COVID-19: cardiovascular manifestations—a review of the cardiac effects

T he coronavirus first reported in China in November 2002 in the form of atypical pneumonia known as the severe acute respiratory syndrome (SARS). The virus then appeared in 2012 in Saudi Arabia as the Middle East respiratory syndrome (MERS). The year 2020 witnessed a novel β-coronavirus related to the previous detected viruses. It was the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) — a positive single stranded RNA virus. It was suspected that bats were the main reservoir, leading to speculation about possible animal to human transmission. The ongoing COVID-19 pandemic caused by SARSCoV-2 has already infected over 450 million people worldwide and has killed more than 6 millions. The pandemic strained the emergency medical services in many countries and led to an increased mortality. Researchers stated that the virus can spread from large respiratory droplets on contaminated surfaces, aerosol transmission of small respiratory droplets and from symptomatic, asymptomatic and presymptomatic patients. The WHO declared the COVID-19 as a pandemic on March 11, 2020. Coronaviruses are named after the spikes on their surface which form a crownlike dome, and they are known to cause respiratory infections in humans and animals. SARS-CoV-2, in particular, clinical pattern progresses from an early infection (Stage I), pulmonary phase (Stage II) to hyperinflammation (Stage III) and can be lethal. This has created multiple challenges since acute respiratory infections are one of the known triggers for cardiovascular diseases (CVD), and the presence of CVD may complicate and worsen the course of the infectious disease. COVID-19 binds via its spike protein the Spike protein receptor-binding domain to the zinc peptidase angiotensin-converting enzyme 2 (ACE2), which acts as a receptor for the virus. ACE2 is a surface molecule found on vascular endothelial cells, arterial smooth muscle, and cardiac myocytes. When COVID-19 attaches to ACE2 receptors on myocardial cells, it causes their down regulation as well as imbalance of Angiotensin II (AII) and Angiotensin 1-7 (A1-7) which is generated by ACE2; unbalanced AII activity leads to endothelial injury, inflammation exacerbation and known thrombotic consequences seen in COVID-19 in addition to the inflammatory pathways provoked by lung viral invasion. It is well established that COVID-19 has many systemic and respiratory manifestations, including major severe cardiovascular consequences. COVID19 has been shown to cause myocarditis, type 1 myocardial infarction (acute coronary syndrome and spontaneous coronary artery dissection), type 2 myocardial infarction, arrhythmias, micro-angiopathy, disseminated intravascular coagulation, systemic infection and cytokine storm.