As we learn more about COVID-19, it has become more evident that cardiovascular (CV) complications are common and may account for up to 40% of deaths. It is the CV complications that appear to provide the best opportunity for an impact from our therapeutic product. Perhaps the most common CV complication in patients with COVID-19 is myocardial injury as reflected by elevation of serum troponin (P. P. Liu et al. 2020). This might reflect myocardial cell death as a direct result of the viral infection; indeed, although uncommon, frank acute myocarditis can develop (F. Zhou et al. 2020; P. P. Liu et al. 2020), (Ruan et al. 2020), with a mononuclear cell infiltration of the myocardium at autopsy. This may be marked enough to result in the development of HF which can be severe. (“ABC News, April 22, 2020,” n.d.) However, a recent study from Israel suggests that the troponin release may originate more from the right ventricle than from the left ventricle (Szekely et al. 2020). This might reflect the severity of the pulmonary infection with resultant pulmonary arterial hypertension. The development of HF in patients with COVID-19, therefore, may be multi-causal and certainly requires further study.
Other patients develop ACS with myocardial cell damage as reflected by enzyme increases and electrocardiographic abnormalities (Huang et al. 2020; P. Zhou et al. 2020). The mechanism of this is not completely clear (Tersalvi et al. 2020). In some patients, it may reflect the development of a supply-demand imbalance caused by the acute infection, hypoxemia and resulting increased heart rate (E. Y. Wang et al. 2020). But another hypothesis is that the extreme inflammation, possibly with a cytokine storm, along with coagulation abnormalities and endothelial dysfunction, cause plaque instability in coronary arteries and results in coronary thrombosis (Tersalvi et al. 2020).
Arrhythmias are also common with atrial fibrillation being most prevalent. The pathogenesis is not clear, but it is interesting that, in general, inflammation of the left atrial tissue is believed to be the common substrate for this arrhythmia. Ventricular arrhythmias also occur with resultant sudden death (P. P. Liu et al. 2020). In some cases, this has been a complication of concomitant therapy – particularly with Chloroquine or Hydroxychloroquine – both of which may prolong the QT interval. However, in a recent study from Northern Italy, investigators found that even out-of-hospital cardiac arrest was twice as common during a six-week period during the 2020 pandemic, compared to a similar period in 2019 (Baldi et al. 2020).
Finally, several recent reports highlight the high incidence of acute renal failure in patients with COVID-19 – particularly in those ill enough to require ICU management (Richardson et al. 2020). Many of these patients require replacement therapy with dialysis and have a poor prognosis. Indeed, recent Centers for Medicare and Medicaid Services (CMS) data suggest that 50% of patients hospitalized with COVID-19 had chronic kidney disease (“CMS Medicare Claims and Encounter Data” 2020).
You might qualify to take part in this study if you meet the following criteria:
- Males and females 18 years of age or older
- Tested positive and hospitalized for COVID-19 within the past 96 hours; illness severity must be less than indicated for intensive care unit (ICU) admission
- Prior history of CVD [cardiovascular (CV), cerebrovascular or peripheral vascular diagnosis], and/or significant risk factors for CVD
- age > 64
- diabetes (DM)
- hypertension (HTN)
- abnormal serum lipids
- obesity (BMI≥30)
Clinical Trial Investigator
Dr. Jose David Suarez, Principal Investigator