What is the impact of coronavirus on the heart?
A novel coronavirus, initially named 2019-nCoV, caused the outbreak of pneumonia in December 2019 in Wuhan, China. The virus was renamed “severe acute respiratory syndrome coronavirus 2” (SARS-CoV-2) by the WHO and is now known as COVID-19. Compared to the SARS-CoV that caused SARS in 2003, SARS-CoV-2 has a stronger transmission capacity. On 30 January 2020, the WHO officially pronounced a Public Health Emergency of International Concern. On 11 March 2020, the WHO decreed the outbreak to be a pandemic. While COVID-19 infection manifests primarily as respiratory symptoms, severe, life-threatening cardiovascular damage is also being noted.
Role of ACE2
Angiotensin-converting enzyme 2 (ACE2) has been identified as a receptor for coronaviruses. Specifically, the spike protein of the virus binds to ACE2 (which is highly present in heart and lungs). Respiratory symptoms resulting from invasion of lung alveolar cells by COVID-19 are worse in patients with cardiovascular disease. Since ACE2 levels can be increased by renin-angiotensin-aldosterone system inhibitors, their continued use in patients with COVID-19 may not be advisable.
Acute cardiovascular symptoms after coronavirus infection
The incidence of cardiovascular symptoms in patients with COVID-19 seems to be high. In fact, some of the infected patients presented initially with heart palpitations and chest tightness (as opposed to respiratory symptoms). This is thought to be due to the systemic inflammatory response and immune system disorders during disease progression. ACE2-related signalling pathways are suspected to play a role in heart injury. In Wuhan, of the first 41 patients diagnosed with COVID-19, 5 showed signs of myocardial injury. Furthermore, 4 out of these 5 patients showed elevated blood pressure (mean systolic blood pressure of 145 mmHg) and increased troponin levels (hs-cTnl >28pg/ml).
Chronic cardiovascular symptoms
The risk of sustaining myocardial damage secondary to COVID-19 infection is not restricted to the acute phase. Patients who recovered from SARS-CoV had evidence of cardiovascular effects 12 years after acute illness. These included hyperlipidemias, “cardiovascular system abnormalities” and impaired glucose metabolism. Given the structural similarity between the two viruses, it is possible that chronic cardiovascular damage might also follow COVID-19 infection.
Pre-existing cardiovascular disease
There exists additional risk for those with pre-existing cardiovascular conditions. Elderly people with comorbidities such as hypertension, coronary artery disease and diabetes are more likely to be infected with SARS-CoV-2. Patients with acute coronary syndrome (ACS) infected with SARS-CoV-2 show a poorer prognosis. In these patients, cardiac functional reserve can be reduced owing to myocardial ischemia or necrosis. When infected with SARS-CoV-2, cardiac insufficiency is more likely to occur. The patients in Wuhan who had previous ACS suffered more severe illness and had a higher mortality rate. Patients with cardiovascular disease account for a large proportion of deaths from COVID-19.
Antivirals and cardiotoxicity
Drug-related heart damage during COVID-19 treatment is also a concern. In a study of 138 patients with COVID-19, 89.9% were given antiviral drugs. However, these drugs can cause cardiac insufficiency, arrhythmia or other cardiovascular disorders. Therefore, patients who are given antivirals must be closely monitored for cardiotoxicity.
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Author: Kelly Schoonderwoerd
Original Article: Zheng et al. Nat Rev Cardiol. 2020 Mar 5.
