Antagonists in Chronic Heart Failure

Prognosis in congestive heart failure is directly linked to neurohormonal activation. Angiotensin II through the activation of the renin angiotensin aldosterone system has been the principal focus of therapy over the last two decades. New agents that target selective blockade of the angiotensin II receptor have been introduced in clinical trials for the treatment of heart failure. Aldosterone has been identified as a critically important neurohormone with direct detrimental effects on the myocardium. Aldosterone antagonists have been utilized in clinical trials to improve mortality in patients with chronic heart failure. Congestive heart failure has emerged as a major public health issue for the new millennium. Currently there are approximately five million patients with this diagnosis in the United States. The prevalence increases with age and mortality and morbidity remain high despite significant advances in pharmacologic therapy. Congestive heart failure symptoms can occur in the presence of systolic dysfunction usually documented by a decrease in ejection fraction or can present with impaired diastolic function occasionally labeled as heart failure with preserved systolic function of the left ventricle. Over the last two decades we have learned that neurohormonal activation primarily mediated through the renin angiotensin aldosterone system, as well as, the sympathetic nervous system is a key determinant in the progression of chronic heart failure. Considerable effort in the form of large scale clinical trials have helped define the current recommendations for pharmacologic treatment of symptomatic patients with heart failure due to left ventricular systolic dysfunction. Diuretics as a drug class appear to be important in symptom relief in congestive heart failure from any etiology. Digitalis appears to be beneficial in many patients again in providing symptomatic benefit. However, it is only until recently where our full comprehension of the role of neurohormonal activation has led to the conclusion that patients with symptomatic heart failure should be treated with agents to decrease angiotensin II, as well as, with beta blocking agents to slow the progression of the disease