What We Know About COVID-19 and the Heart with Gregory Weiss, MD

Gregory Weiss, MD

Over the last year, the global spread of the novel coronavirus COVID-19 has wrought havoc on millions of people and strained the healthcare delivery system. While the vast majority of reports cite respiratory complications as the chief mechanism for morbidity and mortality related to COVID-19 more and more evidence suggests that significant heart damage may be underreported and responsible for significant comorbidity.1 Several small studies looking at troponin I levels in patients admitted with COVID-19 have demonstrated that between 20% and 40% of patients admitted had evidence of cardiac injury.1 Further, patients with evidence of myocardial damage were more likely to die with COVID-19.1

Without a definitive tissue diagnosis, cardiologists often cite myocarditis, or a non-specific cardiac inflammation as a cause for elevated cardiac enzymes in the absence of obstructive coronary anatomy. Compounding an elusive answer to why serologic evidence of heart damage accompanies many COVID-19 cases is the fact that, at autopsy, histological evidence of myocarditis is uncommon.1 Such evidence leads clinicians and researchers to speculate as to what is causing cellular heart damage.

Looking at the pathogenesis of COVID-19 may provide a clue to what is damaging these patient’s hearts. COVID-19 infection and clinical illness is characterized by a dramatic inflammatory response where the body’s immune system, in an effort to combat the coronavirus, damages the lungs by releasing an enormous number of immune mediators. This cytokine “storm” may also be responsible for damaging the heart. Gregg Fonarow, MD, chief of the division of cardiology at the University of California, Los Angeles states, “There is recognition that even some of those COVID-19 patients not hospitalized are experiencing cardiac injury. This raises concerns that there may be individuals who get through the initial infection, but are left with cardiovascular damage and complications."²

Fonarow goes on to postulate that late consequences, even in those who have recovered from or never had symptoms of COVID-19 could be a higher risk for heart failure.² One troubling trend we are seeing is that heart damage seems to be selective. It appears that some patients are affected more than others from a cardiac standpoint^.2 A recent Journal of the American Medical Association Cardiology issue found that 78% of COVID-19 patients scanned with MRI displayed cardiac involvement with 60% of those going on to have persistent myocardial inflammation.³

Important for clinicians is the apparent fact that SARS-CoV-2 (COVID-19) can damage the heart both directly and indirectly. Dr. Eric Topol at Scripps Research Translational Institute in La Jolla, CA describes the close relationship between the COVID-19 spike protein and angiotensin-converting enzyme 2 (ACE2), an enzyme ubiquitous in the human cardiovascular system.⁴ This evidence may explain how COVID-19 first interacts with heart cells and why people with variable risk factors may be affected differently by the infection. Indirect mechanisms are related to severe lung injury. With severe lung damage, heart failure may follow due to pulmonary vascular complications.

During medical training, it is ingrained in our memory that common things occur most commonly. We know that systemic inflammation is the hallmark of infection with COVID-19. As such it is most likely that the same inflammatory response that damages the lungs may lead to myocardial tissue inflammation or myocarditis in those predisposed to such a complication. This last point is what makes navigating these complications difficult for clinicians and researchers. It is clear that the spectrum of COVID-19 disease presentation is extremely variable. Developing an understanding of why some patients exhibit a completely asymptomatic clinical course while others become mortally ill with multi-organ failure leading to death will no doubt aid in our efforts to describe and treat the cardiac manifestations of COVID-19.

For now, experts advise those recovering from COVID-19 to watch for the following symptoms and to consult their physician or a cardiologist if they experience them²:

1. Increasing or extreme shortness of breath with exertion.
2. Chest pain, swelling of the ankles, heart palpitations or an irregular heartbeat.
3. Not being able to lie flat without shortness of breath, waking up at night short of breath.
4. Lightheadedness or dizzy spells.

Patients’ should not wait to seek care and we as clinicians must be vigilant for potential cardiac complications in both clinically acute and recovering COVID-19 patients. While hope is on the horizon we have much to learn about how this dreadful disease affects the heart and human body.

References:

1. Kawakami, R. MD, Sakamoto, A. MD, Kawai, K. MD, et al. Pathological evidence for SARS-CoV-2 as a cause of myocarditis. JACC. Vol 77, No. 3. 2021.
2. https://www.heart.org/en/news/2020/09/03/what-covid-19-is-doing-to-the-heart-even-after-recovery
3. Puntmann VO, Carerj ML, Wieters I, et al. Outcomes of Cardiovascular Magnetic Resonance Imaging in Patients Recently Recovered From Coronavirus Disease 2019 (COVID-19). JAMA Cardiol. 2020;5(11):1265–1273. doi:10.1001/jamacardio.2020.3557
4. Topol, E. J. COVID-19 can affect the heart. Science. 23 Oct 2020, Vol 370, Issue 6515, pp. 408-409.