Abstract

Introduction: High-sensitivity cardiac troponin I (hs-cTnI) assays provide comparable diagnostic information that allow for better detection of myocardial injury. However, hs-cTnI release after cardiac stress testing and its potential utility for identifying inducible myocardial ischemia and risk-stratification are unclear. Aim: This pilot study examined integrating hs-cTnI biomarker testing into cardiac imaging stress testing to improve detection of inducible ischemia and aid in risk-stratification in patients with chest pain being evaluated for acute coronary syndrome (ACS). Methods: We prospectively enrolled 200 consecutive adult patients referred by the Emergency Room for cardiac stress testing for evaluation of possible ACS. A venous blood sample was collected between 0.5 and 2 hours post stress testing; cTnI concentrations were measured in-house by high sensitivity methods. Changes from pre-stress test hs-cTnI concentrations were calculated and association with outcome was explored using a logistic regression model. Results: Patient median age was 62 years, IQR 54-70; 49% were women. ACS known risk factors included hypertension 81.5%, cigarette smoking 49.5% and diabetes 33.5%. Median BMI was 31.63 kg/m 2 , IQR 27.24-35.84. Pre-stress test hs-cTnI median levels were 6 ng/L, IQR 5-9, for women (URL <52 ng/L) and 8 ng/L, IQR 6-12, for men (URL <77 ng/L). A total of 121 patients (60.5%) underwent nuclear stress tests, and 79 (39.5%) received echocardiographic stress tests. Of the 191 samples analyzed, 36% revealed increased hs-cTnI levels from pre-stress test values: 33% in nuclear stress tests (median increase 2 ng/L, IQR 1-5), 41% in echocardiographic stress tests (median increase 2 ng/L, IQR 1-5). In the 155 patients with 6 months of follow-up, changes in post-stress test hs-cTnI levels were not significantly correlated to stress test results, percutaneous coronary interventions or death (p=.85). Conclusion: This study provides insight into the potential of hs-cTnI to aid in identifying inducible myocardial ischemia in a real-world, high-throughput setting. Although a subset of patients exhibited modest increases in hs-cTnI post stress testing, overall, these did not appear to be correlated with inducible myocardial ischemia.

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