Changes in characteristics and management among patients with ST ‐elevation myocardial infarction due to COVID ‐19 infection

Popovic, Batric; Varlot, Jeanne; Metzdorf, Pierre Adrien; Jeulin, Helene; Goehringer, François; Camenzind, Edoardo

doi:10.1002/ccd.29114

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Changes in characteristics and management among patients with ST ‐elevation myocardial infarction due to COVID ‐19 infection

Author(s): Batric Popovic ¹ , Jeanne Varlot ¹ , Pierre Adrien Metzdorf ¹ , Hélène Jeulin ² , François Goehringer ³ , Edoardo Camenzind ¹

Publication date (Electronic): July 15 2020

Journal: Catheterization and Cardiovascular Interventions

Publisher: Wiley

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Abstract

Abstract Objectives To assess changes in characteristics and management among ST‐elevation myocardial infarction (STEMI) patients with coronavirus disease (COVID‐19) who underwent primary percutaneous coronary intervention. Methods Our prospective, monocentric study enrolled all STEMI patients who underwent PPCI during the COVID‐19 outbreak (n = 83). This cohort was first compared with a previous cohort of STEMI patients (2008–2017, n = 1,552 patients) and was then dichotomized into a non‐COVID‐19 group (n = 72) and COVID‐19 group (n = 11). Results In comparison with the pre‐outbreak period, patients during the outbreak period were older (59.6 ± 12.9 vs. 62.6 ± 12.2, p = .03) with a delayed seek to care (mean delay first symptoms‐balloon 3.8 ± 3 vs. .7.4 ± 7.7, p < .001) resulting in a two‐fold higher in‐hospital mortality (non COVID‐19 4.3% vs. COVID‐19 8.4%, p = .07). Among the 83 STEMI patients admitted during the outbreak period, 11 patients were infected by COVID‐19. Higher biological markers of inflammation (C‐reactive protein: 28 ± 39 vs. 98 ± 97 mg/L, p = .04), of fibrinolysis (D‐dimer: 804 ± 1,500 vs. 3,128 ± 2,458 μg/L, p = .02), and antiphospholipid antibodies in four cases were observed in the COVID‐19 group. In this group, angiographic data also differed: a thrombotic myocardial infarction nonatherosclerotic coronary occlusion (MINOCA) was observed in 11 cases (1.4% vs. 54.5%, p < .001) and associated with higher post‐procedure distal embolization (30.6% vs. 72.7%, p = .007). The in hospital mortality was significantly higher in the COVID‐19 group (5.6% vs. 27.3%, p = .016). Conclusion The COVID‐19 outbreak implies deep changes in the etiopathogenesis and therapeutic management of STEMI patients with COVID‐19. The impact on early and long‐term outcomes of systemic inflammation and hypercoagulability in this specific population is warranted.

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Most cited references 8

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High risk of thrombosis in patients with severe SARS-CoV-2 infection: a multicenter prospective cohort study

Julie Helms, Charles Tacquard, François Séverac … (2020)

Little evidence of increased thrombotic risk is available in COVID-19 patients. Our purpose was to assess thrombotic risk in severe forms of SARS-CoV-2 infection.

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Management of Acute Myocardial Infarction During the COVID-19 Pandemic

Ehtisham Mahmud, Harold Dauerman, Frederick Welt … (2020)

The worldwide pandemic caused by the novel acute respiratory syndrome coronavirus 2 (SARS-CoV2) has resulted in a new and lethal disease termed coronavirus disease 2019 (COVID-19). Although there is an association between cardiovascular disease and COVID-19, the majority of patients who need cardiovascular care for the management of ischemic heart disease may not be infected with COVID-19. The objective of this document is to provide recommendations for a systematic approach for the care of patients with an acute myocardial infarction (AMI) during the COVID-19 pandemic. There is a recognition of two major challenges in providing recommendations for AMI care in the COVID-19 era. Cardiovascular manifestations of COVID-19 are complex with patients presenting with AMI, myocarditis simulating a ST-elevation MI presentation, stress cardiomyopathy, non-ischemic cardiomyopathy, coronary spasm, or nonspecific myocardial injury and the prevalence of COVID-19 disease in the US population remains unknown with risk of asymptomatic spread. This document addresses the care of these patients focusing on 1) the varied clinical presentations; 2) appropriate personal protection equipment (PPE) for health care workers; 3) role of the Emergency Department, Emergency Medical System and the Cardiac Catheterization Laboratory; and 4) Regional STEMI systems of care. During the COVID-19 pandemic, primary PCI remains the standard of care for STEMI patients at PCI capable hospitals when it can be provided in a timely fashion, with an expert team outfitted with PPE in a dedicated CCL room. A fibrinolysis-based strategy may be entertained at non-PCI capable referral hospitals or in specific situations where primary PCI cannot be executed or is not deemed the best option.

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Diffuse and active inflammation occurs in both vulnerable and stable plaques of the entire coronary tree: a histopathologic study of patients dying of acute myocardial infarction.

Allison R. Schwartz, L Anemona, Luigi Spagnoli … (2005)

This study was undertaken to define and compare geographic coronary artery inflammation in patients who were dying of acute myocardial infarction (AMI), chronic stable angina (SA), and noncardiac causes (CTRL). Biochemical markers and flow cytometry provide indirect evidence of diffuse coronary inflammation in patients dying of acute coronary syndromes. Yet no histopathologic studies have corroborated these findings. A key unanswered question is whether the inflammatory burden involves the entire coronary tree or is limited to a few plaques. We examined 544 coronary artery segments from 16 patients with AMI, 109 segments from 5 patients with SA, and 304 coronary segments from 9 patients with CTRL. An average of 6.8 +/- 0.5 vulnerable segments per patient were found in the AMI group (in addition to culprit lesions) compared with an average of 0.8 +/- 0.3 and 1.4 +/- 0.3 vulnerable lesions/patient in the SA and CTRL groups, respectively. The AMI group, independent of the type of plaque observed, showed significantly more inflammatory infiltrates compared with the SA and CTRL groups (121.6 +/- 12.4 cell x mm2 vs. 37.3 +/- 11.9 cell x mm2 vs. 26.6 +/- 6.8 cell x mm2, p = 0.0001). In AMI patients, active inflammation was not only evident within the culprit lesion and vulnerable plaques but also involved stable plaques. These showed a three- to four-fold higher inflammation than vulnerable and stable plaques from the SA and CTRL groups, respectively. This histopathologic study found that both vulnerable and stable coronary plaques of patients dying of AMI are diffusely infiltrated by inflammatory cells.