Heart Failure with Normal Ejection Fraction

Epidemiology, Clinical Features, and Pathophysiology. Approximately 30 to 40% of patients with CHF have a normal or well-preserved ejection fraction (the latter usually defined as >.45). The differential diagnosis includes entities such as constrictive pericarditis, restrictive cardiomyopathy, and hypertrophic cardiomyopathy. However, the most common etiologic substrate is concentric left ventricular hypertrophy caused by systolic hypertension in elderly patients, most often women with noncompliant systemic arteries. Many of these patients have concomitant coronary artery disease that undoubtedly contributes to the pathophysiology of CHF, especially since demand ischemia causes increased left ventricular filling pressure with relatively little effect on ejection fraction. Thus, demand ischemia is itself a cause of transient CHF with well-preserved ejection fraction.

The presumption is that patients with CHF and normal ejection fraction have elevated cardiac filling pressures reflecting diastolic dysfunction that is in turn caused by slowed or incomplete myocardial relaxation and/or decreased passive compliance. This is obvious in patients with constrictive pericarditis and restrictive cardiomyopathy, who have major structural impediments to ventricular filling. However, the more commonly encountered patients with underlying concentric hypertrophy also have abnormalities of relaxation and filling, including possible depression of sarcoplasmic reticulum calcium pumping, increased ratio of wall thickness to chamber volume, and very likely increased myocardial connective tissue. In addition, concentric hypertrophy is a substrate for subendocar-dial ischemia when energy demands increase even in the absence of coronary artery disease. Patients with underlying concentric hypertrophy and CHF with normal ejection fraction present typically with acute pulmonary edema in conjunction with markedly elevated blood pressure and often tachycardia. This suggests an important role for increased myocardial energy demands and subendo-cardial ischemia superimposed on resting abnormalities of relaxation and filling.

Echocardiographic-Doppler abnormalities consistent with abnormal dia-stolic function are common in patients with diabetes, and left ventricular mass is increased compared with that in otherwise matched nondiabetic subjects. Moreover, diabetic patients are over-represented in the population of patients with CHF and normal ejection fraction. Thus, although not generally considered an independent etiology of CHF with normal ejection fraction, diabetic cardiomyop-athy may contribute to the pathophysiology of this syndrome.

Management. The general measures described above also apply to patients with CHF and normal ejection fraction. For the vast majority of patients <j with this syndrome and underlying concentric hypertrophy caused by systolic hypertension, therapy is otherwise exclusively pharmacological. The same spe-

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