Peripartum Cardiomyopathy Presenting as Diastolic Heart Failure

Abstract

The authors describe a case of peripartum cardiomyopathy due to diastolic dysfunction. The patient presented postpartum with signs and symptoms of congestive heart failure, pulmonary edema, and cardiomegaly on chest x-ray, elevated levels of B-type natriuretic peptide (BNP), and an echocardiogram demonstrating preserved systolic function with Doppler evidence of impaired left ventricular relaxation. She responded to medical therapy for heart failure. To date, no other investigators have described isolated diastolic dysfunction as a cause of peripartum cardiomyopathy. A 42-year-old woman had a history of pulmonary edema within weeks following 2 uneventful previous pregnancies. The patient became pregnant again and was cared for throughout pregnancy in both the high-risk obstetric clinic and the cardiology section. This pregnancy was uncomplicated, and there was no evidence of gestational hypertension. The patient underwent a cesarean section at another hospital for cephalopelvic disproportion. She developed dyspnea after delivery, was treated with furosemide, and was given metoprolol tartrate at discharge. One week later, she presented to another hospital with dyspnea, orthopnea, and paroxysmal nocturnal dyspnea. Blood pressure was 165/90 mm Hg, heart rate was 50 beats per minute, and respiratory rate was 22 breaths per minute. A computed tomographic scan ruled out a pulmonary embolus and demonstrated significant pulmonary edema. Her pro-BNP level was elevated at 775 pg/mL. She was transferred to our institution, where on arrival, her chest radiograph showed pulmonary edema (Figure 1). An echocardiogram showed no valvular abnormalities and demonstrated normal left ventricular ejection fraction (Figure 2), fractional shortening, and dimensions. The left ventricular filling pattern showed reduced mitral annular early diastolic velocity on Doppler tissue imaging (Figure 3). Her heart failure resolved after treatment with an angiotensin-converting enzyme inhibitor, diuretic, and later a β-adrenergic receptor blocker. Chest radiograph demonstrating pulmonary edema. Apical 4-chamber view with normal left ventricular systolic function. A, end diastole. B, end systole. Tissue Doppler imaging of septal mitral annulus demonstrating reduced early diastolic velocity. The criteria for diagnosis of peripartum cardiomyopathy are: (1) development of cardiac failure in the last month of pregnancy or within 5 months of delivery; (2) absence of an identifiable cause for the cardiac failure; (3) absence of recognizable heart disease before the last month of pregnancy; and (4) an ejection fraction of <45% and/or an M-mode fractional shortening of <30% and an end-diastolic dimension >2.7 cm/m2.1 This modified definition assumes that women with peripartum cardiomyopathy have systolic dysfunction as the source of their heart failure. To date, no other investigators have described peripartum cardiomyopathy in the absence of a reduced ejection fraction. Heart failure with preserved ejection fraction is a clinical syndrome characterized by the signs and symptoms of heart failure, a preserved ejection fraction, and abnormal diastolic function.2 At the bedside, it is difficult to differentiate heart failure due to systolic dysfunction from that caused by diastolic dysfunction. Two-dimensional echocardiography can accurately measure the left ventricular ejection fraction, and the left ventricular diastolic function can be determined by either Doppler-derived mitral and pulmonary venous flow velocities or Doppler tissue imaging. Because abnormal systolic function is one of the criteria for diagnosis, peripartum patients with heart failure who have normal ejection fractions are excluded from series of women with peripartum cardiomyopathy. However, as our case demonstrates, peripartum cardiomyopathy can and does result from diastolic dysfunction. The morbidity, mortality, and risk of recurrence during future pregnancies are unknown in this group.