Background: Acute changes in high-sensitivity troponin T (hs-TnT) are induced by myocardial ischemia during exercise stress testing, but there are no reports of pharmacological stress testing. Hypothesis: The pattern of troponin release by myocardial ischemia-induced pharmacological stress testing differs according to the ischemic burden in stable patients. Methods: In total, 250 patients with suspected coronary artery disease underwent pharmacological stress magnetic resonance imaging (MRI). The amount and degree of myocardial ischemia on MRI and ischemic outcomes at 6 months were determined. hs-TnT levels were measured at baseline and 1 and 3 hours after testing. The 6-month clinical outcome was prespecified. Results: Fifty-one patients had moderate to severe myocardial ischemia (group A), and 199 patients had no or mild myocardial ischemia (group B). hs-TnT levels were significantly higher in group A than B at baseline (11 vs 8 pg/mL, P = 0.016) and at 1 hour (12 vs 8 pg/mL, P = 0.009) and 3 hours after testing (12 vs 9 pg/mL, P = 0.012). Baseline hs-TnT levels of ≥14 pg/mL showed a 43% sensitivity and 77% specificity in predicting moderate to severe ischemia by MRI (P = 0.03; area under the curve: 0.608, P = 0.017). Patients administered dobutamine had a higher acute change in hs-TnT levels 3 hours after testing than did those administered adenosine (21 vs 0 pg/mL, P < 0.001). There was a trend toward a higher incidence of myocardial infarction in patients with baseline hs-TnT levels of ≥14 pg/mL. Conclusions: hs-TnT levels are significantly higher in patients with moderate to severe than no or mild myocardial ischemia.

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Background Indoleamine 2,3 dioxygenase (IDO), the rate-limiting enzyme in the kynurenine (Kyn) pathway of tryptophan (Trp) degradation, is modulated by inflammation, and is regarded as a key molecule driving immunotolerance and immunosuppressive mechanisms. Little is known about IDO activity in patients with active coronary artery disease (CAD). Methods We prospectively enrolled patients who were scheduled to undergo coronary angiography. Measurement of IDO, high-sensitivity troponin T (hs-TnT), and high-sensitivity C-reactive protein (hs-CRP) levels was performed at baseline, and IDO activity was monitored at the 6-month follow-up. Results Three hundred and five patients were enrolled. Ninety-eight patients (32.1%) presented with recent acute coronary syndrome (ACS). Significant difference in IDO, kynurenine, and hs-TnT between patients with and without significant CAD was observed. Baseline IDO activity, kynurenine level, and hs-TnT level were all significantly higher in significant CAD patients with 3-vessel, 2-vessel, and 1-vessel involvement than in those with insignificant CAD [(0.17, 0.13, and 0.16 vs. 0.03, respectively; p = 0.003), (5.89, 4.58, and 5.24 vs. 2.74 µM/g, respectively; p = 0.011), and (18.27, 12.22, and 12.86 vs. 10.89 mg/dL, respectively; p < 0.001)]. One-year mortality was 3.9%. When we compared between patients who survived and patients who died, we found a significantly lower prevalence of left main (LM) disease by coronary angiogram (6.1% vs. 33.3%, p = 0.007), and also a trend toward higher baseline kynurenine (5.07 vs. 0.79 µM/g, p = 0.082) and higher IDO (0.15 vs. 0.02, p = 0.081) in patients who survived. Conclusion Immunometabolic response mediated via IDO function was enhanced in patients with CAD, and correlated with the extent and severity of disease. Patients with LM disease had higher 1-year mortality. Lower level of IDO, as suggested by inadequate IDO response, demonstrated a trend toward predicting 1-year mortality. Trial registration TCTR Trial registration number TCTR20200626001. Date of registration 26 June 2020. “Retrospectively registered”.

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