Section 3.1.1: Myocardial Injury and Heart Failure (from DOI: 10.1007/s11886-020-01293-2)
From publication: "Cardiovascular Risks in Patients with COVID-19: Potential Mechanisms and Areas of Uncertainty" published as Curr Cardiol Rep; 2020 04 29 ; 22 (5) 34. DOI: https://doi.org/10.1007/s11886-020-01293-2
Section 3.1.1: Myocardial Injury and Heart Failure
Several published and unpublished case series have documented elevated serum troponin levels in a significant fraction (5-7%) of hospitalized COVID-19 patients. While the degree of troponin elevation was mild in the majority of cases, the presence of myocardial injury (as manifested by troponins above the upper range of normal) was associated with a significantly worse prognosis . It remains unclear whether the association with worse outcomes is simply reflective of selection of an older, sicker population more prone to demand ischemia with metabolic compromise during critical illness or direct myocardial injury caused by the virus or its inflammatory sequelae (Fig. 2). Relatively high levels of ACE2 protein expression on cardiomyocytes may theoretically lead to increased risk of viral susceptibility and virus mediated injury. However, while there are anecdotal reports of clinical presentations consistent with myocarditis , significant incidence of myocarditis has not been reported in any larger case series thus far. To date, there has been very limited pathologic or radiologic proof of myocarditis as a direct sequelae of COVID-19. Determining the true prevalence of these events is critical. Alternatively, the observed incidence of myocardial injury could be due to the increased risk of myocardial ischemic insult due to the poorly understood pleiotropic pro-thrombotic inflammatory sequelae from viral infections. An increased risk of myocardial infarction as determined by serological evidence of myocardial injuries has been well-documented in influenza infections at similar prevalence. This would suggest that the intravascular prothrombotic effect observed in COVID-19 patients is the consequence of the overall inflammatory state rather than a COVID19-specific phenomenon.
Regardless of the cause of myocardial injuries, early case reports of critically ill patients have found a significant fraction of patients developing clinical heart failure. Zhou et al. from Wuhan found that 28/54 of those who succumbed to the disease had heart failure:albeit the definition of "heart failure" employed was not stated, and a broad definition of acute cardiac injury (cardiac biomarkers > 99th percentile of the upper reference limit or new abnormalities on EKG or echocardiography) was used in this study. The case series of critically ill patients from Seattle showed cardiomyopathy in 7/21 patients, as defined by globally reduced left ventricular ejection function or decreased central venous saturation to < 70%. While the frequency of patient with cardiac dysfunction is notable in these reports, some limitations such as small sample size, very high (44%) baseline history of "CHF", and the lack of clearly defined criteria for heart failure limit the generalizability of these studies. It is worth noting that high incidence of heart failure was not mentioned in a larger case series from China nor in the Italian experience thus far.
