Abstract

A 63-year-old man with a history of hypertension, hyperlipidemia and severe COVID-19 3 months earlier presented with NYHA class III-IV heart failure (HF) and intermittent claudication. Three months before, patient noted increasing dyspnea. SARS-CoV2 was verified. CT scan showed pneumonia; the severity of disease required dexamethasone and tocilizumab. Atrial fibrillation (AF) and LV EF 30% were first detected. CT scan disclosed left atrial appendage (LAA) thrombosis. Despite anticoagulants, 3 weeks later the patient developed lower limbs ischemia. Ultrasound and CT scan showed multiple thrombosis in the abdominal aorta and lower limbs arteries (Figure A). Surgery for limb ischemia was not performed due to a further decrease of LV EF to 18%. At that point, diagnosis was SARSCoV2-induced myocarditis. Нe visited our hospital for second opinion. ECG showed AF with mean heart rate (HR) of 158/min (B). Careful history collection suggested a longer AF duration which was missed and untreated due to lockdown. CRP, troponin were normal. NT-proBNP was 9326 pg/ml. After strict rate control was achieved, LV EF became 23%. Cardiac MRI with delayed gadolinium contrast revealed no fibrosis or active myocarditis (C). Angiography showed stenosis >70% of the left anterior descending artery (D). After PCI, LV EF became 27%. The patient was discharged on guideline-recommended optimal medical therapy. Three months later LV EF became 30%, six months later - 47%. Thrombus in LAA was dissolved. Pulmonary vein isolation and cardioversion were performed. One week later LV EF was 60%. Currently, the patient has stable sinus rhythm and no signs of HF for > 6 months. Thus, COVID-19 could contribute to the progression of atherosclerosis, modify the substrate and aggravate the severity of AF, but it was not the only cause of a serious illness in the patient. COVID-19 also had an indirect negative impact - delay the detection of cardiac pathology and cause its underdiagnosis under the guise of "post-COVID".

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