key: cord-0860877-kp5sc9iv
authors: Popovic, Batric; Varlot, Jeanne; Metzdorf, Pierre Adrien; Jeulin, Hélène; Goehringer, François; Camenzind, Edoardo
title: Changes in characteristics and management among patients with ST‐elevation myocardial infarction due to COVID‐19 infection
date: 2020-07-15
journal: Catheter Cardiovasc Interv
DOI: 10.1002/ccd.29114
sha: 8b7bb54ae2fb296c34ba8522f94f0a50a710f767
doc_id: 860877
cord_uid: kp5sc9iv

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.

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) pandemic, also known as coronavirus disease 2019 (COVID-19), has significantly impacted the healthcare system worldwide. To preserve patients' health and resources, including hospital beds to care for COVID-19 patients, health authorities recommend deferral of elective cardiac procedures, including coronary angiography and percutaneous coronary intervention for stable coronary artery disease. 1 Timely reperfusion of primary percutaneous coronary intervention (PPCI) is the standard of care for patients who develop an ST-elevation myocardial infarction (STEMI). 2 Thus, the Society for Cardiac Angiography and Interventions and the American College of Cardiology continue to recommend primary percutaneous coronary intervention as the standard treatment of STEMI patients during the current pandemic. 3 Despite these recommendations for treatment of STEMI, different reports suggest a reduction in the number of STEMI cases treated in cardiac catheterization laboratories by up to 40%. 4 Moreover, little is known about changes in characteristics and management of STEMI patients who underwent PPCI during the outbreak, and especially in patients infected by COVID-19.

We described the experience concerning STEMI patients during the complete period of the COVID-19 confinement at the University Hospital of Nancy (France) located in the North-Eastern region of France, one of the French epicenters of the pandemia.

We prospectively collected all STEMI patients admitted at the University Hospital of Nancy from February 26, 2020, corresponding to the date of the first patient with COVID-19 was diagnosed in the "Grand Est", the administrative name of the northeastern region of France to May 10th 2020 corresponding to the official end of confinement in Two experienced operators reviewed all coronary angiograms. At least two orthogonal angiographic projections were used to assess the culprit vessel and lesion. The angiographic definition of thrombotic MINOCA was the presence of a thrombus defined as a non-calcified filling defect outlined on at least three sides by contrast media and the absence of coronary lesions (underlying the thrombus as well as throughout the coronary tree) defined as a luminal narrowing >25% by visual estimate.

The case definition of thrombotic MINOCA used in this study consisted of major and minor criteria according to Shibata al as described elsewhere. 5 We excluded myocardial infarction based on 

Continuous variables are presented as mean ± SD or median and interquartile range and compared using a Student t test or Wilcoxon test. Categorical data are presented as numbers and percentages and compared using a χ 2 or Fisher exact test, according to conditions of application. Because of the small sample size and outcome events, multivariable adjustment was considered inappropriate. The significance level was set at .05. All statistical analyses were performed using SPSS software. (Figures 1 and 2) . (Table 3) . Among six COVID-19 patients who experienced STEMI secondary to thrombotic MICOCA, inflammation and recorded coagulation parameters were increased in all cases and antiphospholipid antibodies were observed in three patients.

The major findings of this prospective study evaluating a consecutive series of STEMI patients during the COVID-19 confinement period were: (a) an increase in delay between symptoms onset and PPCI in the overall population with a significant proportion beyond the recommended timelines; (b) although the atherothrombotic mechanism of coronary thrombosis by plaque rupture remains important, a higher prevalence of coronary non-atherosclerotic obstructive disease was observed which concerned more than half of patients in the COVID-19 group, and (c) the incidence of abnormalities in conventional coagulation function parameters was higher in COVID-19 group who experienced nonatherosclerosis induced MI, suggesting that coagulopathy is more frequent. (d) Lastly prognosis in these patients seems worse with more severe early outcomes.

A delayed hospital presentation was the greatest contributor to postponed treatment of acute myocardial infarction (MI) and a critical determinant of short-and long-term mortality. 6 The most significant component in delay from the onset of coronary symptoms to reaching definitive coronary care has been identified in the delay calling for medical assistance because other prehospital medical management delays, that is, call to balloon and door to balloon are unchanged. It is understandable that people are reluctant to go to a hospital during the COVID-19 outbreak, which explains the potential delays in care-seeking. Another concern that we were unable to evaluate is whether some patients with STEMI did not seek care at all. Strategies to reduce patient delay times in a MI setting during this confinement period depend on educating the public on the recognition and diversity of coronary symptoms and the benefits of presenting promptly to the hospital by way of the emergency ambulance service. It will certainly also depend on information campaigns certifying the presence of a COVID-19 free standard care to patients.

Although respiratory distress symptoms were the main clinical manifestation in COVID-19 patients admitted to the intensive care unit, this viral infection may result in acute thrombotic cardiovascular events. Excess in mortality from cardio-vascular disease during bacterial or virus epidemics, such as the influenza epidemic, was first recognized early in the 20th century, and the specific association between a variety of infective pathogens (viral and bacterial) and the development of MI was characterized later. 7, 8 Atherosclerotic plaques contain inflammatory cells, and infection generates circulating inflammatory cytokines, such as interleukin-1, 6, and 8 and tumor necrosis factor-α, that can activate inflammatory cells in atherosclerotic plaques. 9 Studies in animals have shown that warranted. Non-atherosclerotic disease as pathogenesis of MI may also imply specific peri-procedural conditions and therapeutic management. 15 A carefully conducted patient history may also avoid an overaggressive reperfusion strategy, as angioplasty with stenting may be deleterious leading to more distal embolization 15 in addition with antithrombotic drugs. 15 However, the treatment efficiency of antithrombotic drugs in patients with hemodynamic impairment frequently remains challenging.

Our retrospective, monocentric study and the limited number of STEMI patients during the confinement period might have resulted from certain methodological bias. However, it remains, to our knowledge, one of the first series in the literature that has studied the etiopathogenesis of STEMI during this outbreak.

Despite a restrictive thrombotic MINOCA definition, intravascular imaging modalities including optical coherence tomography and intravascular ultrasound may be very helpful tools to identify plaque rupture and ulceration, in proximal coronary lesions especially. However, intravascular imaging may be challenging or inappropriate in the specific clinical settings of STEMI secondary to an extensive occlusive coronary thrombosis requiring multiple balloon inflations to obtain a coronary flow or secondary to a distal coronary occlusion.

Further paradoxical coronary thromboembolism through a patent foramen ovale as the cause of thrombotic MINOCA may have been underestimated by a nonsystematic transesophageal or contrastenhanced echocardiography.

The COVID-19 outbreak implies deep changes in the clinical profile and therapeutic management of STEMI patients who underwent PPCI. Systemic inflammation and hypercoagulability characterized STEMI patients infected with COVID-19 and their impact on early and long-term outcomes should be investigated.

https://orcid.org/0000-0002-2454-6468

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Coronary embolism among ST-segment-elevation myocardial infarction patients: mechanisms and management