Peripartum cardiomyopathy vs. sulprostone-associated heart failure? A case report and analysis of the literature.

A 37-year-old Caucasian woman was referred for a planned cesarean section due to placenta preavia at 38 weeks. The patient has no significant personal history of disease, and was closely monitored throughout the pregnancy. Three hours after surgery, the patient developed postpartum hemorrhage requiring sulprostone administration for uterine atony. Eight hours after surgery, the patient had a sudden cardiogenic shock with biventricular failure requiring intensive care and infusion of noradrenaline (0.3 lg/kg/min) and dobutamine (20 lg/kg/min). Electrocardiography (ECG) showed sinus tachycardia (130 beats/ min) with normal conduction, without any ST segment changes. She desaturated from 91 to 60 % oxygen, the laboratory tests found anemia (Hb = 10.8 g/dL), both metabolic and respiratory acidosis (pH = 7.24; PCO2 = 39 mmHg; PO2 = 70 mmHg; HCO3 = 16.1 mmol/L; lactate = 2.1 mmol/L), no schistocytes, a very low haptoglobin (\0.10 g/L), and increased cardiac enzymes [CPK = 1209 UI/L; troponin = 1.29 lg/L (normal range \0.2 lg/L)]. A transthoracic echocardiography (TTE) found a severe biventricular dysfunction with a left ventricular ejection fraction (LVEF) between 25 and 30 %, without valvular lesion or pericardial effusion. This echocardiographic report was compatible with peripartum cardiomyopathy (PPCM). Chest X-ray showed bilateral diffuse alveolar syndrome. The patient improved rapidly and LVEF increased to 45 % 4 days later. All etiological exams were negative (Parvovirus, EBV, HHV6, CMV, HIV, Coxsackie, Enterovirus serologies, autoimmune thyroid and selenium blood test), and cardiac magnetic resonance imaging showed no evidence of inflammatory process, including any early gadolinium enhancement. The evolution was favorable, and the patient was discharged with long-term treatments (angiotensin-converting-enzyme inhibitors and b-blocking) 12 days later. She was re-evaluated 4 months later, all exams (TTE, biological tests, ECG) were normal and all treatments were stopped. PPCM is a serious dilated cardiomyopathy of unknown origin and occurs in less than 0.1 % of pregnancies, with high mortality rate ranging from 5 to 32 % [1–3]. This is usually a severe heart failure, with sudden onset, in previously healthy women in final month of pregnancy and up to 5 months after delivery. Strong associations have been shown between PPCM and older maternal age, hypertension, multiple pregnancies, and African American background, but precise mechanisms that lead to disease remain poorly defined [1–3]. Cases of major and brutal heart failure associated with sulprostone had been published, as cardiac arrest, pulmonary edema or Takotsubo cardiomyopathy [4–6]. There are few reported cases linking PPCM with the administration of sulprostone [7, 8]. One recently published case is particularly interesting and can support our hypothesis of possible association between PPCM and sulprostone [7]. A 37-year-old Asian woman underwent a cesarean delivery at 37 weeks for failed induction of labor with sulprostone administration for transient uterine atony. Two hours after surgery, heart failure with severe metabolic acidosis and elevated cardiac enzymes were observed requiring M. Vital G. Ducarme (&) Department of Obstetrics and Gynecology, Centre Hospitalier Departemental, 85000 La Roche sur Yon, France e-mail: g.ducarme@gmail.com