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

Abstract

Aims Infection by SARS‐CoV‐2 may result in a systemic disease and a proportion of patients ranging 15%–44% experienced cardiac injury (CI) diagnosed by abnormal troponin levels. The aim of the present study was to analyse the clinical characteristics of a large series of hospitalized patients for COVID‐19 in order to identify predisposing and/or protective factors of CI and the outcome. Methods and results This is an observational, retrospective study on patients hospitalized in two Italian centres (San Raffaele Hospital and Cremona Hospital) for COVID‐19 and at least one high‐sensitivity cardiac troponin (hs‐cTnt) measurement during hospitalization. CI was defined if at least one hs‐cTnt value was above the 99th percentile. The primary end‐point was the occurrence of CI during hospitalization. We included 750 patients (median age 67, IQR 56–77 years; 69% males), of whom 46.9% had history of hypertension, 14.7% of chronic coronary disease and 22.3% of chronic kidney disease (CKD). Abnormal troponin levels (median troponin 74, IQR 34–147 ng/l) were detected in 390 patients (52%) during the hospitalization. At multivariable analysis age, CKD, cancer, C‐reactive protein (CRP) levels were independently associated with CI. Independent predictors of very high troponin levels were chronic kidney disease and CRP levels. Patients with CI showed higher rate of all‐cause mortality (40.0% vs. 9.1%, p = 0.001) compared to those without CI. Conclusion This large, multicentre Italian study confirmed the high prevalence of CI and its prognostic role in hospitalized patients with COVID‐19, highlighting the leading role of systemic inflammation for the occurrence of CI.

A Real Pandora’s Box in Pandemic Times: A Narrative Review on the Acute Cardiac Injury Due to COVID-19

“…Moreover, given the well-established relationship between inflammation and atherosclerosis, a reasonable approach would consist of an assessment of subclinical markers of atherosclerosis, such as carotid intima-media thickness, pulse wave velocity, and ankle-brachial index, which are readily determined and well correlated with multiple cardiovascular risk scores, such as SCORE or Framingham [ 186 ]. Keeping in mind the socioeconomic challenges associated with the pandemic and the increased prevalence of cardiovascular comorbidities among admitted patients, we consider that judicious use of all these available diagnostic and prognostic biomarkers may facilitate the identification of individuals with a high-risk profile, thus allowing a prompt and adequate therapeutic intervention, as the limitation of myocardial injury during SARS-CoV-2 infection is of paramount importance for both short and long-term prognosis [ 134 , 187 ].…”

Cardiovascular Tropism and Sequelae of SARS-CoV-2 Infection

“…Patients with acute COVID-19 display numerous systemic derangements, including marked increases in circulating inflammatory mediators [53,54], activation of the complement cascade [55], impaired fibrinolysis [56], platelet activation and aggregation [57]. While associations between systemic inflammation and acute cardiovascular sequelae of COVID-19 exist [58], a causative relationship is yet to be rigorously established. Much less is known regarding the pathology of PACS.…”

Prothrombotic Phenotype in COVID-19: Focus on Platelets

“…Of course, in the crosstalk between inflammation and thrombosis, platelets are required to talk with other circulating cells, such as monocytes and macrophages, and each of them talks with endothelial cells [11,12]. As documented by reports in patients deceased due to the fact of COVID-19, an extensive platelet-fibrin clot formation in the pulmonary microvasculature was found in 80-100% of lungs and in other organs examined [13] and marked inflammation has been established to be a typical clinicopathological feature that worsens COVID-19 prognosis [7,14,15].…”