key: cord-0741990-pzlhwsb0
authors: Sano, Madoka; Kim, Kitae; Furukawa, Yutaka
title: Extensive Coronary Thrombosis in a COVID-19 Patient
date: 2021-12-28
journal: Intern Med
DOI: 10.2169/internalmedicine.8826-21
sha: f330a767f3a72be24f921f5b706f9d68d3b99760
doc_id: 741990
cord_uid: pzlhwsb0

nan

A 68-year-old man presented with a 7-day history of malaise and 2-day history of worsening chest discomfort. He had had close contact with a person infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) 12 days before admission. On arrival, he was afebrile, hypotensive and hypoxic. Chest X-ray revealed bilateral pulmonary infiltrates. An electrocardiogram showed sinus rhythm with premature atrial contractions, inferior ST-segment elevations and reciprocal changes in the anterolateral leads (Picture 1). A laboratory analysis revealed elevated levels of troponin I (121.94 ng/mL), D-dimer (8.46 μg/mL), C-reactive protein (11.48 mg/dL), blood urea nitrogen (119.7 mg/dL), and creatinine (4.65 mg/dL). Coronary angiography demonstrated proximal right coronary artery (RCA) occlusion. Aspiration thrombectomy was repeated, and multiple thrombi were removed; however, the distal coronary flow could not be restored (Picture 2). Intravascular ultrasound demonstrated hypo-echoic, heterogenous, well-delineated lesions that were consistent with extensive thrombus filling the entire RCA without clear findings of plaque rupture (Picture 3). Histologically the thrombi were composed of fibrin and neutrophilic infiltrates, and no fragments of atherosclerotic plaque were present. After the procedure, a nasopharyngeal swab for SARS-CoV2 reverse polymerase chain reaction (PCR) showed a positive result, indicating that the leading etiology of his hypoxia was coronavirus disease 2019 (COVID-19) pneumonia. COVID-19 causes coagulation abnormalities, in-cluding activation of platelets and the coagulation cascade (1), as well as endothelial cell injury (2) . ST-elevation myocardial infarction (STEMI) in patients with concurrent COVID-19 was associated with an increased thrombus burden (3). In the present case, extensive coronary artery thrombosis rather than plaque rupture, caused by a hypercoagulable state and endothelial injury due to COVID-19 infection, may have been responsible for STEMI.

The authors state that they have no Conflict of Interest (COI).

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