RESUMEN
A 60-year-old male with hypertrophic cardiomyopathy, conduction disorders, post-COVID-19 myopericarditis and heart failure was admitted to the hospital's cardiology department. Blood tests revealed an increase in CPK activity, troponin T elevation and high titers of anticardiac antibodies. Whole exome sequencing showed the presence of the pathogenic variant NM_213599:c.2272C>T of the ANO5 gene. Results of the skeletal muscle biopsy excluded the diagnosis of systemic amyloidosis. Microscopy of the muscle fragment demonstrated sclerosis of the perimysium, moderate lymphoid infiltration, sclerosis of the microvessels, dystrophic changes and a lack of cross striations in the muscle fibers. Hypertrophy of the LV with a low contractile ability, atrial fibrillation, weakness of the distal skeletal muscles and increased plasma CPK activity and the results of the skeletal muscle biopsy suggested a diagnosis of a late form of distal myopathy (Miyoshi-like distal myopathy, MMD3). Post-COVID-19 myopericarditis, for which genetically modified myocardium could serve as a favorable background, caused heart failure decompensation.
Asunto(s)
COVID-19 , Cardiomiopatía Hipertrófica , Miopatías Distales , Insuficiencia Cardíaca , Miocarditis , Masculino , Humanos , Persona de Mediana Edad , Miopatías Distales/diagnóstico , Miopatías Distales/genética , Miopatías Distales/patología , Esclerosis/patología , Anoctaminas/genética , Canales de Cloruro/genética , Mutación , COVID-19/complicaciones , COVID-19/genética , COVID-19/patología , Músculo Esquelético/patología , Cardiomiopatía Hipertrófica/complicaciones , Cardiomiopatía Hipertrófica/genética , Cardiomiopatía Hipertrófica/patología , Insuficiencia Cardíaca/genética , Insuficiencia Cardíaca/patologíaRESUMEN
PURPOSE: To study the clinical signs and mechanisms (viral and autoimmune) of myoendocarditis in the long-term period after COronaVIrus Disease 2019 (COVID-19). METHODS: Fourteen patients (nine male, 50.1 ± 10.2 y.o.) with biopsy proven post-COVID myocarditis were observed. The diagnosis of COVID-19 was confirmed by IgG seroconversion. The average time of admission after COVID-19 was 5.5 [2; 10] months. An endomyocardial biopsy (EMB) of the right ventricle was obtained. The biopsy analysis included polymerase chain reaction diagnosis of viral infection, morphological, immunohistochemical (IHC) examination with antibodies to CD3, CD45, CD68, CD20, SARS-Cov-2 spike, and nucleocapsid antigens. Coronary atherosclerosis was ruled out in all patients over 40 years. RESULTS: The new cardiac symptoms (congestive heart failure 3-4 New York Heart Association class with severe right ventricular involvement, various rhythm, and conduction disturbances) appeared 1-5 months following COVID-19. Magnetic resonance imaging showed disseminated or focal subepicardial and intramyocardial late gadolinium enhancement, hyperemia, edema, and increased myocardial native T1 relaxation time. Antiheart antibodies levels were increased 3-4 times in 92.9% of patients. The mean left ventricular (LV) ejection fraction (EF) was 28% (24.5; 37.8). Active lymphocytic myocarditis was diagnosed in 12 patients, eosinophilic myocarditis in two patients. SARS-Cov-2 RNA was detected in 12 cases (85.7%), in association with parvovirus B19 DNA-in one. Three patients had also endocarditis (infective and nonbacterial, with parietal thrombosis). As a result of steroid and chronic heart failure therapy, the EF increased to 47% (37.5; 52.5). CONCLUSIONS: COVID-19 can lead to long-term severe post-COVID myoendocarditis, that is characterized by prolonged persistence of coronavirus in cardiomyocytes, endothelium, and macrophages (up to 18 months) in combination with high immune activity. Corticosteroids and anticoagulants should be considered as a treatment option of post-COVID myoendocarditis.