Angiographic characteristics of patients with STEMI and COVID-19: Insights from NACMI registry

Payam Dehghani1, Jyotpal Singh1, G B John Mancini2

  • 1Prairie Vascular Research, Regina, Saskatchewan, Canada.

American Heart Journal
|February 23, 2024
PubMed

Insights

COVID-19 and ST-elevation myocardial infarction (STEMI) patients exhibit significant thrombus burden, leading to high rates of multivessel disease and stent thrombosis. Unsuccessful percutaneous coronary intervention (PCI) due to persistent thrombus impacts in-hospital mortality.

Area of Science:

  • Cardiology
  • Infectious Diseases
  • Interventional Cardiology

Background:

  • No prior independent core lab angiographic analysis existed for COVID-19 patients with ST-elevation myocardial infarction (STEMI).
  • This study addresses the gap by characterizing angiographic parameters in this unique patient cohort.

Purpose of the Study:

  • To conduct an independent core laboratory analysis of angiographic findings in patients with COVID-19 and STEMI.
  • To assess culprit lesion characteristics, thrombus burden, and percutaneous coronary intervention (PCI) outcomes.

Main Methods:

  • Angiograms from the North American COVID-19 Myocardial Infarction (NACMI) Registry were analyzed.
  • Key parameters assessed included culprit lesion(s), Thrombolysis In Myocardial Infarction (TIMI) flow, Thrombus Grade Burden (TGB), and PCI outcomes.

Main Results:

  • 74% of 234 patients had one culprit lesion; 27% had multivessel thrombotic disease.
  • Stent thrombosis occurred in 12% of presentations, particularly in those with prior stents (55%).
  • 33% of PCI procedures were unsuccessful, often due to persistent thrombus or suboptimal TIMI flow, and were associated with increased in-hospital mortality.

Conclusions:

  • Patients with COVID-19 and STEMI present with substantial thrombus burden, multivessel disease, and stent thrombosis.
  • Suboptimal PCI outcomes due to persistent thrombus remain a concern and are linked to mortality.
  • These findings highlight the complex interplay between COVID-19 infection and acute coronary syndromes.
Abstract

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