Clinical implications and indicators of mortality among patients hospitalized with concurrent COVID-19 and myocardial infarction

Tavolinejad, Hamed; Hosseini, Kaveh; Sadeghian, Saeed; Pourhosseini, Hamidreza; Lotfi‐Tokaldany, Masoumeh; Masoudkabir, Farzad; Sattartabar, Babak; Masoudi, Maryam; Shafiee, Akbar; Badalabadi, Reza Mohseni; Pashang, Mina; Aein, Afsaneh; Tajdini, Masih

doi:10.5543/tkda.2021.14331

Cited by 3 publications

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“…In one registry-based retrospective analysis of hospitalized patients with COVID-19 who suffered an AMI, the overall mortality was 22.8% (50). The deceased were older than survivors, and patients with hypertension, worsening renal function and higher cardiac troponin T and C-reactive protein levels were more likely to die.…”

Section: Acute Myocardial Infarction/acute Coronary Syndromementioning

confidence: 99%

Emerging Role of Platelet-Endothelium Interactions in the Pathogenesis of Severe SARS-CoV-2 Infection-Associated Myocardial Injury

et al. 2022

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Cardiovascular dysfunction and disease are common and frequently fatal complications of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection. Indeed, from early on during the SARS-CoV-2 virus pandemic it was recognized that cardiac complications may occur, even in patients with no underlying cardiac disorders, as part of the acute infection, and that these were associated with more severe disease and increased morbidity and mortality. The most common cardiac complication is acute cardiac injury, defined by significant elevation of cardiac troponins. The potential mechanisms of cardiovascular complications include direct viral myocardial injury, systemic inflammation induced by the virus, sepsis, arrhythmia, myocardial oxygen supply-demand mismatch, electrolyte abnormalities, and hypercoagulability. This review is focused on the prevalence, risk factors and clinical course of COVID-19-related myocardial injury, as well as on current data with regard to disease pathogenesis, specifically the interaction of platelets with the vascular endothelium. The latter section includes consideration of the role of SARS-CoV-2 proteins in triggering development of a generalized endotheliitis that, in turn, drives intense activation of platelets. Most prominently, SARS-CoV-2–induced endotheliitis involves interaction of the viral spike protein with endothelial angiotensin-converting enzyme 2 (ACE2) together with alternative mechanisms that involve the nucleocapsid and viroporin. In addition, the mechanisms by which activated platelets intensify endothelial activation and dysfunction, seemingly driven by release of the platelet-derived calcium-binding proteins, SA100A8 and SA100A9, are described. These events create a SARS-CoV-2–driven cycle of intravascular inflammation and coagulation, which contributes significantly to a poor clinical outcome in patients with severe disease.

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Section: Acute Myocardial Infarction/acute Coronary Syndromementioning

confidence: 99%

Emerging Role of Platelet-Endothelium Interactions in the Pathogenesis of Severe SARS-CoV-2 Infection-Associated Myocardial Injury

et al. 2022

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“… 18 Sex differences in patients with COVID-19 infection and MI are limited to only 1 small, single-center study ( n = 57) in Iran predominantly composed of patients with NSTEMI that reported no sex difference in in-hospital mortality risk. 19 …”

Section: Introductionmentioning

confidence: 99%

Sex Differences in Clinical Characteristics, Management Strategies, and Outcomes of STEMI With COVID-19: NACMI Registry

Quesada

Hon

Yildiz

et al. 2022

Journal of the Society for Cardiovascular Angiography & Int

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Renin‐Angiotensin Aldosterone System Inhibitors and COVID‐19: A Systematic Review and Meta‐Analysis Revealing Critical Bias Across a Body of Observational Research

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Taylor

Lampa

et al. 2022

JAHA

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Background Renin‐angiotensin aldosterone system (RAAS) inhibitor—COVID‐19 studies, observational in design, appear to use biased methods that can distort the interaction between RAAS inhibitor use and COVID‐19 risk. This study assessed the extent of bias in that research and reevaluated RAAS inhibitor—COVID‐19 associations in studies without critical risk of bias. Methods and Results Searches were performed in MEDLINE, EMBASE, and CINAHL databases (December 1, 2019 to October 21, 2021) identifying studies that compared the risk of infection and/or severe COVID‐19 outcomes between those using or not using RAAS inhibitors (ie, angiotensin‐converting enzyme inhibitors or angiotensin II type‐I receptor blockers). Weighted hazard ratios (HR) and 95% CIs were extracted and pooled in fixed‐effects meta‐analyses, only from studies without critical risk of bias that assessed severe COVID‐19 outcomes. Of 169 relevant studies, 164 had critical risks of bias and were excluded. Ultimately, only two studies presented data relevant to the meta‐analysis. In 1 351 633 people with uncomplicated hypertension using a RAAS inhibitor, calcium channel blocker, or thiazide diuretic in monotherapy, the risk of hospitalization (angiotensin‐converting enzyme inhibitor: HR, 0.76; 95% CI, 0.66–0.87; P <0.001; angiotensin II type‐I receptor blockers: HR, 0.86; 95% CI, 0.77–0.97; P =0.015) and intubation or death (angiotensin‐converting enzyme inhibitor: HR, 0.64; 95% CI, 0.48–0.85; P =0.002; angiotensin II type‐I receptor blockers: HR, 0.74; 95% CI, 0.58–0.95; P =0.019) with COVID‐19 was lower in those using a RAAS inhibitor. However, these protective effects are probably not clinically relevant. Conclusions This study reveals the critical risk of bias that exists across almost an entire body of COVID‐19 research, raising an important question: Were research methods and/or peer‐review processes temporarily weakened during the surge of COVID‐19 research or is this lack of rigor a systemic problem that also exists outside pandemic‐based research? Registration URL: www.crd.york.ac.uk/prospero/ ; Unique identifier: CRD42021237859.

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Clinical implications and indicators of mortality among patients hospitalized with concurrent COVID-19 and myocardial infarction

Cited by 3 publications

References 0 publications

Emerging Role of Platelet-Endothelium Interactions in the Pathogenesis of Severe SARS-CoV-2 Infection-Associated Myocardial Injury

Emerging Role of Platelet-Endothelium Interactions in the Pathogenesis of Severe SARS-CoV-2 Infection-Associated Myocardial Injury

Sex Differences in Clinical Characteristics, Management Strategies, and Outcomes of STEMI With COVID-19: NACMI Registry

Renin‐Angiotensin Aldosterone System Inhibitors and COVID‐19: A Systematic Review and Meta‐Analysis Revealing Critical Bias Across a Body of Observational Research

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