Massive coronary thrombosis in a COVID-19 patient without cardiac history was unresponsive to optimal pharmacological and mechanical treatment, leading to a final TIMI flow of 0/1 and cardiac arrest.
Case Report (n=1)
No
Coronary thrombosis in COVID-19 patients can occur without prior cardiac history and may be unresponsive to optimal pharmacological and mechanical treatment.
This is a case report of a 60-year-old male, without any cardiovascular risk factor and no cardiac history admitted to hospital with a diagnosis of interstitial pneumonia caused by coronavirus disease 2019 (COVID-19). After 7 days, the blood tests showed a significant rise of inflammatory and procoagulant markers, along with a relevant elevation of high-sensitivity Troponin I. Electrocardiogram and transthoracic echocardiogram (TTE) were consistent with a diagnosis of infero-posterolateral acute myocardial infarction and the patient was transferred to the isolated Cath Lab for primary percutaneous coronary intervention (PCI). The angiography showed an acute massive thrombosis of a dominant right coronary artery without clear evidence of atherosclerosis. Despite the optimal pharmacological therapies and different PCI techniques, the final TIMI flow was 0/1 and after 3 hr the clinical condition evolved in cardiac arrest for pulseless electric activity. Acute coronary syndrome-ST-elevation myocardial infarction is a relevant complication of COVID-19. Due to high levels of proinflammatory mediators, diffuse coronary thrombosis could occur even in patients without cardiac history or comorbidities. This clinical case suggests that coronary thrombosis in COVID-19 patients may be unresponsive to optimal pharmacological (GP IIb-IIIa infusion) and mechanical treatment (PCI).
Tedeschi et al. (Fri,) conducted a case report in COVID-19 and acute myocardial infarction (n=1). Primary percutaneous coronary intervention (PCI) and GP IIb-IIIa infusion was evaluated on TIMI flow and clinical evolution. Massive coronary thrombosis in a COVID-19 patient without cardiac history was unresponsive to optimal pharmacological and mechanical treatment, leading to a final TIMI flow of 0/1 and cardiac arrest.
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