Myocardial Injury and COVID-19
In addition to underlying CVD being a risk factor for contracting COVID-19, patients that develop acute myocardial injury have worse outcomes, even in those without baseline cardiovascular dysfunction [25–28]. Acute myocardial injury can be categorized in three varieties: elevated troponin levels above the 99th percentile upper reference limit, development of new or worsening heart failure, and myocarditis. Several studies from China found that elevated troponin levels were significantly associated with higher mortality [26–28]. A case series of 187 patients at the Seventh Hospital of Wuhan City, China, found that patients with elevated troponin T (TnT) levels had a significantly higher mortality rate to those with normal TnT levels (59.6% vs. 8.9%; p < 0.001). Patients with underlying CVD including those with underlying hypertension, coronary heart disease, and cardiomyopathy were more likely to have elevated TnT levels during their hospital course [26]. Lipid metabolism is also observed to be dysregulated in patients with SARS-CoV infection. Serum concentrations of free fatty acids, lysophosphatidylcholine, and phosphatidylglycerol remained elevated and contributed to chronic cardiovascular damage post infection in patients with SARS-CoV [29]. Long-term cardiovascular and atherosclerotic changes in patients who suffer from COVID-19 have not been documented yet given the recent nature of this pandemic.
A case series of 21 critically ill COVID-19 patients from Seattle also found that one-third of their patients developed new cardiomyopathy with cardiogenic shock in the absence of prior systolic dysfunction during the progression of their illness [25]. It is unclear if these patients that developed cardiomyopathy truly had myocarditis or had underlying CVD that predisposed them to this clinical course. However, COVID-19 has been shown to directly cause myocarditis in otherwise healthy individuals in several case reports [30, 31]. Thus, COVID-19 demonstrates various patterns of myocardial injury, with higher mortality risk being associated with elevated troponin levels.
In addition, in the cardio-oncology population, elevated cardiac biomarkers can pose an additional layer of complexity and challenge when dealing with management. Abnormal elevations of troponin and BNP biomarkers can be indicative of cardiotoxicity from cancer physiology or from the treatments themselves [32]. Some elevations may be non-specific and are reflective of subclinical cardiotoxicity in patients receiving anthracyclines and/or anti-HER2 agents in which stable patients can be medically managed [33, 34]. However, some patients receiving other agents such as certain tyrosine kinase inhibitors with prothrombotic risk (i.e., ponatinib) or fluoropyridines (i.e., 5-fluorouracil) may suffer cardiotoxicity in the form of coronary ischemia/vasospasm, which may warrant more invasive diagnostic/treatment strategies [35–37]. Elevated cardiac biomarkers have also been associated with worse outcomes and or cardiac hemodynamic instability, including cytokine release syndrome from chimeric antigen therapy (CAR-T), heart failure from proteasome inhibitor use (i.e., carfilzomib), or myocarditis from immune checkpoint inhibitor therapy [38–41]. Some of these disease processes may confound treatment of a cancer patient also afflicted with COVID-19, and thus, multidisciplinary assessment, particularly by a cardio-oncologist, may be essential to provide optimal care in this high-risk population.