COVID-19 has taken centre stage amongst current medical challenges and now with the rollout of vaccines, the world wants to see the light at the end of the tunnel.
Patients with coronavirus disease (severe acute respiratory syndrome) typically present with symptoms and signs of respiratory tract infection, but cardiac manifestations are common.
Putative causes of myocardial injury include myocarditis, hypoxic injury, stress (takotsubo) cardiomyopathy, ischemic injury caused by cardiac microvascular dysfunction, small vessel cardiac vasculitis, endotheliitis, epicardial coronary artery disease (with plaque rupture or demand ischemia), right heart strain (acute cor pulmonale), and systemic inflammatory response syndrome (cytokine storm).
Symptoms and signs of heart disease in a patient with COVID-19 may result from the acute disease process, haemodynamic demands in the setting of pre-existing heart disease or acute exacerbation of chronic disease.
There is substantial evidence of association between pre-existing cardiovascular disease and the risk and severity of COVID-19 infection. Proposed mechanisms include impaired physiologic reserve, impaired immune response, augmented inflammatory response, vulnerability to SARS-CoV-2-induced endothelial dysfunction and effects mediated by the angiotensin-converting enzyme 2 receptor.
Hypercoagulability and thrombosis are postulated to be due to endothelial injury, stasis and changes in the prothrombotic factors.
Clinical presentations
Most patients with COVID-19 with cardiac test abnormalities (e.g. cardiac troponin elevation and ECG abnormalities) lack symptoms of heart disease. Myocardial injury as detected by troponin elevation can be due to myocarditis, stress cardiomyopathy and myocardial infarction. Heart failure may be precipitated by acute illness in patients with pre-existing heart disease, acute hemodynamic stress or acute myocardial injury. Patients with a known history of HF may suffer an acute decompensation due to the development of COVID-19.
Right heart failure secondary to acute cor pulmonale (acute pulmonary embolism or adult respiratory distress syndrome) has been described. Hypercoagulability leading to venous thromboembolism, pulmonary embolism or arterial thrombosis is seen in patients acutely ill with COVID-19. Cardiogenic shock has been described.
Multisystem inflammatory syndrome (MIS) was initially described in children (Kawasaki-like illness). Similar cases of MIS have been described in young to middle-aged adults presenting with fever, gastrointestinal symptoms, shock with vasoplegia, LV systolic dysfunction and elevated inflammatory markers.
Cardiac arrhythmias can be secondary to myocardial injury, hypoxia, shock, electrolyte disturbances and QT-prolonging drugs. Fever can unmask channelopathies such as Brugada and long QT syndrome.
Investigations
Cardiac troponin and natriuretic peptide are commonly elevated among hospitalised patients and are associated with increased risk of mortality noted in studies from Wuhan, Milan and New York. ECG findings include sinus tachycardia, atrial fibrillation, flutter, RBBB, localised ST elevation, T wave inversion, Q waves, ventricular tachycardia and Torsade de pointes. QTc intervals need to be documented and continuous monitoring or regular ECGs done if QT-prolonging drugs are commenced.
Echocardiogram findings include right ventricular dilatation and dysfunction, LV diastolic dysfunction and LV systolic dysfunction. Femoral deep vein thrombosis was found in 12% of patients with right ventricular failure in one study.
Myocardial histology and viral genome analysis can be utilised for diagnosis of inflammatory myocarditis and viral myocarditis. Other investigations relevant to cardiac outcome include metabolic panel, CK, CRP, prothrombin time and D Dimer.
Management
Supportive cardiac care includes management of heart failure, therapy for arrhythmias and avoidance of cardiotoxins. Heart failure patients will need pharmacologic therapy, careful management of fluid balance and advanced therapy. Early treatment with glucocorticoids, especially dexamethasone, has resulted in better outcome in some studies in patients with fulminant myocarditis.
Even though there is speculation that elevated ACE 2 levels caused by renin angiotensin-aldosterone system may impact susceptibility to SARS-Cov-2, there is no evidence so far that treatment with ACE-I or ARBs worsens clinical course, and treatment with them can be continued. Thrombo-prophylaxis is very important due to the hypercoagulability and risk of DVT and PE.
Trials of IL-6 inhibitor Tocilizumab show a mortality benefit in severe COVID-19. Mechanical circulatory support including intra-aortic balloon pump and extracorporeal membranous oxygenation (ECMO) may be needed in some patients.
Appropriate care should be taken during aerosol-generating procedures (e.g. nebulisation, bronchoscopy, intubation and suctioning). Torsades de pointes can be treated with IV magnesium. If the clinical presentation is suggestive of acute coronary syndrome, timely evaluation and intervention is required.
Paracetamol is the preferred antipyretic. Statins and aspirin can be continued. Remdesevir has shown to hasten time to recovery in patients with COVID- 19.
Key messages
- COVID-19 can have many cardiac manifestations
- Management of COVID-19 clinical conditions are evolving and challenging
- Close monitoring is required to determine clinical severity and escalation of treatments.
– Refences available on request
Author competing interests – nil