Please click here to obtain permission to reproduce this image.
Click on image to view larger version.
Figure 2 The Mechanisms Through Which Cardiac Stresses Incite Ventricular Dilatation Dysfunction
Diverse cardiac stresses, either through direct toxicity to myocytes or through processes such as inflammation and/or aberrant calcium dynamics, result in myocyte apoptosis. The heart initially instigates compensatory responses according to the nature and severity of the inciting influence. If energy deficiency is a prominent feature of the inciting stress, then hypertrophy may initially ensue. If compensatory adaptation through hypertrophy and perhaps stem cell recruitment is inadequate, unchallenged apoptosis will result in myocyte depletion and myocardial decompensation. The resulting low cardiac output state promotes an initially adaptive but a chronically maladaptive neurohormonal state that perpetuates myocyte apoptosis. This common maladaptive chronic heart failure state is, at least in part, independent of the proximate inciting influence and is characterized by neurohormonal activation, metabolic impairment, and maladaptive cardiac remodeling that results in dilated-hypokinetic ventricles. ACE-I = angiotensin-converting enzyme inhibition; DCM = dilated cardiomyopathy; HCM = hypertrophic cardiomyopahy.
|
