A new study investigates whether SARS-CoV-2 targets heart cells in COVID-19 patients.

SARS-CoV-2, the virus that causes COVID-19, exerts well-documented adverse effects on the respiratory system.  These effects can vary significantly between individuals, as some COVID-19 patients require hospitalization while some patients only develop mild symptoms.1  Notably, a growing body of evidence suggests that individuals with underlying cardiovascular issues may be at an increased risk of experiencing poor COVID-19 outcomes.1,2,3

In addition, for some individuals, COVID-19 may further impact the cardiovascular system; some studies suggest an association between COVID-19 and a variety of heart complications.1,2,4  One of these complications is myocarditis, which is a rare yet serious condition where the heart muscle (myocardium) temporarily becomes inflamed and weaker.1,5  Although the mechanism behind this is not fully known, some researchers believe that it may be related to the increased inflammation caused by the body’s immune response to the SARS-CoV-2 virus.1,2,3

This increased inflammation can alter the heart’s environment, which could potentially have effects on the cardiovascular system.  Finally, the respiratory effects of COVID-19 can affect the heart and circulatory system indirectly.

It is unknown whether SARS-CoV-2 infects the heart cells directly; however, one study found SARS-CoV-2 in the myocardial tissues of COVID-19 patients post-mortem.6  An analysis was conducted to determine if and how COVID-19 targets cardiomyocytes, which are heart muscle cells that generate the contractions of the heartbeat.1  The results were analyzed and published in the International Journal of Cardiology.1

To establish a control group, researchers obtained myocardial tissue samples from 14 patients with end-stage heart failure, in addition to post-mortem tissue samples of cardiovascular patients without COVID-19.  Researchers also obtained post-mortem myocardial tissues of 59 deceased patients with confirmed SARS-CoV-2 infections, which were confirmed with a qRT polymerase chain reaction (PCR) test.1  These patients also either had active cardiovascular disease or significant risk factors. 

These samples were compared to screen for any potential associations between SARS-CoV-2 infection and altered structure or function of the cardiomyocytes.  Researchers also scanned for alterations in cardiac enzyme levels and other biomarkers, as this could help indicate the inflammatory responses in these patients.  It could also suggest a potential mechanism behind viral entry into the cardiomyocytes..1 

The cardiomyocytes of the COVID-19 patients functioned differently than the control group post-mortem, showing reduced calcium-activated muscle tension and overall weaker force development in vitro.1  Additionally, the COVID-19 patients had elevated activity of a variety of inflammatory biomarkers, including proteases, matrix metalloproteinase (MMP)-2, MMP-9, and cathepsin.  Notably, cathepsin and proteases may help facilitate viral entry of SARS-CoV-2 into host cells.1,7  Finally, when compared to the control group, the COVID-19 patients had increased activity of IL-6 as well as neutrophils, which release proteases and are an important component of the inflammatory response.1

The results of this study suggest an elevated inflammatory response in the COVID-19 patients, and in theory, this could potentially impact the function of cardiomyocyctes.1  More research is needed to determine how, if at all, this response impacts the function of cardiomyocyctes.1  In addition, more research is needed to determine whether this is a common phenomenon that might occur in a larger general population and how to address it.

References

  1. Tangos, M., Budde, H., Koljin, D., et al (2022, May 25). SARS-CoV-2 infects human cardiomyocytes promoted by inflammation and oxidative stress. International Journal of Cardiology 362: 196-205. Doi: 10.1016/j.ijcard.2022.05.055
  2. Sharma, Y.P., Agstam, S., Yadav, A., et al (2021, January). Cardiovascular manifestations of COVID-19: an evidence-based narrative review. Ind J Med Res 153(1-2): 7-16. Doi: 10.4103/ijmr.IJMR_2450_20
  3. Chung, M.K., Zidar, D.A., Bristow, M.R., et al (2021, April 15). COVID-19 and Cardiovascular Disease. Circulation Research 128: 1214-1236. Doi: 10.1161/CIRCRESAHA.121.317997
  4. Shi, S., Qin, M., Shen, B., et al (2020). Association of cardiac injury with mortality in hospitalized patients with COVID-19 in Wuhan, China. JAMA Cardiol 5: 802-810.
  5. Madjid, M., Safavi-Naeini, P., Solomon, S.D., et al (2020). Potential effects of coronaviruses on the cardiovascular system: a review. JAMA Cardiol 5: 831-840.
  6. Lindner, D., Fitzek, A., Brauninger, H., et al (2020). Association of cardiac infection with SARS-CoV-2 in confirmed COVID-19 autopsy cases. JAMA Cardiol 5: 1281-1285.
  7. Characterization of spike glycoprotein of SARS-CoV-2 on virus entry and its immune cross-reactivity with SARS-CoV. Nat. Commun 11: 1620.

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