Post COVID-19 Coronary Implications

The interaction between the viral spike (S) protein and angiotensin-converting enzyme 2(ACE2) is likely to be involved in the cardiovascular manifestations of COVID-19. The primary function of ACE2 as a peptidase is the metabolism of angiotensin II (ANG II) to angiotensin 1-7 (ANG-(1-7)). The binding of ACE2 to SARS-CoV-2 prevents metabolism and leads to an increased ANG II to ANG-(1-7) ratio, which is detrimental to cardiac function. ACE2 peptidase is expressed in type II alveolar cells, stratified epithelial cells of the upper airway and esophagus, enterocytes of the ileum and colon, myocardial cells, vascular endothelial cells, proximal tubules of the kidney, and urothelial cells. This explains the multi-organ involvement of this infection far beyond the alveolar cells of the lungs, including the cardiovascular system. Future research will undoubtedly be needed to fully understand the long term implications of COVID-19 cardiac effects.

Listed below are the possible cardiovascular abnormalities and manifestations associated with them:

Acute cardiac injury: Identified by significantly elevated levels of cardiac troponins. It is the most commonly reported cardiac abnormality in COVID-19. High-sensitivity troponin I was significantly elevated in over half of fatal COVID-19 cases. Direct myocardial injury due to viral involvement of cardiomyocytes and the effect of systemic inflammation appear to be the most common mechanisms responsible for cardiac injury (Nishiga, M et.al 2020).

Myocarditis: Myocarditis is identified by segmental wall motion abnormality or reduced left ventricular ejection fraction. In patients where ECG/EKG did not have these typical signs, suggesting that observed myocardial injury was secondary to systemic causes rather than direct effect on heart due to viral infection. (Nishiga, M et.al 2020).

Acute coronary syndrome: Although the mechanism underlying covid-19 induced ACS might involve plaque rupture, coronary spam or thrombi due to systemic inflammation or cytokine storm, ACS is observed in individuals even without the presence of substantial systemic inflammation. Direct endothelial or vascular injury caused by SARS-CoV-2 infection might also increase the risk of thrombus formation and ACS (Varga, Z. 2020). Acute myocardial injury and ACS triggered by COVID-19 can also aggravate pre-existing heart disease or provoke contractile dysfunction. Stress- induced cardiomyopathy or cytokine- related myocardial dysfunction, can be triggered in advanced covid-19 as seen with sepsis- associated cardiac dysfunction due to increased immune response towards infection. (Fried, J.A 2020) (Prabhu, 2004).

Heart Failure: Heart failure (HF) is a clinical syndrome caused by structural and functional defects in myocardium resulting in impairment of ventricular filling or the ejection of blood (Inamdar, A.A 2016). Elevated level of amino- terminal pro- B- type natriuretic peptide was observed, indicating of increased pressure on heart (Nishiga, M et.al 2020). In particular, elderly patients with reduced diastolic function might develop heart failure, which can be triggered by high fever, tachycardia, excessive hydration and impaired renal function.

Arrhythmia and sudden cardiac arrest: Arrhythmias and sudden cardiac arrest are common manifestations of COVID-19. Heart palpitations are reported to be the main presenting symptom of COVID-19 in patients without a fever or cough. Elevated levels of troponin T were more likely to develop malignant arrhythmias 24. It is hypothesized that myocardial injury, systemic causes such as fever, sepsis, hypoxia and electrolyte abnormalities can cause cardiac arrhythmias (Nishiga, M et.al 2020).

Coagulation abnormalities and thrombosis: COVID-19 is associated with coagulation abnormalities, which can result in thromboembolic events. Patients with COVID-19 often have elevated levels of d- dimer indicating reduced platelet counts and slightly prolonged prothrombin time. Higher level of d-dimer is directly associated with severity of covid-19. High levels of fibrinogen and factor VIII, in COVID-19 patients indicate a hypercoagulable state. Coagulation abnormalities might contribute to the development of the diverse cvd manifestations of covid-19. Venous thromboembolism, which includes deep vein thrombosis and pulmonary embolism, is a common complication in critically ill patients with COVID-19 (Nishiga, M et.al 2020).

The majority of the COVID-19 patients suffering from cardiovascular complications show a significant elevation of cTnI, NT-proBNP and interleukin-6 (IL-6) or other cytokines [IL1B, IL1RA, IL7, IL8, IL9, IL10, C-X-C motif chemokine 10 (CXCL10), chemokine (C-C motif) ligand 2 (CCL2), granulocyte-macrophage colony-stimulating factor (GM-CSF), and tumor necrosis factor-α (TNF-α)] in their blood stream.