High Thrombus Burden in COVID-19 Patients With STEMI
- Patients with STEMI and COVID-19 experienced high rates of ischemic and thrombotic laboratory markers (e.g., troponin, D-dimer).
- Patients with STEMI and COVID-19 had more thrombus burden and required more anticoagulation than patients with STEMI but no COVID-19 infection.
- Patients with STEMI and COVID-19 experienced worse in-hospital outcomes than patients without COVID-19 infection.
What are the patient and procedural characteristics and clinical outcomes associated with ST-segment elevation myocardial infarction (STEMI) in patients with coronavirus disease 2019 (COVID-19)?
The authors conducted a single-center, consecutive analysis of 115 patients admitted with STEMI and treated with primary percutaneous coronary intervention between March 1 and May 20, 2020. Patients with and without COVID-19 were compared.
Patients with STEMI and concurrent COVID-19 infection (39/115, 33.9%) had higher levels of troponin T (1221 vs. 369 ng/L, p = 0.003), lower lymphocyte count (1.3 vs. 1.7 109/L, p = 0.001), elevated D-dimer (1.86 vs. 0.52 mg/L, p = 0.001), and elevated C-reactive protein levels (50 vs. 12 mg/L, p = 0.010) as compared to patients with STEMI but no concurrent COVID-19 infection. Median door-to-balloon times were the same for both groups (50 vs. 52 minutes, p = 0.248). Patients with concurrent STEMI and COVID-19 had higher rates of multivessel thrombosis (17.9% vs. 0%, p = 0.001), stent thrombosis (10.3% vs. 1.2%, p = 0.045), and higher modified thrombus grade leading to higher use of glycoprotein IIb/IIIa inhibitors (59.0% vs. 9.2%, p < 0.001) and thrombus aspiration (17.9% vs. 1.3%, p = 0.002). Higher doses of heparin were required to achieve therapeutic anticoagulation in patients with STEMI and concurrent COVID-19. These patients required longer mean in-hospital stay and higher rates of intensive care admission.
The authors concluded that patients with STEMI and concurrent COVID-19 experienced higher thrombus burden and worse outcomes than patients without concurrent COVID-19 infection.
While much of the focus in COVID-19 and thrombosis has been on venous thromboembolism, this single-center study highlights the implications in arterial thromboembolism. Specifically, patients presenting with STEMI and concurrent COVID-19 infection experience more thrombus burden and require more anticoagulation. This likely represents a combination of prothrombotic and proinflammatory properties of COVID-19 infection, which have been highlighted in many recent studies. Whether the poor in-hospital outcomes in COVID-19 patients are related to the more extensive coronary thrombosis or concurrent COVID-19 infection are not clear. Nonetheless, this study adds to the growing body of literature calling for efforts to address the varied thrombotic complications associated with COVID-19 infection.
Clinical Topics: Acute Coronary Syndromes, Anticoagulation Management, Invasive Cardiovascular Angiography and Intervention, Prevention, Pulmonary Hypertension and Venous Thromboembolism, Stable Ischemic Heart Disease, Vascular Medicine, ACS and Cardiac Biomarkers, Anticoagulation Management and ACS, Anticoagulation Management and Venothromboembolism, Interventions and ACS, Interventions and Vascular Medicine, Chronic Angina
Keywords: Acute Coronary Syndrome, Anticoagulants, Coronary Thrombosis, Coronavirus Infections, COVID-19, C-Reactive Protein, Critical Care, Heparin, Lymphocyte Count, Myocardial Ischemia, Percutaneous Coronary Intervention, Platelet Glycoprotein GPIIb-IIIa Complex, Secondary Prevention, severe acute respiratory syndrome coronavirus 2, ST Elevation Myocardial Infarction, Troponin T, Vascular Diseases, Venous Thromboembolism
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