Fulminant myocarditis: a comprehensive review from etiology to treatments and outcomes

Abstract

Fulminant myocarditis (FM) is characterized by a rapid progressive decline in cardiac function and a high mortality rate. Since the first report of FM patients in the 1980s, several clinical trials and research studies have been published increasing our knowledge regarding FM. Currently, the diagnosis of FM depends on various techniques including electrocardiography, echocardiography, endomyocardial biopsy, and cardiac magnetic resonance. The development of mechanical circulation support (MCS) devices and progress in our understanding of the pathophysiological mechanisms underlying FM, treatment regimens have evolved from simple symptomatic treatment to a life support-based comprehensive treatment approach. The core mechanism underlying the development of FM is the occurrence of an inflammatory cytokine storm. This review provides a comprehensive account of the current understanding of FM pathophysiology and knowledge regarding its etiology, pathophysiology, treatments, and outcomes.

Focus on Autoimmune Myocarditis in Graves' Disease: A Case-Based Review

“…The conventional treatment for hemodynamically stable patients emphasizes standard anti-heart failure regimens, including positive inotropic drugs, vasoactive drugs, beta-blockade, diuretics, ACEi/ARBs, and also aldosterone antagonists. It is also necessary to prevent and quickly respond to malignant arrhythmias such as malignant tachycardia and high atrioventricular block ( 106 ). Here we focus on the following three aspects on the treatment of hyperthyroidism-induced myocarditis: (1) restraint of thyrotoxicosis, (2) active response to cardiac damage, especially acute circulatory failure in fulminant myocarditis, and (3) immunosuppression or immunomodulatory therapy for excessive inflammatory storms.…”

A Case of Isolated SARS-CoV-2 Fulminant Myopericarditis Without Respiratory Failure

“…Troponin I or T, and also BNP or N-terminal pro-BNP (NT-proBNP) are myocardial injury markers and can be elevated in both acute coronary syndrome and FM [7]. Coronary angiography is used to distinguish these and it is important to differentiate between them as the treatment regimens are completely different [7,11]. The key parts in the management of patients with FM include immunosuppressive therapy with glucocorticoid and supportive measures with circulatory assist devices such as ECMO, LVAD, or IABP to reduce wall stress and inflammation [2,12,13].…”

“…Clinical presentations of COVID-19-induced myocarditis or myopericarditis vary widely. It can manifest itself in different ways, from mild symptoms such as fatigue, dyspnea including chest pain and moderate ventricular dysfunction to life-threatening arrhythmia and serious heart failure requiring mechanical circulatory support [ 7 ]. Diagnostic evaluation includes elevated cardiac biomarkers, images such as echocardiogram or cardiac magnetic resonance (CMR) but endomyocardial biopsy (EMB) remains the gold standard [ 8 ].…”

“…Echocardiography results can vary according to the state of the FM patient’s heart function [ 10 ]. Troponin I or T, and also BNP or N-terminal pro-BNP (NT-proBNP) are myocardial injury markers and can be elevated in both acute coronary syndrome and FM [ 7 ]. Coronary angiography is used to distinguish these and it is important to differentiate between them as the treatment regimens are completely different [ 7 , 11 ].…”

Extracorporeal Membrane Oxygenation for Fulminant Myocarditis: Increase of Cardiac Enzyme and SOFA Score Is Associated with High Mortality

“…and elevated troponin T or I. Coronary angiography was performed to rule out coronary artery diseases. In addition, endomyocardial biopsy or cardiac MRI was performed if possible [ 6 , 7 ]. Fulminant myocarditis is defined as acute myocarditis with hemodynamic instability requiring high doses of vasopressors (≥5 μg/(kg·min) dopamine, dobutamine, or other inotropic equivalents) or mechanical circulatory support, despite maximal medical treatment.…”