5907Not every fulminant lymphocytic myocarditis fully recovers

Introduction: Fulminant lymphocytic myocarditis (FLM), when aggressively supported in a timely manner, is reported to have a complete left ventricular (LV) functional recovery in nearly all cases. Case report: A 28-year-old Cameroonian man with no relevant personal and family medical history suffered a sudden cardiac arrest during a football match. Yearly sports medical screening examinations yielded normal results. Bystander cardiopulmonary resuscitation (CPR) was initiated immediately and continued up to the arrival of the ambulance 7 minutes after. Ventricular fibrillation was the presenting rhythm, refractory to advanced life support measures. Mechanical CPR was started. In hospital veno-arterial extracorporeal membrane oxygenation (ECMO) was placed 50 minutes after the collapse, followed by return of spontaneous circulation. Coronary angiogram was normal. Echocardiogram findings revealed a non-dilated, thickened, severely hypocontractile and hyperechoic LV. Laboratory tests showed massive release of cardiac troponin T (cTnT) (85468 ng/l), elevated leukocytes and C reactive protein. As at the initial ECMO centre right ventricular (RV) endomyocardial biopsy (EMB) was not routinely performed, the procedure was postponed at patient stability. ECMO, counterpulsation and inotropes were discontinued on day 10, 11 and 16, respectively. Blood eosinophils were normal. Autoimmune disorders were ruled out. Viral serologic tests were negative. At clinical stability, the patient was transferred to a heart transplant (HTx) referral hospital. Serial echocardiography showed progressive dysfunction (LV ejection fraction [EF] 20%, LV end-diastolic volume [EDV] 217 ml, RVEF 29%). Cardiac magnetic resonance (CMR) on day 21 confirmed the severe dysfunction with evidence of LV apical thrombus. STIR sequences revealed increased signal intensity located in the inferolateral and septal walls; diffuse biventricular late gadolinium enhancement (LGE) was observed. EMB analysis (day 22) showed severe fibrosis, myocyte degeneration and ongoing lymphocytic myocarditis, excluding giant cells, eosinophilic and granulomatous infiltrates. PCR research for viral genomes was negative. Low-dose oral steroids were prescribed as persistent cTnT release suggested active myocarditis. A second EMB (day 41) showed interstitial fibrosis without inflammatory cells. The patient was added to a HTx waiting list after eligibility screening and discharged in stable condition, with normal neurologic functioning and optimal heart failure medical therapy. CMR on day 71 showed further deterioration (LVEF 9%, LV EDV 256 ml, RVEF 12%). STIR signals were less intense and LGE was unchanged. Differential diagnosis: Drug reactions, including cocaine abuse, were ruled out as well as coronary heart disease and coronary artery dissection. Pre-existing cardiomyopathies were less plausible considering the initial echocardiographic findings of a non-dilated LV and the negative patient's history.