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To the Editor: Peripartum cardiomyopathy is a relatively rare cause of heart failure and is defined as heart failure occurring during the last month of pregnancy or during the first 5 postpartum months.
Although the condition is rare, the incidence of thrombus formation and subsequent embolic events appears to be higher in these women than in the usual heart failure population. However, to our knowledge no report has described embolization to a coronary artery in patients with peripartum cardiomyopathy.
Report of a Case.—A 35-year-old African American woman, gravida 1, para 1, had an uncomplicated vaginal delivery at 38 weeks' gestation after an uneventful pregnancy. She had no contributory medical history, nor was she taking any medications. Her hospitalization was prolonged by 3 days because of dyspnea that was believed to be due to pneumonia.
Three weeks after delivery, she presented with a new complaint of substernal chest pain and exertional dyspnea of 48 hours' duration. An electrocardiogram revealed anterior STwave elevation consistent with an acute anterior myocardial infarction (Figure 1). Her creatine kinase level and CK-MB fraction peaked at 1257 U/L and 160 ng/mL, respectively, with a troponin T level of 170 ng/mL. An echocardiogram showed an ejection fraction of less than 15%, diffuse hypokinesis with anterior akinesis, mild mitral and tricuspid regurgitation, and a left ventricular thrombus. Coronary angiography showed 100% occlusion of the mid left anterior descending artery with a clot; the other coronary arteries appeared normal (Figure 2). Because of hypotension and clinical deterioration, the patient initially required an intra-aortic balloon pump and inotropic therapy. With aggressive diuresis and medical management, her condition improved rapidly. Anticoagulation with heparin was begun followed by conversion to oral anticoagulation prior to discharge. A follow-up echocardiogram 7 days after her primary event showed an improved ejection fraction at 20% with global hypokinesis. At the time of discharge, the physical examination revealed blood pressure of 90/60 mm Hg, heart rate of 60 beats/min, S3 on cardiac examination, no paroxysmal nocturnal dyspnea or orthopnea, but persistent exertional dyspnea.
Figure 1Initial electrocardiogram on presentation. Note the ST-segment elevation in the anterior leads.
Comment.—Peripartum cardiomyopathy is defined as the manifestation of heart failure in the last month of pregnancy or within 5 months of delivery in the absence of any other etiology or prior heart disease.
Its estimated incidence ranges between 1:1300 and 1:15,000 live births in Western countries, and risk factors include African descent, advanced maternal age, multiparity, twinning, and long-term tocolysis.
The cause is currently unknown although some evidence suggests that it is a type of myocarditis arising from an infectious, autoimmune, or idiopathic process.
The diffuse hypokinesis in addition to anterior akinesis on the initial echocardiogram strongly invoked a generalized process such as peripartum cardiomyopathy in our patient. We believe her initial symptoms were in the peripartum period when she complained of dyspnea that was diagnosed as pneumonia. It was only when she subsequently developed a thrombus that embolized to her left anterior descending artery that she had overt symptoms requiring hospitalization. Throm- boembolism has been reported with an incidence of 4% to 30% in peripartum cardiomyopathy, especially in the era before anticoagulation.
The etiology is unclear, but the disorder may occur as a result of the hypercoagulable state during pregnancy (reduction in fibrinolytic activity) or due to stasis and turbulent flow in the dilated heart.
with or without documented deep venous thrombosis, right or left atrial thrombus, or left ventricular mural thrombi. To our knowledge, this is the first report of embolic myocardial infarction due to peripartum cardiomyopathy and an associated left ventricular thrombus. Demakis et al
described a 43-year-old woman with Q waves in leads V1 to V3 but no other clinical or biochemical evidence of myocardial infarction who was asymptomatic at 5-year follow-up. This manifestation of peripartum cardiomyopathy with cardiogenic shock due to embolic myocardial infarction stresses the need for efficient anticoagulation and proposes occult cardiomyopathy as a possible cause of myocardial infarction during the peripartum period.
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