Cardiac Enlargement (cardiac + enlargement)

Distribution by Scientific Domains
Medical Sciences50%

Selected Abstracts

Proteomic profiling of KATP channel-deficient hypertensive heart maps risk for maladaptive cardiomyopathic outcome

PROTEINS: STRUCTURE, FUNCTION AND BIOINFORMATICS, Issue 5 2009
Jelena Zlatkovic
Abstract KCNJ11 null mutants, lacking Kir6.2 ATP-sensitive K+ (KATP) channels, exhibit a marked susceptibility towards hypertension (HTN)-induced heart failure. To gain insight into the molecular alterations induced by knockout of this metabolic sensor under hemodynamic stress, wild-type (WT) and Kir6.2 knockout (Kir6.2-KO) cardiac proteomes were profiled by comparative 2-DE and Orbitrap MS. Despite equivalent systemic HTN produced by chronic hyperaldosteronism, 114 unique proteins were altered in Kir6.2-KO compared to WT hearts. Bioinformatic analysis linked the primary biological function of the KATP channel-dependent protein cohort to energetic metabolism (64% of proteins), followed by signaling infrastructure (36%) including oxidoreductases, stress-related chaperones, processes supporting protein degradation, transcription and translation, and cytostructure. Mapped protein,protein relationships authenticated the primary impact on metabolic pathways, delineating the KATP channel-dependent subproteome within a nonstochastic network. Iterative systems interrogation of the proteomic web prioritized heart-specific adverse effects, i.e., "Cardiac Damage", "Cardiac Enlargement", and "Cardiac Fibrosis", exposing a predisposition for the development of cardiomyopathic traits in the hypertensive Kir6.2-KO. Validating this maladaptive forecast, phenotyping documented an aggravated myocardial contractile performance, a massive interstitial fibrosis and an exaggerated left ventricular size, all prognostic indices of poor outcome. Thus, Kir6.2 ablation engenders unfavorable proteomic remodeling in hypertensive hearts, providing a composite molecular substrate for pathologic stress-associated cardiovascular disease. [source]

DIFFERENCES BETWEEN PATHOLOGICAL AND PHYSIOLOGICAL CARDIAC HYPERTROPHY: NOVEL THERAPEUTIC STRATEGIES TO TREAT HEART FAILURE

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 4 2007
Julie R McMullen
SUMMARY 1In general, cardiac hypertrophy (an increase in heart mass) is a poor prognostic sign. Cardiac enlargement is a characteristic of most forms of heart failure. Cardiac hypertrophy that occurs in athletes (physiological hypertrophy) is a notable exception. 2Physiological cardiac hypertrophy in response to exercise training differs in its structural and molecular profile to pathological hypertrophy associated with pressure or volume overload in disease. Physiological hypertrophy is characterized by normal organization of cardiac structure and normal or enhanced cardiac function, whereas pathological hypertrophy is commonly associated with upregulation of fetal genes, fibrosis, cardiac dysfunction and increased mortality. 3It is now clear that several signalling molecules play unique roles in the regulation of pathological and physiological cardiac hypertrophy. 4The present review discusses the possibility of targeting cardioprotective signalling pathways and genes activated in the athlete's heart to treat or prevent heart failure. [source]

Physiological Society Symposium , the Athlete's Heart

EXPERIMENTAL PHYSIOLOGY, Issue 5 2003
Athlete's heart, effect of age, ethnicity, sporting discipline
Regular physical training is associated with several physiological and biochemical adaptations which enable an increase in cardiac output and widening of the systemic arterio-venous oxygen difference. An increase in cardiac chamber size is fundamental to the generation of a sustained increase in cardiac output for prolonged periods. Echocardiographic studies have shown that the vast majority of athletes have modest cardiac enlargement although a small proportion exhibit substantial increases in heart size. Recognised determinants of cardiac size include age, sex, ethnicity and type of sport. Cardiac dimensions vary considerably amongst athletes, even when allowances are made for these variables, suggesting that genetic, endocrine and biochemical factors also influence heart size. This review discusses the effects of age, sex, ethnicity and sporting discipline on cardiac dimensions in athletic individuals. [source]

Effect of Pimobendan or Benazepril Hydrochloride on Survival Times in Dogs with Congestive Heart Failure Caused by Naturally Occurring Myxomatous Mitral Valve Disease: The QUEST Study

JOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 5 2008
J. Häggström
Background: Myxomatous mitral valve disease (MMVD) continues to be an important cause of morbidity and mortality in geriatric dogs despite conventional therapy. Hypothesis: Pimobendan in addition to conventional therapy will extend time to sudden cardiac death, euthanasia for cardiac reasons, or treatment failure when compared with conventional therapy plus benazepril in dogs with congestive heart failure (CHF) attributable to MMVD. Animals: Two hundred and sixty client-owned dogs in CHF caused by MMVD were recruited from 28 centers in Europe, Canada, and Australia. Methods: A prospective single-blinded study with dogs randomized to PO receive pimobendan (0.4,0.6 mg/kg/d) or benazepril hydrochloride (0.25,1.0 mg/kg/d). The primary endpoint was a composite of cardiac death, euthanized for heart failure, or treatment failure. Results: Eight dogs were excluded from analysis. One hundred and twenty-four dogs were randomized to pimobendan and 128 to benazepril. One hundred and ninety dogs reached the primary endpoint; the median time was 188 days (267 days for pimobendan, 140 days for benazepril hazard ratio = 0.688, 95% confidence limits [CL] = 0.516,0.916, P= .0099). The benefit of pimobendan persisted after adjusting for all baseline variables. A longer time to reach the endpoint was also associated with being a Cavalier King Charles Spaniel, requiring a lower furosemide dose, and having a higher creatinine concentration. Increases in several indicators of cardiac enlargement (left atrial to aortic root ratio, vertebral heart scale, and percentage increase in left ventricular internal diameter in systole) were associated with a shorter time to endpoint, as was a worse tolerance for exercise. Conclusions and Clinical Importance: Pimobendan plus conventional therapy prolongs time to sudden death, euthanasia for cardiac reasons, or treatment failure in dogs with CHF caused by MMVD compared with benazepril plus conventional therapy. [source]