Prompt benefit of early immunosuppressive therapy in acute lymphocytic myocarditis with persistent heart failure

Abstract

Sirs:Myocarditis resolves in about 50 % of cases during 2-4 weeks, but 25 % develop persistent cardiac dysfunction and 12-25 % may deteriorate leading to death or endstage dilated cardiomyopathy [1]. Presentation with heart failure and ventricular dysfunction are strong predictors of adverse outcome [2]. Viral infection is the most commonly identified cause of myocarditis. Mechanisms of injury include direct viral damage or inappropriate immune response. While the initial immune response limits the degree of viral cellular invasion and myocardial damage, non-replicating viral genomic fragments and cardiac epitopes such as myosin and beta-1 receptors might drive an ongoing adverse autoimmune response leading to inflammation through ''anti-heart auto-antibodies'' [3,4].Treatment of myocarditis includes supportive measures, heart failure therapy and treatment of arrhythmias according to current position statements [1]. Immunosuppression is advised with specific rare etiologies such as giant cell and eosinophilic myocarditis, but controversial in the prevalent lymphocytic subtype.A 28-year-old woman was admitted with weakness, dyspnea and nausea for a few days and gastroenteritis 2 weeks earlier. Otherwise, she had no history pertinent to the current illness. On admission, she was pale and nauseous, blood pressure was 90/60, pulse was 130 and ECG showed sinus tachycardia with small complexes. Troponin I was 0.22 mcg/L (normal range \ 0.04), Leukocytes were 10,600 (75 % neutrophils) and hemoglobin was 13 g/dL. She had moderate hepatic transaminase elevation (in the hundreds) and normal renal function; BNP was 2760 pgr/ ml, lactate was 1.29 mmol/L and CRP was 3.5 mg%. Chest X-ray demonstrated mild bilateral congestion. Echocardiogram showed mildly enlarged left ventricle with severe biventricular failure, left ventricular ejection fraction 23 %, normal wall thickness and severe mitral and tricuspid regurgitation. Cardiac MRI showed marked lateral wall edema without late gadolinium enhancement. On catheterization, right atrial pressure was 16 mmHg, pulmonary pressure was 45/25, mean was 30 mmHg, wedge pressure was 20 mmHg and cardiac index was 1.55 l/min/ m 2 . Right ventricular endomyocardial biopsy revealed active lymphocytic myocarditis (CD3? T lymphocyte predominant with CD68? histiocytes and without eosinophils or giant cells) associated with ongoing and wellestablished perivascular and interstitial replacing fibrosis. Electron microscopy showed no viral capsids, no evidence of myofilament loss or mitochondrial pathology.She continued to suffer from persistent weakness and nausea needing continued hospitalization with ongoing tachycardia and low blood pressures, tolerating only low doses of heart failure treatment (Losartan 12.5 mg BID, Bisoprolol 1.25 mg BID, Spironolactone 25 mg and Furosemide). The patient occasionally missed heart failure medication due to low blood pressure, but did not need inotropic support. Repeat echocardiography showed no improvement in ventricular function with a new apical thrombus (tre...

Fulminant Myocarditis Managed by Extracorporeal Life Support (Impella® CP): A Rare Case

“…Our approach was successful in this rare case and although no infectious, immune-mediated, or toxic reason was detectable here, biopsy confirmed our treatment strategy and ensured not to have missed any specifically treatable cause. This is in accordance with current literature [1–10]. …”

A Case of Lymphocytic Myocarditis with Eosinophilic Degranulation Successfully Treated with Steroid Therapy

“…Reiff and Missov recently reported a case of fulminant lymphocytic myocarditis successfully treated with immunosuppressive therapy [ 6 ]. Weitsman et al also reported on the effectiveness of early immunosuppressive therapy in acute lymphocytic myocarditis with persistent heart failure [ 7 ]. In these previous reports, the presence of virus and its association with clinical outcomes were mainly discussed, whereas the presence of eosinophil degranulation was not described.…”