Patients who have a significant loss of cardiac pump function develop progressively severe symptoms of fatigue, dyspnea (shortness of breath), chest pain, syncope (loss of consciousness), and death. The management of these patients requires an understanding that it is an ongoing process in which the response to the initial injury causes damage beyond the insult alone. The challenge of the clinician is to keep the congestive heart failure (CHF) patient out of the hospital while reducing morbidity and mortality in this high-risk population.

Chronic CHF may be defined as the clinical condition in which an individual expels less than 40% of the blood from the left ventricle per heartbeat (ejection fraction [EF] < 40%).A normal individual expels about 55 to 65% of the blood from the left ventricle per heartbeat (EF = 55-65%). The rationale for choosing the 40% EF is based on clinical findings demonstrating pro gressive deterioration and early mortality in individuals who have an EF below 40%.

It is remarkable that the therapeutic approach to a decreased EF is the same regardless of the etiology. The principles that guide the pharmacological management of CHF is the same for patients who had damage from a myocardial infarction (MI), viral infection, valvular disease, alcohol, and so on. This chapter reviews the recommended approach to the pharmacological management of systolic dysfunction. An historic perspective will be followed to provide an appreciation of the evolution in our understanding of the pathophysiology of this condition.

The management of heart failure in the presence of normal systolic function is not reviewed. This form of heart failure commonly occurs in the elderly with chronic hypertension and left ventricular hypertrophy. The failure of the left ventricle to relax during diastole (diastolic dysfunction) results in elevated end diastolic pressures and volumes. The shortness of breath (dyspnea), chest pain, and fatigue that result from elevated pulmonary venous pressures are similar in both systolic and diastolic dysfunction. Also excluded from discussion are nondrug therapies for CHF, such as coronary artery bypass, percutaneous coronary interventions, electronic pacemakers, and cardiac transplantation.

A considerable body of literature supports abnormalities in myocardial excitation-contraction coupling in CHF. An appreciation of the principles involved in this cell signaling process is crucial to understand current and future pharmacotherapies for CHF. A brief overview of myocardial excitation-contraction coupling will be provided.

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