BNP, Serum Troponin and D-dimer as Risk Factors in Patients With COVID-19

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)