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Introduction: Impact on clinical outcome of the patient with calcified nodule remain unknown. Calcified nodule may cause suboptimal stent expansion, stent mal-apposition. Hypothesis: We hypothesized that the presence of calcified nodule in the heavy calcified lesion undergoing rotablator atherectomy (RA) assisted percutaneous coronary intervention (PCI) increased device-oriented composite endpoint (DoCE). Methods: We retrospective reviewed consecutives patient with heavy calcified lesion underwent RA assisted intravascular ultrasound (IVUS) guidance PCI between August 2016-April 2020. Pre-procedural IVUS imaging was mandatory. Calcified nodule was defined as convex shape of luminal surface and luminal side of calcium with protruding in the coronary artery lumen that assessed by IVUS. Primary outcome was cumulative 5-year composite device-oriented composite endpoint (DoCE), define as composite of CV death, myocardial infarction and clinically-driven target lesion revascularization (CDTLR). Results: Two-hundred consecutives patient with heavy calcified lesion underwent RA assisted intravascular ultrasound (IVUS) guidance PCI was enrolled. Calcified nodule was found in 87 patients (43.5%) with heavily calcified lesions. Cumulative 5-year DoCE was significantly higher in the presence of calcified nodule group than in the non-calcified nodule group (20.7% vs 8.8%, P=0.02). Calcified nodule group has the higher incidence of under-expansion and asymmetrical expansion of stent. The patient who had calcified nodule with eccentric calcification has significantly higher cumulative 5-year DoCE compared to calcified nodule with concentric calcification (p Conclusions: The presence of calcified nodule in the heavily calcified lesion underwent RA assisted PCI increased with cumulative 5-year DoCE.

Background Indoleamine 2,3 dioxygenase (IDO), the rate-limiting enzyme in in the kynurenine (Kyn) pathway of tryptophan (Trp) degradation, is modulated by inflammation and regarded as a key molecule driving immunotolerance and immunosuppressive mechanisms. This response accelerates the resolution of inflamed tissues to protect them against collateral damage and facilitate tissue healing. A growing body of evidence indicates that IDO-mediated Trp metabolism is involved directly or indirectly in atherogenesis. Little is known about IDO activity in patients with active coronary artery disease (CAD). Purpose We hypothesized that IDO activity as reflected by Kyn/Trp ratio and Kyn levels correlated with coronary artery disease (CAD) severity and predicted 1-year major adverse cardiac events (MACE). Method We prospectively enrolled the patients whom underwent coronary angiography in our institute. We excluded the patients whom might have other non-cardiac causes of elevated inflammatory biomarkers such as rheumatoid arthritis, allergic asthma, and so on. Measurements of IDO, hs-troponin and hs-CRP levels were performed at baseline and IDO activity was monitored every 6 month at interval. Baseline demographic, coronary angiogram/interventions data were recorded. Significant CAD defined as >70% stenosis in major epicardial vessel. Patients were followed up for 1-year. MACE were pre-specified. Results Three-hundred and five patients were enrolled. Ninety-eight patients (32%) presented with acute coronary syndrome. There was a significant difference in IDO, kynurenine, and hs-troponin between patients with and without significant CAD (Table 1). In addition, baseline IDO activity, kynurenine and hs-troponin levels were significantly higher in significant CAD patients with 3-vessel, 2-vessel and 1-vessel involvements than those with insignificant CAD; (0.17 vs 0.14 vs 0.14 vs 0.04, p Conclusion Immunometabolic response mediated through IDO function were enhanced in patients with CAD and correlated with the severity and extent of the disease. Patient with inadequate IDO response had a higher 1-year mortality. Funding Acknowledgement Type of funding source: Public Institution(s). Main funding source(s): The Siriraj grant for research development and medical education of the Faculty of Medicine Siriraj Hospital

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 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”.