Abstract
We hypothesize that hypoxanthine (HX) is an early biomarker of ischemia. Our goal was to assess early HX values in patients presenting with acute chest pain (ACP) and late troponin elevation (n=27) compared to those with known coronary artery disease (CAD) presenting for elective CABG (n=10) and normal controls without known CAD (n=24). Methods: In a retrospective manner after IRB approval was obtained, we examined residual plasma for HX in 27 patients presenting to the emergency room with troponin samples requested by the clinician as per routine clinical practice. Patients with a non diagnostic troponin level for myocardial infarction (MI) at the time of presentation but who subsequently ruled in for MI (troponin of > .39 μg/L) were included in the study. Significant differences between the groups was determined using a standard t test. Results: Initial sample results for the ACP patient group who subsequently ruled in for MI by troponin show a mean troponin of 0.07+/-0.014(SEM)μg/L and a mean HX level of 27.38 +/- 3.53 μM compared to normal controls whose mean HX was 4.03 +/- 0.32 μM (p<.05). Ten patients without ACP presenting for elective CABG had a mean HX of 5.09+/- 0.67 μM. In the figure below, we demonstrate that HX is elevated in ACP patients who on subsequent sampling rule in by troponin criteria for MI. Reported HX levels in normal volunteers are approximately 3.5 μM consistent with our controls. Conclusion: HX is elevated prior to troponin elevation in patients presenting with ACP that subsequently rule in for MI by troponin criteria. These levels were elevated relative to normal control patients as well as in 10 patients with known CAD without ACP presenting for elective CABG. Therefore, HX is potentially an early maker of ischemia in the acute clinical setting.
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