PHARMACOLOGICAL TREATMENT OF HEART FAILURE (HF)
HF is a clinical syndrome resulting from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with (diastolic dysfunction) or eject blood (systolic dysfunction).
The cardinal manifestations of HF are dyspnea and fatigue, which may limit exercise tolerance, and fluid retention, which may lead to pulmonary and peripheral edema.
Coronary artery disease is the underlying cause of HF in approximately two thirds of patients with left ventricular systolic dysfunction. The remainders have non-ischemic causes of systolic dysfunction and may have an identifiable cause (e.g., hypertension, valvular disease, myocardial toxins, or myocarditis) or may have no discernible cause (e.g., idiopathic dilated cardiomyopathy).
The classification system that is most commonly used to quantify the degree of functional limitation imposed by HF is one first developed by the NYHA1 (New York Heart Association). This system assigns patients to 1 of 4 functional classes depending on the degree of effort needed to elicit symptoms: patients may have symptoms of HF at rest (class IV), on less-than-ordinary exertion (class III), on ordinary exertion (class II), or only at levels that would limit normal individuals (class I).
This functional classification reflects the subjective assessment of physician and patient, may change frequently over short periods of time and the treatments used do not differ significantly across the classes. To overtake these limitations, the joined AHA/ACC committee developed a new staging system that would reliably and objectively identify patients in the course of their disease and would be linked to treatments that were uniquely appropriate at each stage of their illness.
According to this new approach, patients would be expected to advance from one stage to the next unless progression of the disease was slowed or stopped by treatment. Indeed, left ventricular dysfunction, which begins with some injury to the myocardium, is usually a progressive process, even in the absence of a new identifiable insult to the myocardium. The principal manifestation of such progression is a process known as remodeling, which occurs as a homeostatic attempt to decrease wall stress, through increases in wall thickness. This ultimately results in a change in the geometry of the left ventricle such that the chamber dilates, hypertrophies, and becomes more spherical. The process of cardiac remodeling generally precedes the development of symptoms, occasionally by months or even years. The process of remodeling continues after the appearance of symptoms and may contribute importantly to worsening of symptoms despite treatment.
1 The Criteria Committee of the New York Heart Association. Diseases of the Heart and Blood Vessels: Nomenclature and Criteria for Diagnosis. 6th ed. Boston, MA: Little Brown, 1964.