Adverse Cardiovascular Events in Patients Infected with SARS-CoV-2
Cardiovascular symptoms have emerged as a less common but particularly dangerous clinical manifestation of SARS-CoV-2 infection, with a high mortality rate [1]. Because SARS-CoV-2 infection can both exacerbate cardiovascular conditions in patients and promote de novo concerns, research points to a bidirectional interaction between the disease and the cardiovascular system [1]. Adverse cardiovascular events documented in a significant number of the infected population include acute myocardial injury, cardiac arrhythmia, and heart failure [1],[2].
Myocardial injury has been documented in 7 to 17% of patients hospitalized due to COVID-19 and independently contributes to high mortality [1],[2]. The condition is characterized by at least one cardiac troponin value past the 99th percentile upper reference limit and may initially present as acute coronary syndrome (ACS) [2]. Its origin is difficult to distinguish: some evidence points to myocardial injury emerging as a result of ischemia, while a multitude of other causes including sepsis, pulmonary embolism, and tachycardia have also been noted [3]. Cardiac tissue analysis has not yet revealed a definite mechanism — while research has found the viral genome in myocardial tissue, SARS-CoV-2 was not consistent with a myocarditis-causing inflammatory reaction [3]. These findings complicate our understanding of the connection between SARS-CoV-2 and myocardial infection, but they do not rule out the possibility that viral infiltration into myocardial tissues may produce adverse long-term effects [3].
Another prominent cardiovascular symptom associated with SARS-CoV-2 infection is cardiac arrhythmia. In one study of 138 hospitalized COVID-19 patients, cardiac arrhythmia was noted in 16.7% of the sample; another study of 137 patients reported heart palpitations in 7.3% of patients [2]. In the ICU, these rates increase further, with 44% of ICU patients in one Wuhan-based study presenting arrhythmia [1]. Some patients with COVID-19 suffered conditions as severe as atrial fibrillation and complete heart block [2]. The association between SARS-CoV-2 and elevated cytokine levels is may explain atrial and ventricular arrhythmia in COVID-19 patients [2]. Hydroxychloroquine and azithromycin, two common treatments for the disease, can also promote pro-arrhythmic events [1]. Due to these associations with cardiovascular comorbidities, myocardial injury, and medications, it is difficult to predict SARS-CoV-2-produced arrhythmia.
Fulminant myocarditis and cardiac arrhythmias, as well as stress-induced cardiomyopathy and acute coronary syndrome (ACS), have resulted in acute heart failure in some COVID-19 patients [4]. One case study of 191 patients placed the incidence of acute heart failure at 23% of all patients and 52% among non-survivors [4]. Especially in elderly patients with reduced diastolic function, heart failure may also be triggered by ACS, high fever, excessive hydration, tachycardia, and impaired renal function [1]. Some researchers recommend the use of pulmonary artery catheters to diagnose and guide therapy in patients suffering or most likely to suffer from cardiogenic and vasodilatory shock [4]. Another suggested approach is using cardiac MRI to detect and monitor changes in patients’ cardiovascular conditions over time [1]. However, these approaches must be further investigated before widespread implementation.
Other common events observed in parallel with SARS-CoV-2 infection include venous thromboembolism, hyperinflammatory shock resembling Kawasaki disease in children, and cardiogenic shock [1]. As noted, the connection between the virus and adverse cardiovascular effects is not entirely understood at the moment, but scientists suspect that ACE2 expression in the human heart may be the essential link [5]. Clinicians are advised to carefully monitor cardiovascular developments while avoiding pro-arrhythmic medications when treating their patients.
References
[1] M. Nishiga, D. W. Wang, Y. Han, D. B. Lewis, and J. C. Wu,”COVID-19 and Cardiovascular Disease: From Basic Mechanisms to Clinical Perspectives,” Nature Reviews Cardiology, vol. 17, no. 1, p. 543-558, July 2020. [Online]. Available: https://doi.org/10.1038/s41569-020-0413-9. [Accessed September 7, 2020].
[2] B. P. Dhakal, N. K. Sweitzer, J. H. Indik, D. Acharya, and P. William, “SARS-Cov-2 Infection and Cardiovascular Disease: COVID-19 Heart,” Heart, Lung, and Circulation, vol. 29, no. 7, p. 973-987, June 2020. [Online]. Available: https://doi.org/10.1016/j.hlc.2020.05.101. [Accessed September 7, 2020].
[3] D. Lindner et al., “Association of Cardiac Infection With SARS-CoV-2 in Confirmed COVID-19 Autopsy Cases,” JAMA Cardiology, July 2020. [Online]. Available: https://doi.org/10.1001/jamacardio.2020.3551. [Accessed September 7, 2020].
[4] A. S. Rali and A. J. Sauer,”COVID-19 Pandemic and Cardiovascular Disease,” US Cardiology Review, vol. 14, no. 1, March 2020. [Online]. Available: https://doi.org/10.15420/usc.2020.14. [Accessed September 7, 2020].
[5] L. Chen et al., “The ACE2 Expression in Human Heart Indicates New Potential Mechanism of Heart Injury Among Patients Infected with SARS-CoV-2,” Cardiovascular Research, vol. 116, no. 6, p. 1097-1100, May 2020. [Online]. Available: https://doi.org/10.1093/cvr/cvaa078. [Accessed September 7, 2020].