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pubmed:abstractText |
Chronic heart failure results from two processes, i.e., myocardial and congestive failure. Myocardial failure is clinically silent, most often progresses slowly, and is documented by a depressed left ventricular ejection fraction. Multiple etiologic factors include systolic and diastolic overloads, myocardial necrosis and/or ischemia, and, perhaps, microvascular spasm. Myocardial failure ultimately leads to exaggerated neurohumoral compensatory mechanisms and derangements of the peripheral circulation, which are the hallmarks of congestive heart failure. At that stage of the syndrome, patients have symptoms, initially, with exercise and, later, at rest. Objective assessment of severity is afforded by determination of maximal oxygen uptake during maximal exercise testing. When congestive heart failure supervenes, the prognosis is poor. Current medical therapy is aimed at improving the derangements of the peripheral circulation, which relieves the symptoms but leaves the primary myocardial process unaffected. The goal of future therapy is to intervene at an earlier stage of the syndrome to halt or even partially reverse the myocardial failure.
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