Cardiomyopathy of Overload
MORE than 80 years ago, Sir James MacKenzie noted: “The more I study the symptoms of heart failure, and the more I reflect on the part played by the heart muscle, the more convinced I am that… heart failure is due to the exhaustion of the reserve force of the heart muscle.” Except for the cardiac glycosides, however, therapy for congestive heart failure generally has focused on the systemic signs and symptoms that appear when the failing heart becomes unable to meet the hemodynamic demands of the body, rather than on abnormalities in the heart muscle itself, which both cause and exacerbate the clinical disability.
A new understanding of the pathophysiology of congestive heart failure has led to the identification of important cellular and molecular alterations in the failing heart. Although often masked by prominent systemic compensations for depressed cardiac performance, notably salt and water retention and vasoconstriction, the heart-muscle disorders play a major part in determining the poor prognosis in this condition, which a few years ago had a five-year mortality of approximately 50 percent. Stimulated by a growing realization that medical therapy can alter this grim outlook, applications of new knowledge of the pathophysiology of the heart in congestive heart failure are increasingly affecting strategies for the clinical care of patients with the condition.
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Although myocardial hypertrophy, one of the most important responses of the failing heart, is an adaptive process that enables the heart to compensate for overloading, the cells of the hypertrophied, failing heart are not normal. This review of the cellular abnormalities in the failing myocardium describes a cardiomyopathy of overload that appears to be among the chief causes of deterioration and death in patients with congestive heart failure.
Clinical Syndromes in Heart Failure
The hemodynamic abnormalities that result from heart failure are conceptually simple because, as a pump, the heart has but two ways to fail: through inadequate emptying of the venous reservoirs (backward failure) and through reduced ejection of blood under pressure into the aorta and pulmonary artery (forward failure). However, the response of the body to these abnormalities is complex and varies from person to person. Furthermore, because blood flows in a circle, forward failure and backward failure generally coexist, although the highly variable circulatory adjustments in response to impaired pump performance may cause one or the other to dominate the clinical picture in any given patient.
In patients with left ventricular dysfunction, by far the most common cause of heart failure, an increase in left atrial pressure (backward failure) leads to dyspnea, to pulmonary congestion, and when severe, to pulmonary edema. Reduced cardiac output (forward failure) causes poor tissue perfusion and fatigue; since the body tends to protect blood pressure at the expense of cardiac output (because of vasoconstriction), hypotension is uncommon in chronic heart failure, usually appearing only in the very late stages when pump function has become severely impaired.