Several recent studies have supported the growing hypothesis that coronavirus disease 2019 (COVID-19) is primarily a cardiovascular, and not a pulmonary virus. The narrative that those affected are usually asymptomatic and have very mild or no disease may be false. Many of those who are asymptomatic may actually fall victim to myocarditis, a sinister, stealth-like disease, whose resulting disability may take decades to manifest.
Concerns for cardiovascular involvement of SARS-CoV-2 have been present since the early genesis of the pandemic. A research paper from China found that 20% of COVID-19 hospitalized patients developed heart disease and thromboembolic events happened in 31% of those in the ICU. Another from Germany reported ongoing myocardial inflammation in 60% of 100 recently recovered patients with COVID-19.
However, cardiovascular disease has been assumed by many to be a manifestation of severe COVID-19; and not from direct infection of the virus but instead from small vessel disease caused by the hypercoagulation of the blood.
All of that changed last week with the publication of three reports. The first was from Penn State Health which reported that 15% of Penn State athletes who tested positive for COVID-19 had myocarditis. These were young athletes and included both mildly symptomatic and asymptomatic individuals. As a result of these findings, the Big 10 and Pac 12 postponed their football season.
Myocarditis does not have specific symptoms and most patients can be asymptomatic. Myocarditis can produce fibrosis of the heart which may present years later with heart failure from dilated cardiomyopathy. However, in 50% of cases the cause of dilated cardiomyopathy is unknown, but there is strong evidence that past viral infections play a role. And myocarditis can occur in children.
The second was a study by Perez-Bermejo, et al. which provided evidence that COVID-19 heart disease was a direct effect on the heart by SARS-CoV-2. This was suspected since cardiac myocytes express the ACE2 protein needed for viral entry into the cells. The authors described robust and specific change in cell cultured cardiomyocytes which corresponded to the changes they observed in autopsies of patients with COVID-19. Thus, the virus can also attack and destroy the heart directly, not just indirectly with hemodynamic stress, hypoxemia and small vessel thrombosis.
The third report was by Reynolds, et al., and offered an explanation for the perplexing clinical finding that COVID-19 asymptomatic patients have no pulmonary symptoms but are still hypoxic, indicating something major may be taking place. This finding is so common, that there was even discussion in the news media regarding pulse oximeters and if they should be purchased to detect infections with SARS-CoV-2.
Reynolds, et al. noted that there is a “disconnect between gas exchange and lung mechanics in COVID-19 pneumonia.” In other words, the patient’s decreased oxygenation does not correspond to the patient’s ability to breathe. Much like what has been observed in asymptomatic patients. The authors drew similarities to what is observed in hepatopulmonary syndrome and using a contrast enhanced doppler they were able to postulate pulmonary vascular dilatation with resultant increased blood flow which could account for the “ventilation-perfusion mismatch and hypoxemia.”
Thus, the once thought asymptomatic patients who luckily dodged a bullet and were spared from the ravages of the disease, may indeed be truly sick. A significant portion of them may develop myocarditis along with vascular vasodilation with resultant hypoxemia. This pathological process could easily be more significant than the pulmonary effects of the virus, since it is present in both symptomatic and asymptomatic patients. And could explain the debilitating symptoms of fatigue and mental fog which “long-haulers” are experiencing, many of which had a mild initial illness.
