It has become apparent that unlike other coronaviruses, COVID-19 can impact the heart and lead to cardiovascular disease. Individuals with pre-existing heart disease are at greater risk to mortality if infected with COVID-19. Hereby, we review:
- What is known about the link between COVID-19 and the heart?
- COVID-19 and the risk of cardiovascular complications
- Case report of a patient with COVID-19 and myocarditis
What is known about the link between COVID-19 and the heart?
COVID-19 binds angiotensin-converting enzyme 2 (ACE2). ACE2 is widely expressed in the heart and lungs, providing a critical link between COVID-19 and heart disease. Although COVID-19, also known as SARS-CoV-2 shares a close evolutionary link to SARS-CoV (the SARS outbreak of 2003), the diseases they each cause are quite different. Key differences in amino acid residues, in other words slight chemical structural differences, allows COVID-19 to bind the human ACE2 receptor much more strongly than SARS-CoV. The stronger binding affinity of COVID-19 to ACE2 may be the reason it is more pathogenic than SARS-CoV-2.1 Once COVID-19 binds ACE2, there is a loss of ACE2 function.
The ACE2 system has an important protective role against:
- Heart failure
- Myocardial infarction
- Hypertension
- Lung disease
- Diabetes
Loss of ACE2 function due to COVID-19 binding may be the reason patients with heart diseases, diabetes and hypertension are at greater risk of death.
ACE2 has also been linked to gut dysbiosis and vascular permeability; these are important factors in pulmonary hypertension and diabetic cardiovascular disease and complications.1 Therefore, the loss of ACE2 function due to COVID-19 binding may be the reason patients with heart diseases, diabetes and hypertension are at greater risk of death. The descriptive clinical characteristics of COVID-19 have clearly shown that patients with pre-existing cardiovascular disease, hypertension and diabetes are more vulnerable to having severe symptoms if infected with COVID-19.
Does COVID-19 cause cardiovascular complications?
The most commonly reported cardiovascular complication due to COVID-19 has been acute myocardial injury.2 Approximately 8-10% of COVID-19 positive cases develop acute myocardial injury, defined by elevated high-sensitivity cardiac troponin I levels (above the 99th percentile upper reference limit). Cardiovascular complications due to COVID-19 infection can be caused by any of the following mechanisms:
- Systemic inflammation
- Direct myocardial injury
- Insufficient myocardial oxygen supply
- Acute coronary event
- Complications due to COVID-19 treatment
The impact of COVID-19 on the heart can also result from treatment methods used. Cardiovascular complications can also arise from antiviral drugs used to treat COVID-19 infection. Antiviral drugs used to fight COVID-19 infection have been suggested to have cardiotoxicity effects.
COVID-19 and myocarditis case report
There have been numerous cases of COVID-19 and myocarditis. Hereby we review one case report. Hu et al.3 report on a 37 year old male who was admitted to hospital with a 3 day history of chest pain, dyspnea and diarrhea. He had hypotension, cardiac enlargement, and elevated markers of myocardial injury (troponin T, creatine kinase isoenzyme, natriuretic peptide). Chest CT scan demonstrated pulmonary infection and pleural effusion. His sputum was tested for 13 viral nucleic acids; all were negative except for coronavirus. He was diagnosed with coronavirus fulminant myocarditis with cardiogenic shock and pulmonary infection. He was treated with methylprednisone, immunoglobulin, norepinephrine, a diuretic, milrinone, an antibiotic, and pantoprazole. After 7 days, his heart had returned to normal size and function; after 3 weeks, his myocardial injury markers had returned to normal. Some patients infected with COVID-19 may experience heart damage as opposed to only respiratory problems. Practitioners must be able to quickly recognize and effectively manage this presentation of COVID-19 illness.
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Author: Kelly Schoonderwoerd & Nazanin Hakimzadeh
Original articles:
1. Gheblawi et al. Circ Res. 2020 Apr 8.
2. Bansal M. Diabetes Metab Syndr. 2020 May-June; 14(3): 247–250.
