title: Coronary vascular mechanisms involved in decompensation from hypertrophy to heart failure.
abstract: One potential mechanism for the eventual failure of the hypertrophied ventricle to maintain compensation may involve impaired coronary reserve. Reduced coronary reserve is one of the hallmarks of ventricular hypertrophy. Although this reduced coronary reserve may not affect baseline left ventricular function, it could be of greater importance during periods of stress, such as occur during exercise, where increased metabolic demands induced by the stress may not be fully met by an increase in coronary blood flow. The impaired subendocardial coronary reserve is caused not only by the hypertrophy but also by the hemodynamic changes (for example, the left ventricular subendocardial wall stress that increases markedly on exercise). In the severely hypertrophied heart, there are impaired subendocardial wall function and reduced subendocardial coronary perfusion in response to exercise. It is hypothesized that these episodes occur frequently under normal activity (for example, in response to exercise, excitement, eating) and that they become severe enough to induce myocyte necrosis and replacement fibrosis. This in turn will impair left ventricular systolic function. Furthermore, myocardial ischemia and left ventricular fibrosis as well as the altered loading conditions result in impaired diastolic function, which in turn diminishes systolic function. All of these mechanisms working in concert act to further impair systolic function and accelerate the progression of compensated left ventricular hypertrophy to failure.
authors.affiliation: Department of Medicine, Harvard Medical School, Brigham & Women's Hospital, Boston, Massachusetts.
authors.forename: S F
authors.initials: SF
authors.lastname: Vatner
authors.forename: L
authors.initials: L
authors.lastname: Hittinger
mesh_terms: D000319:Adrenergic beta-Antagonists / Q000627:therapeutic use; D000818:Animals; D003094:Collagen / Q000378:metabolism; D003326:Coronary Circulation / Q000187:drug effects; D003331:Coronary Vessels / Q000187:drug effects / Q000503:physiopathology*; D004195:Disease Models, Animal; D004285:Dogs; D004353:Drug Evaluation, Preclinical; D006321:Heart / Q000187:drug effects / Q000503:physiopathology; D006333:Heart Failure / Q000188:drug therapy / Q000209:etiology* / Q000503:physiopathology; D006439:Hemodynamics / Q000187:drug effects; D017379:Hypertrophy, Left Ventricular / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology; D009206:Myocardium / Q000378:metabolism; D013312:Stress, Physiological / Q000503:physiopathology
chemical_list: D000319:Adrenergic beta-Antagonists; D003094:Collagen