Dissemin is shutting down on January 1st, 2025

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Aterotromboz = Atherothrombosis, 1, p. 6-24, 2021

DOI: 10.21518/2307-1109-2021-11-1-6-24

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Cardiomyopathy and multiple arterial thrombosis in a patient with severe tachyform atrial fibrillation after COVID-19

This paper was not found in any repository; the policy of its publisher is unknown or unclear.
This paper was not found in any repository; the policy of its publisher is unknown or unclear.

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Abstract

We present a case of cardiomyopathy with a reduced left ventricular ejection fraction of up to 18%, multivessel arterial thrombosis in a patient who had undergone severe COVID-19 3.5 months earlier. The cardiopathy was initially considered as an outcome of SARSCoV2-induced myocarditis, but MRI with delayed gadolinium contrast revealed no fibrosis or evidence of active myocarditis. A detailed collection of the medical history showed that the duration of tachyform atrial fibrillation exceeded the 4 months indicated in the medical records. Oligosymptomatic manifestation of arrhythmia occurred 8 months earlier, the patient did not consult a physician due to epidemic conditions. Coronary angiography revealed subtotal stenosis of the anterior descending artery. Most probably, the cardiopathy was arrhythmogenic and ischemic. After achieving normosystole and coronary stenting, the left ventricular ejection fraction was 25-27%. At the first hospitalization 4 months ago, left atrial auricular thrombus was detected. After COVID-19 the patient received inadequately low dose of apixaban 5 mg per day. Three weeks after COVID-19, the patient was diagnosed with infarction of the right kidney, wall thrombosis in the abdominal aorta, thrombosis of the superficial femoral, deep femoral, popliteal, anterior tibial arteries on the left, right popliteal artery; thrombotic complications could have developed both in situ and as a result of cardioembolism. Administration of dabigatran 300 mg per day and aspirin helped to dissolve the thrombus in the left atrial auricle, improve the course of intermittent claudication, and avoid recurrent thrombotic complications. COVID-19 could contribute to the progression of atherosclerosis, more malignant course of atrial fibrillation, development of thrombosis, but coronavirus infection is not the only cause of severe disease in a patient. СOVID-19 can not only be the cause of direct lesions of the heart and vessels, but also have an indirect negative effect - to delay the detection of cardiac pathology and be the cause of its hypodiagnosis under the mask of “postcovid”.