COVID-19 and Cardiovascular Disease – respiratory syndrome coronavirus

respiratory syndrome coronavirus

Table of Contents


Coronavirus disease 2019 (COVID-19) is a global pandemic affecting 185 countries and >3 000 000 patients worldwide as of April 28, 2020. COVID-19 is caused by severe acute respiratory syndrome coronavirus 2, which invades cells through the angiotensin-converting enzyme 2 receptors. Among patients with COVID-19, there is a high prevalence of the cardiovascular disease, and >7% of patients experience myocardial injury from the infection (22% of critically ill patients). Although angiotensin-converting enzyme 2 serves as the portal for infection, the role of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers requires further investigation. COVID-19 poses a challenge for heart transplantation, affecting donor selection, immunosuppression, and post-transplant management. There are a number of promising therapies under active investigation to treat and prevent COVID-19.

COVID-19, myocardial injury, pandemic, heart transplant


Coronavirus disease 2019 (COVID-19) is a global pandemic. As of April 28, 2020, infected patients were present in 185 countries and there were >3 000 000 cases reported worldwide, with more than 210 000 fatalities.1 The outbreak began in China, but the number of cases outside of China exceeded those in China by March 15, 2020, and rose at an exponential rate. The number of fatalities in several countries now exceeds the total in China. COVID-19 interacts with the cardiovascular system on multiple levels, increasing morbidity in patients with underlying cardiovascular conditions and provoking myocardial injury and dysfunction.

COVID-19 is caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). This novel single-stranded enveloped RNA virus is the 7th known human coronavirus. SARS-CoV-2 is unlike the coronaviruses known to cause the common cold (229E, OC43, NL63, and HKU1), but similar to the zoonotic severe acute respiratory syndrome (SARS) coronavirus (SARS-CoV) from 20022 and the Middle East respiratory syndrome (MERS) coronavirus from 2012.3 SARS-CoV-2 is believed to have originated in bats, similar to many other coronaviruses, because it shares 89% to 96% nucleotide identity with bat coronaviruses.4 Similar to SARS and MERS, it is believed that SARS-CoV-2 moved from bats to an intermediate host (possibly a Malayan pangolin, which shares 91% nucleotide identity) and then to humans5 (Figure 1).

respiratory syndrome coronavirus
Figure 1. Suspected transmission pathway of severe acute respiratory syndrome coronavirus 2 to humans.
SARS-CoV-2 infection is caused by binding of the viral surface spike protein to the human angiotensin-converting enzyme 2 (ACE2) receptor after activation of the spike protein by transmembrane protease serine 2.6 ACE2 is expressed in the lung (principally type II alveolar cells7) and appears to be the predominant portal of entry. ACE2 is highly expressed in the heart as well, counteracting the effects of angiotensin II in states with excessive activation of the renin-angiotensin system, such as hypertension, congestive heart failure, and atherosclerosis.8 In addition to the heart and lung, ACE2 is expressed in the intestinal epithelium, vascular endothelium, and kidneys, providing a mechanism for the multiorgan dysfunction that can be seen with SARS-CoV-2 infection.8,9 There is increasing evidence linking COVID-19 with increased morbidity and mortality from cardiovascular disease (CVD). In this review, we summarize the rapidly evolving data in this field.


COVID-19, caused by SARS-CoV-2, is a global pandemic evolving in real-time. Cardiovascular comorbidities are common in patients with COVID-19 and these patients are at higher risk of morbidity and mortality. It is not known if the presence of cardiovascular comorbid conditions pose independent risk or whether this is mediated by other factors (eg, age). Myocardial injury is present in >25% of critical cases and presents in 2 patterns: acute myocardial injury and dysfunction on presentation and myocardial injury that develops as illness severity intensifies. Continuation of clinically indicated angiotensin-converting enzyme inhibitor and angiotensin receptor blocker medications is recommended based on the available evidence at this time. A number of promising treatments are under investigation, but none with proven clinical efficacy to date.

About KSRA

The Kavian Scientific Research Association (KSRA) is a non-profit research organization to provide research / educational services in December 2013. The members of the community had formed a virtual group on the Viber social network. The core of the Kavian Scientific Association was formed with these members as founders. These individuals, led by Professor Siavosh Kaviani, decided to launch a scientific / research association with an emphasis on education.

KSRA research association, as a non-profit research firm, is committed to providing research services in the field of knowledge. The main beneficiaries of this association are public or private knowledge-based companies, students, researchers, researchers, professors, universities, and industrial and semi-industrial centers around the world.

Our main services Based on Education for all Spectrum people in the world. We want to make an integration between researches and educations. We believe education is the main right of Human beings. So our services should be concentrated on inclusive education.

The KSRA team partners with local under-served communities around the world to improve the access to and quality of knowledge based on education, amplify and augment learning programs where they exist, and create new opportunities for e-learning where traditional education systems are lacking or non-existent.

FULL Paper PDF file:




The authors thank Deborah Burkhoff for graphical support.


Nir Uriel, MD, MSc, Director of New York-Presbyterian Heart Failure, Heart Transplant & Mechanical Circulatory Support Programs, Columbia University Irving Medical Center, Weill Cornell Medicine, 622 West 168th Street, PH4-129, New York, NY 10032. Email 

PDF reference and original file: Click here

Website | + posts

Professor Siavosh Kaviani was born in 1961 in Tehran. He had a professorship. He holds a Ph.D. in Software Engineering from the QL University of Software Development Methodology and an honorary Ph.D. from the University of Chelsea.