Objective
The role of oxidative stress and inflammation in acute coronary syndrome (ACS) pathophysiology is well established. Bilirubin is the end-product of the heme catabolism including heme oxygenase enzyme which degrades heme leading production of carbon monoxide, Fe+2, biliverdin. As a result of this catabolic process, biliverdin is then converted to an anitoxidant bilirubin by biliverdin reductase. It was shown that bilirubin levels were elevated in acute stress such as acute ST elevation myocardial infarction. The data is scant regarding the serum bilirubin levels in non-ST elevation acute coronary syndrome (NSTE-ACS). In this study, we evaluated the role of serum bilirubin levels in predicting troponin positivity in NSTE-ACS.
Methods
We enrolled 782 patients (mean age 60.4±10.2 years, 61.4 % male) who presented to the emergency service with acute chest pain. Patients were divided into 2 groups based on the troponin positivity. NSTE-ACS patients with troponin positivity were included in group 1 (n:382) and the group 2 consisted of the control patients with negative troponin values (n:400). The serum bilirubin levels (total bilirubin, direct bilirubin) were compared between the group 1 and group 2.
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