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.