A clinical case of SARS-CoV-2 infection complicated by acute respiratory distress syndrome, pulmonary edema, and heart failure in the presence of chronic venous congestion in a patient with chronic rheumatic heart disease

Abstract

The article presents a clinical case of SARS-CoV-2 infection complicated by acute respiratory distress syndrome, pulmonary edema, and heart failure in the presence of chronic venous congestion in a patient with chronic rheumatic heart disease. A female patient R., 65 years old, was hospitalized at the Republican Cardiological Dispensary with a diagnosis of novel coronavirus infection COVID-19 (severe course); the virus was identified. Competing diagnosis: (1) acute viral myocarditis;(2) chronic rheumatic heart disease with combined mitral-aortic disease. Complications of the underlying disease included viral interstitial pneumonia (75%) and pulmonary edema. The patient was admitted at day 8 from the onset of the disease with complaints of increase in body temperature up to 38.5 °C, chest pain, and shortness of breath. She was treated in the outpatient setting without visible improvement. The patient had a history of chronic rheumatic heart disease. Due to persistent fever, patient received computed tomography showing interstitial pneumonia of viral etiology. The diagnosis of COVID-19 was based on a typical clinical presentation and a positive PCR test in nasopharyngeal swabs. Nonspecific changes were observed in the electrocardiogram. Treatment was initiated without positive dynamics, and a fatal outcome occurred. According to the autopsy data, the organs showed signs of chronic venous congestion (brown induration of the lungs, nutmeg fibrosis, cyanotic induration of the spleen and kidneys). The infiltrates consisting of lymphocytes and eosinophils were detected in the myocardium. Also, edema of the intercellular space, plethora of microvasculature vessels, and dystrophic changes in cardiomyocytes were detected. The presence of Aschoff-Talalaev granulomas with fibrinoid necrosis and avulsion of the chorda of the mitral valve leaflet was observed. Morphologically, there were signs of pulmonary infarction with a polysegmental character. Thus, in the presented case, the scientific novelty was the extremely rare development of mitral valve chord avulsion in aortic-mitral disease after infection with SARS-CoV-2, which was the cause of acute heart failure. It is likely that the process was aggravated by concomitant diffuse interstitial serous myocarditis and fibrinoid necrosis in granulomas.