Relation of pathophysiologic mechanisms to outcome in heart failure

Advances in the treatment of heart failure with angiotensin-converting enzyme inhibitors have been accompanied by an improved understanding of the pathophysiology of heart failure. The inability of the heart to act as a pump is determined in some patients by alterations to the architecture of the heart and changes in the extracellular space, particularly fibrosis. The degree to which the failure of the heart as a pump can be attributed to a reduced ability of the myocyte to contract is contentious. The origin of symptoms is still uncertain but does relate to identified changes in the lung, increased peripheral resistance and atrophy of skeletal muscle. The mechanisms of action of angiotensin-converting enzyme inhibitors are numerous and do not yet account easily for the clinical benefits. Further epidemiologic studies are needed to ascertain the proportion of patients who manifest progressive heart failure rather than deterioration due to further cardiac events. Understanding the pathophysiology of heart failure will allow therapy to be tailored to the requirements of the individual patient.