Myocardial injury and COVID-19: Possible mechanisms

Abstract

Coronavirus Disease 2019 (COVID-19) has quickly progressed to a global health emergency. Respiratory illness is the major cause of morbidity and mortality in these patients with the disease spectrum ranging from asymptomatic subclinical infection, to severe pneumonia progressing to acute respiratory distress syndrome. There is growing evidence describing pathophysiological resemblance of SARS-CoV-2 infection with other coronavirus infections such as Severe Acute Respiratory Syndrome coronavirus and Middle East Respiratory Syndrome coronavirus (MERS-CoV). Angiotensin Converting Enzyme-2 receptors play a pivotal role in the pathogenesis of the virus. Disruption of this receptor leads to cardiomyopathy, cardiac dysfunction, and heart failure. Patients with cardiovascular disease are more likely to be infected with SARS-CoV-2 and they are more likely to develop severe symptoms. Hypertension, arrhythmia, cardiomyopathy and coronary heart disease are amongst major cardiovascular disease comorbidities seen in severe cases of COVID-19. There is growing literature exploring cardiac involvement in SARS-CoV-2. Myocardial injury is one of the important pathogenic features of COVID-19. As a surrogate for myocardial injury, multiple studies have shown increased cardiac biomarkers mainly cardiac troponins I and T in the infected patients especially those with severe disease. Myocarditis is depicted as another cause of morbidity amongst COVID-19 patients. The exact mechanisms of how SARS-CoV-2 can cause myocardial injury are not clearly understood. The proposed mechanisms of myocardial injury are direct damage to the cardiomyocytes, systemic inflammation, myocardial interstitial fibrosis, interferon mediated immune response, exaggerated cytokine response by Type 1 and 2 helper T cells, in addition to coronary plaque destabilization, and hypoxia.

Cardiac involvement in COVID-19 patients: mid-term follow up by cardiac magnetic resonance imaging

“…The persistence of visual LGE at 3-month follow-up re ecting necrosis (persistent in ammation) or scar ( brosis) might be caused by COVID-19 and needs to be elucidated further 21 . Yet, visual LGE indicated that up to 30% COVID-19 patients have irreversible myocardial injury 22,23 , which is consistent with the ndings of the previous study and can con rm one of the main mechanisms of COVID-19 induced direct myocardial injury-myocarditis [24][25][26] . In addition, the presence of LGE has been proven to be an independent predictor of all-cause mortality and cardiac mortality in myocarditis 27,28 .…”

Clinical Characteristics and Prognosis of Patients with COVID-19 Combineded with or without Diabetes, Hypertension or Coronary

“…Middle East respiratory syndrome coronavirus (MERS-CoV) cases suggests that diabetes and hypertension are equally prevalent in approximately 50% of the patients while coronary heart disease are present in 30% [17]. However, the mechanisms for destabilization, and hypoxia [27][28][29]. We suggest that myocardial injury is a problem that cannot be ignored in patients with COVID-19.…”

Acute Cardiac Injury and COVID-19 – A Systematic Review and Meta-analysis

“…Potential mechanisms currently proposed either invoke a direct damage to myocytes as a result of systemic in ammation, myocardial interstitial brosis, interferon mediated immune response, exaggerated cytokine response by Type 1 and 2 helper T cells or the secondary effect of coronary plaque destabilization as well as the profound hypoxia these patients have as a result of the overwhelming pneumonia. 4 Furthermore, Zhou et 5 al have also demonstrated the relationship existing between COVID-19 and angiotensin-converting enzyme 2 (ACE2), which is a monocarboxypeptidase renin-angiotensinaldosterone system enzyme that metabolizes several peptides, to enter ACE2-expressing cells. ACE2 is widely expressed in the endothelium of the heart and kidneys, 6 and that might explain the prevalence of ACI and acute kidney injury among patients with COVID-19.…”