Myocardial Injury in COVID-19 Patients: Association with Inflammation, Coagulopathy and In-Hospital Prognosis

Abstract

The exact mechanisms leading to myocardial injury in the coronavirus disease 2019 (COVID-19) are still unknown. In this retrospective observational study, we include all consecutive COVID-19 patients admitted to our center. They were divided into two groups according to the presence of myocardial injury. Clinical variables, Charlson Comorbidity Index (CCI), C-reactive protein (CRP), CAC (COVID-19-associated coagulopathy), defined according to the ISTH score, treatment and in-hospital events were collected. Between March and April 2020, 331 COVID-19 patients were enrolled, 72 of them (21.8%) with myocardial injury. Patients with myocardial injury showed a higher CCI score (median (interquartile range), 5 (4–7) vs. 2 (1–4), p = 0.001), higher CRP values (18.3 (9.6–25.9) mg/dL vs. 12.0 (5.4–19.4) mg/dL, p ˂ 0.001) and CAC score (1 (0–2) vs. 0 (0–1), p = 0.001), and had lower use of any anticoagulant (57 patients (82.6%) vs. 229 patients (90.9%), p = 0.078), than those without. In the adjusted logistic regression, CRP, myocardial injury, CCI and CAC score were positive independent predictors of mortality, whereas anticoagulants resulted as a protective factor. Myocardial injury in COVID-19 patients is associated with inflammation and coagulopathy, resulting in a worse in-hospital prognosis. Treatment with anticoagulant agents may help to improve in-hospital outcomes.

COVID-19 and Heart Failure: From Epidemiology During the Pandemic to Myocardial Injury, Myocarditis, and Heart Failure Sequelae

“…Indeed, during the acute phase of the infection, an imbalanced response of types 1 and 2 T helper cells may lead to a hyperinflammatory response (35,36), resulting in an excessive release of cytokines: in particular, higher levels of interleukin-1β (IL-1β), interleukin-6, interferon-γ, tumor necrosis factor (TNF), macrophage inflammatory protein, and vascular endothelial growth factor (VEGF) have been described in patients affected by severe COVID-19 (16)(17)(18), and are independently associated with a severe course of the infection and eventually death (16,37). In addition, the hyperinflammation syndrome seems to be pivotal in the development of cardiac injury, since a positive correlation has been described between the increase in inflammatory markers and myocardial damage in COVID-19 (38)(39)(40)(41). Consistently, previous in-vitro studies have shown that the release of proinflammatory cytokines such as TNF and IL-1β, in other septic conditions, were responsible for myocardial cells depression (42)(43)(44), through modulation of calcium channel activity and nitric oxide production (43,44).…”

Myocardial injury in patients with SARS‐CoV‐2 pneumonia: Pivotal role of inflammation in COVID‐19

“…The clinical variables were selected a priori based on previous clinically studies on prognosis of COVID‐19 patients. 9 Prognostic properties of cardiovascular chronic treatments were assessed based on the uncertainty regarding the effects of ACEI, ARB and mineralocorticoid antagonist in COVID‐19 patients 10 and the potentially beneficial effects of beta blockers and calcium‐channel blockers on myocardial injury. Antithrombotic treatments were included in the regression as coagulopathy is a common part of the systemic inflammatory response syndrome in COVID‐19 patients.…”

“…Logistic regression analysis and Cox regression analysis was performed to identify the predictors of myocardial injury and all‐cause death, respectively. The clinical variables were selected a priori based on previous clinically studies on prognosis of COVID‐19 patients 9 . Prognostic properties of cardiovascular chronic treatments were assessed based on the uncertainty regarding the effects of ACEI, ARB and mineralocorticoid antagonist in COVID‐19 patients 10 and the potentially beneficial effects of beta blockers and calcium‐channel blockers on myocardial injury.…”

Acute and Chronic Effects of COVID-19 on the Cardiovascular System

“…The cytokines probably act by recruiting inflammatory cells through increased expression of adhesion molecules [28,29]. Observational studies have reported that elevated inflammatory biomarkers such as C-reactive protein (CRP), IL-6, and ferritin were related to higher incidences of myocardial injury in COVID-19 patients [30,31]. Furthermore, cardiomyocytes express receptors for the TNF and IL-6, and the binding of these molecules leads to a decreased inotropic response secondary to catecholamine signaling alteration and cytotoxic lesion [32].…”

“…The elevation of cardiac injury biomarkers in blood was related to worse in-hospital outcomes in COVID-19 patients. These markers more frequently rose in patients with cardiovascular risk factors and prior cardiovascular disease, including ischemic heart disease, chronic heart failure, peripheral vascular disease, and history of stroke [21,22,31].…”