Covid-19 is caused by a strain of coronavirus known as Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2). It has become a global pandemic that has impacted the lives of many people.

Studies have shown that SARS-CoV-2 shares many biological features with SARS-CoV, a virus that was the reason of the 2002 outbreak of SARS, including the system of cell entry that is triggered by holding together the viral spike protein to angiotensin-converting enzyme 2. Studies have also spoken of a link between Covid-19 and cardiovascular problems. Pre-existing cardiovascular diseases seem to be linked with worsening of outcomes and in increased death risk in patients with Covid-19. However, Covid-19 itself can also induce myocardial injury, arrhythmia, acute coronary syndrome, and venous thromboembolism.

SARS-CoV-2 is a member of the genus Betacoronavirus like the two other coronaviruses that have caused pandemic diseases (severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV)). As with SARS-CoV and MERS-CoV, SARS-CoV-2 causes a respiratory infection, which leads to viral pneumonia and acute respiratory distress syndrome (ARDS) in some patients.

However, in addition to respiratory symptoms, uncontrolled SARS-CoV-2 infection can trigger a cytokine storm, whereby pro-inflammatory cytokines and chemokines are overproduced by the immune system, resulting in multi-organ damage. Furthermore, Covid-19 causes coagulation abnormalities in a substantial proportion of patients, which can lead to thromboembolic events.

Pathogenic considerations

SARS-CoV-2 is caused by a novel enveloped RNA beta-coronavirus. Direct myocardial injury due to SARS-CoV-2 enters the human cells by binding to angiotensin-converting enzyme 2 (ACE2), a membrane bound aminopeptidase which is highly expressed in the heart and lungs. ACE2 plays an important role in neurohumoral regulation of CV system in normal health as well as in various disease conditions. The binding of SARS-CoV-2 to ACE2 can result in alteration of ACE2 signalling pathways, leading to acute myocardial and lung injury.

Systemic inflammation: More severe forms of Covid-19 are characterised by acute systemic inflammatory response and cytokine storm, which can result in injury to multiple organs leading to multiorgan failure. Studies have shown high circulatory levels of pro-inflammatory cytokines in patients with severe/critical Covid-19.

Altered myocardial demand-supply ratio: Increased cardiometabolic demand associated with the systemic infection coupled with hypoxia caused by acute respiratory illness can impair myocardial oxygen demand-supply relationship and lead to acute myocardial injury.

Plaque rupture and coronary thrombosis: Systemic inflammation as well as increased stress due to increased coronary blood flow can precipitate plaque rupture resulting in acute myocardial infarction. Prothrombotic milieu created by systemic inflammation further increases the risk. Adverse effects of various therapies: Various antiviral drugs, corticosteroids and other therapies aimed at treating Covid-19 can also have deleterious effects on the CV system.

Electrolyte imbalances: Electrolyte imbalances can occur in any critical systemic illness and precipitate arrhythmias, especially in patients with underlying cardiac disorder. There is particular concern about hypokalemia in Covid-19, due to interaction of SARS-CoV-2 with renin-angiotensin-aldosterone system. Hypokalemia increases vulnerability to various tachyarrhythmias.

Although respiratory illness is the dominant clinical manifestation of Covid-19, the sheer burden of the illness implies that a large number of patients with Covid-19 would present with pre-existing CVD or cardiovascular diseases or develop new-onset cardiac dysfunction during the course of the illness. Considering this, the current understanding about the interplay between CVD and Covid-19 is grossly inadequate. It is therefore highly desirable that the future studies on Covid-19 specifically describe the incidence, mechanisms, clinical presentation and outcomes of various CVD manifestations in these patients. The diagnostic and therapeutic challenges posed by the concurrence of these two illnesses also need to be adequately studied.

(The author is an interventional cardiologist)