High Thrombus Burden in Patients With COVID-19 Presenting With ST-Segment Elevation Myocardial Infarction

Abstract

Background: Coronavirus disease-2019 (COVID-19) is thought to predispose patients to thrombotic disease. To date there are few reports of ST-segment elevation myocardial infarction (STEMI) caused by type 1 myocardial infarction in patients with COVID-19.

Objectives: The aim of this study was to describe the demographic, angiographic, and procedural characteristics alongside clinical outcomes of consecutive cases of COVID-19-positive patients with STEMI compared with COVID-19-negative patients.

Methods: This was a single-center, observational study of 115 consecutive patients admitted with confirmed STEMI treated with primary percutaneous coronary intervention at Barts Heart Centre between March 1, 2020, and May 20, 2020.

Results: Patients with STEMI presenting with concurrent COVID-19 infection had higher levels of troponin T and lower lymphocyte count, but elevated D-dimer and C-reactive protein. There were significantly higher rates of multivessel thrombosis, stent thrombosis, higher modified thrombus grade post first device with consequently higher use of glycoprotein IIb/IIIa inhibitors and thrombus aspiration. Myocardial blush grade and left ventricular function were significantly lower in patients with COVID-19 with STEMI. Higher doses of heparin to achieve therapeutic activated clotting times were also noted. Importantly, patients with STEMI presenting with COVID-19 infection had a longer in-patient admission and higher rates of intensive care admission.

Conclusions: In patients presenting with STEMI and concurrent COVID-19 infection, there is a strong signal toward higher thrombus burden and poorer outcomes. This supports the need for establishing COVID-19 status in all STEMI cases. Further work is required to understand the mechanism of increased thrombosis and the benefit of aggressive antithrombotic therapy in selected cases.

Keywords: COVID-19; ST-segment elevation myocardial infarction; primary percutaneous coronary intervention; thrombosis.

Graphical abstract

Figure 1

Increased Arterial Thrombogenicity Associated With D-Dimer Levels (A) Correlation between D-dimer and thrombus grade in all patients (p = 0.068). (B) Correlation between D-dimer and myocardial blush grade for all patients (p = 0.0003). ∗p < 0.01, †p < 0.05, ‡p<0.001.

Figure 2

Requirement for Heparin During Primary PCI (A) Correlation between D-dimer and total heparin dose U/kg/min required to maintain activated clotting time (ACT) >250 s during primary percutaneous coronary intervention (PCI) procedure for all patients (p = 0.0029). (B) Correlation between baseline heparin dose and first ACT measured after a 10- to 15-min interval in all patients (p = 0.0002). (C) Correlation between baseline heparin dose and first ACT measured after a 10- to 15-min interval in coronavirus disease-2019 (COVID-19) group (p = 0.144). (D) Correlation between baseline heparin dose and first ACT measured after a 10- to 15-min interval in non-COVID-19 group (p = 0.0004). ∗p < 0.01, †p < 0.05, ‡p<0.001.

Figure 3

In-Hospital Outcomes for Non-COVID-19 and COVID-19 Groups In-hospital outcomes including intensive care admission, in-hospital mortality, and admission length. COVID-19 = coronavirus disease-2019. ∗p < 0.01, †p < 0.05, ‡p<0.001.

Central Illustration

Characteristics of ST-Segment Elevation Myocardial Infarction in COVID-19 Infection ST-segment elevation myocardial infarction (STEMI) in coronavirus disease-2019 (COVID-19) infection is associated with significantly higher rates of stent thrombosis (p = 0.0445), multivessel thrombus (p = 0.0003), modified thrombus grade 4 to 5 (p = 0.0006), lower rates of myocardial blush grade 2 to 3 (p = 0.0001), and raised D-dimer levels (p = 0.012). ∗p < 0.01, †p < 0.05, ‡p < 0.001.