Characteristics and Pattern of Calcified Nodule and/or Nodular Calcification Detected by Intravascular Ultrasound on the Device-Oriented Composite Endpoint (DoCE) in Patients with Heavily Calcified Lesions Who Underwent Rotational Atherectomy-Assisted Percutaneous Coronary Intervention.

Objectives: This study aimed to determine characteristics and pattern of a calcified nodule (CN) and/or nodular calcification (NC) detected by intravascular ultrasound (IVUS) on the device-oriented composite endpoint (DoCE) in patients with calcified lesions who underwent rotational atherectomy (RA)-assisted percutaneous coronary intervention (PCI). Background: The characteristics and pattern of a CN and/or NC on clinical outcome remain unknown. Methods: We retrospectively enrolled patients who underwent RA-assisted PCI at Siriraj Hospital during August 2016 to April 2020. Preprocedural IVUS imaging was mandatory. CN/NC was defined as convex shape of luminal surface and luminal side of calcium with protrusion into the coronary artery lumen as assessed by IVUS. The primary outcome was cumulative of DoCE, defined as the composite of cardiovascular death, myocardial infarction, and clinically-driven target lesion revascularization. Results: Two hundred patients were included. Primary outcome occurred in 14%. The cumulative DoCE was significantly higher in the CN/NC group than that in the non-CN/NC group (20.7% vs. 8.8%, p = 0.022). CN/NC (p = 0.023) and MSA ≤ 5.5 mm2 (p = 0.047) were correlated with a significantly higher cumulative DoCE. CN/NC was the independent predictor for the cumulative DoCE (HR = 2.96, 95% CI 1.08-8.11, p = 0.035). Pattern and characteristic of CN/NC have a prognostic value. Patients with an eccentric CN/NC had a significantly higher cumulative DoCE compared to those CN/NC with concentric calcification (p = 0.014). Conclusion: The presence of a CN/NC in patients with heavily calcified lesions who underwent RA-assisted PCI was found to be associated with increased cumulative 5 year DoCE, especially in patients with an eccentric CN/NC. The clinical trial is registered with TCTR20210616001.

Indoleamine 2,3 dioxygenase (IDO) level as a marker for significant coronary artery disease.

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".