Cellular and signaling mechanisms of cardiac hypertrophy.
Left ventricular hypertrophy (LVH) is an important independent risk factor for cardiovascular morbidity and mortality. Initially LVH improves contractility and pump function; however, over time a sequence of events occurs including disintegration of myofibrils, interstitial fibrosis, adenosine triphosphate depletion, and altered gene expression. Eventually the hypertrophied myocardium outgrows its capillary bed, subendocardial ischemia develops, and the heart fails. Hemodynamic (pressure) and nonhemodynamic signals (catecholamines, angiotensin II, thyroid hormone) have been identified that stimulate hypertrophic growth of the myocardium. Evidence is also accumulating that the induction of immediate early genes such as c-fos and c-myc may participate in the development of LVH.
Piano
M R
MR
Department of Medical-Surgical Nursing, College of Nursing, University of Illinois at Chicago.
D000255:Adenosine Triphosphate / Q000172:deficiency; D000804:Angiotensin II / Q000502:physiology; D002318:Cardiovascular Diseases / Q000453:epidemiology / Q000209:etiology; D002395:Catecholamines / Q000502:physiology; D015870:Gene Expression / Q000502:physiology; D016762:Genes, fos / Q000502:physiology; D016259:Genes, myc / Q000502:physiology; D006439:Hemodynamics; D006801:Humans; D017379:Hypertrophy, Left Ventricular / Q000150:complications / Q000451:nursing / Q000473:pathology / Q000503:physiopathology*; D010347:Patient Care Planning; D012307:Risk Factors; D015398:Signal Transduction / Q000502:physiology*; D013963:Thyroid Hormones / Q000502:physiology
D002395:Catecholamines; D013963:Thyroid Hormones; D000804:Angiotensin II; D000255:Adenosine Triphosphate