COVID-19 and cardiovascular disease - a Research Digest by Brian
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CORONAVIRUS DISEASE 2019 (COVID-19) was first identified in Wuhan, the capital of Hubei, China, in December 2019. To date, it has led to restrictions on the movement and social contact of over a quarter of the world’s total population. Relatively little is known about the interplay between the disease with cardiovascular disease (CVD). Here, I outline what is known about the susceptibility of patients with CVDs to COVID-19, and the likelihood of patients with CVDs succumbing to severe illness.


Disease transmission

COVID-19 IS AN INFECTIOUS DISEASE caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), phylogenetically related to the beta coronavirus SARS that led to a global outbreak in 2002-2004. Viruses belonging to the beta coronavirus family attach to the host receptor angiotensin-converting enzyme 2 (ACE2) present in the lungs. In this way, coronaviruses are able to anchor to the lower respiratory tract. 10-14 days following infection by SARS-CoV-2, patients may suffer from severe viral pneumonia and potentially fatal respiratory failure.1

Prognosis of COVID-19 patients with CVD


A STUDY was conducted based on patient data up to 29th January from 552 hospitals in China. This study investigated the outcomes of 1,099 patients with laboratory confirmation of COVID-19 infection.2They identified the incidence of severe illness using three primary end points – intensive care admission, use of a mechanical ventilator, and death. The study identified that 5% of patients with COVID-19 were admitted to an intensive care unit, 2.3% of patients required a mechanical ventilator, and 1.4% died. Of the 261 patients with coexisting disorders, these three primary end points were identified in 15% (39 patients), much greater than the population without comorbidities. Hypertension was diagnosed in 165 patients, of which 24 patients had the primary end points (14.5%). Strikingly, of the 27 patients with coronary heart disease (CHD), 22% (6 patients) were positive for the primary end points. This provided initial evidence that patients with cardiovascular comorbidities were more likely to suffer from a severe illness.


A MUCH LARGER STUDY identified that among 44,672 patients confirmed to have COVID-19 as of 11th February, 2020, 2,683 patients (12.8%) had hypertension and 873 (4.2%) had CVD. Importantly, 10.5% of patients with CVDs and 6.0% with hypertension died, compared to the 0.9% in patients with no comorbidities.This provides evidence that CVD greatly increases the susceptibility of patients to severe illness.


ALTHOUGH THE EVIDENCE in these studies suggest that there a large number of hospital patients with COVID-19, it is important to consider the limitations in extrapolating this to determine the susceptibility within the general population. Two of the typical symptoms of coronavirus infection, dyspnoea and shortness of breath, are commonly experienced by people with pre-existing CVD. How many people in the community with CVD infected with COVID-19 go undetected because they attribute their symptoms to poor control of their disease? Greater testing of the wider population will help us understand the presence of the virus beyond the hospital inpatients.

Cardiovascular complications of COVID-19


THE STUDIES INDICATE that individuals with underlying CVDs are more susceptible to COVID-19 and these patients are more prone to critical conditions and death. It is well known that acute pulmonary infection, particularly with viral pathogens, can destabilise cardiac disease. Any deterioration of these diseases would, in turn, complicate the management of COVID-19. A local infection to the viral antigens can propagate into a systemic response. In patients with pneumonia, the most frequent causes of death are respiratory failure, sepsis and cardiac arrhythmias.4A study presented by Wang and colleagues showed that of the 138 patients, while 27 (19.6%) had acute respiratory distress syndrome, there was acute cardiac injury in 10 (7.2%) patients.5Although this was stated as being defined as troponin I elevation or new abnormalities on imaging, they did not provide clear classification of echocardiography parameters. 


VIRAL INFECTION can also lead to heart rhythm abnormalities. The study by Wang and colleagues identified that arrhythmia was reported in 23 (16.7%) patients with COVID-19. 5Similar to the echocardiography findings, arrhythmia classification parameters were not clearly outlined by the study. However, if COVID-19 does follow the trends of other beta coronaviruses, then arrhythmias are likely to be a common dysfunction in patients – Yu et al reported that in patients with SARS, tachycardia was present in 71.9% and bradycardia occurred in 14.9% as a transient event. 6


TO DATE, there is limited published data on the features of the myocardium in patients infected with SARS-CoV-2. Future studies must identify, via biopsies, the histological features of the myocardium. Alternatively, cardiac magnetic resonance imaging could provide crucial non-invasive insight into the nature of the cardiac injury in these patients.

CVD medications

AN AREA POORLY UNDERSTOOD but may unlock knowledge about COVID-19 is how does the medication come into the susceptibility and prognosis of disease? As explained, ACE2 is the receptor for the virus. ACE inhibitors and Angiotensin II receptor blockers (ARBs) are favoured medications for treatment of CVDs as well as other comorbidities associated with COVID-19 susceptibility, including diabetes and chronic kidney disease. As these medications increase ACE2 expression, are patients taking these medications daily at an increase risk of contracting the disease? 


COVID-19 HAS EMERGED as an acute infectious disease. However, as it may become a chronic epidemic similar to influenza, even if infections do become controlled, we must prepared for re-emergence of COVID-19 as well as future outbreaks with other coronaviruses.


1.      Xu X, Chen P, Wang J, Feng J, Zhou H, Li X, Zhong W, Hao P. Evolution of the novel coronavirus from the ongoing Wuhan outbreak and modeling of its spike protein for risk of human transmission. Sci China Life Sci2020;63:457–460. 

2.      Guan W-J, Ni Z-Y, Hu Y, Liang W-H, Ou C-Q, He J-X, Liu L, Shan H, Lei C-L, Hui DSC, Du B, Li L-J, Zeng G, Yuen K-Y, Chen R-C, Tang C-L, Wang T, Chen P-Y, Xiang J, Li S-Y, Wang J-L, Liang Z-J, Peng Y-X, Wei L, Liu Y, Hu Y-H, Peng P, Wang J-M, Liu J-Y, Chen Z, et al. Clinical characteristics of coronavirus disease 2019 in China. N Engl J Med2020;1–13. 

3.      Novel Coronavirus Pneumonia Emergency Response Epidemiology Team. The epidemiological characteristics of an outbreak of 2019 novel coronavirus diseases (COVID-19) in China. Zhonghua liuxingbingxue zazhi2020;41:145–151. 

4.      Strålin K, Holmberg H, Mortensen E, Obrosky DS, Fine MJ. Causes of death for patients with community-acquired pneumonia. Arch Intern Med2002;162:2491–2493.

5.      Wang D, Hu B, Hu C, Zhu F, Liu X, Zhang J, Wang B, Xiang H, Cheng Z, Xiong Y, Zhao Y, Li Y, Wang X, Peng Z. Clinical characteristics of 138 hospitalized patients with 2019 novel coronavirus-infected pneumonia in Wuhan, China. JAMA - J Am Med Assoc2020;323:1061–1069. 

6.     Yu CM, Wong RSM, Wu EB, Kong SL, Wong J, Yip GWK, Soo YOY, Chiu MLS, Chan YS, Hui D, Lee N, Wu A, Leung CB, Sung JJY. Cardiovascular complications of severe acute respiratory syndrome. Postgrad Med J2006;82:140–144. 

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Originally published 26 March 2020 , updated 03/04/2020

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