2021 Scientific Sessions

Acute MI in the COVID Era: Extent of CAD, Presence of Thrombus and MINOCA

Presenter

Zoltan G. Turi, M.D., MSCAI, Hackensack University Medical Center, Cambridge, MA
Zoltan G. Turi, M.D., MSCAI1, David B Landers, MD2, Steven M. Hollenberg, M.D.3, Jana Tancredi, BSN3, Aref Obagi, MD4 and Joseph E Parrillo, MD3, (1)Hackensack University Medical Center, Cambridge, MA, (2)Hackensack Meridian Health, Edison, NJ, (3)Hackensack University Medical Center, Hackensack, NJ, (4)University of Florida College of Medicine Jacksonville, Jacksonville, FL

Keywords: Acute Coronary Syndromes (ACS), COVID-19 and Coronary

Background


The first wave of the COVID 19 pandemic had substantial impact on cardiac catheterization for acute myocardial infarction (MI). We sought to determine the influence on the angiographic appearance of coronary disease (CAD) in MI patients undergoing cardiac cath.

Methods


COVID positive patients presenting with MI to the cardiac cath lab during the first wave of the pandemic (Index period (IP) = March – June 2020) were compared with a representative sample of those presenting with MI during the same period in 2019 (Baseline). Angiograms were analyzed for SYNTAX score, presence of thrombus, and MI without coronary disease (MINOCA) by an investigator blinded to group assignment.

Results


1,289 COVID patients were hospitalized during the IP. Cardiac cath volume fell 55%: 1,179 (Baseline) v 527 (IP). Comparing angiography during Baseline (representative MI sample March – June 2019, n=49) vs IP (all Mis brought to the cath lab March – June 2020, n=19), median SYNTAX scores were lower in the IP (13.0 [IQR 2-19] vs 5.0 [IQR 0-15.5]), presence of thrombus was also lower (55.1% vs 31.6%) while MINOCA was more prevalent (22.5% vs 36.8%). The differences were largely accounted for by the Baseline (n=17) vs IP (n=9) STEMI subgroups: SYNTAX score 16.5 [IQR 13-27.5] vs 8.0 [IQR 0-12], P=0.03; thrombus 88.2% vs 33.3%, P=0.004; and MINOCA 5.9% vs 33%, P=0.06.

Conclusions


Our findings suggest that the mechanisms responsible for COVID-associated MI may involve less extensive CAD and less thrombus. This was most apparent in the STEMI population.