COVID-19 vs. Classical Myocarditis Associated Myocardial Injury Evaluated by Cardiac Magnetic Resonance and Endomyocardial Biopsy.

Radu Tanacli,Burkert Pieske,Alessandro Faragli,Victoria Zieschang,Sophie Van Linthout,Carsten Tschöpe,Martin Witzenrath,Franziska Seidel,Sebastian Kelle,Grigorios Korosoglou,Dominik Geisel,Philipp Stawowy,Karin Klingel,Patrick Doeblin,Alexander Berger,Jennifer Erley,Felix Pröpper,Fridolin Steinbeis,Collin Götze,Christian Stehning,Titus Kühne,Karl Jakob Weiß ,Thula Walter

doi:10.3389/fcvm.2021.737257

Abstract

Background: Despite the ongoing global pandemic, the impact of COVID-19 on cardiac structure and function is still not completely understood. Myocarditis is a rare but potentially serious complication of other viral infections with variable recovery, and is, in some cases, associated with long-term cardiac remodeling and functional impairment.Aim: To assess myocardial injury in patients who recently recovered from an acute SARS-CoV-2 infection with advanced cardiac magnetic resonance imaging (CMR) and endomyocardial biopsy (EMB).Methods: In total, 32 patients with persistent cardiac symptoms after a COVID-19 infection, 22 patients with acute classic myocarditis not related to COVID-19, and 16 healthy volunteers were included in this study and underwent a comprehensive baseline CMR scan. Of these, 10 patients post COVID-19 and 13 with non-COVID-19 myocarditis underwent a follow-up scan. In 10 of the post-COVID-19 and 15 of the non-COVID-19 patients with myocarditis endomyocardial biopsy (EMB) with histological, immunohistological, and molecular analysis was performed.Results: In total, 10 (31%) patients with COVID-19 showed evidence of myocardial injury, eight (25%) presented with myocardial oedema, eight (25%) exhibited global or regional systolic left ventricular (LV) dysfunction, and nine (28%) exhibited impaired right ventricular (RV) function. However, only three (9%) of COVID-19 patients fulfilled updated CMR–Lake Louise criteria (LLC) for acute myocarditis. Regarding EMB, none of the COVID-19 patients but 87% of the non-COVID-19 patients with myocarditis presented histological findings in keeping with acute or chronic inflammation. COVID-19 patients with severe disease on the WHO scale presented with reduced biventricular longitudinal function, increased RV mass, and longer native T1 times compared with those with only mild or moderate disease.Conclusions: In our cohort, CMR and EMB findings revealed that SARS-CoV-2 infection was associated with relatively mild but variable cardiac involvement. More symptomatic COVID-19 patients and those with higher clinical care demands were more likely to exhibit chronic inflammation and impaired cardiac function compared to patients with milder forms of the disease.

Highlights

Despite the ongoing global pandemic, the impact of COVID-19 on cardiac structure and function is still not completely understood
Cough, and loss of taste or smell were dominant in COVID-19 patients, some of them suffered from palpitations (1, 3%), chest pain (8, 25%), arrhythmia (9, 28%), or had elevated troponin (9, 28%) or NT-proBNP (6, 24%)
Our findings indicate that both left ventricular (LV) and right ventricular (RV) long-axis deformation are decreased in more severe forms of COVID-19

Summary

Introduction

Despite the ongoing global pandemic, the impact of COVID-19 on cardiac structure and function is still not completely understood. A three-phase model of pathogenesis of COVID-19 has been proposed [1] where a significant minority of patients progress to a critical hyperinflammation phase characterized by a systemic host response with elevated IL-2, IL6, IL-7, TNF-α, C-reactive protein, and D-dimer levels. Several studies [2,3,4] demonstrated cardiac pathologic modifications reflected by elevated troponin and N-terminal pro B-type natriuretic peptide in 10–28% of COVID-19 patients, requiring hospitalization. In a large multicentre study [5], myocardial injury was diagnosed in 62% of cases presenting with troponin elevation and was associated with higher percentage of abnormal echocardiographic findings and higher mortality. Several pathogenic mechanisms may explain the specific cardiac findings post-COVID-19: triggered pan-endotheliitis [4] or macrophage activation [6] precipitating acute plaque rupture and coronary events [7], imbalanced activation of helper T cells leading to cytokine storm and direct myocardial injury [3], sepsis, or hypoxia-induced myocyte apoptosis [8]

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