**12. Coronavirus and thromboembolic problems**

The patients with COVID 19 have shown a higher risk of forming arterial and venous thrombus and embolic complications. The patient with severe clinical infection shows the neurological components and the increment level of the D – dimer values, indicating that thromboembolic complications increase mortality among the COVID 19 patients. Among thromboembolic difficulties, VTE (Venous Thromboembolic complication) was a common problem in hospitalized patients [32].

## **13. Potential mechanisms of SARS-CoV-2-instigated endothelial injury**

The organ damage from the coronavirus was mainly related to the inflammatory response; the stimulation of the inflammatory mediator such as cytokine leads to endothelial injury. The virus damages the endothelial cell, directly and indirectly, leading to the endothelial cell's dysfunction and the formation of the clots. Endothelial cell damage increases the permeability of the cell membrane, leading to complications such as acute respiratory distress syndrome and pulmonary fibrosis and pulmonary edema, which is not related to the cardiac problem but due to the increase in vascular permeability. Thus, endothelial injury due to the COVID virus can affect the patient's respiratory function and impacts the patient's recovery [33].

#### **14. Myocardial injury related with COVID-19**

There are different types of cardiovascular problems observed in the patient of COVID-19. The issues include congestive cardiac heart failure, dysrhythmia, cardiogenic shock, myocardial infarction, and myocarditis. The studies also stated that the diagnostic studies related to cardiac system problems such as cardiac injury in COVDI-19 patients indicated a positive test of Troponin T, changes in the ECG, and 2d echo. The pathogenesis of the myocardial injury is indescribable in the situation of COVID 19. Due to the viral infection, the inflammatory mediator triggers the inflammatory process, leading to the rupture of the plaque and development of the thrombus and ending in atherosclerotic diseases. The production of the inflammatory mediator comprises of cytokine causes instability in the plaque results in atherosclerosis, and myocardial dysfunction shows clinical conditions like inflammation of myocardium and cardiomyopathy [33].

Apart from this, essential risk factors such as smoking, obesity, hypertension, diabetes, etc., cause atherosclerosis. It increases the viral load in circulation causes hypoxemia and unusual hemodynamic changes in patients with COVID-19. This mechanism probably acts in corresponding to cause the damage to the cardiovascular system, leads myocardial infarction, ventricular arrhythmias, and congestive cardiovascular failure. Viral infection also affects the respiratory system, which reduces the oxygen levels in the blood. This process alters the hemodynamic parameters, including saturation level, blood pressure changes, leading to cardiovascular complications and atherosclerosis plaque formation. This process of pathogenesis causes significant cardiac damage and significant complications such as myocardial infarction, dysrhythmias, and the cardiac failure [34].
