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.