Introduction: Maternal cardiac arrest, during or early after childbirth, is a rare and frightening event that can be favoured by various causes: heart failure, heart attack, peripartum cardiomyopathy, myocarditis, preeclampsia, amniotic fluid embolism, excessive bleeding or blood infection. Early diagnosis and optimal treatment of the triggering disease significantly reduce maternal and fetal morality.
Case presentation: 22-year-old woman, without any cardiovascular risk factors and hereditary or perso-nal history, with an episode of acute upper respiratory infection one week ago, with spontaneous remission, suffered a sudden cardiac arrest caused by ventricu-lar fibrillation, resuscitated in hospital, 5 hours after childbirth by cesarean delivery in the 39th week of pregnancy. After electric conversion, the patient developed signs and symptoms of acute heart failure and ECG showed sinus tachycardia with ST segment horizontal depression in anterolateral leads. Laboratory tests revealed an important inflammatory syndrome, leukocytosis with neutrophilia, mild anemia, elevated myocardial necrosis enzymes and no electrolyte disturbance. Emergency angiography showed normal epicardial coronary arteries.
Ecocardiography revealed a normal sized left ventri-cle (LV), with severe reduced LV ejection fraction (EF), global diffuse LV hypokinesia, moderate mitral regur-gitation, and secondary mild pulmonary hyperten-sion. Treatment included prophylactic LMWH, loop and antialdosterone diuretic, beta-blockers, angioten-sin-converting enzyme inhibitor, antibiotherapy and gynecological post-surgery monitoring determined a favorable clinical evolution. At discharge, the second echocardiography revealed an improved LVEF (45%), with mild mitral regurgitation.
The clinical and paraclinical presentation suggested two underlying causes for acute heart failure and ventricular arrhythmia: myocarditis or peripartum cardi-omyopathy.
Performed 10 days after discharge, cardiac magne-tic resonance showed a normal sized LV with normal systolic function (LVEF 70%) with no signal in T2 edema sequence. Early gadolinium enhancement (GE) T1 sequence was normal, but late Gadolinium Enhancement diagnosed myocardial scar of inferior septum and lateral myocardial walls. Thereby, all this data suggest peripartum cardiomyopathy as etiology of acute heart failure and ventricular fibrillation, but an episode of myocarditis could not be excluded. The patient undergone ICD implantation in secondary prevention 1 week later.
Case particularity: Young patient with cardiac arrest and heart failure in which cardiac imaging had criterias for both myocarditis and peripartum cardiomyopathy. Conclusion: Peripartum cardiomyopathy and myocar-ditis during or after childbirth are slightly clinical similar and sometimes may coexist, making the diagnosis even more difficult. Both can lead to life-threatening complication such as cardiac arrest and acute heart fa-ilure. Therefore, an accurate diagnosis and treatment reduce the risk of maternal mortality.