AnatomyDiseasesAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPhenomena and ProcessesInformation ScienceNamed GroupsHealth CareGeographicals
CardiomegalyHydrops FetalisCardiomegaly, Exercise-InducedJamaicaRadiography, ThoracicCardiomyopathiesArteriovenous FistulaPericardial EffusionChagas CardiomyopathyFetal DiseasesUltrasonography, PrenatalHeart NeoplasmsHeart FailureFatal OutcomeElectrocardiographyEchocardiographyHeart Defects, CongenitalMyocardiumPregnancyRetrospective StudiesInfant, NewbornHypertensionPrognosisScleroderma, SystemicScleroderma, LocalizedScleroderma, DiffuseLymphangioleiomyomatosisMultiple SclerosisScleroderma, LimitedHistiocytosis, Langerhans-Cell
Cardiomegaly
Enlargement of the HEART, usually indicated by a cardiothoracic ratio above 0.50. Heart enlargement may involve the right, the left, or both HEART VENTRICLES or HEART ATRIA. Cardiomegaly is a nonspecific symptom seen in patients with chronic systolic heart failure (HEART FAILURE) or several forms of CARDIOMYOPATHIES.
Hydrops Fetalis
Abnormal accumulation of serous fluid in two or more fetal compartments, such as SKIN; PLEURA; PERICARDIUM; PLACENTA; PERITONEUM; AMNIOTIC FLUID. General fetal EDEMA may be of non-immunologic origin, or of immunologic origin as in the case of ERYTHROBLASTOSIS FETALIS.
Cardiomegaly, Exercise-Induced
Heart enlargement and other remodeling in cardiac morphology and electrical circutry found in individuals who participate in intense repeated exercises.
Jamaica
An island in the Greater Antilles in the West Indies. Its capital is Kingston. It was discovered in 1494 by Columbus and was a Spanish colony 1509-1655 until captured by the English. Its flourishing slave trade was abolished in the 19th century. It was a British colony 1655-1958 and a territory of the West Indies Federation 1958-62. It achieved full independence in 1962. The name is from the Arawak Xaymaca, rich in springs or land of springs. (From Webster's New Geographical Dictionary, 1988, p564 & Room, Brewer's Dictionary of Names, 1992, p267)
Radiography, Thoracic
X-ray visualization of the chest and organs of the thoracic cavity. It is not restricted to visualization of the lungs.
Cardiomyopathies
A group of diseases in which the dominant feature is the involvement of the CARDIAC MUSCLE itself. Cardiomyopathies are classified according to their predominant pathophysiological features (DILATED CARDIOMYOPATHY; HYPERTROPHIC CARDIOMYOPATHY; RESTRICTIVE CARDIOMYOPATHY) or their etiological/pathological factors (CARDIOMYOPATHY, ALCOHOLIC; ENDOCARDIAL FIBROELASTOSIS).
Arteriovenous Fistula
An abnormal direct communication between an artery and a vein without passing through the CAPILLARIES. An A-V fistula usually leads to the formation of a dilated sac-like connection, arteriovenous aneurysm. The locations and size of the shunts determine the degree of effects on the cardiovascular functions such as BLOOD PRESSURE and HEART RATE.
Pericardial Effusion
Fluid accumulation within the PERICARDIUM. Serous effusions are associated with pericardial diseases. Hemopericardium is associated with trauma. Lipid-containing effusion (chylopericardium) results from leakage of THORACIC DUCT. Severe cases can lead to CARDIAC TAMPONADE.
Chagas Cardiomyopathy
A disease of the CARDIAC MUSCLE developed subsequent to the initial protozoan infection by TRYPANOSOMA CRUZI. After infection, less than 10% develop acute illness such as MYOCARDITIS (mostly in children). The disease then enters a latent phase without clinical symptoms until about 20 years later. Myocardial symptoms of advanced CHAGAS DISEASE include conduction defects (HEART BLOCK) and CARDIOMEGALY.
Fetal Diseases
Pathophysiological conditions of the FETUS in the UTERUS. Some fetal diseases may be treated with FETAL THERAPIES.
Ultrasonography, Prenatal
The visualization of tissues during pregnancy through recording of the echoes of ultrasonic waves directed into the body. The procedure may be applied with reference to the mother or the fetus and with reference to organs or the detection of maternal or fetal disease.
Heart Neoplasms
Tumors in any part of the heart. They include primary cardiac tumors and metastatic tumors to the heart. Their interference with normal cardiac functions can cause a wide variety of symptoms including HEART FAILURE; CARDIAC ARRHYTHMIAS; or EMBOLISM.
Heart Failure
A heterogeneous condition in which the heart is unable to pump out sufficient blood to meet the metabolic need of the body. Heart failure can be caused by structural defects, functional abnormalities (VENTRICULAR DYSFUNCTION), or a sudden overload beyond its capacity. Chronic heart failure is more common than acute heart failure which results from sudden insult to cardiac function, such as MYOCARDIAL INFARCTION.
Fatal Outcome
Death resulting from the presence of a disease in an individual, as shown by a single case report or a limited number of patients. This should be differentiated from DEATH, the physiological cessation of life and from MORTALITY, an epidemiological or statistical concept.
Electrocardiography
Recording of the moment-to-moment electromotive forces of the HEART as projected onto various sites on the body's surface, delineated as a scalar function of time. The recording is monitored by a tracing on slow moving chart paper or by observing it on a cardioscope, which is a CATHODE RAY TUBE DISPLAY.
Echocardiography
Ultrasonic recording of the size, motion, and composition of the heart and surrounding tissues. The standard approach is transthoracic.
Heart Defects, Congenital
Developmental abnormalities involving structures of the heart. These defects are present at birth but may be discovered later in life.
Myocardium
The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.
Pregnancy
The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.
Retrospective Studies
Studies used to test etiologic hypotheses in which inferences about an exposure to putative causal factors are derived from data relating to characteristics of persons under study or to events or experiences in their past. The essential feature is that some of the persons under study have the disease or outcome of interest and their characteristics are compared with those of unaffected persons.
Infant, Newborn
An infant during the first month after birth.
Hypertension
Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.
Prognosis
A prediction of the probable outcome of a disease based on a individual's condition and the usual course of the disease as seen in similar situations.
Scleroderma, Systemic
A chronic multi-system disorder of CONNECTIVE TISSUE. It is characterized by SCLEROSIS in the SKIN, the LUNGS, the HEART, the GASTROINTESTINAL TRACT, the KIDNEYS, and the MUSCULOSKELETAL SYSTEM. Other important features include diseased small BLOOD VESSELS and AUTOANTIBODIES. The disorder is named for its most prominent feature (hard skin), and classified into subsets by the extent of skin thickening: LIMITED SCLERODERMA and DIFFUSE SCLERODERMA.
Scleroderma, Localized
A term used to describe a variety of localized asymmetrical SKIN thickening that is similar to those of SYSTEMIC SCLERODERMA but without the disease features in the multiple internal organs and BLOOD VESSELS. Lesions may be characterized as patches or plaques (morphea), bands (linear), or nodules.
Scleroderma, Diffuse
A rapid onset form of SYSTEMIC SCLERODERMA with progressive widespread SKIN thickening over the arms, the legs and the trunk, resulting in stiffness and disability.
Lymphangioleiomyomatosis
A disease characterized by the progressive invasion of SMOOTH MUSCLE CELLS into the LYMPHATIC VESSELS, and the BLOOD VESSELS. The majority of the cases occur in the LUNGS of women of child-bearing age, eventually blocking the flow of air, blood, and lymph. The common symptom is shortness of breath (DYSPNEA).
Multiple Sclerosis
An autoimmune disorder mainly affecting young adults and characterized by destruction of myelin in the central nervous system. Pathologic findings include multiple sharply demarcated areas of demyelination throughout the white matter of the central nervous system. Clinical manifestations include visual loss, extra-ocular movement disorders, paresthesias, loss of sensation, weakness, dysarthria, spasticity, ataxia, and bladder dysfunction. The usual pattern is one of recurrent attacks followed by partial recovery (see MULTIPLE SCLEROSIS, RELAPSING-REMITTING), but acute fulminating and chronic progressive forms (see MULTIPLE SCLEROSIS, CHRONIC PROGRESSIVE) also occur. (Adams et al., Principles of Neurology, 6th ed, p903)
Scleroderma, Limited
The least progressive form of SYSTEMIC SCLERODERMA with skin thickening restricted to the face, neck and areas distal to the elbows and/or knees, sparing the trunk. The CREST SYNDROME is a form of limited scleroderma.
Histiocytosis, Langerhans-Cell
A group of disorders resulting from the abnormal proliferation of and tissue infiltration by LANGERHANS CELLS which can be detected by their characteristic Birbeck granules (X bodies), or by monoclonal antibody staining for their surface CD1 ANTIGENS. Langerhans-cell granulomatosis can involve a single organ, or can be a systemic disorder.

Gender-related differences in myocyte remodeling in progression to heart failure. (1/3277)

Gender-related differences responsible for the better prognosis of females with heart failure have not been clearly established. To address this issue, we investigated potential gender-related differences in myocyte remodeling in spontaneously hypertensive heart failure rats. Echocardiograms and myocyte growth were compared between males and females at compensated (2, 4, and 6 months) and decompensated (18 months in males and 24 months in females) stages of cardiac hypertrophy. Although left ventricular diastolic dimensions did not differ significantly between failing male and female rats, fractional shortening declined significantly only in failing males. Myocyte cross-sectional area did not change after 4 months of age in both genders, which is likely to be responsible for the absence of a change in left ventricular wall thickness during the progression to heart failure. Myocyte volume and cross-sectional area were significantly larger in males than females at 2, 4, and 6 months of age, although there were no significant differences at the failing stage. Reduced adaptive hypertrophic reserve was observed in males, which is likely to contribute to the higher morbidity and mortality of males with chronic heart failure.  (+info)

Cardiomegaly in the juvenile visceral steatosis (JVS) mouse is reduced with acute elevation of heart short-chain acyl-carnitine level after L-carnitine injection. (2/3277)

The long-term administration of L-carnitine was very effective in preventing cardiomegaly in juvenile visceral steatosis (JVS) mice, which was confirmed by heart weight as well as the lipid contents in heart tissue. After i.p. injection of L-carnitine, the concentration of free carnitine in heart remained constant, although serum free carnitine level increased up to 80-fold. On the other hand, a significant increase in short-chain acyl-carnitine level in heart was observed. These results suggest that increased levels of short-chain acyl-carnitine, not free carnitine, might be a key compound in the protective effect of L-carnitine administration in JVS mice.  (+info)

Cellular mechanisms of altered contractility in the hypertrophied heart: big hearts, big sparks. (3/3277)

To investigate the cellular mechanisms for altered Ca2+ homeostasis and contractility in cardiac hypertrophy, we measured whole-cell L-type Ca2+ currents (ICa,L), whole-cell Ca2+ transients ([Ca2+]i), and Ca2+ sparks in ventricular cells from 6-month-old spontaneously hypertensive rats (SHRs) and from age- and sex-matched Wistar-Kyoto and Sprague-Dawley control rats. By echocardiography, SHR hearts had cardiac hypertrophy and enhanced contractility (increased fractional shortening) and no signs of heart failure. SHR cells had a voltage-dependent increase in peak [Ca2+]i amplitude (at 0 mV, 1330+/-62 nmol/L [SHRs] versus 836+/-48 nmol/L [controls], P<0.05) that was not associated with changes in ICa,L density or kinetics, resting [Ca2+]i, or Ca2+ content of the sarcoplasmic reticulum (SR). SHR cells had increased time of relaxation. Ca2+ sparks from SHR cells had larger average amplitudes (173+/-192 nmol/L [SHRs] versus 109+/-64 nmol/L [control]; P<0.05), which was due to redistribution of Ca2+ sparks to a larger amplitude population. This change in Ca2+ spark amplitude distribution was not associated with any change in the density of ryanodine receptors, calsequestrin, junctin, triadin 1, Ca2+-ATPase, or phospholamban. Therefore, SHRs with cardiac hypertrophy have increased contractility, [Ca2+]i amplitude, time to relaxation, and average Ca2+ spark amplitude ("big sparks"). Importantly, big sparks occurred without alteration in the trigger for SR Ca2+ release (ICa,L), SR Ca2+ content, or the expression of several SR Ca2+-cycling proteins. Thus, cardiac hypertrophy in SHRs is linked with an alteration in the coupling of Ca2+ entry through L-type Ca2+ channels and the release of Ca2+ from the SR, leading to big sparks and enhanced contractility. Alterations in the microdomain between L-type Ca2+ channels and SR Ca2+ release channels may underlie the changes in Ca2+ homeostasis observed in cardiac hypertrophy. Modulation of SR Ca2+ release may provide a new therapeutic strategy for cardiac hypertrophy and for its progression to heart failure and sudden death.  (+info)

Rho family small G proteins play critical roles in mechanical stress-induced hypertrophic responses in cardiac myocytes. (4/3277)

-Mechanical stress induces a variety of hypertrophic responses, such as activation of protein kinases, reprogramming of gene expression, and an increase in protein synthesis. In the present study, to elucidate how mechanical stress induces such events, we examined the role of Rho family small GTP-binding proteins (G proteins) in mechanical stress-induced cardiac hypertrophy. Treatment of neonatal rat cardiomyocytes with the C3 exoenzyme, which abrogates Rho functions, suppressed stretch-induced activation of extracellular signal-regulated protein kinases (ERKs). Overexpression of the Rho GDP dissociation inhibitor (Rho-GDI), dominant-negative mutants of RhoA (DNRhoA), or DNRac1 significantly inhibited stretch-induced activation of transfected ERK2. Overexpression of constitutively active mutants of RhoA slightly activated ERK2 in cardiac myocytes. Overexpression of C-terminal Src kinase, which inhibits functions of the Src family of tyrosine kinases, or overexpression of DNRas had no effect on stretch-induced activation of transfected ERK2. The promoter activity of skeletal alpha-actin and c-fos genes was increased by stretch, and these increases were completely inhibited by either cotransfection of Rho-GDI or pretreatment with C3 exoenzyme. Mechanical stretch increased phenylalanine incorporation into cardiac myocytes by approximately 1.5-fold compared with control, and this increase was also significantly suppressed by pretreatment with C3 exoenzyme. Overexpression of Rho-GDI or DNRhoA did not affect angiotensin II-induced activation of ERK. ERKs were activated by culture media conditioned by stretch of cardiomyocytes without any treatment, but not of cardiomyocytes with pretreatment by C3 exoenzyme. These results suggest that the Rho family of small G proteins plays critical roles in mechanical stress-induced hypertrophic responses.  (+info)

TAFII250, Egr-1, and D-type cyclin expression in mice and neonatal rat cardiomyocytes treated with doxorubicin. (5/3277)

Differential display identified that gene fragment HA220 homologous to the transcriptional activator factor II 250 (TAFII250) gene, or CCG1, was increased in hypertrophied rodent heart. To determine whether TAFII250 gene expression is modified after cardiac damage, we measured TAFII250 expression in vivo in mouse hearts after injection of the cardiotoxic agent doxorubicin (DXR) and in vitro in DXR-treated isolated rat neonatal cardiomyocytes. In vivo atrial natriuretic factor (ANF), beta-myosin heavy chain (beta-MHC), Egr-1, and TAFII250 expression increased with dose and time after a single DXR injection, but only ANF and beta-MHC expression were increased after multiple injections. After DXR treatment of neonatal cardiomyocytes we found decreased ANF, alpha-MHC, Egr-1, and TAFII250 expression. Expression of the TAFII250-regulated genes, the D-type cyclins, was increased after a single injection in adult mice and was decreased in DXR-treated cardiomyocytes. Thus expression of Erg-1, TAFII250, and the D-type cyclins is modulated after cardiotoxic damage in adult and neonatal heart.  (+info)

Heart hypertrophy induced by levothyroxine aggravates ischemic lesions and reperfusion arrhythmias in rats. (6/3277)

AIM: To develop a cardiac hypertrophic model in rats. METHODS: Rats were i.p. levothyroxine 0.5 mg.kg-1.d-1 x 10 d. The action potentials of right papillary muscles were recorded by standard glass-microelectrode technique. The left coronary artery was ligated followed by reperfusion and the apparent infarcted zone (AIZ) was determined by tetracycline fluoresence, and the superoxide dismutase (SOD) activity and malondialdehyde (MDA) product in myocardium were also measured. RESULTS: In the rats treated by levothyroxine, the heart was hypertrophic and the action potential duration (APD) and effective refractory period (ERP) were prolonged, the APD20, APD50, APD90, and ERP were prolonged by 80%, 79%, 74%, and 68%, respectively. No changes in resting potential (RP), action potential amplitude (APA), and Vmax were produced. The incidence of heart arrest (8/8) and the risk of death (67 +/- 0) induced by ischemia-reperfusion in rats with hypertrophic heart was higher than those in normal rats (4/10 and 44 +/- 19, respectively). The AIZ was expanded markedly in hypertrophic heart, and attenuated by lidocaine and propranolol. CONCLUSION: Levothyroxine-induced heart hypertrophy is a suitable model for severe ischemia and arrhythmias in rats.  (+info)

A case of eosinophilic myocarditis complicated by Kimura's disease (eosinophilic hyperplastic lymphogranuloma) and erythroderma. (7/3277)

This report describes a patient with eosinophilic myocarditis complicated by Kimura's disease (eosinophilic hyperplastic lymphogranuloma) and erythroderma. A 50-year-old man presented with a complaint of precordial pain. However, the only abnormal finding on examinatioin was eosinophilia (1617 eosinophils/microl). Three years later, the patient developed chronic eczema, and was diagnosed with erythroderma posteczematosa. One year later, a tumor was detected in the right auricule, and a diagnosis of Kimura's disease was made, based on the biopsy findings. The patient developed progressive dyspnea 6 months later and was found to have cardiomegaly and a depressed left ventricular ejection fraction (17%). A diagnosis of eosinophilic myocarditis was made based on the results of a right ventricular endomyocardial biopsy. The eosinophilic myocarditis and erythrodrema were treated with steroids with improvement of both the eosinophilia and left ventricular function.  (+info)

Transcriptional activation of the glucose transporter GLUT1 in ventricular cardiac myocytes by hypertrophic agonists. (8/3277)

Myocardial hypertrophy is associated with increased basal glucose metabolism. Basal glucose transport into cardiac myocytes is mediated by the GLUT1 isoform of glucose transporters, whereas the GLUT4 isoform is responsible for regulatable glucose transport. Treatment of neonatal cardiac myocytes with the hypertrophic agonist 12-O-tetradecanoylphorbol-13-acetate or phenylephrine increased expression of Glut1 mRNA relative to Glut4 mRNA. To study the transcriptional regulation of GLUT1 expression, myocytes were transfected with luciferase reporter constructs under the control of the Glut1 promoter. Stimulation of the cells with 12-O-tetradecanoylphorbol-13-acetate or phenylephrine induced transcription from the Glut1 promoter, which was inhibited by cotransfection with the mitogen-activated protein kinase phosphatases CL100 and MKP-3. Cotransfection of the myocytes with constitutively active versions of Ras and MEK1 or an estrogen-inducible version of Raf1 also stimulated transcription from the Glut1 promoter. Hypertrophic induction of the Glut1 promoter was also partially sensitive to inhibition of the phosphatidylinositol 3-kinase pathway and was strongly inhibited by cotransfection with dominant-negative Ras. Thus, Ras activation and pathways downstream of Ras mediate induction of the Glut1 promoter during myocardial hypertrophy.  (+info)

Microtubule Stabilization in Pressure Overload Cardiac Hypertrophy | JCBMicrotubule Stabilization in Pressure Overload Cardiac Hypertrophy | JCB
The cardiocyte contractile dysfunction characteristic of pressure overload cardiac hypertrophy is accounted for to a remarkable degree by increased density of the cellular microtubule network (Tsutsui et al., 1993, 1994), which imposes a primarily viscous load on active myofilaments; that is, structural damping via intracellular frictional dissipation that impedes sarcomere shortening (Tagawa et al., 1997). This is accompanied by persistent increases in α- and β-tubulin on both the mRNA and protein levels (Tagawa et al., 1996). Thus, increased synthesis of αβ-tubulin heterodimers, effecting in turn microtubule formation, is one apparent cause for this greater microtubule density. Given, however, that the αβ-tubulin heterodimer-microtubule system is in dynamic equilibrium, enhanced microtubule stability is a second, and potentially synergistic, candidate mechanism for augmented microtubule density. This study was designed to evaluate this second potential mechanism.. The restriction of the ...
http://jcb.rupress.org/content/139/4/963
Mineralocorticoid Receptor Deficiency in T Cells Attenuates Pressure Overload-Induced Cardiac Hypertrophy and Dysfunction...Mineralocorticoid Receptor Deficiency in T Cells Attenuates Pressure Overload-Induced Cardiac Hypertrophy and Dysfunction...
Although functions of MR in several other cell types have been elucidated in pathologic cardiac hypertrophy and heart failure,15-17,19,36-38 the roles of MR in T cells have not been illuminated. Through this study, we demonstrated that eplerenone and TMRKO attenuated POL-induced cardiac remodeling and dysfunction in parallel with attenuated cardiac inflammation, as well as decreased T-cell accumulation and activation in the heart. Moreover, in vitro results illustrated direct regulation of T-cell activation by MR.. This study implies that MR blockade in T cells is a feasible approach to treat pathologic cardiac hypertrophy and heart failure. MR deficiency in T cells was sufficient to suppress POL-induced cardiac hypertrophy, cardiac fibrosis, and cardiac dysfunction, as well as cardiac inflammation in mice. Particularly, TMRKO completely abrogated parts of the phenotype 1 week after POL, indicating that MR in T cells may be more important than MR in other cellular compartments in the early stage ...
http://hyper.ahajournals.org/content/70/1/137
c-Myc alters substrate utilization and O-GlcNAc protein posttranslational modifications without altering cardiac function...c-Myc alters substrate utilization and O-GlcNAc protein posttranslational modifications without altering cardiac function...
The protooncogene C-Myc (Myc) regulates cardiac hypertrophy. Myc promotes compensated cardiac function, suggesting that the operative mechanisms differ from those leading to heart failure. Myc regulation of substrate metabolism is a reasonable target, as Myc alters metabolism in other tissues. We hypothesize that Myc-induced shifts in substrate utilization signal and promote compensated hypertrophy. We used cardiac specific Myc-inducible C57/BL6 male mice between 4-6 months old that develop hypertrophy with tamoxifen (tam). Isolated working hearts and 13Carbon (13C )-NMR were used to measure function and fractional contributions (Fc) to the citric acid cycle by using perfusate containing 13C-labeled free fatty acids,more » acetoacetate, lactate, unlabeled glucose and insulin. Studies were performed at pre-hypertrophy (3-days tam, 3dMyc), established hypertrophy (7-days tam, 7dMyc) or vehicle control (cont). Non-transgenic siblings (NTG) received 7-days tam or vehicle to assess drug effect. ...
https://www.osti.gov/pages/biblio/1229960-myc-alters-substrate-utilization-glcnac-protein-posttranslational-modifications-without-altering-cardiac-function-during-early-aortic-constriction
Inhibition of angiotensin II-induced cardiac hypertrophy and associated ventricular arrhythmias by a p21 activated kinase 1...
Cardiac hypertrophy increases the risk of morbidity and mortality of cardiovascular disease and thus inhibiting such hypertrophy is beneficial. In the present study, we explored the effect of a bioactive peptide (PAP) on angiotensin II (Ang II)-induced hypertrophy and associated ventricular arrhythmias in in vitro and in vivo models. PAP enhances p21 activated kinase 1 (Pak1) activity by increasing the level of phosphorylated Pak1 in cultured neonatal rat ventricular myocytes (NRVMs). Such PAP-induced Pak1 activation is associated with a significant reduction of Ang II-induced hypertrophy in NRVMs and C57BL/6 mice, in vitro and in vivo, respectively. Furthermore, PAP antagonizes ventricular arrhythmias associated with Ang II-induced hypertrophy in mice. Its antiarrhythmic effect is likely to be involved in multiple mechanisms to affect both substrate and trigger of ventricular arrhythmogenesis. Thus our results suggest that Pak1 activation achieved by specific bioactive peptide represents a potential
https://www.cardioscience.ox.ac.uk/publications/475681
Growth Arrest-Specific 6 Exacerbates Pressure Overload-Induced Cardiac HypertrophyNovelty and Significance | HypertensionGrowth Arrest-Specific 6 Exacerbates Pressure Overload-Induced Cardiac HypertrophyNovelty and Significance | Hypertension
Pathological cardiac hypertrophy is a complicated dynamic process that ultimately leads to heart failure. At present, we still have few effective methods to reverse pathological cardiac hypertrophy. Because the cardiovascular mortality increased 6- to 10-fold because of the development of pathological cardiac hypertrophy,21 it is of great importance to elucidate the underlying molecular mechanism of cardiac hypertrophy and discover potential target molecules to regulate pathological cardiac hypertrophy. Using genetic loss-of-function and gain-of-function animal models, the present study provides the systemic direct evidence that selective inhibition of GAS6 may be a therapeutic target for treating cardiac hypertrophy and congestive heart failure.. Mechanical stress and neurohormone stimuli are the 2 major causes for pathological cardiac hypertrophy.22 Both of these initially cause number of extracellular molecules to bind with their receptors and subsequently activate intrinsic signaling ...
http://hyper.ahajournals.org/content/67/1/118
Abstract 18184: Deficiency in the Novel Small Leucin-Rich Repeat Protein Podocan Promotes Pressure Load-Induced Cardiac...Abstract 18184: Deficiency in the Novel Small Leucin-Rich Repeat Protein Podocan Promotes Pressure Load-Induced Cardiac...
Background: Extracellular matrix (ECM) molecules have been increasingly implicated in cardiac remodeling, and in particular the myocardial response to pressure overload. Podocan is a novel member of the small leucin-rich-repeat protein family of ECM proteins. We recently have characterized podocan as an inhibitor of the migration and proliferation of vascular smooth muscle cells. Now we are testing if podocan deficiency has an effect on pressure load-induced cardiac hypertrophy.. Methods and Results: We induced pressure overload cardiac hypertrophy using aortic banding (AB) in mice (age 10-12 weeks) with podocan-/- (n=6) and wild-type (WT) (n=7) genotype. Four weeks after AB, cardiac anatomy and function were assessed by echocardiography. In addition, histological analysis was used to assess the myocardial response to AB. Podocan-deficient mice showed significantly greater cardiac hypertrophy compared with WT mice after AB, whereas no significant differences were observed when comparing ...
http://circ.ahajournals.org/content/128/Suppl_22/A18184
Neuron-derived orphan receptor-1 modulates cardiac gene expression and exacerbates angiotensin II-induced cardiac hypertrophy |...Neuron-derived orphan receptor-1 modulates cardiac gene expression and exacerbates angiotensin II-induced cardiac hypertrophy |...
Hypertensive cardiac hypertrophy (HCH) is a common cause of heart failure (HF), a major public health problem worldwide. However, the molecular bases of HCH have not been completely elucidated. Neuron-derived orphan receptor-1 (NOR-1) is a nuclear receptor whose role in cardiac remodelling is poorly understood. The aim of the present study was to generate a transgenic mouse over-expressing NOR-1 in the heart (TgNOR-1) and assess the impact of this gain-of-function on HCH. The CAG promoter-driven transgenesis led to viable animals that over-expressed NOR-1 in the heart, mainly in cardiomyocytes and also in cardiofibroblasts. Cardiomyocytes from TgNOR-1 exhibited an enhanced cell surface area and myosin heavy chain 7 (Myh7)/Myh6 expression ratio, and increased cell shortening elicited by electric field stimulation. TgNOR-1 cardiofibroblasts expressed higher levels of myofibroblast markers than wild-type (WT) cells (α 1 skeletal muscle actin (Acta1), transgelin (Sm22α)) and were more prone to ...
https://www.portlandpress.com/clinsci/article-abstract/134/3/359/221950/Neuron-derived-orphan-receptor-1-modulates-cardiac?redirectedFrom=fulltext
Parsing the roles of the transcription factors GATA-4 and GATA-6 in the adult cardiac hypertrophic response<...Parsing the roles of the transcription factors GATA-4 and GATA-6 in the adult cardiac hypertrophic response<...
TY - JOUR. T1 - Parsing the roles of the transcription factors GATA-4 and GATA-6 in the adult cardiac hypertrophic response. AU - Van Berlo, Jop H.. AU - Aronow, Bruce J.. AU - Molkentin, Jeffery D.. PY - 2013/12/31. Y1 - 2013/12/31. N2 - The transcriptional code that programs cardiac hypertrophy involves the zinc finger-containing DNA binding factors GATA-4 and GATA-6, both of which are required to mount a hypertrophic response of the adult heart. Here we performed conditional gene deletion of Gata4 or Gata6 in the mouse heart in conjunction with reciprocal gene replacement using a transgene encoding either GATA-4 or GATA-6 in the heart as a means of parsing dosage effects of GATA-4 and GATA-6 versus unique functional roles. We determined that GATA-4 and GATA-6 play a redundant and dosage-sensitive role in programming the hypertrophic growth response of the heart following pressure overload stimulation. However, non-redundant functions were identified in allowing the heart to compensate and ...
https://experts.umn.edu/en/publications/parsing-the-roles-of-the-transcription-factors-gata-4-and-gata-6-
Carnitine palmitoyltransferase-1b deficiency aggravates pressure overload-induced cardiac hypertrophy caused by lipotoxicity. ...Carnitine palmitoyltransferase-1b deficiency aggravates pressure overload-induced cardiac hypertrophy caused by lipotoxicity. ...
Circulation. 2012 Oct 2;126(14):1705-16. doi: 10.1161/CIRCULATIONAHA.111.075978. Epub 2012 Aug 29. Research Support, N.I.H., Extramural
https://www.ncbi.nlm.nih.gov/pubmed/22932257?dopt=Abstract
Cardiomegaly - WikipediaCardiomegaly - Wikipedia
Cardiomegaly is a medical condition in which the heart is enlarged. It is more commonly referred to as an enlarged heart. The causes of cardiomegaly may vary. Many times this condition results from high blood pressure (hypertension) or coronary artery disease. An enlarged heart may not pump blood effectively, resulting in congestive heart failure. Cardiomegaly may improve over time, but many people with an enlarged heart need lifelong treatment with medications. Having an immediate family member who has or had cardiomegaly may indicate that a person is more susceptible to getting this condition. Cardiomegaly is not a disease but rather a condition that can result from a host of other diseases such as obesity or coronary artery disease. Recent studies suggest that cardiomegaly is associated with a higher risk of sudden cardiac death (SCD). Cardiomegaly is a condition affecting the cardiovascular system, specifically the heart. This condition is strongly associated with congestive heart failure. ...
https://en.wikipedia.org/wiki/Cardiomegaly
Cardiomegaly - WikipediaCardiomegaly - Wikipedia
The causes of cardiomegaly are not well understood and many cases of cardiomegaly are idiopathic (having no known cause). Prevention of cardiomegaly starts with detection. If a person has a family history of cardiomegaly, one should let ones doctor know so that treatments can be implemented to help prevent worsening of the condition. In addition, prevention includes avoiding certain lifestyle risk factors such as tobacco use and controlling ones high cholesterol, high blood pressure, and diabetes. Non-lifestyle risk factors include family history of cardiomegaly, coronary artery disease (CAD), congenital heart failure, Atherosclerotic disease, valvular heart disease, exposure to cardiac toxins, sleep disordered breathing (such as sleep apnea), sustained cardiac arrhythmias, abnormal electrocardiograms, and cardiomegaly on chest X-ray. Lifestyle factors which can help prevent cardiomegaly include eating a healthy diet, controlling blood pressure, exercise, medications, and not abusing alcohol ...
https://en.m.wikipedia.org/wiki/Enlarged_heart
Abstract 13685: Toll-Like Receptor 2 Mediates Cardiac Adaptive Response to Pressure Overload | CirculationAbstract 13685: Toll-Like Receptor 2 Mediates Cardiac Adaptive Response to Pressure Overload | Circulation
Background: Toll-like receptors (TLRs) are a class of proteins that play a key role in the innate immune system. TLR2 is a member of the TLR family, and has been shown to recognize not only foreign substances, but also endogenous ligands, which induce inflammatory response called homeostatic inflammation. Recently, homeostatic inflammation has been revealed to contribute to the pathophysiology of various diseases. However, the role of homeostatic inflammation mediated by TLR2 on pressure overload-induced cardiac hypertrophy remains unclear.. Methods and Results: Pressure overload was induced in 8- to 12-week-old wild-type (WT) and TLR2 knock-out (KO) mice by transverse aortic constriction (TAC). In WT mice, TLR2 mRNA expression at 2 weeks after TAC was up-regulated compared with that after sham operation (1.32±0.18 versus 0.50±0.03, n=4, p=0.004). At 2 weeks after TAC, KO mice showed reduced cardiac hypertrophy and fibrosis with more left ventricular dilatation and impaired systolic function ...
http://circ.ahajournals.org/content/126/Suppl_21/A13685
cardiomegaly - Symptoms, Treatments and Resources for cardiomegalycardiomegaly - Symptoms, Treatments and Resources for cardiomegaly
cardiomegaly - MedHelps cardiomegaly Center for Information, Symptoms, Resources, Treatments and Tools for cardiomegaly. Find cardiomegaly information, treatments for cardiomegaly and cardiomegaly symptoms.
http://www.medhelp.org/tags/show/1502/cardiomegaly
Genetic Manipulation of Periostin Expression Reveals a Role in Cardiac Hypertrophy and Ventricular Remodeling | Circulation...Genetic Manipulation of Periostin Expression Reveals a Role in Cardiac Hypertrophy and Ventricular Remodeling | Circulation...
Here we observed that Pn contributes to the cardiac hypertrophic response, an observation that was not anticipated, given its primary function as an ECM cellular adhesion protein. That a cellular adhesion protein might affect the cardiac hypertrophic response is not without precedence, especially given the known importance of integrins in regulating cardiac reactive signaling4,35 and given the known role of Pn as a substrate for multiple combinations of integrins. For example, both focal adhesion kinase and integrin-linked kinase, which are intracellular signaling components of the integrin complex, function as important regulators of the cardiac hypertrophy response.36,37 Indeed, mice lacking the protein osteopontin, which is another cardiac inducible and secreted ECM protein that binds integrins, showed less pressure overload hypertrophy compared with wild-type mice.38 Based on these results, it is tempting to speculate that Pn alters the cardiac hypertrophic response by affecting signaling ...
http://circres.ahajournals.org/content/101/3/313
Activation of Hypoxia-Inducible Factor-2 in Adipocytes Results in Pathological Cardiac Hypertrophy | Journal of the American...Activation of Hypoxia-Inducible Factor-2 in Adipocytes Results in Pathological Cardiac Hypertrophy | Journal of the American...
Our findings presented herein have uncovered a previously unappreciated transcription factor pathway, mediated by HIF-2 in adipocytes, that plays a critical role in the regulation of adipocyte functions. Chronic activation of HIF-2, but not HIF-1, in adipocytes leads to adipose inflammation and pathological hypertrophy in the heart. The hypertrophic heart conditions presented by our mouse models are reminiscent of the cardiac hypertrophy observed in severely obese persons.2 Our solid genetic evidence strongly suggests that adipose hypoxia, observed under the condition of pathological obesity,5-7 may facilitate the development of obesity-related cardiac hypertrophy via sustained activation of HIF-2 in adipocytes.. Our findings demonstrate that HIF activation in adipocytes exerts its cardiac effects in a manner distinct from other purported mechanisms linked to obesity-associated cardiomyopathy. The pathological cardiomegaly observed herein occurs in the absence of lipid accumulation in blood ...
http://jaha.ahajournals.org/content/2/6/e000548
Speckle Tracking Based Strain Analysis Is Sensitive for Early Detection of Pathological Cardiac Hypertrophy - pdf descargar
Speckle Tracking Based Strain Analysis Is Sensitive for Early Detection of Pathological Cardiac Hypertrophy. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.
http://libros.duhnnae.com/2017/jun9/149853919176-Speckle-Tracking-Based-Strain-Analysis-Is-Sensitive-for-Early-Detection-of-Pathological-Cardiac-Hypertrophy.php
Regulation of fetal gene expression in heart failure<...
TY - JOUR. T1 - Regulation of fetal gene expression in heart failure. AU - Dirkx, Ellen. AU - da Costa Martins, Paula A.. AU - De Windt, Leon J.. PY - 2013/12. Y1 - 2013/12. KW - Gene regulation. KW - Transcription factors. KW - Epigenetics. U2 - 10.1016/j.bbadis.2013.07.023. DO - 10.1016/j.bbadis.2013.07.023. M3 - Article. VL - 1832. SP - 2414. EP - 2424. JO - Biochimica et Biophysica Acta-Molecular Basis of Disease. JF - Biochimica et Biophysica Acta-Molecular Basis of Disease. SN - 0925-4439. IS - 12. ER - ...
https://cris.maastrichtuniversity.nl/en/publications/regulation-of-fetal-gene-expression-in-heart-failure
Plus itPlus it
Physiological cardiac growth occurs during postnatal development, and in response to long-term exercise training (15). This form of hypertrophy is associated with normal or enhanced cardiac function and normal cardiac structure. In contrast, pathological cardiac hypertrophy may arise as a compensatory mechanism against increased myocyte stress in many disease states. Any initial benefit is however overridden by eventual derangement of myocardial architecture and deterioration of function (15). Diabetic cardiomyopathy is characterized by adverse structural changes to the heart, including increased cardiac fibrosis (pathological in nature) and cardiomyocyte hypertrophy. Our results show that diabetes increased several markers of cardiomyocyte hypertrophy, including cardiomyocyte width as well as gene expression of β-myosin heavy chain, ANP, and BNP as previously described (13). No changes in heart weight-to-body weight or heart weight-to-tibia length ratios were observed in Ntg diabetic mice, ...
http://diabetes.diabetesjournals.org/content/59/6/1512
glossary:cardiomegaly [Lymphedema People]glossary:cardiomegaly [Lymphedema People]
An abnormal enlargement of the heart; mild cardiomegaly is common in athletes. Cardiomegaly is a condition wherein the heart enlarges in a cardiothoracic ratio of more than 0.50. It can be attributed to a lot of causes, but mostly it is because of low heart output, otherwise referred to as a cardiac failure. A cardiothoracic ratio is the way to measure the size of a persons heart. In this case, cardiomegaly occurs if the heart is more than 50 percent bigger than the inner diameter of ones rib cage. Cardiomegaly is assumed to be the direct effect of the thickening of the heart muscles and that happens when the heart is given an increased workload. This increase workload on the other hand, may be due to other health conditions present in the body. Viral illnesses and previous heart attacks can cause the heart to overwork. Drug abuse, inflammation of the heart, and uncontrolled hypertension are the known issues that may give rise to cardiomegaly. ...
http://lymphedemapeople.com/wiki/doku.php?id=glossary:cardiomegaly
glossary:cardiomegalyglossary:cardiomegaly
An abnormal enlargement of the heart; mild cardiomegaly is common in athletes. Cardiomegaly is a condition wherein the heart enlarges in a cardiothoracic ratio of more than 0.50. It can be attributed to a lot of causes, but mostly it is because of low heart output, otherwise referred to as a cardiac failure. A cardiothoracic ratio is the way to measure the size of a persons heart. In this case, cardiomegaly occurs if the heart is more than 50 percent bigger than the inner diameter of ones rib cage. Cardiomegaly is assumed to be the direct effect of the thickening of the heart muscles and that happens when the heart is given an increased workload. This increase workload on the other hand, may be due to other health conditions present in the body. Viral illnesses and previous heart attacks can cause the heart to overwork. Drug abuse, inflammation of the heart, and uncontrolled hypertension are the known issues that may give rise to cardiomegaly. ...
http://www.lymphedemapeople.com/wiki/doku.php?id=glossary:cardiomegaly
Cardiac hypertrophy is stimulated by altered training intensity and correlates with autophagy modulation in male Wistar rats |...Cardiac hypertrophy is stimulated by altered training intensity and correlates with autophagy modulation in male Wistar rats |...
The mechanism for cardiac hypertrophy process that would be a benefit for improvement of cardiovascular endurance needed to be investigated throughly. Specific intensity of training may play a role for homeostasis process in cardiac during training. In the present study, we examine the effect of different intensity of treadmill training on cardiac hypertrophy process and autophagy related gene expression in male wistar rats. Three different intensities of treadmill training were conducted on 15 male wistar rats (Low Intensity: 10 m/minute, Moderate Intensity: 20 m/minute, and High Intensity: 30 m/minute) compared to 5 sedentary rats as control. Training duration was 30 min per day, frequency was 5 days per week, during 8 weeks period. Heart weight and heart weight/body weight ratio were measured after the experiments. Left ventricle myocardium was taken for microscopic analysis with HE staining. mRNA was extracted from left ventricle myocardium for examining αMHC and autophagy related gene expression
https://bmcsportsscimedrehabil.biomedcentral.com/articles/10.1186/s13102-019-0121-0/email/correspondent/c1/new
Estrogen receptor-β mediates male-female differences in the development of pressure overload hypertrophy | Heart and...
We found that hypertrophy induced secondary to pressure overload was significantly less in female WT mice compared with age-matched male WT mice at 2 wk postsurgery. We were therefore interested in determining whether this male/female difference was mediated via the ER and, if so, which receptor.. Direct effects of estrogen on the myocardium have been demonstrated (7, 14, 26), but the physiological roles of ER-α and ER-β in the myocardium remain largely unexplored. For the first time, we report the response of ERKO mice to pressure overload hypertrophy. We found that homozygous α-ERKO female mice exhibit a response to TAC that is identical to the response of WT females. This finding indicates that ER-α is not essential for the attenuation of the hypertrophic response. In contrast, we found that homozygous β-ERKO female mice subjected to TAC exhibited an increased degree of hypertrophy compared with WT female mice, comparable to WT males, indicating a role for ER-β in mediating an ...
http://ajpheart.physiology.org/content/288/2/H469.long
Phenotyping Hypertrophy | Circulation ResearchPhenotyping Hypertrophy | Circulation Research
The widespread use of the term hypertrophy to describe one or a few specific pathophysiological conditions is a holdover from the earliest scientific work on cardiac response to stress, in which cardiac enlargement was largely assumed to be the result of increased cardiomyocyte size and was qualitatively predictable based on the nature of the provocative stimulus.4 Hence, morphogenic changes in the heart were classified by the nature of the inciting hemodynamic stress as pressure-overload or volume-overload hypertrophy, referring to concentric hypertrophy (increased thickness of ventricular walls with little or no change in chamber volume) and eccentric hypertrophy (increased chamber volume with ventricular wall thickness increased in proportion with chamber dimensions), respectively. Note that, in both forms of hypertrophy, cardiac dry mass is increased. These etiologic/morphometric descriptors could be further categorized as compensated or decompensated, based on left ventricular ...
http://circres.ahajournals.org/content/92/11/1171
日本超音波医学会会員専用サイト
阿部 美保1, 福田 信夫2, 井形 次郎1, 稲山 久美1, 福田 保1, 篠原 尚典2, 添木 武2, 酒部 宏一2, 小野瀬 由紀子2, 田村 禎通2. Miho ABE1, Nobuo FUKUDA2, Ziro IKATA1, Kumi INAYAMA1, Tamotsu FUKUDA1, Hisanori SHINOHARA2, Takeshi SOEKI2, Kouichi SAKABE2, Yukiko ONOSE2, Yoshiyuki TAMURA2. 1公立学校共済組合四国中央病院内科, 2国立善通寺病院循環器科・臨床研究部. 1Depertment of Internal Medicine Shikoku Central Hospital, 2Division of Cardiology, and Clinical Research, Zentsuji National Hospital. キーワード : acute myocarditis, diastolic dysfunction of the ventricle, echocardiography, mitral annular velocity, left ventricular inflow velocity A man aged 27 years was admitted to the hospital because of fever and general fatigue. The electrocardiogram showed abnormal Q wave in leads II, III, and aVF, and poor R-wave progression in leads V3 through V6 at time of admission. The chest roentgenogram showed cardiac enlargement and no ...
https://www.jsum.or.jp/journals/2474
Role of serotonin 5-HT2A receptors in the development of cardiac hypertrophy in response to aortic constriction in mice.
Serotonin, in addition to its fundamental role as a neurotransmitter, plays a critical role in the cardiovascular system, where it is thought to be involved in the development of cardiac hypertrophy and failure. Indeed, we recently found that mice with deletion of monoamine oxidase A had enhanced levels of blood and cardiac 5-HT, which contributed to exacerbation of hypertrophy in a model of experimental pressure overload. 5-HT2A receptors are expressed in the heart and mediate a hypertrophic response to 5-HT in cardiac cells. However, their role in cardiac remodeling in vivo and the signaling pathways associated are not well understood. In the present study, we evaluated the effect of a selective 5-HT2A receptor antagonist, M100907, on the development of cardiac hypertrophy induced by transverse aortic constriction (TAC). Cardiac 5-HT2A receptor expression was transiently increased after TAC, and was recapitulated in cardiomyocytes, as observed with 5-HT2A in situ labeling by immunohistochemistry.
http://www.hal.inserm.fr/inserm-00852242
Support the Hypertrophic Heart Center | Tufts Medical CenterSupport the Hypertrophic Heart Center | Tufts Medical Center
Support the Hypertrophic Heart Center at Tufts Medical Center in Boston by making a donation to help improve patient care, research, and clinical trials.
https://www.tuftsmedicalcenter.org/patient-care-services/Departments-and-Services/Hypertrophic-Cardiomyopathy-Center/Support-HCM-Center
Difference Between Cardiomegaly and Cardiomyopathy | Cardiomegaly vs CardiomyopathyDifference Between Cardiomegaly and Cardiomyopathy | Cardiomegaly vs Cardiomyopathy
What is the difference between Cardiomegaly and Cardiomyopathy? Cardiomegaly, the abnormal enlargement of heart, is a clinical manifestation of cardiomyopathies
http://www.differencebetween.com/difference-between-cardiomegaly-and-vs-cardiomyopathy/
Weight Loss Workout Without Cardiomegaly
An enlarged heart, or cardiomegaly, is a symptom of another medical condition it is not a. Physicians at the Mayo Clinic advise that patients with cardiomegaly get modest exercise, after. How to Reduce Estrogen in Men Through the Diet. Adherence to an appropriate diet and regular exercise. Diet should. Cardiomegaly. A nine pound weight loss was re-. vascular markings, and normal exercise tol erance without stridor. The patient. ale due to airway obstruction but without.
http://pacifichealthedu.info/weight-loss-workout-without-cardiomegaly_rc.htm
Biochemistry of Hypertrophy and Heart Failure by Danny P. Goel, David A. Ford (auth.), Lorrie A. Kirshenbaum, - Library
Yet not much is known about patients with PA, VSD at a cellular level, so any available new data for this group is taken along in the understanding of this disease. As mentioned earlier, we studied limited numbers of patients and controls. Therefore the conclusions can only be drawn with caution. It may be added here that the limited clinical data on normal myocardium in young healthy children is a limitation of our study as well. We are currently accumulating appropriate tissue biopsies to increase the number of contro ls. Two of these mutations are found within a troponin T binding site, located at amino acids 175 and 180. In this study, we analyze a transgenic mouse model for one of the mutations that occur at codon 180: a substitution of a glutami c acid for a glycine. These mice develop severe cardiac hypertrophy, substantial interstitial fibrosis, and have an increased heart weight! body weight ratio . Results show that calcium-handling proteins associated with the sarcoplasmic reticulum ...
http://mamenchica.com/index.php/download/biochemistry-of-hypertrophy-and-heart-failure
DDiT4L promotes autophagy and inhibits pathological cardiac hypertrophy in response to stress | Science SignalingDDiT4L promotes autophagy and inhibits pathological cardiac hypertrophy in response to stress | Science Signaling
Thank you for your interest in spreading the word about Science Signaling.. NOTE: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address.. ...
https://stke.sciencemag.org/content/10/468/eaaf5967/tab-article-info
heart hypertrophyheart hypertrophy
Disrupted organ growth leads to disease development. Hypertrophy underlies postnatal heart growth and is triggered after stress, but the molecular mechanisms involved in these processes are largely unknown.. Here we show that cardiac activation of p38γ and p38δ increases during postnatal development and by hypertrophy-inducing stimuli. p38γ/δ promote cardiac hypertrophy by phosphorylating the mTORC1 and mTORC2 inhibitor DEPTOR, which leads to its degradation and mTOR activation. Hearts from mice lacking one or both kinases are below normal size, have high levels of DEPTOR, low activity of the mTOR pathway and reduced protein synthesis. The phenotype of p38γ/δ−/− mice is reverted by overactivation of mTOR with amino acids, shRNA-mediated knockdown of Deptor, or cardiomyocyte overexpression of active p38γ and p38δ. Moreover, in WT mice, heart weight is reduced by cardiac overexpression of DEPTOR.. Our results demonstrate that p38γ/δ control heart growth by modulating mTOR pathway ...
http://www.sabiolab.com/tag/heart-hypertrophy/
JCI - The H3K9 dimethyltransferases EHMT1/2 protect against pathological cardiac hypertrophyJCI - The H3K9 dimethyltransferases EHMT1/2 protect against pathological cardiac hypertrophy
Cardiac hypertrophic growth in response to pathological cues is associated with reexpression of fetal genes and decreased cardiac function and is often a precursor to heart failure. In contrast, physiologically induced hypertrophy is adaptive, resulting in improved cardiac function. The processes that selectively induce these hypertrophic states are poorly understood. Here, we have profiled 2 repressive epigenetic marks, H3K9me2 and H3K27me3, which are involved in stable cellular differentiation, specifically in cardiomyocytes from physiologically and pathologically hypertrophied rat hearts, and correlated these marks with their associated transcriptomes. This analysis revealed the pervasive loss of euchromatic H3K9me2 as a conserved feature of pathological hypertrophy that was associated with reexpression of fetal genes. In hypertrophy, H3K9me2 was reduced following a miR-217-mediated decrease in expression of the H3K9 dimethyltransferases EHMT1 and EHMT2 (EHMT1/2). miR-217-mediated, genetic, ...
https://www.jci.org/articles/view/88353/pdf
Top Cardiomegaly Hospitals in Bangalore | CredihealthTop Cardiomegaly Hospitals in Bangalore | Credihealth
View details of top cardiomegaly hospitals in Bangalore. Get guidance from medical experts to select best cardiomegaly hospital in Bangalore
https://www.credihealth.com/hospitals/bangalore/cardiomegaly
Tolerance of the hypertrophic heart to ischemia. Studies in compensated and failing dog hearts with pressure overload...
Tolerance of the canine heart to prolonged ischemic arrest was studied in 10 hearts from normal control dogs and 15 hearts from dogs with left ventricular hypertrophy (LVH); experiments were performed 1 year after banding the aorta in 8-week-old pupp
http://www.biomedsearch.com/nih/Tolerance-hypertrophic-heart-to-ischemia/2139593.html
PTEN-inducible kinase 1 (PINK1)/Park6 is indispensable for normal heart function | PNASPTEN-inducible kinase 1 (PINK1)/Park6 is indispensable for normal heart function | PNAS
We present several noteworthy observations from our genetic deletion studies supporting the importance of PINK1 in the murine heart during postnatal development. In particular, PINK1−/− mice develop LV dysfunction with a reduced fractional shortening and evidence of pathological cardiac hypertrophy as early as 2 mo of age. Associated with this baseline cardiac phenotype we have shown that the PINK1−/− mice have higher degrees of cardiomyocyte apoptosis with fibrosis and reciprocal reduction in capillary density. In addition, the PINK1−/− mice have greater levels of oxidative stress as reflected by higher levels of lipid peroxidation, DNA damage, and decreased aconitase activity in conjunction with reduced activity of several cytoplasmic and mitochondrial antioxidative systems. In response to biomechanical stress, the PINK1−/− mice developed a further exaggeration in the degree of cardiac hypertrophy compared with their littermate controls. Of clinical relevance is the finding ...
https://www.pnas.org/content/108/23/9572?ijkey=c75d6d6ee87f87916243fa7f11b1f334c25118da&keytype2=tf_ipsecsha
WNBAs Atlanta Dream sold to real estate group following pressure on Kelly Loeffler - The Globe and MailWNBAs Atlanta Dream sold to real estate group following pressure on Kelly Loeffler - The Globe and Mail
The three-member investor group also includes former Dream guard Renee Montgomery and Suzanne Abair, president of Gottesdieners Northland Investment Corp. in Massachusetts
https://www.theglobeandmail.com/sports/basketball/article-wnbas-atlanta-dream-sold-to-real-estate-group-following-pressure-on/
Application Of Gene Expression Data And Cellular Automata To Predict Disease Progress In A Cardiac Hypertrophy ModelApplication Of Gene Expression Data And Cellular Automata To Predict Disease Progress In A Cardiac Hypertrophy Model
The discernment of gene expression changes at the molecular level presents great opportunities to conquer human disease; therefore it is important that...
https://www.witpress.com/elibrary/dne-volumes/6/1/499
Hypertensive Heart Disease | The Virtual Physiological Rat ProjectHypertensive Heart Disease | The Virtual Physiological Rat Project
Hypertension can lead to hypertrophic heart disease is a multi-factorial, multi-scale problem in which altered whole body hemodynamics and neurohormonal factors lead to a complex growth and remodeling response in the heart. The cells and extracellular matrix in the myocardium initially compensate to the abnormal environmental factors with altered gene expression, changes in contractile and mechanoenergetic function, cell and tissue structural remodeling, in turn further affecting circulatory dynamics and often leading to decompensation and failure. The goal of this project is to integrate novel cell signaling models of myocyte hypertrophy into organ-level continuum models of ventricular growth, remodeling and mechanoenergetics coupled to hemodynamic models of systemic hypertension, and validate these multi-scale models with experiments in rats subjected to ventricular hemodynamic overload and treated with drugs that target key response pathways. The resulting model systems will enable ...
http://vpr.sites.uofmhosting.net/research-projects/hypertensive-heart-disease
Sex- and oestrogen-dependent regulation of miRNAs in cardiac hypertrophySex- and oestrogen-dependent regulation of miRNAs in cardiac hypertrophy
The present study aimed to identify sex-differently expressed miRNAs in a late stage of hypertrophy (9 weeks) and the possible role of ERs in the regulation of these differences. Our previous studies identified ERbeta as an important determinant factor of the observed sex differences in pressure overload, playing different roles in males and females. This report identified a total of 30 miRNAs with sex and/or sex*surgery interaction effect 9 weeks after TAC in WT mice. The same effects were not observed in ERbeta-/- animals partially due to the higher expression of these miRNAs in ERbeta-/- females than in their WT counterparts. This study reveals a repression of a number of miRNAs by estradiol and its receptors alpha and beta in female cardiomyocytes, confirming the in vivo results and accentuating the important protective role of oestrogen and ERbeta in the female heart. Six of the miRNAs with sex differences in WT but not in ERbeta-/- hypertrophy models were found to be possible fibrosis ...
https://edoc.hu-berlin.de/handle/18452/17817
NO TABOO: The treatmentNO TABOO: The treatment
They asked themselves, how can something as commonplace and benign as a fruit extract reverse so many aspects of coronary artery disease, simultaneously, as it was evidenced by the study above? They say that the answer might be found in the fact that our ancestors evolved together with certain foods (fruits in particular) for so long that a lack of adequate quantities of these foods may directly result in deteriorating organ function. The journal Atherosclerosis published an interesting study in which they confirm that pomegranate extract may reverse or/and prevent the primary pathology associated with cardiac mortality: the accumulation of fatty materials on the coronary arteries known as atherosclerosis.What really surprised the researchers,were the other beneficial effects of the pomegranate extract treatment: Reduced lipid accumulation in the heart muscle Reduced ECG abnormalities Reduced levels of oxidative stress Reduced cardiac enlargement Reduced monocytie chemotactic protein-1, a ...
http://notaboohere.blogspot.com/2017/04/the-treatment.html
The effects of FABP4 on cardiac hypertrophy ended up investigated in the presence of an ERK signaling inhibitor PD098059 | www...
Notably, the Ang II-induced expression of hypertrophic hall marks had been also profoundly enhanced in Advertisement-FABP4-infected NRCMs compared with
http://www.nrtisinhibitor.com/2016/06/21/the-effects-of-fabp4-on-cardiac-hypertrophy-ended-up-investigated-in-the-presence-of-an-erk-signaling-inhibitor-pd098059/
Rationale Rescuing adverse myocardial redesigning can be an unmet clinical goal - Outlook on PI3K/AKT/mTOR inhibitionRationale Rescuing adverse myocardial redesigning can be an unmet clinical goal - Outlook on PI3K/AKT/mTOR inhibition
Rationale Rescuing adverse myocardial redesigning can be an unmet clinical goal and, correspondingly, pharmacological opportinity for its meant reversal are urgently required. cardiac redesigning without influencing the vasculature. Increasing the arsenal of remodeling-reversing medicines to pathways apart from RAAS, a particular inhibitor of 11-hydroxy-steroid dehydrogenase type 1 (11 HSD1), an integral enzyme necessary for producing active glucocorticoids, completely rescued myocardial hypertrophy. This is connected with mitigating the hypertrophy-associated gene personal, including reversing the myosin weighty chain isoform change however in a design distinguishable from that connected with neovascularization-induced reversal. Conclusions Something was developed ideal for determining novel remodeling-reversing medicines operating in various pathways as well as for getting insights to their systems of actions, exemplified right here by uncoupling their vascular impacts. Introduction Cardiac ...
http://www.gasyblog.com/2018/09/29/rationale-rescuing-adverse-myocardial-redesigning-can-be-an-unmet-clinical-goal/
Sodium Ferulate Protects against Angiotensin II-Induced Cardiac Hypertrophy in Mice by Regulating the MAPK/ERK and JNK PathwaysSodium Ferulate Protects against Angiotensin II-Induced Cardiac Hypertrophy in Mice by Regulating the MAPK/ERK and JNK Pathways
|i|Background and Objective|/i|. It has been reported that sodium ferulate (SF) has hematopoietic function against anemia and immune regulation, inflammatory reaction inhibition, inhibition of tumor cell proliferation, cardiovascular and cerebrovascular protection, and other functions. Thus, this study aimed to investigate the effects of SF on angiotensin II- (AngII-) induced cardiac hypertrophy in mice through the MAPK/ERK and JNK signaling pathways.|i| Methods|/i|. Seventy-two male C57BL/6J mice were selected and divided into 6 groups: control group, PBS group, model group (AngII), model + low-dose SF group (AngII + 10 mg/kg SF), model + high-dose SF group (AngII + 40 mg/kg SF), and model + high-dose SF + agonist group (AngII + 40 mg/kg SCU + 10 mg/kg TBHQ). After 7 d/14 d/28 days of treatments, the changes of blood pressure and heart rates of mice were compared. The morphology of myocardial tissue and the apoptosis rate of myocardial cells were observed. The mRNA and protein expressions of atrial
https://www.hindawi.com/journals/bmri/2017/3754942/
Left atrial enlargement: Causes, signs and symptoms, and treatment - Latin-Hearts
Detecting left atrial enlargement is frequently suspected in line with the presentation of signs and symptoms of the underlying cardiogenic condition. Once other tests addressing other complications are carried out to assist eliminate any potentially existence-threatening disorders, additional testing searching in the structure from the heart can be achieved to find out if left atrial enlargement exists.. Probably the most generally done test to identify left atrial enlargement is applying imaging methods known as echocardiograms. To control your emotions by utilizing seem waves to consider images of the center structures. Using other imaging tests, namely CT or MRI scans, may also be used to identify left atrial enlargement.. With respect to the underlying condition, treatment will normally follow. For instance, treating high bloodstream pressure calls for the effective use of bloodstream pressure medication for example beta-blockers and diuretics. Also, maintaining a healthy diet plan, ...
http://latin-hearts.com/left-atrial-enlargement-causes-signs-and-symptoms-and-treatment/
Cellular interplay via cytokine hierarchy causes pathological cardiac hypertrophy in RAF1-mutant Noonan syndrome. | Nat Commun...Cellular interplay via cytokine hierarchy causes pathological cardiac hypertrophy in RAF1-mutant Noonan syndrome. | Nat Commun...
Noonan syndrome (NS) is caused by mutations in RAS/ERK pathway genes, and is characterized by craniofacial, growth, cognitive and cardiac defects. NS patients with kinase-activating RAF1 alleles typically develop pathological left ventricular hypertrophy (LVH), which is reproduced in Raf1L613V/+ knock-in mice. Here, using inducible Raf1L613V expression, we show that LVH results from the interplay of cardiac cell types. Cardiomyocyte Raf1L613V enhances Ca2+ sensitivity and cardiac contractility without causing hypertrophy. Raf1L613V expression in cardiomyocytes or activated fibroblasts exacerbates pressure overload-evoked fibrosis. Endothelial/endocardial (EC) Raf1L613V causes cardiac hypertrophy without affecting contractility. Co-culture and neutralizing antibody experiments reveal a cytokine (TNF/IL6) hierarchy in Raf1L613V-expressing ECs that drives cardiomyocyte hypertrophy in vitro. Furthermore, postnatal TNF inhibition normalizes the increased wall thickness and cardiomyocyte hypertrophy ...
https://pesquisa.bvsalud.org/portal/resource/pt/mdl-28548091
Taxifolin protects against cardiac hypertrophy and fibrosis during biomechanical stress of pressure overload (Journal Article) ...Taxifolin protects against cardiac hypertrophy and fibrosis during biomechanical stress of pressure overload (Journal Article) ...
Cardiac hypertrophy is a key pathophysiological component to biomechanical stress, which has been considered to be an independent and predictive risk factor for adverse cardiovascular events. Taxifolin (TAX) is a typical plant flavonoid, which has long been used clinically for treatment of cardiovascular and cerebrovascular diseases. However, very little is known about whether TAX can influence the development of cardiac hypertrophy. In vitro studies, we found that TAX concentration-dependently inhibited angiotensin II (Ang II) induced hypertrophy and protein synthesis in cardiac myocytes. Then we established a mouse model by transverse aortic constriction (TAC) to further confirm our findings. It was demonstrated that TAX prevented pressure overload induced cardiac hypertrophy in mice, as assessed by ventricular mass/body weight, echocardiographic parameters, myocyte cross-sectional area, and the expression of ANP, BNP and β-MHC. The excess production of reactive oxygen species (ROS) played ...
https://www.osti.gov/scitech/biblio/22465817-taxifolin-protects-against-cardiac-hypertrophy-fibrosis-during-biomechanical-stress-pressure-overload
Frontiers | Toll-Like Receptor 4 Inhibition Improves Oxidative Stress and Mitochondrial Health in Isoproterenol-Induced Cardiac...Frontiers | Toll-Like Receptor 4 Inhibition Improves Oxidative Stress and Mitochondrial Health in Isoproterenol-Induced Cardiac...
Background- Inflammation remains a crucial factor for progression of cardiac diseases and cardiac hypertrophy remains an important cause of cardiac failure over all age groups. As a key regulator of inflammation, toll like receptor 4 (TLR4) plays an important role in pathogenesis of cardiac diseases. Being an important regulator of innate immunity, the precise pathway of TLR4 mediated cardiac complications is yet to be established. Therefore, the primary objective of the present study was to find the role of TLR4 in cardiac hypertrophy and the molecular mechanism thereof. Methods- Cardiac hypertrophy was induced with administration of isoproterenol (5mg/kg/day, sc). TLR4 receptor inhibitor RS-LPS (lipopolysaccharide from the photosynthetic bacterium Rhodobacter sphaeroides; 5 microgram/day) and agonist LPS (Lipopolysaccharide from Escherichia coli; 3.12 microgram/day) were administered through osmotic pump along with isoproterenol. Cardiac hypertrophy as well as oxidative stress and mitochondrial
https://www.frontiersin.org/articles/10.3389/fimmu.2017.00719/full
Effect of SKF‑96365 on cardiomyocyte hypertrophy induced by angiotensin II
Angiotensin II (Ang II) is an important bioactive peptide in the renin‑angiotensin system, and it can contribute to cell proliferation and cardiac hypertrophy. Dysfunctions in transient receptor potential canonical (TRPC) channels are involved in many types of cardiovascular diseases. The aim of the present study was to investigate the role of the TRPC channel inhibitor SKF‑96365 in cardiomyocyte hypertrophy induced by Ang II and the potential mechanisms of SKF‑96365. H9c2 cells were treated with different concentrations of Ang II. The expression levels of cardiomyocyte hypertrophy markers and TRPC channel‑related proteins were also determined. The morphology and surface area of the H9c2 cells, the expression of hypertrophic markers and TRPC channel‑related proteins and the [3H] leucine incorporation rate were detected in the Ang II‑treated H9c2 cells following treatment with the TRPC channel inhibitor SKF‑96365. The intracellular Ca2+ concentration was tested by flow cytometry. ...
https://tessera.spandidos-publications.com/10.3892/mmr.2019.10877/abstract
Collaborative Regulation of LRG1 by TGF-beta 1 and PPAR-beta/delta Modulates Chronic Pressure Overload-Induced Cardiac FibrosisCollaborative Regulation of LRG1 by TGF-beta 1 and PPAR-beta/delta Modulates Chronic Pressure Overload-Induced Cardiac Fibrosis
BACKGROUND:Despite its established significance in fibrotic cardiac remodeling, clinical benefits of global inhibition of TGF (transforming growth factor)-β1 signaling remain controversial. LRG1 (leucine-rich-α2 glycoprotein 1) is known to regulate endothelial TGFβ signaling. This study evaluated the role of LRG1 in cardiac fibrosis and its transcriptional regulatory network in cardiac fibroblasts. METHODS:Pressure overload-induced heart failure was established by transverse aortic constriction. Western blot, quantitative reverse transcription polymerase chain reaction, immunofluorescence, and immunohistochemistry were used to evaluate the expression level and pattern of interested targets or pathology during fibrotic cardiac remodeling. Cardiac function was assessed by pressure-volume loop analysis. RESULTS:LRG1 expression was significantly suppressed in left ventricle of mice with transverse aortic constriction-induced fibrotic cardiac remodeling (mean difference, -0.00085 [95% CI, -0.0013 ...
https://scholars.latrobe.edu.au/display/publication834819
cardiac hypertrophy treatment
Right ventricular hypertrophy is a heart disorder characterized by thickening of the walls of the right ventricle. Introduction. Cardiac hypertrophy refers to the cardiac remodeling process in response to a variety of intrinsic and extrinsic stimuli that stress the heart . Abstract Cardiac hypertrophy is the hearts response to a variety of extrinsic and intrinsic stimuli that impose increased biomechanical stress. Doxorubicin (DOX) is regarded as one of the most potent anthracycline antibiotic agents; however, its clinical usage has some limitations because it has serious … In this article I deal with only clinical aspects of LVH, because LVH is common, among all types of hypertrophies of the heart. HPE administration may thus be an effective approach to the treatment of cachexia, cardiac hypertrophy and fibrosis. This intervention study has the potential to discover a new strategy for the treatment of cardiac hypertrophy and fibrosis in patients on maintenance hemodialysis. Therefore, BA can ...
https://web.re-nova.net/donut-bags-jacj/cardiac-hypertrophy-treatment-cb42cd
Pituitary Adenylate Cyclase Activating Peptide Receptors | Selective Sirt2 inhibition by ligand-induced rearrangementPituitary Adenylate Cyclase Activating Peptide Receptors | Selective Sirt2 inhibition by ligand-induced rearrangement
Supplementary MaterialsSupplementary Information 41598_2019_44331_MOESM1_ESM. in CACNA1H the denseness of DHPR and RyR2 clusters with pressure-overload cardiac hypertrophy and a rise in the denseness of SERCA2A proteins clusters. PLN proteins clusters reduced in denseness in 2-week TAC but came back to sham amounts Meptyldinocap by 4-week TAC. Furthermore, 2D-FFT evaluation revealed adjustments in molecular firm during pathological hypertrophy, with RyR2 and DHPR becoming dispersed while both SERCA2A and PLN sequestered into dense clusters. Our function reveals molecular adaptations that happen in important SR protein at an individual molecule during pressure overload-induced cardiomyopathy. Nanoscale modifications in proteins localization and patterns of manifestation of important SR proteins inside the cardiomyocyte offered insights in to the pathogenesis of cardiac hypertrophy, and particular proof that cardiomyocytes go through significant structural redesigning during the development of ...
http://themodernsolution.com/category/pituitary-adenylate-cyclase-activating-peptide-receptors/
Mitoquinone Ameliorates Pressure Overload-Induced Cardiac Fibrosis and by Kah Yong Goh, Li He et al.Mitoquinone Ameliorates Pressure Overload-Induced Cardiac Fibrosis and by Kah Yong Goh, Li He et al.
Increasing evidence indicates that mitochondrial-associated redox signaling contributes to the pathophysiology of heart failure (HF). The mitochondrial-targeted antioxidant, mitoquinone (MitoQ), is capable of modifying mitochondrial signaling and has shown beneficial effects on HF-dependent mitochondrial dysfunction. However, the potential therapeutic impact of MitoQ-based mitochondrial therapies for HF in response to pressure overload is reliant upon demonstration of improved cardiac contractile function and suppression of deleterious cardiac remodeling. Using a new (patho)physiologically relevant model of pressure overload-induced HF we tested the hypothesis that MitoQ is capable of ameliorating cardiac contractile dysfunction and suppressing fibrosis. To test this C57BL/6J mice were subjected to left ventricular (LV) pressure overload by ascending aortic constriction (AAC) followed by MitoQ treatment (2 µmol) for 7 consecutive days. Doppler echocardiography showed that AAC caused severe LV
https://scholarcommons.usf.edu/intmed_facpub/15/
The Effect of 12-Week Resistance Training on Cardiac Hypertrophy Glucose Level Insulin and Insulin Resistance Index in STZ...
Background and Objectives: Type 2 diabetes is a risk factor for heart disease and has a major contribution in mortality due to cardiovascular diseases. In the present study, the effect of 12-week resistance training was investigated on cardiac hypertrophy, glucose, level, insulin, and insulin resistance index in STZ-induced diabetic rats. Methods: A total of ...
http://journal.muq.ac.ir/article-1-436-en.html
381 Does the BNP may be used as a biochemical marker for assessing severity of left ventricular hypertrophy in aortic stenosis?
54 Downregulation Erb2 and Erb4 receptors in patients with congestive cardiomyopathy and in patients with pressure overload hypertrophy due to aortic stenosis is related to diastolic load. Delrue, L.; Bartunek, J.; Goethals, M.; De Bruyne, B.; De Beenhouwer, H.; Vanderheyden, M. // European Journal of Heart Failure. Supplements;Jun2004, Vol. 3 Issue 1, p12 An abstract of the study Downregulation Erb2 and Erb4 Receptors in Patients With Congestive Cardiomyopathy and in Patients With Pressure Overload Hypertrophy Due to Aortic Stenosis Is Related to Diastolic Load, by L. Delrue and colleagues is presented. ...
http://connection.ebscohost.com/c/abstracts/14270528/381-does-bnp-may-be-used-as-biochemical-marker-assessing-severity-left-ventricular-hypertrophy-aortic-stenosis
Aging | Circular RNA expression in isoproterenol hydrochloride-induced cardiac hypertrophy - Figure
Circular RNA (circRNA) is a novel class of noncoding RNAs, and the roles of circRNAs in the development of cardiac hypertrophy remain to be explored. Here, we investigate the potential roles of circRNAs in cardiac hypertrophy. By circRNA sequencing in left ventricular specimens collected from 8-week-old mice with isoproterenol hydrochloride-induced cardiac hypertrophy, we found 401 out of 3323 total circRNAs were dysregulated in the hypertrophic hearts compared with the controls. Of these, 303 circRNAs were upregulated and 98 were downregulated. Moreover, the GO and KEGG analyses revealed that the majority of parental gene of differentially expressed circRNAs were not only related to biological process such as metabolic process and response to stimulus, but also related to pathway such as circulatory system and cardiovascular diseases. On the other hand, total 1974 miRNAs were predicted to binding to these differentially expressed circRNAs, and the possible target mRNAs of those miRNAs were also
https://www.aging-us.com/figure/102761/f10
ECG: left atrial enlargement | DiagnosaurusECG: left atrial enlargement | Diagnosaurus
ECG: left atrial enlargement answers are found in the Diagnosaurus powered by Unbound Medicine. Available for iPhone, iPad, Android, and Web.
https://im.unboundmedicine.com/medicine/view/Diagnosaurus/114633/all/ECG:_left_atrial_enlargement
JCI - Regulator of G protein signaling 2 mediates cardiac compensation to pressure overload and antihypertrophic effects of...JCI - Regulator of G protein signaling 2 mediates cardiac compensation to pressure overload and antihypertrophic effects of...
The heart initially compensates for hypertension-mediated pressure overload by enhancing its contractile force and developing hypertrophy without dilation. Gq protein-coupled receptor pathways become activated and can depress function, leading to cardiac failure. Initial adaptation mechanisms to reduce cardiac damage during such stimulation remain largely unknown. Here we have shown that this initial adaptation requires regulator of G protein signaling 2 (RGS2). Mice lacking RGS2 had a normal basal cardiac phenotype, yet responded rapidly to pressure overload, with increased myocardial Gq signaling, marked cardiac hypertrophy and failure, and early mortality. Swimming exercise, which is not accompanied by Gq activation, induced a normal cardiac response, while Rgs2 deletion in Gαq-overexpressing hearts exacerbated hypertrophy and dilation. In vascular smooth muscle, RGS2 is activated by cGMP-dependent protein kinase (PKG), suppressing Gq-stimulated vascular contraction. In normal mice, but not ...
https://www.jci.org/articles/view/35620/pdf
Myocardial and Coronary Effects of Propofol in Rabbits with Compensated Cardiac Hypertrophy | Anesthesiology | ASA PublicationsMyocardial and Coronary Effects of Propofol in Rabbits with Compensated Cardiac Hypertrophy | Anesthesiology | ASA Publications
In the current study, we used an experimental model of compensated cardiac hypertrophy induced by pressure overload over a 12-week period. The degree of hypertrophy induced in our study (136 ± 21%) was consistent with previous studies using the same model and reported a mean cardiac hypertrophy of 127%11 and 136%. 32 These authors reported noncardiac abnormalities associated with cardiac hypertrophy, including skeletal and diaphragmatic muscle abnormalities, without any physical signs of congestive heart failure, but they did not perform accurate evaluation of myocardial performance. 11 Our results showed a preserved state of contractility as indicated by the absence of significant difference in indexed Emaxbetween SHAM and LVH groups but an alteration of the diastolic compliance in the LVH group (fig. 1). These results explain significant differences in the inotropic and lusitropic baseline values between SHAM and LVH1groups. In the latter group, by altered diastolic compliance, the value of ...
http://anesthesiology.pubs.asahq.org/article.aspx?articleid=1944520
Role of cyclin-dependent Kinase 9 in the zebrafish embryonic heart
Cardiac hypertrophy leading to heart failure remains a leading cause of morbidity and mortality in the 21st century despite major therapeutic advances. Improved understanding of novel molecular and cellular processes contributing to cardiac hypertrophy therefore continues to be important. Cyclin-dependent Kinase 9 (CDK9), part of a family of proteins controlling cell cycle and growth, has emerged as one such potential candidate over the last 5 years. CDK9 is the catalytic subunit of the CDK9/CyclinT complex and acts by phosphorylating the carboxy-terminal domain of RNA polymerase II. Hypertrophic signals, such as Endothelin-1 (ET-1) and phenylephrine, have been shown to cause CDK9 activation leading to a hypertrophic response in cultured mouse cardiomyocytes associated with reactivation of the foetal gene program. CDK9 also forms a complex with GATA4 to play a role in differentiation of mouse ES cells into cardiomyocytes. These findings suggest a specific role for CDK9 in controlling growth and ...
https://www.era.lib.ed.ac.uk/handle/1842/11820
IP3 Receptor Linked to Cardiac Hypertrophy - Drug Discovery OpinionIP3 Receptor Linked to Cardiac Hypertrophy - Drug Discovery Opinion
Cardiac hypertrophy is a thickening of the heart muscle - characterized by increased cell size rather than number - in response to conditions such as high blood pressure and coronary heart disease, which results in a decrease in size of the chambers of the heart, including the left and right ventricles. Since hypertrophy is associated with heart failure, irregular heart rhythms and an increased risk of angina and heart attack, understanding the mechanisms underlying this abnormal thickening is of great importance. Scientists at the Babraham Institute have now identified a new signalling process in the heart which contributes to cardiac hypertrophy. Rhythmical Ca2+ increases are fundamental to contraction of the heart muscle, but elevated Ca2+ levels also regulate the gene transcription that leads to hypertrophy. The Babraham team found that it is localised increases in Ca2+ concentrations in the cell nucleus that activate the genes responsible for hypertrophy. These nuclear Ca2+ signals, which ...
http://drugdiscoveryopinion.com/2009/03/ip3-receptor-linked-to-cardiac-hypertrophy/
ACROMEGALY AND THE HEART: A CLINICAL AND PATHOLOGIC STUDY* | Annals of Internal Medicine | American College of PhysiciansACROMEGALY AND THE HEART: A CLINICAL AND PATHOLOGIC STUDY* | Annals of Internal Medicine | American College of Physicians
Heart disease has long been known as a frequent complicating factor and a common cause of exitus in acromegaly. Only nine years after the recognition of the features of acromegaly by Marie1 in 1886, Huchard2 reported cardiac enlargement in the clinical and autopsy findings of three patients with the disease. Fournier3 drew particular attention to the features of cardiac failure in a series of 25 patients, pointing out the frequent association of cardiomegaly with hypertrophy of all the viscera. Similar reports, consisting usually of one or two cases, have appeared from time to time in the French and German literature, ...
http://annals.org/aim/article-abstract/674692/acromegaly-heart-clinical-pathologic-study
Plus it
Four weeks of aortic banding resulted in significant hypertrophy in rats. This was evident from a significant increase in LVm/BW ratios. Furthermore, the hypertrophy was concentric in nature as evident from significant increases in the IVS and LVPW, an indication of increased septal and posterior wall thickness, respectively, at both systole and diastole. There was no change observed in LVID, an indication of increased chamber size, at systole and diastole. Results of the current study are consistent with results from our previous study (4). Treatment of aortic-banded rats with 2.5 mg·kg−1·day−1 resveratrol completely prevented development of hypertrophy because there was a normalization of the increase in left ventricle-to-body weight ratio. Resveratrol treatment also prevented concentric remodeling by normalizing IVS and LVPW at both systole and diastole. The beneficial effects of resveratrol in preventing PO-induced cardiac hypertrophy are consistent with another recent study, which ...
http://ajpheart.physiology.org/content/292/5/H2138
cNMA and Fuzzy -Logic Based Ligand Screening for Preventing Myocardial Lipid Accumulation in Pressure-Overload Cardiac...cNMA and Fuzzy -Logic Based Ligand Screening for Preventing Myocardial Lipid Accumulation in Pressure-Overload Cardiac...
Inherited and acquired cardiomyopathy due to obesity and diabetes results in impaired lipid accumulation in the myocyte. Lipid accumulation in the heart leads t
https://papers.ssrn.com/sol3/papers.cfm?abstract_id=3529895
left ventricular hypertrophy - Heartbeats of Licking County
September 29th is World Heart Day, that is held and arranged through the world heart foundation. The objective of this occasion would be to inform people about cardiovascular illnesses, which cause most cases of avoidable dying on the planet. To higher facilitate this purpose, weve compiled a summary of articles to assist enable you to get began on what causes cardiovascular disease. Youll find info on what can cause an enlarged heart and fluid round the heart, diabetes and cardiovascular disease, and what to anticipate throughout a massive cardiac arrest. Hopefully these details might help our readers and potentially save a existence later on.. Cardiomegaly (enlarged heart) isnt an illness by itself, but instead an indicator of some other condition. An enlarged heart is visible on X-ray images, but additional exams are needed to look for the exact reason for cardiomegaly.. Cardiomegaly could be temporary or chronic, based on its underlying cause. Oftentimes, cardiomegaly is really a ...
http://heartbeats-olc.org/tag/left-ventricular-hypertrophy/
A change of heart: Epigenetic basis of cardiac hypertrophy uncoveredA change of heart: Epigenetic basis of cardiac hypertrophy uncovered
Their research, published in the Journal of Clinical Investigation, compared the differences between hypertrophic heart growth in rats as a result of exercise - which is beneficial - and heart growth induced by pathology - in this case increased load. Specifically, they compared epigenetic marks responsible for locking cells in their final developed state - important for preventing cells from switching to a less differentiated state. Notably for their analysis, the researchers employed a powerful cell sorting technique to allow them to study pure populations of heart muscle cells (cardiomyocytes) rather than a mix of all cell types in the heart - which, due to an alteration in composition during disease, would confound analysis ...
http://www.vib.be/en/news/Pages/A-change-of-heart.aspx
RhoA signaling in cardiomyocytes protects against stress-induced heart failure but facilitates cardiac fibrosis | Science...RhoA signaling in cardiomyocytes protects against stress-induced heart failure but facilitates cardiac fibrosis | Science...
Over time, overloaded hearts typically become larger (a process called compensatory hypertrophy) to deal with the increased pressure. If prolonged, as occurs in untreated hypertension, the pressure overload leads to pathological hypertrophy and fibrosis, and ultimately leading to heart failure. Lauriol et al. found that mice with a cardiomyocyte-specific deficiency of RhoA, a GTP (guanosine 5′-triphosphate)-regulated protein, developed increased pathological hypertrophy but reduced fibrosis with chronic cardiac stress. These results suggest that targeting downstream effectors of RhoA, rather than RhoA itself, may be better for treating pathologies associated with heart failure.. ...
https://stke.sciencemag.org/content/7/348/ra100.editor-summary
ESC calls for renaming of term cardiac hypertrophy | Cardiovascular News
The term myocardial hypertrophy, say the working group, lacks precision. In cell biology the term hypertrophy describes growth via cell enlargement as opposed to growth by cell division, where hyperplasia is the correct term. Currently in cardiology the term hypertrophy is commonly applied to the situation in the whole heart where myocardial enlargement is accompanied by both hypertrophy and hyperplasia. In addition the term hypertrophy does not take account of the fact that non myocytes in the heart are not passive bystanders and also change in number when the heart remodels. Additionally there may be an invasion of inflammatory cells into the heart, and angiogenesis may occur.. The advantage of the term cardiac remodelling is that it simply defines reorganisation of the different cardiac tissue components, and can be used to describe an increase, or decrease in the size of the left ventricle, as well as a change to the cellular components, explained the first author of the paper, Ralph ...
https://cardiovascularnews.com/esc-calls-for-renaming-of-term-cardiac-hypertrophy/
Apocynin attenuates oxidative stress and cardiac fibrosis in angiotensin II-induced cardiac diastolic dysfunction in mice.
To investigate whether apocynin, a NADPH oxidase inhibitor, produced cardioproteictive effects in Ang II-induced hypertensive mice, and to elucidate the underlying mechanisms. C57BL/6 mice were subcutaneously infused Ang II for 4 weeks to mimic
http://www.biomedsearch.com/nih/Apocynin-attenuates-oxidative-stress-cardiac/23334241.html
Most recent papers with the keyword Transverse aortic constriction | Read by QxMDMost recent papers with the keyword Transverse aortic constriction | Read by QxMD
Dipeptidyl peptidase-4 (DPP-4) inhibitors are hypoglycemic agents. DPP-4 inhibitor has cardioprotective effects after transverse aortic constriction (TAC), but role of DPP-4 on cardiac fibrosis after TAC is not well known. Our aim was to determine the effects of DPP-4 on cardiac fibrosis in murine TAC model. Wild-type mice and DPP-4 knockout mice were subjected to TAC. Wild-type mice were then treated with vehicle or DPP-4 inhibitor. DPP-4 activities in serum and heart tissue were significantly increased at 2 weeks after TAC, but they were significantly decreased by DPP-4 inhibitor treatment ...
https://www.readbyqxmd.com/keyword/53493
Signs or symptoms hematomacrosis - Tips and Tricks From DoctorsSigns or symptoms hematomacrosis - Tips and Tricks From Doctors
Signs or symptoms hematomacrosis - What are the symptoms of hemochromatosis? Varies. Many times, it is only presented with high iron saturation and or iron storage without having any symptoms. However, the clinical manifestations of iron accumulation can include liver disease, elevation of liver enzymes, skin pigmentation, diabetes mellitus, arthropathy, impotence in males, and cardiac enlargement with or without heart failure or conduction defects etc.
https://www.healthtap.com/topics/signs-or-symptoms-hematomacrosis
Plus itPlus it
Although cardiac hypertrophy is an important condition that usually precedes heart failure (Carreno et al., 2006), there are limited reports of altered expression of P450 genes during cardiac hypertrophy. The expression of P450 has been studied in SHRs as compared with SD rats (Thum and Borlak, 2002) and the expression of sEH has been studied in spontaneously hypertensive heart failure (SHHF) rats as compared with normal strains (Monti et al., 2008). Nevertheless, there are no data about the effect of experimentally induced cardiac hypertrophy on the expression of P450 and sEH genes and their associated P450-derived metabolites of AA. To the best of our knowledge, this work demonstrates for the first time the effect of experimentally induced cardiac hypertrophy on the expression of several P450 genes and P450-dependent AA metabolism in rats. In addition, the current study demonstrates the tissue-specific expression of many P450 genes and sEH in male SD rats.. Tissue-specific expression of P450 ...
http://dmd.aspetjournals.org/content/36/11/2277
Therapeutic inhibition of the miR-34 family (miR-34a -b -c) or miR-34a - BRAF inhibitors on Immune-based antitumor therapyTherapeutic inhibition of the miR-34 family (miR-34a -b -c) or miR-34a - BRAF inhibitors on Immune-based antitumor therapy
Therapeutic inhibition of the miR-34 family (miR-34a -b -c) or miR-34a only have emerged as encouraging strategies for the treating cardiac pathology. safety this approach will probably result in much less potential off-target results. Subsequently silencing of miR-34a only may be inadequate in configurations of founded cardiac pathology. We lately proven Cobicistat that inhibition from the miR-34 family members however not miR-34a only provided benefit inside a chronic style of myocardial infarction. Inhibition of miR-34 also attenuated cardiac redesigning and improved center function pursuing pressure overload nevertheless silencing of miR-34a only was not analyzed. The purpose of this research was to assess whether inhibition of miR-34a could attenuate cardiac redesigning inside a mouse model with pre-existing pathological hypertrophy. Mice had been put through pressure overload via constriction from the transverse aorta for a month and echocardiography was performed to verify remaining ...
http://www.bioinbrief.com/2017/05/29/therapeutic-inhibition-of-the-mir-34-family-mir-34a-b-c-or-mir-34a/
CardiomegalyCardiomegaly
Prevention of cardiomegaly starts with detection. If a person has a family history of cardiomegaly, one should let one's doctor ... Cardiomyopathy is also associated with cardiomegaly. Cardiomegaly can be serious depending on what part of the heart is ... Recent studies suggest that cardiomegaly is associated with a higher risk of sudden cardiac death. Cardiomegaly may improve ... and cardiomegaly on chest X-ray. Lifestyle factors that can help prevent cardiomegaly include eating a healthy diet, ...
https://en.wikipedia.org/wiki/Cardiomegaly
Riaz HaiderRiaz Haider
A rare cause of cardiomegaly". British Heart Journal. 35 (9): 981-984. doi:10.1136/hrt.35.9.981. ISSN 0007-0769. PMC 458738. ...
https://en.wikipedia.org/wiki/Riaz_Haider
John Maurice Hardman CampbellJohn Maurice Hardman Campbell
with Margaret Turner-Warwick: Campbell, M.; Turner-Warwick, M. (July 1956). "Two more families with cardiomegaly". Br Heart J. ...
https://en.wikipedia.org/wiki/John_Maurice_Hardman_Campbell
MegacolonMegacolon
Koeberle F (1963). "Enteromegaly and cardiomegaly in Chagas disease". Gut. 4 (4): 399-405. doi:10.1136/gut.4.4.399. PMC 1413478 ...
https://en.wikipedia.org/wiki/Megacolon
Cameron Moore (basketball)Cameron Moore (basketball)
In late May 2015, he collapsed and spent a few hours in a coma for what was diagnosed as cardiomegaly. Moore did not play pro ... "Cameron Moore in coma for a cardiomegaly". sportando.com. Retrieved 3 November 2016. Brutta avventura per Cameron Moore (in ...
https://en.wikipedia.org/wiki/Cameron_Moore_(basketball)
Left ventricular hypertrophyLeft ventricular hypertrophy
Cardiomegaly Primary hyperparathyroidism Ventricular hypertrophy Maron, Barry J; Maron, Martin S (2013-01-19). "Hypertrophic ...
https://en.wikipedia.org/wiki/Left_ventricular_hypertrophy
Ernest BethellErnest Bethell
He died of cardiomegaly on 1 May 1909. The Korean people erected a monument in his honour, though it was defaced by the ...
https://en.wikipedia.org/wiki/Ernest_Bethell
Fritz KöberleFritz Köberle
Koeberle, F. Enteromegaly and cardiomegaly in Chagas disease. Gut. 1963 Dec;41:399-405. Rezende, J.M.: Fritz Köberle and his ... cardiomegaly, heart ventricular aneurysm, achalasia, etc., and the mechanism of the causation of these several pathologies. By ...
https://en.wikipedia.org/wiki/Fritz_Köberle
Left atrial enlargementLeft atrial enlargement
Articles with short description, Short description matches Wikidata, Cardiomegaly). ... and is a form of cardiomegaly. Left atrial enlargement can be mild, moderate or severe depending on the extent of the ...
https://en.wikipedia.org/wiki/Left_atrial_enlargement
Rh factor testingRh factor testing
Splenomegaly, cardiomegaly and hepatomegaly may occur in the baby. Excessive tissue fluid may accumulate in the stomach, lungs ...
https://en.wikipedia.org/wiki/Rh_factor_testing
Mark HainesMark Haines
He died of congestive heart failure due to cardiomegaly. Just after the market opened on May 25, CNBC broadcast that Haines had ...
https://en.wikipedia.org/wiki/Mark_Haines
The Shangri-La DietThe Shangri-La Diet
... occlusive coronary artery disease and cardiomegaly contributed to his death. List of diets Interview with Author Dr. Seth ...
https://en.wikipedia.org/wiki/The_Shangri-La_Diet
Seth RobertsSeth Roberts
Occlusive coronary artery disease and cardiomegaly contributed to his death. Seth Roberts Blog. "Seth", 27 April 2014. ...
https://en.wikipedia.org/wiki/Seth_Roberts
Left atrial volumeLeft atrial volume
Enlargement of the left atrium is a form of cardiomegaly. Moderately increased LAVI (63 to 73 mL/m2) is associated with ...
https://en.wikipedia.org/wiki/Left_atrial_volume
Cantú syndromeCantú syndrome
The main features of this condition are hypertrichosis, osteochondrodysplasia, and cardiomegaly. There is also a characteristic ... Cantú syndrome is a rare condition characterized by hypertrichosis, osteochondrodysplasia, and cardiomegaly. Less than 50 cases ...
https://en.wikipedia.org/wiki/Cantú_syndrome
Ebsteins anomalyEbstein's anomaly
Joseph Prescher was cyanotic with dyspnea, palpitations, jugular venous distension, and cardiomegaly. At autopsy, "Ebstein ...
https://en.wikipedia.org/wiki/Ebstein's_anomaly
Ventricular remodelingVentricular remodeling
... may include ventricular hypertrophy, ventricular dilation, cardiomegaly, and other changes. It is an ...
https://en.wikipedia.org/wiki/Ventricular_remodeling
OrganomegalyOrganomegaly
For example, clitoromegaly is the enlargement of the clitoris, and cardiomegaly is enlargement of the heart. Visceromegaly is ... Tracy, Richard Everett (2011). "Association of Cardiomegaly with Coronary Artery Histopathology and its Relationship to ...
https://en.wikipedia.org/wiki/Organomegaly
Emmanuel Badu KobiEmmanuel Badu Kobi
The actor was reported suffering from enlargement of the heart or cardiomegaly. In February 2019, Abronye DC of the ruling New ...
https://en.wikipedia.org/wiki/Emmanuel_Badu_Kobi
Right atrial enlargementRight atrial enlargement
... (RAE) is a form of cardiomegaly, or heart enlargement. It can broadly be classified as either right ... v t e (Articles with short description, Short description matches Wikidata, Cardiomegaly, All stub articles, Circulatory ...
https://en.wikipedia.org/wiki/Right_atrial_enlargement
Ortners syndromeOrtner's syndrome
This cardiomegaly, or enlargement of the heart, led to compression of the LRLN. Atrial Myxoma Aorta: Traumatic injury Incidence ...
https://en.wikipedia.org/wiki/Ortner's_syndrome
Hypoplastic left heart syndromeHypoplastic left heart syndrome
Chest x-ray may show a large heart (cardiomegaly) or increased pulmonary vasculature. Neonates with HLHS do not typically have ...
https://en.wikipedia.org/wiki/Hypoplastic_left_heart_syndrome
Cor bovinumCor bovinum
Cardiomegaly Left ventricular hypertrophy Syphilitic aortitis Ventricular hypertrophy Kumar, V et al. Robbins and Colran ...
https://en.wikipedia.org/wiki/Cor_bovinum
Max BarrettMax Barrett
Barrett, A. M. (1963). "Arterial measurements in the interpretation of cardiomegaly at necropsy: Cardiac hypertrophy and ...
https://en.wikipedia.org/wiki/Max_Barrett
HeartHeart
"Comparing fist size to heart size is not a viable technique to assess cardiomegaly". Cardiovascular Pathology. 36: 1-5. doi: ...
https://en.wikipedia.org/wiki/Heart
Aziz ShavershianAziz Shavershian
An autopsy revealed a previously undiagnosed congenital heart defect and cardiomegaly which triggered cardiac arrest. His ...
https://en.wikipedia.org/wiki/Aziz_Shavershian
Infantile free sialic acid storage diseaseInfantile free sialic acid storage disease
... cardiomegaly). ISSD is a rare autosomal recessive disorder and affects 1 in 528,000 live births worldwide. Symptoms present by ... cardiomegaly).[citation needed] A diagnosis can be made by measuring cultured tissue samples for increased levels of free ...
https://en.wikipedia.org/wiki/Infantile_free_sialic_acid_storage_disease
PalpitationsPalpitations
Evidence of cardiomegaly and peripheral edema may indicate heart failure and ischemia or a valvular abnormality. Blood tests, ... cardiomegaly, aortic aneurysm, or acute left ventricular failure), and miscellaneous sources (postural orthostatic tachycardia ...
https://en.wikipedia.org/wiki/Palpitations
TafazzinTafazzin
A patient with a frame shift mutation of c.227delC displayed symptoms of neutropenia, cardiomegaly, and other common symptoms ... Another c.C153G mutation resulted in severe metabolic acidosis, cardiomegaly, and other major symptoms of Barth syndrome. There ...
https://en.wikipedia.org/wiki/Tafazzin
Juan LoyolaJuan Loyola
He died suddenly on April 27, 1999, in Catia la Mar, Venezuela, after a long battle with cardiomegaly. This article was ...
https://en.wikipedia.org/wiki/Juan_Loyola
Idiopathic cardiomegaly*Idiopathic cardiomegaly*
Unknown author (‎1968)‎. Idiopathic cardiomegaly*. Bulletin of the World Health Organization, 38 (‎6)‎, 979 - 992. https:// ...
https://extranet.who.int/iris/restricted/handle/10665/266571
A to Z: Cardiomegaly (for Parents) - Print Version - NemoursA to Z: Cardiomegaly (for Parents) - Print Version - Nemours
If cardiomegaly is found, tests will be done to find and treat its cause. Not treating the condition causing cardiomegaly can ... Cardiomegaly (kar-dee-oh-MEG-uh-lee) is the medical term for an enlarged heart. ... Sometimes, such as with athletes and pregnant women, cardiomegaly is normal and reversible, meaning that the heart can go back ... Successfully treating the condition causing the heart to enlarge will often treat the cardiomegaly as well. ...
https://kidshealth.org/nemours/en/parents/az-cardiomegaly.html?view=ptr&WT.ac=p-ptr
Cardiomegaly with left atrial enlargement | Radiology Case | Radiopaedia.orgCardiomegaly with left atrial enlargement | Radiology Case | Radiopaedia.org
Gross cardiomegaly, even allowing for projection. Splaying of the carina noted and the impression of double density sign, both ... Knipe H, Cardiomegaly with left atrial enlargement. Case study, Radiopaedia.org (Accessed on 06 Dec 2022) https://doi.org/ ...
https://radiopaedia.org/cases/cardiomegaly-with-left-atrial-enlargement?iframe=true&lang=us
Coxsackie group B fatal neonatal myocarditis associated with cardiomegaly | Journal of Clinical PathologyCoxsackie group B fatal neonatal myocarditis associated with cardiomegaly | Journal of Clinical Pathology
Coxsackie group B fatal neonatal myocarditis associated with cardiomegaly Message subject: (Your Name) has forwarded a page to ...
https://jcp.bmj.com/content/19/4/325.share
CardiomegalyCardiomegaly
... - the standard term for designation of the increased heart ... Anamnesis of a cardiomegaly. In details collected anamnesis can not always give help in a cardiomegaly reason explanation. Very ... The cardiomegaly is found at physical inspection or is more often at a thorax X-ray analysis. Usually increase in heart is ... Cardiomegaly - the standard term for designation of the increased heart. Increased can be one or all four cameras of heart. To ...
http://infomeds.net/kardiomegaliya.html
IMSEAR at SEARO: Cardiomegaly with pericardial effusion in myxoedema.
Chandrasekaran M, Murugaiyan R, Gopinath KR, Kasirajan N. Cardiomegaly with pericardial effusion in myxoedema. Indian Heart ...
https://imsear.searo.who.int/handle/123456789/4272
Results of search for 'su:{Cardiomegaly.}' › WHO HQ Library catalog
Text; Format: print Publication details: Paris : INSERM, 1990Availability: Items available for loan: WHO HQ (1)Call number: WG 200 90CA. ...
https://kohahq.searo.who.int/cgi-bin/koha/opac-search.pl?q=su:%7BCardiomegaly.%7D
MeSH | Cardiomegaly (D006332)MeSH | Cardiomegaly (D006332)
Cardiomegaly is a nonspecific symptom seen in patients with chronic systolic heart failure (HEART FAILURE) or several forms of ...
https://www.cdek.liu.edu/mesh/D006332/
Treatment options for cardiomegalyTreatment options for cardiomegaly
Cardiomegaly is basically an enlarged heart and an indicative symptom of cardiomyopathy. ... The treatment for cardiomegaly will depend on the type of cardiomegaly affecting the individual as well as the underlying ... Treatment options for cardiomegaly. Leave a Comment / Circulatory Emergencies / By S. Black ... Cardiomegaly is basically an enlarged heart and an indicative symptom of cardiomyopathy. It is important to note that ...
https://www.stmarkjamestraining.ca/treatment-options-for-cardiomegaly/
cardiomegaly Archives - Sock-Doccardiomegaly Archives - Sock-Doc
cardiomegaly. Its Not "Natural", and Definitely Not Normal, to Die From Cardiac Arrest: The Death of Caballo Blanco. Its ...
https://sock-doc.com/tag/cardiomegaly/
Fire Fighter Fatality Investigation Report F2008-04 | NIOSH | CDCFire Fighter Fatality Investigation Report F2008-04 | NIOSH | CDC
Cardiomegaly/Left Ventricular Hypertrophy (LVH). On autopsy, the Trainee was found to have LVH and an enlarged heart. These ... Cardiomegaly (enlarged heart)(heart weighed 550 grams [g]; normal weight is ,400 g) [Siegel 1997a] ... Siegel RJ [1997a]. Cardiomegaly. In: Bloom S, ed. Diagnostic criteria for cardiovascular pathology acquired diseases. ...
https://www.cdc.gov/niosh/fire/reports/face200804.html
RXQ RX H
Cardiomegaly. I51.9. Heart disease, unspecified. I51.9P. Prevent heart disease. I63. Cerebral infarction. ...
https://wwwn.cdc.gov/Nchs/Nhanes/2013-2014/RXQ_RX_H.htm
Heart Failure Medication: Beta-Blockers, Alpha Activity, Beta-Blockers, Beta-1 Selective, ACE Inhibitors, ARBs, Inotropic...Heart Failure Medication: Beta-Blockers, Alpha Activity, Beta-Blockers, Beta-1 Selective, ACE Inhibitors, ARBs, Inotropic...
Pulmonary edema, visceral congestion, or cardiomegaly at autopsy. Source: Ho KK, Pinsky JL, Kannel WB, Levy D. The epidemiology ...
https://www.medscape.com/answers/163062-86726/which-medications-in-the-drug-class-beta-blockers-beta-1-selective-are-used-in-the-treatment-of-heart-failure
Top Ranked Doctors for Cardiomegaly in Arizona - DexurTop Ranked Doctors for Cardiomegaly in Arizona - Dexur
Cardiomegaly Top Ranked Most Experience - Arizona Cardiomegaly Top Ranked Most Experience - Maricopa County, AZ Cardiomegaly ... Cardiomegaly Top Ranked Most Experience - Arizona Cardiomegaly Top Ranked Most Experience - Maricopa County, AZ Cardiomegaly ... Cardiomegaly Top Ranked Most Experience - Arizona Cardiomegaly Top Ranked Most Experience - Maricopa County, AZ Cardiomegaly ... Cardiomegaly Top Ranked Most Experience - Arizona Cardiomegaly Top Ranked Most Experience - Maricopa County, AZ Cardiomegaly ...
https://dexur.com/gpsr/et/6/p/0/cat/01/rc/0104/st/az/
Cantú syndrome: MedlinePlus GeneticsCantú syndrome: MedlinePlus Genetics
Many infants with Cantú syndrome are born with a heart defect such as an enlarged heart (cardiomegaly) or patent ductus ... Congenital hypertrichosis, osteochondrodysplasia, and cardiomegaly: further delineation of a new genetic syndrome. Am J Med ... and cardiomegaly). Am J Med Genet. 2000 Oct 23;94(5):421-7. doi: 10.1002/1096-8628(20001023)94:53.0.co;2-9. Citation on PubMed ... and cardiomegaly: Cantu syndrome. Am J Med Genet. 1999 Aug 6;85(4):395-402. Citation on PubMed ...
https://medlineplus.gov/genetics/condition/cantu-syndrome
Lysosomal Storage Disease: Overview, Classification of Lysosomal Storage Diseases, Glycogen Storage Disease Type IILysosomal Storage Disease: Overview, Classification of Lysosomal Storage Diseases, Glycogen Storage Disease Type II
This manifestation is also characterized by macroglossia; progressive cardiomegaly; and rapidly progressive motor weakness with ... cardiomegaly, weakness, and cardiac failure were frequently reported but percentages were not specified. Progression of the ... arrhythmia or cardiomegaly), hepatosplenomegaly, ophthalmologic signs (corneal clouding or macular cherry-red spot), and ...
https://emedicine.medscape.com/article/1182830-overview
Browsing Journal Articles - Bulletin by Title
Kalter, H. D.; Schillinger, J. A.; Hossain, M.; Burnham, G.; Saha, S.; de Wit, V.; Khan, N. Z.; Schwartz, B.; Black, R. E. (‎World Health Organization, 1997)‎ ...
https://apps.who.int:80/iris/handle/10665/260543/browse?rpp=20&sort_by=1&type=title&etal=-1&starts_with=I&order=ASC
Aortic Arch Calcification and Cardiomegaly Are Associated with Overall and Cardiovascular Mortality in Hemodialysis Patients. ...Aortic Arch Calcification and Cardiomegaly Are Associated with Overall and Cardiovascular Mortality in Hemodialysis Patients. ...
The patients who had a high AoAC score and cardiomegaly had the highest overall and cardiovascular mortality among the four ... Aortic Arch Calcification and Cardiomegaly Are Associated with Overall and Cardiovascular Aortic Arch Calcification and ... Cardiomegaly Are Associated with Overall and Cardiovascular Mortality in Hemodialysis Patients. Ou, Shih-Hsiang; Liu, Yi-Hsueh ...
https://pesquisa.bvsalud.org/portal/resource/pt/mdl-34357124
SafeBeat Initiative: Mild Cardiomegaly: Causes And How To Reduce A Slightly Enlarged HeartSafeBeat Initiative: Mild Cardiomegaly: Causes And How To Reduce A Slightly Enlarged Heart
Mild cardiomegaly refers to a less severe form of cardiomegaly, which is an enlargement of the heart. ... This extra work leads to cardiomegaly.. Symptoms and diagnosis of mild cardiomegaly. Generally speaking, mild cardiomegaly does ... Mild Cardiomegaly: Causes And How To Reduce A Slightly Enlarged Heart. Mild cardiomegaly refers to a less severe form of ... Treating mild cardiomegaly. It is important to understand that problems with the heart, especially cases of cardiomegaly, ...
https://safebeat.org/cardiac/heart_health/mild_cardiomegaly_causes_and_how_to_reduce_a_slightly_enlarged_heart/
Probiotic administration attenuates myocardial hypertrophy and heart failure after myocardial infarction in the ratProbiotic administration attenuates myocardial hypertrophy and heart failure after myocardial infarction in the rat
Cardiomegaly / etiology * Cardiomegaly / physiopathology * Cardiomegaly / prevention & control* * Coronary Occlusion / ...
https://pubmed.ncbi.nlm.nih.gov/24625365/
Dr. Brian Friedman, MD - Interventional Cardiology Specialist in Overland Park, KS | HealthgradesDr. Brian Friedman, MD - Interventional Cardiology Specialist in Overland Park, KS | Healthgrades
Cardiomegaly. *Cardiomyopathy. *Cardiomyopathy, Dilated. *Cardiomyopathy, Hypertrophic. *Cardiovascular Diagnostic Test. * ...
https://www.healthgrades.com/physician/dr-brian-friedman-xnhds
Dr. Michael Wood, MD | Cardiothoracic Surgery in Chester, VA | Healthline FindCareDr. Michael Wood, MD | Cardiothoracic Surgery in Chester, VA | Healthline FindCare
Q Fever Endocarditis in HIV-Infected Patient - Volume 10, Number 3-March 2004 - Emerging Infectious Diseases journal - CDC
Chest x-ray showed cardiomegaly and congestive heart failure. An electrocardiogram showed a left anterior hemiblock and a first ...
https://wwwnc.cdc.gov/eid/article/10/3/03-0971_article
Advanced Search Results - Public Health Image Library(PHIL)Advanced Search Results - Public Health Image Library(PHIL)
Categories: Cardiomegaly Image Types: Photo, Illustrations, Video, Color, Black&White, PublicDomain, CopyrightRestricted 3 ...
https://phil.cdc.gov/AdvancedSearchResults.aspx?Search=Cardiomegaly&parentid=12355&catid=12356
Norco • NORCO: Find More Information here • oxycodone drugNorco • NORCO: Find More Information here • oxycodone drug
Cardiomegaly flaring in patients cartilaginous with narcotics. A NORCO has a rhineland abuse darvon. I want to get my ...
https://www.angelfire.com/ak3/3alamy/norco/oxycodone-drug.html
Cardiomegaly a sign of Heart Issue can be diagnosed by Deeptek's path-breaking innovative machine learning technique - MP...
Cardiomegaly refers to the thickening of the heart muscles or the expansion of the chambers. Cardiomegaly is a sign of another ... Cardiomegaly a sign of Heart Issue can be diagnosed by Deepteks path-breaking innovative machine learning technique. Akhil ... Cardiomegaly a sign of Heart Issue can be diagnosed by Deepteks path-breaking innovative machine learning technique. ... Cardiomegaly can be caused by many conditions, including hypertension, coronary artery disease, infections, inherited disorders ...
https://mpguardian.com/index.php/2022/07/12/cardiomegaly-a-sign-of-heart-issue-can-be-diagnosed-by-deepteks-path-breaking-innovative-machine-learning-technique/
DailyMed - GLATOPA- glatiramer acetate injection, solutionDailyMed - GLATOPA- glatiramer acetate injection, solution
6 Types of Heart Doctors You Should Know About | Healthfully6 Types of Heart Doctors You Should Know About | Healthfully
What Are the Treatments for Cardiomegaly? * The Best Exercises for a Deconditioned Heart ...
https://healthfully.com/6-types-of-heart-doctors-you-should-know-about-3352355.html
Systemic Sclerosis Imaging: Practice Essentials, Radiography, Computed TomographySystemic Sclerosis Imaging: Practice Essentials, Radiography, Computed Tomography
Pulmonary artery enlargement and cardiomegaly Ancillary findings include diffuse esophageal dilation with a resultant "air ...
https://emedicine.medscape.com/article/362660-overview
Diagnosing and Classifying Pulmonary Hypertension - Renal and Urology NewsDiagnosing and Classifying Pulmonary Hypertension - Renal and Urology News
Figure 1. Chest radiograph from a patient with suspected pulmonary hypertension; notable findings include cardiomegaly, and ...
https://www.renalandurologynews.com/home/decision-support-in-medicine/cardiology/diagnosing-and-classifying-pulmonary-hypertension/
Pericardial effusionCardiomyopathyPulmonaryEnlargementCongenitalHypertrophicBilateralSymptomsAcuteDiseaseSignsDiagnosisComplicationsRefersCardiovascularTypicallyChamberMusclesPatientsSyndromeNormalConditionSearchTermHeart failureReasonNaturalFoundCases
Pericardial effusion3
  • IMSEAR at SEARO: Cardiomegaly with pericardial effusion in myxoedema. (who.int)
  • Chandrasekaran M, Murugaiyan R, Gopinath KR, Kasirajan N. Cardiomegaly with pericardial effusion in myxoedema. (who.int)
  • Chest X-ray showed cardiomegaly suggestive of pericardial effusion. (springer.com)
Cardiomyopathy1
  • Cardiomegaly is basically an enlarged heart and an indicative symptom of cardiomyopathy. (stmarkjamestraining.ca)
Pulmonary4
  • a) CXR showed cardiomegaly with pulmonary congestion and bilateral pleural effusion. (hindawi.com)
  • b) CT chest with contrast showed moderately large bilateral pleural effusions, right greater than left, with cardiomegaly and reflux of IV contrast into the IVC, consistent with cardiogenic pulmonary vascular congestion. (hindawi.com)
  • The [chest X-ray] demonstrated cardiomegaly and pulmonary vascular congestion. (the-hospitalist.org)
  • Patient may not have cardiomegaly or bilateral pulmonary infiltrates on chest radiograph. (knowcancer.com)
Enlargement2
  • Knipe H, Cardiomegaly with left atrial enlargement. (radiopaedia.org)
  • Mild cardiomegaly refers to a less severe form of cardiomegaly, which is an enlargement of the heart. (safebeat.org)
Congenital2
  • Congenital hypertrichosis, osteochondrodysplasia, and cardiomegaly: further delineation of a new genetic syndrome. (medlineplus.gov)
  • Any children showing an abnormal heart condition such as central cyanosis, cardiac murmur, cardiomegaly, arrhythmia or those with non-cardiac congenital abnormality were examined later in hospital by a cardiologist and given a 12-lead electrocardiogram and chest X-ray. (who.int)
Hypertrophic1
  • There are three forms of cardiomegaly with each resulting to an enlarged heart -restrictive, dilated and hypertrophic. (stmarkjamestraining.ca)
Bilateral2
  • Chest X-ray (CXR) and computed tomography (CT) of the chest showed cardiomegaly and moderate pleural effusion in bilateral lung fields (Figure 2 ). (hindawi.com)
  • Chest radiograph showed bilateral pleural effusion (right>left) without any cardiomegaly. (saudija.org)
Symptoms3
  • Often heart disease symptoms are found in patients with a cardiomegaly. (infomeds.net)
  • Take note that controlling the fluid volume can help maintain a stable blood pressure as well as relieves symptoms of fatigue , shortness of breath and cough caused by cardiomegaly. (stmarkjamestraining.ca)
  • Generally speaking, mild cardiomegaly does not present with any noticeable symptoms, as real problems typically appear once cardiomegaly had reached moderate to severe status. (safebeat.org)
Acute1
  • Usually it is easier to find a cardiomegaly in subacute or chronic, than in initial or acute stages of a disease. (infomeds.net)
Disease3
  • However over time most of patients with an explicit cardiomegaly has accessory clinical signs of a heart disease. (infomeds.net)
  • The treatment for cardiomegaly will depend on the type of cardiomegaly affecting the individual as well as the underlying disease process. (stmarkjamestraining.ca)
  • Cardiomegaly is a sign of another heart issue, not a disease. (mpguardian.com)
Signs1
  • Signs of myocardial ischemia and cardiomegaly are the predominate manifestations of this lesion. (uwi.edu)
Diagnosis3
  • As upper limits of the sizes of heart are strictly not defined, the diagnosis of a cardiomegaly is more subjective, than is considered to be. (infomeds.net)
  • Thus, the diagnosis of a cardiomegaly causes the necessity of systematic research of cardiovascular system. (infomeds.net)
  • In this chapter it is not given full differential diagnosis of a cardiomegaly. (infomeds.net)
Complications1
  • Ensure these conditions are treated properly to help reduce complications like cardiomegaly. (safebeat.org)
Refers1
  • Cardiomegaly refers to the thickening of the heart muscles or the expansion of the chambers. (mpguardian.com)
Cardiovascular2
  • Aortic Arch Calcification and Cardiomegaly Are Associated with Overall and Cardiovascular Mortality in Hemodialysis Patients. (bvsalud.org)
  • The patients who had a high AoAC score and cardiomegaly had the highest overall and cardiovascular mortality among the four groups. (bvsalud.org)
Typically1
  • The treatment for cardiomegaly typically includes controlling the blood pressure with the help of medications such as angiotensin-receptor blockers and angio-converting enzymes. (stmarkjamestraining.ca)
Chamber1
  • A form of mild cardiomegaly that affects only one chamber of the heart, the left ventricle. (safebeat.org)
Muscles1
  • Always bear in mind that cardiomegaly deteriorates the heart muscles and diminishes the pumping ability to the entire body. (stmarkjamestraining.ca)
Patients2
  • Cardiomegaly is a nonspecific symptom seen in patients with chronic systolic heart failure ( HEART FAILURE ) or several forms of CARDIOMYOPATHIES . (liu.edu)
  • The medical term for this condition is cardiomegaly, although most patients will hear that their hearts are enlarged or dilated . (heart-valve-surgery.com)
Syndrome1
  • Many infants with Cantú syndrome are born with a heart defect such as an enlarged heart (cardiomegaly) or patent ductus arteriosus (PDA). (medlineplus.gov)
Normal1
  • Sometimes, such as with athletes and pregnant women, cardiomegaly is normal and reversible, meaning that the heart can go back to its normal size. (kidshealth.org)
Condition4
  • Not treating the condition causing cardiomegaly can lead to heart failure and other serious problems. (kidshealth.org)
  • Successfully treating the condition causing the heart to enlarge will often treat the cardiomegaly as well. (kidshealth.org)
  • Cardiomegaly is a condition where the heart becomes larger or hypertrophied due to being overworked. (safebeat.org)
  • Mild cardiomegaly may provide an opportunity to manage the condition on your own to prevent its progression. (safebeat.org)
Search1
  • Results of search for 'su:{Cardiomegaly. (who.int)
Term2
  • Cardiomegaly (kar-dee-oh-MEG-uh-lee) is the medical term for an enlarged heart . (kidshealth.org)
  • Cardiomegaly - the standard term for designation of the increased heart. (infomeds.net)
Heart failure1
  • Congestive heart failure results in the heart having to work harder to maintain the perfusion of blood, however, it often is insufficient and leads to cardiomegaly. (safebeat.org)
Reason1
  • If the reason for cardiomegaly is a dysfunctional heart valve, the affected valve might be repaired surgically or completely replaced. (stmarkjamestraining.ca)
Natural1
  • Natural cardiomegaly cures may prove useful when combined with a healthy diet and active lifestyle. (safebeat.org)
Found1
  • If cardiomegaly is found, tests will be done to find and treat its cause. (kidshealth.org)
Cases1
  • It is important to understand that problems with the heart, especially cases of cardiomegaly, should be treated with the aid of a trained medical professional. (safebeat.org)