Although we often think of Covid-19 as a respiratory disease, cardiovascular complications are not uncommon.

Myocardial injury based on elevated cardiac troponin levels have been reported in ~20% of patients with Covid-19.^1,2 Among deceased patients with Covid-19 without underlying cardiovascular disease, ~12.0% have been reported to have “substantial heart damage” based on elevated levels of troponins or cardiac arrest.¹  

Arrythmias have also been reported in a significant number of patients (~20.0% in those on invasive mechanical ventilation). ^3,4

Reports of Covid-19-associated acute onset heart failure, myocardial infarction, myocarditis and pericarditis have also appeared in the literature. ^4-6

Proposed mechanisms of acute myocardial injury include direct binding of the virus to ACE2 receptors which are present not only in the lungs but also cardiac endothelial and smooth muscle cells of myocardial vessels as well as in cardiac myocytes. ^1,7,8 Myocardial injury may also be a consequence of Covid-19-related cytokine storm or respiratory insufficiency.¹

Interestingly, patient with heart failure have increased expression of ACE2 which may make them particularly vulnerable to myocardial injury and failure after Covid-19 infection. ⁸

Bonus Pearl: Did you know that a type of perivascular mural cell called “pericyte” makes up a significant part of the myocardium and—in contrast to relatively low expression of ACE2 in cardiac myocytes— expresses ACE2 at high levels, potentially serving as an important target for Covid-19 virus? ⁸

Liked this post? Download the app on your smart phone and sign up below to catch future pearls right into your inbox, all for free!

 References

1. Zheng YY, Ma YT, Zhang JY, et al. Covid-19 and the cardiovascular system. Nature Rev 2020, May. https://www.nature.com/articles/s41569-020-0360-5
2. Yang xz, Yu Y, Xu J, et al. Clinical course and outcomes of critically ill patients with SARS-CoV-2 pneumonia in Wuhan, China: a single-centered, retrospective, observational study. Lancet Respir Med 2020, Feb 24. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7102538/
3. Goyal P, Choi JJ, Pinheiro LC, et al. Clinical characteristics of Covid-19 in New York City 2010. N Engl J Med 2020. DOI: 10.1056/NEJMc2010419 https://www.nejm.org/doi/full/10.1056/NEJMc2010419
4. Covid-19 clinical guidance for the cardiovascular care team. American College of cardiology 2020. https://www.acc.org/~/media/665AFA1E710B4B3293138D14BE8D1213.pdf
5. Hu H, Ma F, Wei X, et al. Coronavirus fulminant myocarditis treated with glucocorticoid and human immunoglobulin. Eur Heart J 2020. https://pubmed.ncbi.nlm.nih.gov/32176300/
6. Hua A, O’Gallaher KO, Sado D. Life-threatening cardiac tamponade complicating myo-pericarditis in Covid-19. Eur Heart J 2020. https://academic.oup.com/eurheartj/article/doi/10.1093/eurheartj/ehaa253/5813280
7. Gallager PE, Ferrario CM, Tallant EA. Regulation of ACE2 in cardiac myocytes and fibroblasts. Am J Physiol heart Circ Physiol 2008;295:H2373-9. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2614534/
8. Chen L, Li X, Chen M, et al. The ACE2 expression in human heart indicates new potential mechanism of heart injury among patients infected with SARS-CoV-2. Cardiovasc Res 2020, March 13. https://academic.oup.com/cardiovascres/article/doi/10.1093/cvr/cvaa078/5813131

Disclosures: The listed questions and answers are solely the responsibility of the author and do not necessarily represent the official views of Massachusetts General Hospital, Harvard Catalyst, Harvard University, its affiliate academic healthcare centers, or its contributors. Although every effort has been made to provide accurate information, the author is far from being perfect. The reader is urged to verify the content of the material with other sources as deemed appropriate and exercise clinical judgment in the interpretation and application of the information provided herein. No responsibility for an adverse outcome or guarantees for a favorable clinical result is assumed by the author. Thank you!