The Heartbreaking Story of SARS-CoV-2

Illustrated by Alexandra Laufer

Etiologically, SARS-CoV-2 is a virus that predominantly affects the respiratory tract: that is, our lungs and intricate airways. In the year that COVID-19 spread to every corner of our world, an increasing body of research demonstrates that this virus can wreak havoc on cardiac and vascular tissue. The ability for SARS-CoV-2 to lead to prolonged vascular implications, even years after recovery from typical viral symptoms renders SARS-CoV-2 research incredibly relevant [8].

In the early months of the pandemic, many researchers agreed that heart health was only compromised in cases of high viral load or severity of infection. In a study published in July, Valentina Puntmann et al. found that of 100 SARS-CoV-2 patients, 78% of them showed continued cardiac involvement while 60% of patients showed ongoing myocarditis [6]. Cardiac involvement includes abnormal cardiovascular magnetic resonance (CMR) readings, which measures irregularities, injury and inflammation to the heart tissue, while myocarditis is inflammation in the tissues of the heart that can result in arrhythmias or irregular pumping patterns [5]. The implications of these data are alarming; our heart health is in danger even in recovered patients [3]. While the recency of the SARS-CoV-2 pandemic has limited the study of long-term effects on cardiac health, the concern that heart failure could affect the younger infected population decades from now still remains [3].

There are a few methods to measure the cardiac implications of SARS-CoV-2. One way to measure the degree of cardiac inflammation is to measure the blood levels of troponin, an enzyme that is released from injured cardiac tissue. Mitrani et al. showed that 20-30% of hospitalized patients with SARS-CoV-2 had elevated levels of troponin, indicating worse short term effects due to cardiac problems, and increased presence of ventricular arrhythmias [4]. Arrhythmias and other rhythmic and electrical abnormalities of the heart can be monitored using electrocardiograms [4]. Interestingly, research has demonstrated that myocarditis can occur through both direct viral infections and immune inflammatory responses, enabling the possibility for asymptomatic individuals to potentially develop cardiac defects [4].  

While poor cardiovascular health can be a downstream effect of SARS-CoV-2, it can also serve as a risk factor for severe illness. The angiotensin converting enzyme 2 (ACE-2) receptor is the main receptor that allows host cell invasion for SARS-CoV-2. That is to say, ACE-2 receptors serve as the “gateway” of infection into our bodies. ACE-2 receptors are also known for their extensive role in modulating blood pressure and establishing homeostasis by negatively feedbacking on the renin-angiotensin-aldosterone system [3]. Since ACE-2 is known to increase blood pressure, many individuals afflicted with hypertension use ACE-2 inhibitors to lower their chronically high blood pressure [4]. In turn, “ACE inhibitors (ACEIs)… may upregulate ACE-2 [receptor] expression, thus increasing the availability of target molecules for SARS-CoV-2,” thereby increasing host cell invasion and propagation [1]. This leads to the concern that individuals medicated with ACE inhibitors could be at a higher risk of contracting SARS-CoV-2 [1]. Another risk factor for SARS-CoV-2 that leads to poorer cardiac outcomes is obesity due to the presence of ACE-2 receptors in adipose tissues. In obese individuals, the contiguity of the myocardium and the epicardial adipose tissue leads to more infiltration of the SARS-CoV-2 via ACE-2 receptors and an overall increased inflammatory response, leading to tissue damage and long term cardiac damage [4]. In this way, obese patients are more at risk for tissue damage than non-obese patients. 

One area of further study would center around developing protocols for prognostic techniques for individuals post-COVID-19 infection. Patients with baseline elevated troponin levels and other risk factors like obesity should be monitored more closely to assess long term cardiac damage [3]. However, regardless of risk factors and presence of symptoms, vascular health and SARS-CoV-2 are more intimately related than early research indicated them to be. 

Edited by: Caelan Miller
Illustrated by: Alexandra Laufer

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