempting to explain the variability. Metaanalyses were identified by electronic search and citation tracking. Included were those conducted prior to 1995 that dealt with cholesterol reduction and total mortality, cardiovascular mortality, or nonfatal cardiovascular disease. In addition to extracting odds ratios for total mortality, cardiovascular mortality, and nonfatal cardiovascular disease, the authors encoded methodological variables, publication variables, and data concerning investigators' backgrounds. Twenty-three meta-analyses were reviewed, and 15 concluded that cholesterol reduction was beneficial. Summary odds ratios for total mortality were heterogeneous, generally failing to support the value of cholesterol reduction. Odds ratios depended on inclusion criteria and investigator variables. Odds ratios for cardiovascular mortality and for nonfatal cardiovascular disease were more homogeneous and supported the value of cholesterol reduction. Methodologically better meta-analyses tended to report more beneficial odds ratios. Although "supportiveness" of the value of cholesterol reduction was associated with inclusion/exclusion criteria and publication variables, the primary outcome variable related to supportiveness was the statistical significance of the odds ratios for cardiovascular mortality.  (+info)

TY - JOUR. T1 - T helper-cell phenotype regulates atherosclerosis in mice under conditions of mild hypercholesterolemia. AU - Huber, Sally Ann. AU - Sakkinen, P.. AU - David, C.. AU - Newell, M. K.. AU - Tracy, R. P.. PY - 2001/5/29. Y1 - 2001/5/29. N2 - Background - T cells are implicated in atherosclerosis, but little is known about the genetic control or molecular pathways, especially under conditions of mild hypercholesterolemia. Methods and Results - BALB/c mice, making a CD4+ Th2 (IL-4+) cell response, express both MHC class II antigens (IAd, IEd) and are atherosclerosis-resistant. C57B1/6 mice produce a CD4+ Th1 (interferon [IFN]γ+) response, express IAb but no IE, and are atherosclerosis-prone. To evaluate T helper-cell phenotype in fatty streak formation, wild-type C57B1/6 mice (IAb+IE-) and transgenic mice, either ABo, IAb-IE-; ABEα, IA-IEk+; or B1.Tg.Eα, IAb+IEk+, were fed a high-cholesterol diet for 16 weeks and evaluated histomorphometrically for aortic lesions. Lesion size in ...
The present study demonstrates that pathogenic events in fetal arteries associated with maternal hypercholesterolemia are capable of enhancing the susceptibility to atherosclerosis later in life, and that cholesterol-lowering interventions or antioxidant treatment of hypercholesterolemic mothers during pregnancy have long-term beneficial effects in their offspring.. As previously demonstrated in the same rabbit model,13 diet-induced maternal hypercholesterolemia during pregnancy markedly increased fatty streak formation during fetal development, whereas maternal treatment with vitamin E or cholestyramine significantly reduced lesion sizes in their offspring, compared with untreated mothers. In the present study, a higher dose of vitamin E (1000 IU) was used than in the preceding one (100 IU). This yielded a greater reduction of lesion sizes and intimal content in lipid peroxidation products at birth. After weaning and five months on the mildly hypercholesterolemic diet, lesion sizes in aortic ...
Autosomal recessive hypercholesterolemia (ARH) is a rare disorder characterized by elevated low-density lipoprotein (LDL) serum levels, xanthomatosis, and premature coronary artery disease. Several dyslipidemias have been identified which lead to severe primary hypercholesterolemia. Among them, ARH is characterized by clinical symptoms and plasma cholesterol levels intermediate between those found in heterozygous and homozygous familial hypercholesterolemia (FH) [DS:H00155] individuals. ARH patients develop symptomatic coronary artery disease later in life and their xanthomas tend to be large and bulky. In 2001, ARH was found to be caused by mutations in the LDL receptor adaptor protein 1 (LDLRAP1). In ARH, the internalization of the ligand-receptor complex cannot occur and all the LDL receptors accumulate on the cell membrane. In general, ARH patients show a better response to lipid-lowering therapy than the FH patients, and they rarely require LDL apheresis ...
TY - JOUR. T1 - Resistance to diet-induced hypercholesterolemia and gallstone formation in ACAT2-deficient mice. AU - Buhman, Kimberly K.. AU - Accad, Michel. AU - Novak, Sabine. AU - Choi, Rebekah S.. AU - Wong, Jinny S.. AU - Hamilton, Robert L.. AU - Turley, Stephen. AU - Farese, Robert V.. PY - 2000/12/1. Y1 - 2000/12/1. N2 - The importance of cholesterol ester synthesis by acyl CoA:cholesterol acyltransferase (ACAT) enzymes in intestinal and hepatic cholesterol metabolism has been unclear. We now demonstrate that ACAT2 is the major ACAT in mouse small intestine and liver, and suggest that ACAT2 deficiency has profound effects on cholesterol metabolism in mice fed a cholesterol-rich diet, including complete resistance to diet-induced hypercholesterolemia and cholesterol gallstone formation. The underlying mechanism involves the lack of cholesterol ester synthesis in the intestine and a resultant reduced capacity to absorb cholesterol. Our results indicate that ACAT2 has an important role in ...
The current study investigated the effects of hyperglycemia, hypertension, and hypercholesterolemia on the severity of sequelae related to traumatic brain injury. Existing data of 209 participants was utilized from an urban hospital, which included neuropsychological evaluations following traumatic brain injury. Specific areas examined included measures of executive functioning, both immediate and delayed memory, and learning. Each participant was placed into a group based on the number of documented diagnoses (hyperglycemia, hypercholesterolemia, and hypertension). The control group consisted of patients that did not carry a record of these health risks. Each of these groups was further stratified according to age. An interaction between the variables of health risk factors and neuropsychological assessment results was predicted specified by decreasing standard scores with the increase in number of health risk factors. Furthermore, age was hypothesized to be a main effect, with the prediction of a
Inclusion criteria :. - Participants with primary hypercholesterolemia treated with atorvastatin at stable dose of 5-20 mg for at least 6 weeks prior to screening and likely to have LDL-C ≥100 mg/dL (≥2.59 mmol/L) at the screening visit.. OR. - Participants with primary hypercholesterolemia who were receiving a lipid-lowering treatment other than atorvastatin, or who were not at stable dose of atorvastatin 5-20 mg for at least 6 weeks prior to screening if they were likely to have LDL-C ≥100 mg/dL (≥2.59 mmol/L) after a 6-week run-in treatment period on atorvastatin therapy.. Exclusion criteria:. ...
Low levels of high-density lipoproteins (HDLs) may constitute an independent risk factor that may be as important as elevated low-density lipoproteins (LDLs) in coronary artery disease (CAD). Concentrations and distributions of lipids, apolipoprotein (apo) B, and apoA-I in the plasma and lipoprotein subfractions of two groups of swine, one with familial hypercholesterolemia (FHC) and the other with diet-induced hypercholesterolemia (DHC), were examined. Normolipidemic (NL) animals served as controls. All pigs carried the Lpb5 apoB mutation, which is known to influence the formation of atherosclerotic lesions. Mean concentrations of serum total cholesterol in NL, DHC, and FHC were 80.0 +/- 9.3, 774.3 +/- 54.5, and 316.5 +/- 36.1 mg/dL, respectively; HDL cholesterol (HDL-C), 33.5 +/- 1.9, 137.0 +/- 9.9, and 22.3 +/- 2.2 mg/dL; triglycerides, 33.0 +/- 16.3, 40.3 +/- 11.7, and 56.8 +/- 7.2 mg/dL; apoB, 35.7 +/- 3.1, 142.0 +/- 4.8, and 169.3 +/- 13.9 mg/dL; and apoA-I, 62.4 +/- 9.3, 170.9 +/- 6.9, ...
Hypercholesterolemia: High blood cholesterol. This can be sporadic with no family history) or familial. Familial hypercholesterolemia is the most common inherited type of hyperlipidemia (high lipid levels in blood). It predisposes to premature arteriosclerosis including coronary artery disease with heart attacks at an unusually young age. About half of men and a third of women suffer a heart attack by age 60. Persons with familial hypercholesterolemia can reduce their risk by adhering to a very low cholesterol diet under a doctors supervision, and may also need to take medications that reduce their cholesterol level. Familial hypercholesterolemia is recognizable in childhood. Children and other relatives at risk for familial hypercholesterolemia can be screened (checked) for the condition. Familial hypercholesterolemia is due to a geneticdefect in the receptor (the dock on the surface of cells) for LDL (low density lipoprotein). ...
This study compared the efficacy and pharmacodynamics of atorvastatin versus rosuvastatin in hypercholesterolaemic patients with or without the
CYP7A1 encodes the rate limiting enzyme for the conversion of cholesterol to bile acids. Several studies have demonstrated that elevated expression of CYP7A1 confers protection from hypercholesterolemia. CYP7A1 expression is regulated by two nuclear receptors, farnesoid X receptor (FXR) and small heterodimer (SHP). Here we demonstrate that although FXR−/ − and SHP−/ − mice have similarly elevated levels of CYP7A1, FXR−/ − mice have elevated serum cholesterol and triglyceride levels and serum markers of hepatic inflammation whereas the SHP−/ − mice do not. This suggestion of a beneficial lipid effect of the loss of SHP was confirmed in a cholesterol/cholic acid diet model, in which SHP−/ − mice were strongly protected form diet-induced hypercholesterolemia and hepatic inflammation. To examine the effects of the loss of SHP in a model relevant to human dyslipidemia, we generated LDLR−/ −SHP−/ − mice. The LDLR−/ −SHP−/ − mice were highly resistant to Western ...
METHODS AND RESULTS Normal or hypercholesterolemic rabbits received intravenous L-arginine (10 mg/kg/min) or vehicle for 70 minutes. Subsequently, animals were killed, thoracic aortas were harvested, and vascular rings were studied in vitro. Rings were contracted by norepinephrine and relaxed by acetylcholine chloride or sodium nitroprusside. Vasorelaxation was quantified by determining the maximal response (expressed as percent relaxation of the contraction) and the ED50 (dose of drug inducing 50% relaxation; expressed as -log M). In vessels from hypercholesterolemic animals receiving vehicle, there was a fivefold rightward shift in sensitivity to acetylcholine compared with normal animals (p = 0.05, n = 5 in each group). In vessels from hypercholesterolemic animals, L-arginine augmented the maximal response to acetylcholine (83 +/- 16% versus 60 +/- 15%, p = 0.04 versus vehicle) and increased the sensitivity to acetylcholine (ED50 value: 6.7 +/- 0.2 versus 6.2 +/- 0.2, p less than 0.05 versus ...
Hypercholesterolemia is common in older adults and less treated, but little is known about correlates of untreated hypercholesterolemia. Using a standard interview method we examined a random sample of 7,572 participants aged 60 years in a community-based household survey across 7 provinces of China during 2007-2012, and documented 328 cases of hypercholesterolemia from self-reported doctor diagnosis. Compared to participants with normal cholesterol, older adults with hypercholesterolemia had higher socioeconomic position and larger body mass index. In patients with hypercholesterolemia, 209 were not treated using lipid-lowering medications (63.7%, 95% confidence interval (CI) 58.5%- 68.9%). Untreated hypercholesterolemia was significantly associated with female sex (adjusted odds ratio 2.13, 95%CI 1.17-3.89), current smoking (3.48, 1.44-8.44), heavy alcohol drinking (3.13,1.11-8.84), chronic bronchitis (2.37,1.14-4.90) and high level of meat consumptions (2.85,1.22-6.65). Although having ...
KEGG : 36 Autosomal recessive hypercholesterolemia (ARH) is a rare disorder characterized by elevated low-density lipoprotein (LDL) serum levels, xanthomatosis, and premature coronary artery disease. Several dyslipidemias have been identified which lead to severe primary hypercholesterolemia. Among them, ARH is characterized by clinical symptoms and plasma cholesterol levels intermediate between those found in heterozygous and homozygous familial hypercholesterolemia (FH) [DS:H00155] individuals. ARH patients develop symptomatic coronary artery disease later in life and their xanthomas tend to be large and bulky. In 2001, ARH was found to be caused by mutations in the LDL receptor adaptor protein 1 (LDLRAP1). In ARH, the internalization of the ligand-receptor complex cannot occur and all the LDL receptors accumulate on the cell membrane. In general, ARH patients show a better response to lipid-lowering therapy than the FH patients, and they rarely require LDL apheresis ...
TY - JOUR. T1 - Altered myocardial microvascular 3D architecture in experimental hypercholesterolemia. AU - Rodriguez-Porcel, Martin. AU - Lerman, Amir. AU - Ritman, Erik L.. AU - Wilson, Stephanie H.. AU - Best, Patricia J.M.. AU - Lerman, Lilach O.. PY - 2000/10/24. Y1 - 2000/10/24. N2 - Background - Experimental hypercholesterolemia (HC) impairs intramyocardial microvascular function. However, whether this is associated with alterations in microvascular architecture remained unknown. Using a novel 3D micro-CT scanner, we tested the hypothesis that HC is associated with an alteration in the microvascular architecture. Methods and Results - Pigs were euthanized after 12 weeks of either normal (n=6) or 2% HC (n=6) diet. The hearts were excised and the coronary arteries injected with a radiopaque contrast material. Myocardial samples were scanned with micro-CT, and 3D images were reconstructed with 21-μm cubic voxels. The myocardium was tomographically subdivided into subepicardium and ...
We investigated whether primary hypercholesterolaemia per se affects glucose homeostasis and insulin secretion in low-density lipoprotein receptor knockout mice (LDLR(-/-)). Glucose plasma levels were increased and insulin decreased in LDLR(-/-) compared to the wild-type mice. LDLR(-/-) mice presented impaired glucose tolerance, but normal whole body insulin sensitivity. The dose-response curve of glucose-stimulated insulin secretion was shifted to the right in LDLR(-/-) islets. Significant reductions in insulin secretion in response to L-leucine or 2-ketoisocaproic acid were also observed in LDLR(-/-). Islet morphometric parameters, total insulin and DNA content were similar in both groups. Glucose uptake and oxidation were reduced in LDLR(-/-) islets. Removal of cholesterol from LDLR(-/-) islets corrected glucos-estimulated insulin secretion. These results indicate that enhanced membrane cholesterol content due to hypercholesterolaemia leads to a lower insulin secretion and glucose intolerance ...
P8 We have studied the effect of valsartan treatment (3 and 10 mg/kg/day) on plasma fibrinolytic balance in normo- and hypercholesterolemic rabbits. Animals were fed a normal chow or an experimental diet containing 1% cholesterol for 10 weeks. Systolic blood pressure, as well as plasma cholesterol, dimer D, plasminogen activator inhibitor-1 (PAI-1) and tissue plasminogen activator (tPA) were measured. Plasma cholesterol concentrations were higher in rabbits fed the experimental diet compared with control ones. None of the doses of valsartan were able to affect either plasma cholesterol or blood pressure levels in any group.As compared with control animals hypercholesterolemic rabbits presented lower dimer D (0.37±0.07 mg/ml vs 0.96±0.13, p,0.05) and tPA levels (0.27±0.003 ng/ml vs 0.31±0.007, p,0.05) but higher PAI-1 levels (11.1±0.9 ng/ml vs 8.84±0.04, p,0.05). In cholesterol-fed rabbits, valsartan treatment (3 or 10 mg/kg/day) significantly increased both dimer D (0.73±0.1 mg/ml and, ...
During homeostasis hematopoietic stem and progenitor stem cells (HSPCs) give rise to lymphoid and myeloid cells as well as platelets and erythrocytes. However, during chronic inflammatory conditions hematopoiesis is often skewed towards the myeloid lineage, thereby potentially aggravating the ongoing inflammation. Here we investigated the effects of hypercholesterolemia on HSPCs during atherogenesis.. Hypercholesterolemia increased HSPCs, defined as Lin-Sca1+cKit-, in the bone marrow (BM) of LDLr-/- mice by 253.1%. The number of granulocyte-monocyte progenitors, BM granulocytes and BM monocytes was increased by 18.1%, 34.8% and 13.2%, respectively. In accordance, the myeloid colony forming potential of hypercholesterolemic BM was increased by 25.8%. Peripheral blood monocytes and granulocytes were increased by 203.0% and 161.1%, respectively.. Competitive bone marrow transplantations (cBMT) in which we compared the effects of normo- vs. hypercholesterolemia primed HSPCs confirmed that the ...
Evidence-based recommendations on evolocumab (Repatha) for treating primary hypercholesterolaemia (high cholesterol) and mixed dyslipidaemia
Evidence-based recommendations on evolocumab (Repatha) for treating primary hypercholesterolaemia (high cholesterol) and mixed dyslipidaemia
Hypo and hypercholesterolemic rats strains were selected (Lyon) and compared to a normocholesterolemic one issued from the same race (Sprague-Dawley). The arterial tissue of these three strains at three ages (10-19-25 months) and their reactivity to an hyperlipidic diet (2 and 6 month duration) were studied using histological and histochemical technics. There were neither histological nor histochemical differences between the three strains whatever the ages. Therefore, at the present stage of selection, the genetic differences have not changed the arterial metabolism or its evolution during ageing. However the arterial reactivity of hypo and hypercholesterolemic strains towards an hyperlipidic diet was different: indeed both strains developed hypercholesterolemia, liver steatosis and diffuse intimal lipoidosis, but on the other hand the hypercholesterolemic rat alone demonstrated arterial cell proliferation. These data suggest that a same genetic trait can give rise to both a spontaneous
High Blood cholesterol. What Are High Blood Cholesterol and Triglycerides? Learn about high blood cholesterol and why it is damaging to your health.
Looking for a low fat, high fiber ingredient to add to your cholesterol-lowering diet? Look no further. Lentils are a good legume to have on-hand.
Extracorporeal methods of therapy are used only to severe forms of pathology. Special innovative devices change the composition of blood and its properties (outside the human body).. Natural remedies for hypercholesterolemia should be used only with the permission of the physician and together with the methods of traditional medicine. The most effective natural remedies: the root of the Dioscorean of Nippon; berries of a dogrose; immortelle sandy; leaves watch three-leafed; a powder of seeds of a thistle; the roots of blue cyanosis; grasses; celandine; artichoke prickly.. Possible Complications:. Hypercholesterolemia may cause atherosclerotic changes in the vessels.. Prevention:. Prevention of hypercholesterolemia can be divided into primary and secondary. Primary prevention is a method that should be used to prevent an increase in amounts of cholesterol in the blood. Such events include:. ...
Behavioral and psychosocial factors have been shown to influence cardiovascular disease. While interventions targeting these risk factors demonstrate clinical improvement, mechanisms underlying these effects remain to be determined. Research has also defined a relationship between psychosocial stress and immune function, and revealed stress related increases in lymphatic sympathetic nerve density. Considering that inflammation characterizes the various stages of heart disease, the current study assessed whether social stress could influence vascular sympathetic innervation in the presence or absence of hypercholesterolemia. We found dense sympathetic innervation extending into the vascular media and intima throughout the aortic arch and thorax in diseased as well as non-diseased animals. To our knowledge, this is the first demonstration of extensive sympathetic innervation in all layers of normal vessels. Compared to NZW animals, WHHL rabbits displayed increased sympathetic innervation and a
The role of the endothelium was examined in the response to aggregating platelets in cerebral arteries from normal and hypercholesterolemic animals. Male Yorkshire pigs were fed either a normal diet or a 2% high-cholesterol diet for 10 weeks. Endothelium-dependent responses were examined in vitro. In rings of basilar arteries from control animals aggregating platelets caused endothelium-dependent relaxations, which were significantly inhibited by apyrase, an adenosine diphosphatase and triphosphatase, but were augmented by methiothepin, a combined S1- and S2-serotonergic blocker. In quiescent rings platelets induced contractions that were inhibited by the presence of the endothelium; these contractions were significantly inhibited by methiothepin, but not by ketanserin (an S2-serotonergic blocker) or dazoxiben (a thromboxane-synthetase blocker) in the presence or absence of SQ29548 (a thromboxane-receptor blocker). Adenosine diphosphate but not serotonin caused endothelium-dependent relaxations. ...
Inclusion criteria:. Cohort 1: Alirocumab-Exposed:. Currently pregnant - Diagnosed with primary hypercholesterolemia and atherosclerotic cardiovascular disease, or primary hypercholesterolemia associated with familial hypercholesterolemia - Exposed to alirocumab for any number of days, at any dose, and at any time from the first day of the last menstrual period up to and including the end of pregnancy - Agree to the conditions and requirements of the study and provide informed consent.. Cohort 2: Disease-Matched Comparison:. Currently pregnant - Diagnosed with primary hypercholesterolemia and atherosclerotic cardiovascular disease, or primary hypercholesterolemia associated with familial hypercholesterolemia - Unexposed to alirocumab or any biologic medication during pregnancy or any time within 10 weeks prior to the first day of the last menstrual period - Agree to the conditions and requirements of the study and provide informed consent.. Cohort 3: Non-Diseased Comparison:. Currently pregnant ...
Pedigree of an infant with severe hypercholesterolemia who presented with cutaneous xanthomas. (A) Pictures taken at presentation of cutaneous (planar) xanthoma
Alnylam Pharmaceuticals, Inc., a leading RNAi therapeutics company, announced today positive results from its Phase I clinical trial of ALN-PCS, an RNAi therapeutic targeting PCSK9 for the treatment of severe hypercholesterolemia.
Persons with familial hypercholesterolemia can reduce their risk by adhering to a very low cholesterol diet under a doctor​s supervision,​ and may also need to take medications that reduce their cholesterol level. Familial hypercholesterolemia is recognizable in childhood. Children and other relatives at risk for familial hypercholesterolemia can be screened (checked) for the condition ...
Looking for medication to treat heterozygous+inherited+high+blood+cholesterol? Find a list of current medications, their possible side effects, dosage, and efficacy when used to treat or reduce the symptoms of heterozygous+inherited+high+blood+cholesterol
TY - JOUR. T1 - Prostacyclin, thromboxane A2, and atherosclerosis in young hypercholesterolemic swine. AU - Norman, J. F.. AU - Miller, C. W.. PY - 1994/10. Y1 - 1994/10. N2 - Plasma 6-keto-prostaglandin F1α and thromboxane B2 levels were determined to evaluate their role as predictive indicators for the development and progression of coronary atherosclerosis in young hypercholesterolemic swine. 32 young swine were randomly assigned to the control or atherogenic diet group for 10, 30, 90, or 180 days. Lipid profiles were obtained at the onset and repeated throughout the study. Radioimmunoassays of plasma 6-keto-prostaglandin F1α and thromboxane B2 were recorded at 10 day intervals in the 10 and 30 day subjects and at 30 day intervals in the 90 and 180 day subjects. Sections from the proximal left anterior descending coronary artery were classified based on their histological evidence of atherosclerosis by light microscopy. Hypercholesterolemia was positively correlated with development of ...
List of drugs used to treat hypercholesterolemia, including various medications for hypercholesterolemia treatments. These medical treatments that are used to fight...
Do You Have Hypercholesterolemia? Join friendly people sharing true stories in the I Have Hypercholesterolemia group. Find support forums, advice and chat with groups who share this life experience. Hypercholesterolemia anonymous support group with i...
Dowload Sample Page for Hypercholesterolemia analysis. This report contains Hypercholesterolemia companies, epidemiology, drugs and market forecast upto 2030
Cholesterol is a lipid or fat that is produced by the liver. It is crucial for body function and metabolism. However, there is a certain amount of this compound that should be present in human body. High cholesterol level can harm your health in
Colantonio L, Cermignani E, Ciapponi A, Calcagno JI. Ezetimibe for primary hypercholesterolemia. Cochrane Database of Systematic Reviews 2015, Issue 6. Art. No.: CD006298. DOI: 10.1002/14651858.CD006298. ...
There are conflicting results regarding the erythrocyte membrane cholesterol and phospholipid content in patients with primary hypercholesterolemia (PHC), due to methodological problems in obtaining haemoglobin-free ghosts. At the same time, the diff
Greater than normal Cholesterol levels in blood. The tendency of developing high Cholesterol levels is effected by genetic factors, nutrition, age, body weight and others.. High Cholesterol level is one of the risk factors for the development of Ischemic heart disease.. ...
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EDITORIAL COMMENTS. http://dx.doi.org/10.5546/aap.2016.eng.398. Genetic and epigenetic, the case of hypercholesterolemia. To size up how important the human genome description is, the researchers who described it illustrated the relevance of genes in the development of conditions that create a large burden on public health. The authors reported on ApoE genetic variations and their role in the development of hypercholesterolemia and cardiovascular disease. This is an important issue, which calls upon us to reflect on how knowledge has evolved in the past decades.. Morbidity and mortality from cardiovascular disease (CVD) across Europe between 1990 and 1992 was greatly dissimilar among countries. Mortality among 45-74-year-old men was 655/100 000 inhabitants per year in Scotland, whereas it was 142/100 000 inhabitants per year in France, i.e., 4.5 times higher. The mortality rate among Scottish women in the same age group was 7.5 times higher than among their French counterparts.1 Subsequent ...
Help patients follow treatment plans for high blood cholesterol and other lipids. This booklet reviews risk factors and emphasizes making lifestyle changes.
High blood cholesterol is a leading risk factor in the development of atherosclerosis and coronary heart disease (CHD) (1,2). The risks associated with high blood cholesterol can be reduced by screening and early intervention (3). Current clinical practice guidelines provide evidenced-based standards for detection, treatment, and control of high blood cholesterol (4). Healthy People 2020 monitors national progress related to screening and controlling high blood cholesterol through the National Health Interview Survey and the National Health and Nutrition Examination Survey (NHANES). State-level estimates of self-reported cholesterol screening and high blood cholesterol prevalence are available using Behavioral Risk Factor Surveillance System (BRFSS) data. To assess recent trends in the percentage of adults aged ≥18 years who had been screened for high blood cholesterol during the preceding 5 years, and the percentage among those who had been screened within the previous 5 years and who were ...
TY - JOUR. T1 - The severe hypercholesterolemia phenotype. T2 - Clinical diagnosis, management, and emerging therapies. AU - Sniderman, Allan D.. AU - Tsimikas, Sotirios. AU - Fazio, Sergio. N1 - Funding Information: Dr. Tsimikas is supported by National Institutes of Health/National Heart, Lung, and Blood Institute grants R01-HL119828 , R01-HL093767 , and P01-HL055798 ; has received royalties from patents held by the University of California; has received research grants from Pfizer, ISIS, and Genentech; and is a consultant to ISIS, Genzyme, and Sanofi. Dr. Fazio is supported by NIH/NHLBI grants R01-HL106845 and R01-HL57986 ; has received research grants from ISIS, Merck, Pfizer, and Amarin; and is a consultant for Merck, Roche, Kowa, Sanofi, Gilead, Aegerion, Genzyme, and Amarin. Dr. Sniderman has received honoraria from Merck and Genzyme. Copyright: Copyright 2018 Elsevier B.V., All rights reserved.. PY - 2014/5/20. Y1 - 2014/5/20. N2 - The severe hypercholesterolemia phenotype includes all ...
The effect of lovastatin on serum lipids and its tolerability in patients with non-familial primary hypercholesterolemia (type II-A and type II-B) during a six-month period were evaluated in this open-label study. Thirty-eight patients were enrolled in the study; tolerability was assessed in all 38 patients. Thirty patients completed the study, and the effect of lovastatin on serum lipids in these patients was assessed. Some patients had been treated for hypercholesterolemia with long-term dietary and other non-pharmacologic means before entry into the study. All patients were unresponsive to a six-week program of intensive dietary therapy and other nonpharmacologic treatment to lower their blood cholesterol levels before receiving lovastatin. While maintaining intensive dietary therapy, administration of lovastatin was instituted at a dosage of 20 mg/day, which was increased by 20-mg increments monthly, as necessary, to a maximum of 80 mg/day. In an effort to achieve goal levels of low-density ...
High blood cholesterol increases your risk of cardiovascular complications such as a heart attack or stroke. Your doctor may periodically evaluate your risk for these complications by using a calculator such as the Atherosclerotic Cardiovascular Disease Estimator. This calculator estimates your risk of having a heart attack or stroke in the next 10 years. It considers your total and good high-density lipoprotein (HDL) cholesterol levels, age, and systolic blood pressure. It also factors in whether you have diabetes, smoke, or use medicines to control high blood pressure. Your doctor will consider how unhealthy your blood cholesterol levels are and your 10-year risk calculation when deciding how best to treat your high blood cholesterol and to manage your risk of cardiovascular complications. Your doctor may recommend aspirin to prevent a first heart attack or stroke.. Keep in mind that this 10-year cardiovascular risk calculator may not accurately estimate risk in certain situations, such as ...
The present randomised cross-over clinical trial investigated the effects of two intervention diets (non-soya legume-based therapeutic lifestyle change (TLC) diet v. isoenergetic legume-free TLC diet) on inflammatory biomarkers among type 2 diabetic patients. A group of thirty-one participants (twen …
For those suffering heart disease or at high risk, consider making dietary changes with the Therapeutic Lifestyle Changes Diet. Look up easy-to-cook TLC diet recipes.
The CDCs National Health and Nutrition Examination Survey results1 highlight recent trends associated with cholesterol-lowering medications. Among adults in the US aged 40 and over during 2003-2012, the percentage using a cholesterol-lowering medication in the past 30 days increased from 20% to 28%. Statin use overall increased from 18% to 26%, and by 2011-2012, 93% of adults who were using a cholesterol-lowering medication used a statin. The use of cholesterol-lowering medications increased with age, with 17% of adults aged 40-59 and 48% of adults aged 75 and over taking them. Cholesterol-lowering medications were used by approximately 71% of adults with cardiovascular disease and 54% of adults with hypercholesterolemia. Use of cholesterol-lowering medications was more prevalent among adults aged 40-64 with health insurance than those without it. Of prescription cholesterol-lowering medications, the most commonly used product was simvastatin, with 42% reporting its use. Following this was ...
Ackermann RT, Mulrow CD, Ramirez G, Gardner CD, Morbidoni L, Lawrence VA. Garlic shows promise for improving some cardiovascular risk factors. Arch Intern Med. 2001;161:813-824.. Anderson JW, Davidson MH, Blonde L, et al. Long-term cholesterol-lowering effects on Psyllium as an adjunct to diet therapy in the treatment of hypercholesterolemia. Am J Clin Nutr. 2000a;71:1433-1438.. Anderson JW, Allgood LD, Lawrence A, et al. Cholesterol-lowering effects of psyllium intake adjunctive to diet therapy in men and women with hypercholesterolemia: meta-analysis of 8 controlled trials. Am J Clin Nutr. 2000b;71:472-479.. Becker DJ, Gordon RY, Morris PB, Yorko J, Gordon YJ, Li M, Iqbal N. Simvastatin vs therapeutic lifestyle changes and supplements: randomized primary prevention trial. Mayo Clin Proc. 2008 Jul;83(7):758-764.. Birketvedt GS, Aaseth J, Florholmen JR, Ryttig K. Long-term effect of fibre supplement and reduced energy intake on body weight and blood lipids in overweight subjects. Acta Medica. ...
Pictured Recipe: Avocado Pesto. A. It depends. Most people absorb about half the cholesterol they consume through foods, but absorption rates vary (from 20 to 60 percent) from person to person. This variation may help explain why dietary cholesterol seems to increase levels of unhealthy LDL blood cholesterol in some people more than others, says EatingWell advisor Alice Lichtenstein.. In any case, saturated and trans fats have a bigger detrimental effect on blood cholesterol levels, and heart health in general, than dietary cholesterol does. Trans and saturated fats not only affect how much plaque is deposited in blood vessels, but also may damage the tissue of blood vessels, says Susan Moores, M.S., R.D., a spokesperson for the American Dietetic Association. With a few exceptions-notably eggs and shellfish-foods high in cholesterol, such as fatty meats and whole-milk dairy, also tend to be high in saturated fat. Cutting back on sources of saturated fat automatically limits intake of dietary ...
On the 8th October our Scientific & Medical Manager, Dr Marta Carrera, attended as a key speaker at the Spanish Familial Hypercholesterolemia (FH) Foundation Conference presenting the Utility of genetics in the clinical and therapeutic management of FH. Familial hypercholesterolemia (FH) is the most common genetic condition globally. FH causes high cholesterol and increases the risk of cardiovascular disease and heart attack. However, 90% of patients born with FH are undiagnosed.. The Fundación Hipercolesterolemia Familiar (FHF) is a Spanish nationwide organisation, created to raise awareness of genetic induced high cholesterol, and the need to promote early detection in families, as well as treatment and control to prevent cardiovascular mortality in people with Familial Hypercholesterolemia (FH).. The FHF results from the combined effort of patients and health care professionals giving their knowledge, support, commitment and dedication to raise FH awareness. The FHF relies on experts, both ...
TY - JOUR. T1 - Molecular basis of familial hypercholesterolemia. AU - Russell, D. W.. AU - Esser, V.. AU - Hobbs, H. H.. PY - 1989. Y1 - 1989. N2 - Familial hypercholesterolemia (FH) is a genetic disease characterized by an elevated level of low density lipoprotein (LDL), xanthomas, and an increased frequency of heart attacks. One of the first descriptions of this disease was reported some 50 years ago by the Norwegian physician, Carl Muller. Research and clinical studies in the ensuing half century have shown that FH is caused by mutations in the gene for the LDL receptor. In this article, we review our studies of the last 5 years that have focused on the molecular genetics of the LDL receptor locus and its pathogenesis in FH.. AB - Familial hypercholesterolemia (FH) is a genetic disease characterized by an elevated level of low density lipoprotein (LDL), xanthomas, and an increased frequency of heart attacks. One of the first descriptions of this disease was reported some 50 years ago by the ...
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A family history of hypercholesterolemia is very, very important. Familial hypercholesterolemia means that an individual has a very high circulating cholesterol concentration. Cholesterol is a major risk factor for the development of atherosclerosis, by that I mean furring up of the coronary arteries. People with familial hypercholesterolemias usually have heart attacks in their twenties and thirties. A family history of familial hypercholesterolemia should mean rapid assessment of ones cholesterol because there are fantastic drugs on the market known as the statins that can bring down the cholesterol level and reduce the risk of heart attacks significantly. These blood tests are offered on the National Health Service.. ...
A family history of hypercholesterolemia is very, very important. Familial hypercholesterolemia means that an individual has a very high circulating cholesterol concentration. Cholesterol is a major risk factor for the development of atherosclerosis, by that I mean furring up of the coronary arteries. People with familial hypercholesterolemias usually have heart attacks in their twenties and thirties. A family history of familial hypercholesterolemia should mean rapid assessment of ones cholesterol because there are fantastic drugs on the market known as the statins that can bring down the cholesterol level and reduce the risk of heart attacks significantly. These blood tests are offered on the National Health Service.. ...
What is High Blood Cholesterol?. As the name suggests, High Blood Cholesterol refers to a condition characterized by a high level of cholesterol in the bloodstream. Cholesterol is a fatty substance found in the walls or membranes of cells. It is carried in the blood in small packages known as lipoproteins. These lipoproteins are of two types, namely Low Density Lipoprotein (LDL) and High Density Lipoprotein (HDL). The risk of developing heart problems increases with an increase in the level of LDL.. On the other hand, High Density Lipoprotein is considered good as it helps in carrying the cholesterol to the liver from where it can be easily removed. Hence, an increase in the level of HDL is favorable as it decreases the risk of potential heart problems and diseases.. When cholesterol builds up along the walls of arteries, it increases the probability of developing heart diseases. In case the accumulated cholesterol or plaque bursts, it releases the cholesterol and fat content in the blood. As ...
The effects of age, atherosclerosis, hypertension, and hypercholesterolemia on vascular function of the coronary circulation were studied by subselective intracoronary infusions of acetylcholine, which releases endothelium-derived relaxing factor, and papaverine, which directly relaxes vascular smooth muscle, in normal patients (n = 18; no risk factors for coronary artery disease), in patients with evidence of early atherosclerosis but normal cholesterol levels and normal blood pressure (n = 12), in patients with hypertension without left ventricular hypertrophy (n = 12), and in patients with hypercholesterolemia (n = 20). Papaverine-induced maximal increases in coronary blood flow were significantly greater in normals, but no differences were noted between the groups of patients with early atherosclerosis, with hypertension, and with hypercholesterolemia. The capacity of the coronary system to increase blood flow in response to acetylcholine was similar in normal and normocholesterolemic ...
The current study examined the attenuating influence of dietary carrot pomace powder (CaPP) on hypercholesterolemia and various oxidative stress-associated with biochemical parameters in hypercholesterolemic rats. Thirty two male albino rats weighing 110±10 g were divided into four groups, the first group received the basal diet only and served as (negative control), the second group received the hypercholesterolemic diet and served as positive control, the other groups received hypercholesterolemic diet supplemented with 10%, 20% CaPP for six weeks. The obtained results revealed that groups supplemented with 10% and 20% CaPP significantly decrease total lipid, total cholesterol, triglycerides, low density lipoprotein cholesterol, liver enzymes: alanine aminotransferase, aspartate aminotransferase compared to positive and negative groups. Organs weight, body weight gain significantly decreased compared with positive control. Moreover dietary carrot pomace powder can used to reduce the body ...
Swiss drug major Novartis AG (NVS) announced Friday that the Committee for Medicinal Products for Human Use (CHMP) of the European Medicines Agency (EMA) has adopted a positive opinion and recommended granting marketing authorization of Leqvio (inclisiran) for the treatment of adults with hypercholesterolemia or mixed dyslipidemia.. The CHMP recommended granting inclisiran marketing authorization for the treatment of adults with primary hypercholesterolemia (heterozygous familial and non-familial) or mixed dyslipidemia.. If approved, inclisiran will be the first and only small interfering RNA (siRNA) in Europe for patients with hypercholesterolemia or mixed dyslipidemia.. Inclisiran is a potential first-in-class small interfering RNA (siRNA) with a new mechanism of action which delivers effective and sustained low-density lipoprotein cholesterol (LDL-C) reduction for patients with atherosclerotic cardiovascular disease (ASCVD).. ASCVD corresponds to the accumulation of lipids over time mainly ...
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The theory that iron may play a significant role in atherogenesis by promoting the formation of free radicals is controversial. Previous results using the new technique of nuclear microscopy showed a seven-fold increase in iron concentrations within newly formed atherosclerotic lesions in hypercholesterolemic rabbits compared to healthy artery tissue. In a follow- up time sequence study described here, we show that iron accumulation occurs at the onset of lesion formation. In addition, weekly bleeding decreases the iron uptake into the artery wall and delays the onset of atherogenesis. These results provide direct evidence for a key role of iron in initiating atherogenesis ...
Cholesterol is a fatty substance produced by your liver. Its also found in foods high in saturated fat, such as meat, eggs, some shellfish, and whole-milk dairy products.. Your cells need some cholesterol to functional normally. But too much cholesterol in your blood can be harmful. High blood cholesterol levels can cause fatty deposits to build up on the walls of your arteries. This condition is known as atherosclerosis (sometimes called hardening of the arteries). Over time, the fatty deposits can decrease the amount of blood flowing in the arteries and eventually block blood flow entirely. This narrowing of the arteries can lead to heart disease, heart attack, and stroke. People who are overweight, eat a lot of foods high in saturated fat, or who have a family history of high cholesterol have an increased risk of high cholesterol levels. There are few symptoms of high cholesterol levels and a blood test is almost always needed to confirm it.. There are two kinds of cholesterol:. ...
In a new study, NYU Langone Medical Center researchers have discovered how cholesterol-lowering drugs called statins promote the breakdown of plaque in the arteries. The study was published online by the journal PLoS One on December 6, 2011.. The findings support a large clinical study that recently showed patients taking high-doses of the cholesterol-lowering medications not only reduced their cholesterol levels but also reduced the amount of plaque in their arteries. However, until now researchers did not fully understand how statins could reduce atherosclerosis, the accumulation of fat and cholesterol that hardens into plaque in arteries, a major cause of mortality in Western countries. High blood cholesterol is a major culprit in atherosclerosis. As a result of narrowing arteries, blood clots can form or plaque can break off causing blockages in vessels. This can lead to a potentially fatal heart attack or stroke.. Our new research shows statins actually promote the regression of ...
50 APPENDIX A CHOLESTEROL HANDOUT High Blood Cholesterol What you need to know US Department of Health and Human Services National Institutes of Health (June, 2005) Why Is Cholesterol Important? Your blood cholesterol level has a lot to do with your chances of getting heart disease. High blood cholesterol is one of the major risk factors for heart disease. A risk factor is a condition that increases your chance of getting a disease. In fact, the higher your blood cholesterol level, the greater your risk for developing heart disease or having a h eart attack. Heart disease is the number one killer of women and men in the United States. Each year, more than a million Americans have heart attacks, and about a half million people die from heart disease. How Does Cholesterol Cause Heart Disease? When there is too much cholesterol (a fat like substance) in your blood, it builds up in the walls of narrowed and blood flow to the heart is slowed down or b locked. The blood carries oxygen to the heart, ...
Several studies have shown that elevated plasma cholesterol levels (i.e. hypercholesterolemia) serve as a risk factor for late-onset Alzheimers disease (AD). However, it remains unclear how hypercholesterolemia may contribute to the onset and progression of AD pathology. In order to determine the role of hypercholesterolemia at various stages of AD, we evaluated the effects of high cholesterol diet (5% cholesterol) in wild-type (WT; C57BL6) and triple-transgenic AD (3xTg-AD: Psen1, APPSwe, tauB301L) mice at 7, 14, and 20 months. The transgenic APP-Swedish/Dutch/Iowa AD mouse model (APPSwDI) was used as a control since these animals are more pathologically-accelerated and are known to exhibit extensive plaque deposition and cerebral amyloid angiopathy. Here, we describe the effects of high cholesterol diet on: (1) cognitive function and stress, (2) AD-associated pathologies, (3) neuroinflammation, (4) blood-brain barrier disruption and ventricle size, and (5) vascular dysfunction. Our data show ...
However, the research about familial hypercholesterolemia actually disproves the hypothesis that elevated cholesterol levels are responsible for cardiovascular disease.
Low saturated fat diets have been recommended as a means of reducing blood cholesterol levels for decades. However, for many years it has also been recognized that reducing the saturated fat content of the diet alone isnt sufficient to markedly lower blood cholesterol levels. To this point, since 2002, Dr. David Jenkins of the University of Toronto and his colleagues have published a series of studies showing that the combination of cholesterol-lowering foods called the portfolio diet lowers cholesterol to a much greater extent than any single food. Not surprisingly, soyfoods have been an integral part of this combination since they are low in saturated fat and soy protein itself lowers blood cholesterol levels. Subjects following the test diet are instructed to consume 22 grams of soy protein from soymilk, tofu and soy meat analogues per 1000 calories or about 35 grams per participant. Other components of the portfolio diet included nuts, soluble fiber and phytosterols.. In the latest study ...
The efficiency and efficacy of low-density lipoprotein (LDL) apheresis performed with a dextran sulphate cellulose (DSC) regenerating unit were tested in five familial hypercholesterolaemic patients. LDL apheresis was repeated four times at both bi-weekly and weekly intervals, processing one plasma volume each time. The efficiency of the procedure (i.e., the extent of lipoprotein removal) was nearly identical with both schedules. Efficacy parameters, i.e., decreases of plasma total and LDL cholesterol (TC and LDL-C) and apo B, were highly correlated (r , 0.96) with pre-apheresis levels, allowing an accurate prediction of the absolute lipid removal in the single individual. Plasma triglycerides, high-density lipoprotein cholesterol, apo A-I and apo A-II recovered rather rapidly, reaching 91-96% of the pre-apheresis values in 48 hours; the recovery of TC, LDL-C and apo B was much slower, with a relatively rapid early phase (80% recovery after about 7 days) followed by a successive slower rise. ...
Despite recent national pediatric guidelines recommending identification and treatment of children with familial hypercholesterolemia, the use of lipid-lowering treatment has been flat over the past decade in real-world pediatric practice, finds a large multicenter study.. Justin Zachariah, MD, MPH, a pediatric cardiologist at Boston Childrens Hospital, presented the findings this week at the 2013 American Heart Association (AHA) Scientific Sessions. He believes they dispel some critiques of the recent guidelines, particularly concerns that more screening would result in overmedicating the pediatric population.. Extending beyond 2008 recommendations from the American Academy of Pediatrics, the 2011 National Heart, Lung and Blood Institutes pediatric guidelines call for universal lipid screening and medical treatment for children at highest risk for early cardiovascular disease. One such high-risk condition is familial hypercholesterolemia, a genetic disorder characterized by high blood ...
Define familial hypercholesterolemia: an inherited metabolic disorder marked by excess accumulation of LDL cholesterol in the blood resulting…
Genetic testing of familial hypercholesterolemia (FH). Although awareness of familial hypercholesterolemia (FH) is increasing, this common, potentially fatal, treatable condition remains underdiagnosed. Despite FH being a genetic disorder, genetic testing is rarely used. With costs of next-generation DNA sequencing continuing to fall, genetic testing for FH has become more accessible. Most importantly, genetic testing provides a window of opportunity whereby we can identify those individuals at significantly higher risk than the general population for CAD at a given LDL-C level. Early recognition of FH leading to guideline-based therapy will alter the natural history of this highly morbid genetic condition. Read the full article. ...
Mellies, M.J.; Stein, E.A.; Khoury, P.; Lamkin, G.; Glueck, C.J., 1987: Effects of fenofibrate on lipids lipoproteins and apolipoproteins in 33 subjects with primary hypercholesterolemia
Familial hypercholesterolemia is an autosomal recessive disease caused by pathogenic variants in the LDLR gene. Although it has been diagnosed in individuals worldwide, the disease is more prevalent in individuals of Ashkenazi Jewish, Finnish, or French Canadian descent, as well as South African Afrikaners. For patients who inherit two mutant alleles, age of onset is in childhood or adolescence. The disease is characterized by high levels of cholesterol in the bloodstream and cholesterol deposits on the tendons (xanthomas). Due to the high levels of cholesterol, hardening of the arteries can occur at a young age and most patients have severe coronary heart disease by their mid-20s. Many patients have either coronary bypass surgery, or a fatal heart attack, in adolescence. Individuals who carry one mutant allele also have hypercholesterolemia, although not to the same extent. These individuals have a 20-fold increased risk of coronary heart disease compared to the general public. Without ...
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Primary objective of this article is to explain Symptoms of Familial Hypercholesterolemia. The most prevalent symptom of Familial Hypercholesterolemia is e
Definition of familial hypercholesterolemia, with etymology, pronunciation (phonetic and audio), synonyms, antonyms, derived terms and more about the word familial hypercholesterolemia.
Remember: cholesterol-free does not mean fat-free.. Dietary cholesterol is a fat-like substance found in all foods of animal origin: egg yolks, meat, poultry, fish, milk, and milk products.. Because our bodies make cholesterol, it is not required in our diets. However, because most people eat foods that contain cholesterol, it is important to avoid excessive amounts.. The amount of cholesterol you consume can affect your blood cholesterol levels.. Fatty acids are the basic chemical units in fat. They may be saturated, polyunsaturated, monounsaturated, or trans fats.. These fatty acids differ in their chemical compositions and structures, and in the way in which they affect your blood cholesterol levels.. Saturated fat is used by the liver to manufacture cholesterol.. It is considered the most dangerous kind of fat because it has been shown to raise blood cholesterol levels, particularly the LDL, and should comprise no more than 10 percent of your daily calorie intake.. Examples include: ...
Remember: cholesterol-free does not mean fat-free.. Dietary cholesterol is a fat-like substance found in all foods of animal origin: egg yolks, meat, poultry, fish, milk, and milk products.. Because our bodies make cholesterol, it is not required in our diets. However, because most people eat foods that contain cholesterol, it is important to avoid excessive amounts.. The amount of cholesterol you consume can affect your blood cholesterol levels.. Fatty acids are the basic chemical units in fat. They may be saturated, polyunsaturated, monounsaturated, or trans fats.. These fatty acids differ in their chemical compositions and structures, and in the way in which they affect your blood cholesterol levels.. Saturated fat is used by the liver to manufacture cholesterol.. It is considered the most dangerous kind of fat because it has been shown to raise blood cholesterol levels, particularly the LDL, and should comprise no more than 10 percent of your daily calorie intake.. Examples include: ...
Review of medications for reducing high cholesterol levels. Outlines effect, side effect, drug interactions, and mechanism of statins and other drugs used for managing cholesterol.
QUESTION: I am diabetic patient having high cholesterol level. So tell me about my diet and food. Some time I feel pain on my left hand, my blood sugar
Question - Diagnosed with frontal lobe atrophy. Taking medicine for HBP and high cholesterol level. Concerned. Ask a Doctor about when and why MRI is advised, Ask a Neurologist
High cholesterol levels can have a serious effect on your health as the years go by. In this post, well run down how you can manage this situation.
We are pleased to announce we have added new panels for dyslipidemias and familial hypercholesterolemia to our testing menu! Dyslipidemias are a clinically and genetically heterogenous group of disorders associated with abnormal levels of lipids and lipoproteins, including increased or decreased levels of LDL or HDL cholesterol or increased levels of triglycerides. The most common subset of monogenic dyslipidemia is familial hypercholesterolemia (FH), which has an estimated prevalence of 1 in 200 in the Caucasian population. More information about these new panel options can be found on the individual test pages on our website: Dyslipidemia Sequencing Panel (23 genes) ...
APOB Hypercholesterolemia, familial; 143890; LDLR Hypercholesterolemia, familial, 3; 603776; PCSK9 Hypercholesterolemia, ... TJP2 Hypercholesterolemia, due to ligand-defective apo B; 144010; ... familial, autosomal recessive; 603813; LDLRAP1 Hypercholesterolemia, familial, modification of; 143890; APOA2 ...
It is also known as "normotriglyceridemic hypobetalipoproteinemia". Familial hypercholesterolemia Braunwald, Eugene; Hauser, ... such as familial hypercholesterolemia. Treatment may include, niacin or statin or ezetimibe. ...
... inhibitor drugs are now approved by the FDA to treat familial hypercholesterolemia. Drugs can inhibit PCSK9, leading to ... Reduced LDLR levels result in decreased metabolism of LDL-particles, which could lead to hypercholesterolemia. When LDL binds ... Lopez D (2008). "Inhibition of PCSK9 as a novel strategy for the treatment of hypercholesterolemia". Drug News Perspect. 21 (6 ... The drugs are approved by the FDA for treatment of hypercholesterolemia, notably the genetic condition heterozygous familial ...
In familial hypercholesterolemia, a mutation in the LDLR, PCSK9, or APOB is usually the reason for this and these mutations ... Some common genetic disorders associated with primary dyslipidemias are homozygous or heterozygous hypercholesterolemia, ... Rosenson, Robert S; Durrington, Paul (September 21, 2020). "Familial hypercholesterolemia in adults: Overview". UpToDate. ... "Inherited disorders of LDL-cholesterol metabolism other than familial hypercholesterolemia". UpToDate. Retrieved April 22, 2021 ...
Familial hypercholesterolemia Ileojejunal bypass Buchwald H, Stoller DK, Campos CT, Matts JP, Varco RL (September 1990). " ... Chalstrey LJ, Winder AF, Galton DJ (November 1982). "Partial ileal bypass in treatment of familial hypercholesterolaemia". J R ... "Partial ileal bypass for hypercholesterolemia. 20- to 26-year follow-up of the first 57 consecutive cases". Ann. Surg. 212 (3 ... the procedure is used to treat a number of hyperlipidemias including familial hypercholesterolemia. The only randomized ...
In children statins are effective at reducing cholesterol levels in those with familial hypercholesterolemia. Their long term ... Statins may be less effective in reducing LDL cholesterol in people with familial hypercholesterolemia, especially those with ... Braamskamp MJ, Wijburg FA, Wiegman A (April 2012). "Drug therapy of hypercholesterolaemia in children and adolescents". Drugs. ... Rader DJ, Cohen J, Hobbs HH (June 2003). "Monogenic hypercholesterolemia: new insights in pathogenesis and treatment". The ...
The presence of palmar xanthomata, like the presence of tendinous xanthomata, is indicative of hypercholesterolaemia. ... Also associated with familial hypercholesterolemia (FH). Eruptive xanthoma (ILDS E78.220) is clinically characterized by small ... Tendon Xanthoma in Familial Hypercholesterolemia". New England Journal of Medicine. 338 (22): 1591. doi:10.1056/ ...
"OMIM Entry #144010 - HYPERCHOLESTEROLEMIA, FAMILIAL, 2; FCHL2". www.omim.org. Retrieved 2019-07-01. Simons, M.; Walz, G. ( ...
It is associated with hypercholesterolemia (typically 8-12 mmol/L), hypertriglyceridemia (typically 5-20 mmol/L), a normal ApoB ... Hyperlipidemias are also classified according to which types of lipids are elevated, that is hypercholesterolemia, ... These unclassified forms are extremely rare: Hyperalphalipoproteinemia Polygenic hypercholesterolemia Acquired hyperlipidemias ... is a commonly occurring form of hypercholesterolemia (elevated cholesterol levels) characterized by increased LDL and ...
"Sitosterolemia Presenting as Pseudohomozygous Familial Hypercholesterolemia". Clin Med Res. 14 (2): 103-8. doi:10.3121/cmr. ...
Familial hypercholesterolemia: this disorder is characterized by the absence of functional receptors for LDL. Deficiencies in ... "Novel Therapies for Treating Familial Hypercholesterolemia". Current Atherosclerosis Reports. 16 (1): 382. doi:10.1007/s11883- ...
Desai NR, Sabatine MS (Feb 2015). "PCSK9 inhibition in patients with hypercholesterolemia". Trends in Cardiovascular Medicine. ... its role in causing some cases of familial hypercholesterolaemia when some mutations are present, and its role in causing very ... from the identification of a new gene in familial hypercholesterolemia towards a potential new class of anticholesterol drugs ... added an indication for alirocumab to treat adults with homozygous familial hypercholesterolemia (HoFH), a genetic condition ...
January 2007). "Inhibition of microsomal triglyceride transfer protein in familial hypercholesterolemia". The New England ... "FDA Approves Aegerion Pharmaceuticals' Juxtapid (lomitapide) Capsules for Homozygous Familial Hypercholesterolemia (HoFH)" ( ... is a medication used as a lipid-lowering agent for the treatment of familial hypercholesterolemia, developed by Aegerion ... in patients with homozygous familial hypercholesterolemia (HoFH)." In a Phase III study, lomitapide led to elevated ...
Mannu GS, Zaman MJ, Gupta A, Rehman HU, Myint PK (October 2012). "Update on guidelines for management of hypercholesterolemia ... There are several international guidelines on the treatment of hypercholesterolaemia. Human trials using HMG-CoA reductase ... PMID 28864697.CS1 maint: multiple names: authors list (link) "Familial Hypercholesterolemia (FH)". www.heart.org. Retrieved 2 ... November 1995). "Prevention of coronary heart disease with pravastatin in men with hypercholesterolemia. West of Scotland ...
2003). "Autosomal recessive hypercholesterolemia in a Sicilian kindred harboring the 432insA mutation of the ARH gene". ... 2002). "Autosomal recessive hypercholesterolaemia in Sardinia, Italy, and mutations in ARH: a clinical and molecular genetic ... 2001). "Autosomal recessive hypercholesterolemia caused by mutations in a putative LDL receptor adaptor protein". Science. 292 ... 2005). "A novel ARH splice site mutation in a Mexican kindred with autosomal recessive hypercholesterolemia". Hum. Genet. 116 ( ...
Yamamoto, Akira; Sudo, Hiroshi; Endo, Akira (March 1980). "Therapeutic effects of ML-236B in primary hypercholesterolemia". ...
"27-Hydroxycholesterol links hypercholesterolemia and breast cancer pathophysiology". Science. 342 (6162): 1094-8. doi:10.1126/ ...
Endocrinology Hypercholesterolemia is associated with significant retinal microvascular dysfunction as evidenced in a study ... Nägele MP et al.: Retinal microvascular dysfunction in hypercholesterolemia.J Clin Lipidol. 2018;12:1523-1531 Hanssen, H; et al ... based on 67 patients with hypercholesterolemia without known cardiovascular disease by a reduction in flicker-induced ...
Zech LA, Hoeg JM (March 2008). "Correlating corneal arcus with atherosclerosis in familial hypercholesterolemia". Lipids in ...
Qin Y, Niu K, Zeng Y, Liu P, Yi L, Zhang T, Zhang QY, Zhu JD, Mi MT (2013). "Isoflavones for hypercholesterolaemia in adults". ...
Heterozygous familial hypercholesterolemia in children Homozygous familial hypercholesterolemia Hypertriglyceridemia ( ... May 1995). "Reduction of LDL cholesterol by 25% to 60% in patients with primary hypercholesterolemia by atorvastatin, a new HMG ... August 2006). "The anti-atherosclerotic effects of lipid lowering with atorvastatin in patients with hypercholesterolemia". ... Hypercholesterolemia (heterozygous familial and nonfamilial) and mixed dyslipidemia (Fredrickson types IIa and IIb) to reduce ...
Past nine months of age, hypercholesterolemia may be seen. In the final stages of the disease, at around 15 months of age for ...
"Effect of torcetrapib on carotid atherosclerosis in familial hypercholesterolemia". The New England Journal of Medicine. 356 ( ...
INMEGEN also works on identifying the biomarkers for hypercholesterolemia. INMEGEN has established collaborations with both ...
Paillard F (May 1999). "A novel soluble chimera for the treatment of familial hypercholesterolemia". Human Gene Therapy. 10 (7 ...
Mutations in the gene encoding the LDL receptor are known to cause familial hypercholesterolaemia. There are 5 broad classes of ... Hobbs HH, Brown MS, Goldstein JL (1993). "Molecular genetics of the LDL receptor gene in familial hypercholesterolemia". Human ... Barrett PH, Watts GF (March 2002). "Shifting the LDL-receptor paradigm in familial hypercholesterolemia: novel insights from ... or Medicine for their identification of LDL-R and its relation to cholesterol metabolism and familial hypercholesterolemia. The ...
... is mainly used for primary hypercholesterolemia or mixed dyslipidemia. Fenofibrate appears to decrease the risk of ... in adults with primary hypercholesterolemia or mixed dyslipidemia. Severe hypertriglyceridemia type IV or V It is used in ...
Atherosclerosis Cholesterol Hypercholesterolemia Saturated fat and cardiovascular disease Ahrens EH Jr (July 1976). "The ... Steinberg D (2002). "Atherogenesis in perspective: hypercholesterolemia and inflammation as partners in crime". Nature Medicine ...
Paillard F (1999). "A novel soluble chimera for the treatment of familial hypercholesterolemia". Hum. Gene Ther. 10 (7): 1093-4 ...
... stress reduction and hypercholesterolemia in African Americans: a review". Ethnicity & Disease. 9 (3): 451-462. ISSN 1049-510X ...
Familial hypercholesterolaemia is an inherited (genetic) condition in which affected members of a family have high levels of ... Treatment for familial hypercholesterolaemia. If you have familial hypercholesterolaemia, treatment will be directed at ... Familial hypercholesterolaemia affects about one in 500 people. Children of affected people have a 50 per cent chance of having ... People with familial hypercholesterolaemia usually have a strong personal or family history of early-onset of diseases caused ...
Background Hypercholesterolaemia is an important modifiable risk factor for cardiovascular disease (CVD) which requires ... Control of hypercholesterolaemia was defined as LDL-C below the guideline target in conjunction with the use of lipid-lowering ... Hypercholesterolaemia according to CVD risk status. A subgroup analysis was conducted on those aged 50-64 years, in whom ... Failure to control hypercholesterolaemia in the Irish adult population: cross-sectional analysis of the baseline wave of The ...
Genetics of Familial Hypercholesterolemia. Familial hypercholesterolemia (FH) can be caused by inherited changes (mutations) in ... How do I know if I have familial hypercholesterolemia?. One of the main signs of FH is LDL cholesterol levels over 190 mg/dL in ... Familial hypercholesterolemia (FH) is a genetic disorder that affects about 1 in 250 people and increases the likelihood of ... Coronavirus Disease 2019 (COVID-19) and Familial Hypercholesterolemia (FH). COVID-19 is a new disease and information on risk ...
Cascade Screening for Familial Hypercholesterolemia. By R Ned and E Sijbrands. PLoS Currents EGT 2011External. ...
Familial hypercholesterolemia is an inherited condition characterized by very high levels of cholesterol in the blood. Explore ... Familial hypercholesterolemia resulting from mutations in the LDLR, APOB, or PCSK9 gene have an autosomal dominant pattern. of ... Mutations in the APOB, LDLR, LDLRAP1, or PCSK9 gene cause familial hypercholesterolemia. Changes in the LDLR gene are the most ... When familial hypercholesterolemia is caused by mutations in the LDLRAP1 gene, the condition is inherited in an autosomal ...
Individuals with hypercholesterolemia are therefore advised to adopt lifestyle changes such as a healthy, balanced diet and ... Hypercholesterolemia or raised blood cholesterol is a risk factor for cardiovascular events such as stroke or heart attack. ... Hypercholesterolemia or raised blood cholesterol is a risk factor for cardiovascular events such as stroke or heart attack. ... A diagnosis of hypercholesterolemia is based on routine blood analysis to check levels of "bad" cholesterol, which includes ...
... to help further lower cholesterol in patients with homozygous familial hypercholesterolemia. The approval comes with a box ... The safety and effectiveness of JUXTAPID have not been established in patients with hypercholesterolemia who do not have HoFH. ... The safety and effectiveness of JUXTAPID have not been established in patients with hypercholesterolemia who do not have HoFH. ... FDA Approves Aegerion Pharmaceuticals JUXTAPID(TM) (lomitapide) Capsules for Homozygous Familial Hypercholesterolemia (HoFH). ...
Familial hypercholesterolaemia is a genetic disorder affecting 1 in 250 people. But how do you diagnose and treat it? We talk ... What is familial hypercholesterolemia?. Familial hypercholesterolaemia (or FH) is a genetic condition thought to affect roughly ... Familial hypercholesterolemia is a hereditary condition characterised by high cholesterol in your blood, increasing the risk of ... How do you diagnose and treat familial hypercholesterolaemia?. FH is diagnosed through a simple blood test that detects the ...
Thus, if the role of LOL in the pathogenesis of hypercholesterolemia was well established a great deal of information appears ... The Help-System in the Treatment of Severe Hypercholesterolaemia: Acute and Long-Term Experience ... increase and of LOL receptor deficiency or malfunctions in familial hypercholesterolemia has been largely enlightened by the ... Band/or LOL receptor The opening topic is devoted to these new avenues outlined in the field of hypercholesterolemia. The first ...
Download Familial Hypercholesterolaemia and enjoy it on your iPhone, iPad and iPod touch. ... Read reviews, compare customer ratings, see screenshots and learn more about Familial Hypercholesterolaemia. ... Familial hypercholesterolaemia (FH) - inherited high cholesterol - is one of the most common genetic conditions, affecting ... Targeting Familial Hypercholesterolaemia: EAS Guidance for Detection & Management - Børge G. Nordestgaard, John Chapman, ...
Familial hypercholesterolemia definition, an inherited metabolic disorder caused by a lack or malfunction of receptors for the ... familial hypercholesterolemia. in Medicine. familial hypercholesterolemia. n.. *. .css-10rk44a{font-size:15px;line-height:24px ...
Considering taking a vitamin or supplement to treat Familial+Hypercholesterolemia? Below is a list of common natural remedies ... used to treat or reduce the symptoms of Familial+Hypercholesterolemia. Follow the links to read common uses, side effects, ...
hypercholesterolemia synonyms, hypercholesterolemia pronunciation, hypercholesterolemia translation, English dictionary ... definition of hypercholesterolemia. n. 1. An excess of cholesterol in the blood. 2. A familial disorder characterized by high ... hypercholesterolemia. Also found in: Thesaurus, Medical, Acronyms, Encyclopedia, Wikipedia. hy·per·cho·les·ter·ol·e·mi·a. (hī′ ... Familial hypercholesterolemia: clues to catching it early: heres how to spot the red flags that could signal your patient is ...
Thus, the endothelium is a source of02 in hypercholesterolemia probably via xanthine oxidase activa-tion. Increased endothelial ... title = {Hypercholesterolemia increases endothelial superoxide production},. journal = {J Clin Invest},. year = {1993}. }. ... Thus, the endothelium is a source of02 in hypercholesterolemia probably via xanthine oxidase activa-tion. Increased endothelial ...
Familial hypercholesterolemia (FH) is an autosomal dominant disorder that causes severe elevations in total cholesterol and low ... Autosomal recessive hypercholesterolemia (ARH) and homozygous familial hypercholesterolemia (FH): a phenotypic comparison. ... Familial Hypercholesterolemia Clinical Presentation. Updated: Mar 07, 2017 * Author: Mose July, MD, CCD; Chief Editor: Romesh ... Familial hypercholesterolemia: a challenge of diagnosis and therapy. Cleve Clin J Med. 2006 Jan. 73(1):57-64. [Medline]. ...
H. P. Wu, Y. L. Hua, P. L. Xi et al., "Anti-oxidant effect of ming dang shen in rats with hypercholesterolemia," Journal of ... Y. Fu, "Clinical assessment of hypercholesterolaemia," Chinese Journal of Information on Traditional Chinese Medicine, vol. 6, ... W. H. Ren, G. Q. Huang, D. M. Xu et al., "Research on the effect of pu huang and its preparations on hypercholesterolemia and ... C. Stevinson, M. H. Pittler, and E. Ernst, "Garlic for treating hypercholesterolemia: a meta-analysis of randomize clinical ...
Hypercholesterolemia. (June 2011). "Familial hypercholesterolemia: screening, diagnosis and management of pediatric and adult ... Clinical guideline 71: Familial hypercholesterolaemia. London, 2008. *^ Kastelein JJ, Akdim F, Stroes ES, et al. (April 2008 ... Familial hypercholesterolemia (FH) is a genetic disorder characterized by high cholesterol levels, specifically very high ... 2003). "Mutations in PCSK9 cause autosomal dominant hypercholesterolemia". Nat. Genet. 34 (2): 154-6. doi:10.1038/ng1161. PMID ...
27-Hydroxycholesterol links hypercholesterolemia and breast cancer pathophysiology.. Nelson ER1, Wardell SE, Jasper JS, Park S ... Hypercholesterolemia is a risk factor for estrogen receptor (ER)-positive breast cancers and is associated with a decreased ... Genetic or pharmacological inhibition of 27-hydroxycholesterol production attenuates hypercholesterolemia-promoted tumor growth ...
Gene Therapy Strategies for Hypercholesterolemia. What is Hypercholesterolemia?. Researchers at our world-class Gene Therapy ... One form of hypercholesterolemia is due to inherited mutations in the cell receptor molecule that binds and absorbs low density ... Gaos gene therapy strategy on Hypercholesterolemia To avoid this problem, Drs. Flotte, Gao, and Zamore used an alternative to ... Even when these mice are kept on a normal diet, they have high cholesterol levels as seen in humans with hypercholesterolemia. ...
One form of hypercholesterolemia is due to inherited mutations in the cell receptor molecule that binds and absorbs low density ... Hypercholesterolemia. Researchers at our world-class Gene Therapy Center are continuously developing new methods to safely ... Even when these mice are kept on a normal diet, they have high cholesterol levels as seen in humans with hypercholesterolemia. ... High blood cholesterol levels, known as hypercholesterolemia, are a major risk factor for cardiovascular disease, the most ...
AHA: Biggest Hypercholesterolemia Challenge Is Nonadherence. by Ed Susman, Contributing Writer, MedPage Today November 11, 2007 ...
Russian Familial Hypercholesterolemia Registry. *Familial Hypercholesterolemia. Observational. *Russian Cardiology Research and ... Study of Awareness and Detection of Familial Hypercholesterolemia. *Hypercholesterolemia. Observational. *The Familial ... A Registration Study for Familial Hypercholesterolemia in Taiwan. *Familial Hypercholesterolemia. Observational. *National ... Greek Registry - Familial Hypercholesterolaemia. *Familial Hypercholesterolemia. Observational. *Hellenic College of Treatment ...
... Allen J. Orehek Dementia Prevention Center, 1 ... R. R. Williams, S. C. Hunt, M. C. Schumacher et al., "Diagnosing heterozygous familial hypercholesterolemia using new practical ... R. Beigel and Y. Beigel, "Homozygous familial hypercholesterolemia: long term clinical course and plasma exchange therapy for ...
Synonyms of Familial Hypercholesterolemia. *APOB-related familial hypercholesterolemia, autosomal dominant. *autosomal dominant ... LDLR-related familial hypercholesterolemia, autosomal dominant. *PCSK9-related familial hypercholesterolemia, autosomal ... Subdivisions of Familial Hypercholesterolemia. *heterozygous familial hypercholesterolemia. *homozygous familial ... Wilemon K and Knowles JW Proceedings of the Familial Hypercholesterolemia Foundations Inaugural Familial Hypercholesterolemia ...
NHS England and Public Health England are working to raise the profile of familial hypercholesterolaemia (FH) and break down ... clinical commissioning groups to provide adequate access to genetic cascade testing services for familial hypercholesterolemia ...
Healthy, HypercholesterolemiaPharmacokinetic and Pharmacodynamic Study of Bococizumab Alone and When Combined With Recombinant ... bococizumab 300 mg co-mixed with rHuPH20 and administered subcutaneously to subjects with hypercholesterolemia receiving a ... bococizumab 300 mg + rHuPH20 administered SC to subjects with hypercholesterolemia receiving a statin ...
Hypercholesterolemia. Introduction. Hypercholesterolemia, or high cholesterol, occurs when there is too much cholesterol in the ... Long-term cholesterol-lowering effects on Psyllium as an adjunct to diet therapy in the treatment of hypercholesterolemia. Am J ... Bravo E, Napolitano M, Lopez-Soldado I, Valeri M, Botham KM, Stefanutti C. Hypercholesterolaemia alters the responses of the ... Time- and dose-dependent effect of psyllium on serum lipids in mild-to-moderate hypercholesterolemia: a meta-analysis of ...
Our data demonstrate a relationship between hypercholesterolemia and the development of CSVD. Ldlr-/- mice appear to be an ... We thus aimed to understand the detailed relationship between hypercholesterolemia and CSVD using the well described Ldlr-/- ... Conclusions In Ldlr-/- mice, hypercholesterolemia is related to a thrombotic CSVD phenotype, which is different from ... Background While hypercholesterolemia plays a causative role for the development of ischemic stroke in large vessels, its ...
Familial hypercholesterolemia (FH) is a special form of high cholesterol . It is passed down through families. FH increases ... Familial hypercholesterolemia (FH) is a special form of high cholesterol . It is passed down through families. FH increases ... Familial hypercholesterolemia. EBSCO DynaMed Plus website. Available at: http://www.dynamed.com/topics/dmp~AN~T115368/Familial- ... hypercholesterolemia . Updated January 8, 2018. Accessed March 26, 2018. Familial hypercholesterolemia. National Institutes of ...
Genetic testing should become the standard of care for patients with definite or probable familial hypercholesterolemia (FH), ... Genetic Testing Recommended for Familial Hypercholesterolemia. Print this page FRIDAY, Sept. 14, 2018 -- Genetic testing should ... and colleagues from the JACC Scientific Expert Panel were convened by the Familial Hypercholesterolemia Foundation to assess ... become the standard of care for patients with definite or probable familial hypercholesterolemia (FH), according to a statement ...

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