Progressive chronic SARS-CoV-2-positive giant cell myoendocarditis with atrial standstill and sudden cardiac death

Abstract

Giant cell myocarditis (GCM) is a rare condition. Its association with SARS-CoV-2 has not been described before. The 46-year-old female patient was admitted to the clinic on September 2020. She had 7 year adrenal insufficiency history and infarct-like debut of myocardial disease in November 2019. After COVID-19 in April 2020, cardiac disease progressed. The examination showed low QRS voltage, QS complexes in V₁ -V₅ leads, atrial standstill, left ventricular systolic and restrictive dysfunction, elevated anti-heart antibodies, and subepicardial late gadolinium enhancement by magnetic resonance imaging. Endomyocardial biopsy and pacemaker implantation were performed, but the patient died suddenly due to ventricular tachycardia or ventricular fibrillation (the resuscitation was ineffective). The autopsy revealed GCM, SARS-CoV-2, and Parvovirus B19 were detected in the myocardium. The role of SARS-CoV-2 in the pathogenesis of autoimmune myocarditis is discussed.

Keywords: Atrial standstill; Endomyocardial biopsy; Giant cell myoendocarditis; SARS-CoV-2; Sudden cardiac death.

Figure 1

Electrocardiograms of patient. (A) Electrocardiogram (ECG) at the admission to the clinic dated 10.09.2020 (nodal rhythm without signs of atrial activity, narrow QRS complex, heart rate 55 per min, right axis deviation, low QRS voltage, QS in V₁–V₅ leads). (B) ECG dated 14.09.2020 (change to left axis deviation). (C) ECG dated 25.10.2020 (no atrial activity, ventricular pacing with 60 per min rate). (D) ECG from 28.10.2020 during unsuccessful resuscitation (ventricular fibrillation with pacing spikes). Paper speed 25 mm/s.

Figure 2

Cardiac visualization of patient. (A–C) Echocardiograms. (A) Enlangered right ventricle and normal size of left ventricle; (B) restrictive dysfunction of left ventricle; (C) sever tricuspid regurgitation by Doppler. (D–F) Cardiac MRI with gadolinium. (D) Short axis view at mid‐level, arrows show fluid in the pericardial cavity, E ‐ short axis view, foci of late gadolinium enhancement along posterior wall of LV and posterior septal segment, F ‐ four‐chamber view, areas of late gadolinium enhancement along the right atrium myocardium.

Figure 3

Post‐mortem morphological study of the myocardium. (A) Macroscopic study (myocardium is flabby, patchy, red‐brown, without any focal lesions). (B,C) Microscopic study of right ventricle, (D–I) microscopic study of left ventricle; haematoxylin and eosin staining: thrombotic masses adhered to the endocardium (B), endocardium is thickened, with lymphocytic infiltrates (C, blue arrows), interstitial oedema, massive lymphocytic infiltration of the myocardium (blue arrows) with focal fibrosis, cardiomyocyte dystrophy and necrosis (D,E), lymphocytic pericarditis, severe substitutive fibrosis in the myocardium (F), diffuse lymphocytic infiltration of the myocardium with giant cells (G,H, yellow arrows), focal lipomatosis in the myocardium, microvasculitis (I). Low series—immunohistochemical (IHC) study with antibodies to CD3, CD45 lymphocytes and CD68 macrophages (massive clusters of IHC‐positive cells in the left ventricular myocardium). Magnification 50× (E), 100× (B), 200× (C, D, & F), and 400× (G, I, IHS).