Tako-tsubo syndrome soon after caesarean delivery: two case reports.

First case: a 35-year-old primigravida at 40 weeks of gestation was admitted to our hospital for spontaneous delivery. Her past medical history was negative for cardiovascular disease, and no risk factors or family history of cardiac disease was reported. After 10 h of labour, she underwent cesarean section because of cephalopelvic disproportion. Spinal anesthesia with 0.75% hyperbaric bupivacaine 10 mg, fentanyl 20 μg, and morphine 0.25 mg was performed. Intravenous oxytocin 10 IU bolus, followed by continuous infusion, was administered in order to stimulate uterine contraction. The day after delivery of her healthy child, the patient complained of increasing dyspnea. On physical examination, tachycardia (120/min) and cyanosis were noted. Pulmonary rales were detected in both lungs. Her blood pressure was 85/55 mmHg and body temperature was 36 °C. An initial arterial blood gas analysis revealed severe hypoxemia (pO2 = 62 mmHg), hypercapnia (pCO2 = 44 mmHg) and respiratory acidosis (pH = 7.3). Laboratory tests showed elevated troponin I (0.173 ng/ml; normal value 0.00–0.10 ng/ml) and creatine kinase (231 U/L; n.v. < 145 U/L). The electrocardiogram (ECG) disclosed sinus tachycardia with left-axis deviation and negative T waves in D1 and aVL without ST-segment changes. The patient was transferred to the intensive care unit and mechanical ventilation support was started after endotracheal intubation. Chest X-ray showed diffuse consolidation consistent with pulmonary edema. Two-dimensional transthoracic echocardiography (TTE) showed LV dilatation with akinesis of the midventricular segments. LV ejection fraction (LVEF, calculated by modified Simpson's rule) was 30%. No obstruction of LV outflow tract was observed. Furosemide (600 mg/day) and heparin were given intravenously. Dobutamine (6 γ/kg/min), levosimendan (0.02 γ/kg/min) and norepinephrine (0.05 γ/kg/min) were used for inotropic support. In the cath lab, normal coronary arteries and midventricular ballooning were documented at angiography. Owing to the lack of clinical improvement, intra-aortic balloon pumping (IABP) was instituted. Oxygen saturation was maintained above 90%. After 24 h, the patient was weaned from the ventilator and extubated, and inotropic agents were tapered gradually. Because of persistent tachycardia and hypotension, IABP was maintained for 3 days. Then, the patient's vital signs became stable, with no respiratory distress or other complications related to heart failure. She was discharged after 12 days in good health under beta-blocker therapy (bisoprolol 1.25 mg/day). At discharge, the ECG was normal and echocardiography showed complete recovery of LV systolic function (LVEF 67%). At 6-month follow-up, the patient remained asymptomatic with no evidence of ECG and TTE abnormalities. Second case: a 24-year-old multiparous Caucasian woman at 38 weeks of gestation was admitted to a peripheral hospital for cesarean section delivery under spinal anesthesia. She had a previous elective cesarean section. She was heterozygous for methylenetetrahydrofolate reductase mutation, a gene involved in the metabolism of homocysteine that predisposes to thrombophilia. No typical cardiovascular risk factors or preexisting cardiomyopathy was reported. A few hours after delivery of a healthy boy, the patient complained of severe shortness of breath and palpitations. Heart rate was 140 bpm, blood pressure 95/60 mmHg, oxygen saturation < 50% (pO2 46 mmHg). Hypercapnia (pCO2 50 mmHg) and acidosis (pH = 7.21) were documented. On cardiac auscultation, a grade 2/6 pansystolic murmur at the apex was present. Bilateral basal pulmonary rales were detected on lung fields. The ECG showed sinus tachycardia (140 bpm) and right bundle branch block (RBBB). Laboratory tests revealed elevated troponin I (11 ng/ml; normal value 0.00–0.10 ng/ml) and myoglobin (400 ng/ml; n.v. 10–92 ng/ml). Computed tomography angiography excluded pulmonary embolism. Owing to worsening of dyspnea and oxygen saturation, mechanical ventilation support was applied after endotracheal intubation. A second ECG revealed ST-segment depression of 1 mm in DII, DIII e aVF and a slight ST-segment elevation in V1–V3, with disappearance of RBBB. TTE showed severe LV systolic dysfunction, LVEF 30%, severe hypokinesis of the mid and basal segments of the anterior, posterior and lateral walls, with preserved contractility of the apical segments. Mild mitral regurgitation was detected. LV intraventricular gradient was absent. The right chambers were within normal limits. Pulmonary artery systolic pressure estimated by the simplified Bernoulli equation of the tricuspid regurgitant jet was 50 mmHg. With the suspicion of an acute coronary syndrome, the patient was transferred to our tertiary center for urgent coronary angiography that showed normal coronary arteries. Left ventriculography confirmed severe systolic dysfunction with akinesis of the mid segments and normal contractility of the apex, compatible with midventricular ballooning and apical-sparing variant form of TTS (Fig. 1). After IABP placement, the patient was admitted to the coronary care unit and received inotropic agents. Following hemodynamic improvement patient was extubated and IABP was removed after 2 days; inotropic agents were tapered gradually. TTE performed on day 5 showed complete recovery of myocardial function (LVEF 70%). After 10 days, the ECG was normal, and the patient was discharged in stable clinical conditions on ramipril (2.5 mg/day) and bisoprolol (1.25 mg/day). At a 6-month follow-up, she was in good health, ECG and TTE findings were unchanged, and ramipril administration was discontinued. TTS is most prevalent among women, in particular after menopause, suggesting that lowered estrogen levels may play a role, [1], [2] and [3]. TTS in the postpartum period especially after cesarean delivery has been previously reported, [4] and [5]. Of note, in late pregnancy the placenta produces high estradiol levels that decrease suddenly after placenta expulsion in the early postpartum favoring a higher myocardium susceptibility to adrenergic stimuli, [6]. In conclusion, women in the postpartum may represent another vulnerable group for TTS onset which should be considered as a peculiar entity with specific characteristics related to clinical presentation, LV function and morphology in the acute phase along with time to recovery of myocardial contraction. Prompt recognition of TTS in the postpartum period has immediate therapeutic implications (use of inotropic agents, IABP support) as well as prognostic importance in the long term, including the likelihood of future pregnancies.