Coronavirus disease-2019 (COVID-19), a contagious novel coronavirus now called severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2; formerly called 2019-nCoV).~Cardiac injury is a common condition among the hospitalized patients with COVID-19. It t was recently reported that 19.7% patients with COVID-19 had cardiac injury with more adverse clinical outcomes compared to those without cardiac injury (Shi S, et al, 2020) Fulminant myocarditis due to direct viral infection can certainly occur, but in patients with increased oxygen demands due to tachycardia and fever and reduced oxygen delivery due to hypotension and hypoxemia, COVID 19 disease can cause myocardial injury indirectly. Cytokines released during the acute infection can elicit activation of cells within pre-existing atherosclerotic lesions, augmenting thrombotic risk and risk of ischemic syndromes. Moreover, microvascular activation by cytokines can cause not only myocardial injury but can also harm other organ systems commonly involved in COVID-19 infections including the kidneys.(Peter,2020) Treatment in intensive care units (ICU) has become a major challenge; therefore, early recognition of severe forms is absolutely essential for timely triaging of patients. Several laboratory parameters may facilitate the assessment of disease severity. The recognized risk factors such as old age and underlying comorbidities-particularly cardiovascular diseases, diabetes, respiratory diseases, and other conditions (Zhou et al,2020) Several markers have been identified that modulate the course of COVID-19. The heart failure marker, N terminal pro B type natriuretic peptide (NT-proBNP), increased significantly during the course of hospitalization (Guo T, et al ,2020) The sensitivity of cardiac troponin testing that ensures it is one of the earliest and most precise indicators of end organ dysfunction. Cardiac troponin testing could prompt early initiation of measures to improve tissue oxygenation and perfusion.~COVID-19 infection is associated with intra-alveolar fibrin deposition, leading to lethal respiratory failure; reports suggesting that anticoagulation or fibrinolytic therapy can improve clinical outcomes (Wang J, et Al , 2020) ; case series implying that large percentages of severely affected COVID-19 patients suffer clinically significant thrombosis (Porfidia A , et al ,2020)
To evaluate the role of N terminal pro B type natriuretic peptide (NTproBNP), D-Dimer, and Troponin - I as risk factors in COVID-19 patients and to correlate these markers with in-hospital death in patients with COVID-19