The abnormalities of myocardial structure and function that underlie heart failure can activate biological responses that drive disease progression. Drugs that reduce ventricular wall stress or inhibit the renin-angiotensin system (e.g., selected vasodilators, ACE inhibitors, and aldosterone antagonists) or the sympathetic nervous system (e.g., p adrenergic antagonists) can decrease pathological ventricular remodeling, attenuate disease progression, and decrease mortality in patients with heart failure due to systolic dysfunction. As a result, these drugs have become mainstays in the long-term treatment of heart failure. Some of the drugs that slow progression afford an immediate beneficial impact on hemodynamic function and symptoms (e.g., vasodilators and ACE inhibitors). Other agents that attenuate disease progression can adversely affect hemodynamic function and worsen symptoms in the short term and must therefore be used with caution (e.g., p receptor antagonists). Figure 33-1 provides an overview of the pathophysiological mechanisms of heart failure and the sites of action of the major drug classes used in treatment.
The current approach to therapy for CHF involves preload reduction, afterload reduction, and enhancement of inotropic state. A variety of vasodilators will reduce preload and afterload (Table 33-1). Although a vasodilator's more prominent effect may be to reduce either preload or afterload, most agents affect both.
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