ABSTRACT
Heart failure has traditionally been considered a clinical syndrome in which the symptoms define the disorder. Indeed, the clinical syndrome is often designated as “congestive heart failure” because symptoms are usually accompanied by fluid retention leading to peripheral edema and pulmonary congestion. The structural change in the left ventricle that characterizes heart failure involves myocytes and interstitium, and perhaps the vasculature. The myocyte hypertrophy of pressure overload is characterized by an increase in the transverse diameter of individual myocytes, an increase in the cross-section area, a consequent increase in wall thickness, an increase in mass with a normal chamber dimension, and a normal ejection fraction. As myocytes and fibers lengthen, the left ventricular chamber enlarges and a physiologically appropriate stroke volume can be delivered with considerably less shortening. Thus, a low ejection fraction is an obligatory accompaniment of a dilated ventricle in the absence of gross valvular regurgitation.
