Coronavirus disease 2019 (COVID-19) is associated with an increased risk of thromboembolic events in the acute setting. However, the abnormal thrombotic diathesis is not known to persist into the recovery phase of COVID-19 infection. We described 3 cases of ST-segment elevation myocardial infarction in healthy male patients who recovered from COVID-19 with no prior cardiovascular risk factors. They shared features of elevated von Willebrand factor antigen, factor VIII and D-dimer level. One patient had a borderline positive lupus anticoagulant. Intravascular ultrasound of culprit vessels revealed predominantly fibrotic plaque with minimal necrotic core. Clot waveform analysis showed parameters of hypercoagulability. They were treated with dual antiplatelet therapy, angiotensin-converting-enzyme inhibitor, beta blocker and statin. These cases highlight the strong thrombogenic nature of COVID-19 that persisted among patients who recovered from infection. Several suspected mechanisms could explain the association between vascular thrombosis in the convalescent period (endothelial dysfunction, hypercoagulability, systemic inflammatory response and vasculopathy). Additional studies on “long COVID” are essential for identifying endotheliopathy and thrombotic sequalae.
Coronavirus disease 2019 (COVID-19) has been associated with thromboembolic phenomenon in the early phase of disease. Growing evidence suggests a hypercoagulable state as well as abnormal platelet activation, impaired fibrinolysis, and endothelial dysfunction in COVID-19 patients, resulting in thrombosis. The lungs are thought to be the epicentre of thrombosis, where thrombosis may manifest as in situ pulmonary thrombosis, as well as systemic microand macrovascular thrombosis. Little is known about post-COVID-19 thrombotic complications.
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