Background and Objectives: Cigarette smoking is a major risk factor for atherosclerosis.Nicotine, a crucial constituent of tobacco, contributes to atherosclerosis development and progression. However, evidence of the association between nicotine and neointima formation is limited. We aimed to evaluate whether nicotine enhances neointimal hyperplasia in the native epicardial coronary arteries of pigs after percutaneous coronary intervention (PCI) with drug-eluting stents (DES). Methods: After coronary angiography (CAG) and quantitative coronary angiography (QCA), we implanted 20 DES into 20 pigs allocated to 2 groups: no-nicotine (n=10) and nicotine (n=10) groups. Post-PCI CAG and QCA were performed immediately. Follow-up CAG, QCA, optical coherence tomography (OCT), and histopathological analyses were performed 2 months post-PCI. Results: Despite intergroup similarities in the baseline QCA findings, OCT analysis showed that the nicotine group had a smaller mean stent and lumen areas, a larger mean neointimal area, greater percent area stenosis, and higher peri-strut fibrin and inflammation scores than the no-nicotine group. In immunofluorescence analysis, the nicotine group displayed higher expression of CD68 and α-smooth muscle actin but lower CD31 expression than the no-nicotine group. Conclusions Nicotine inhibited re-endothelialization and promoted inflammation and NIH after PCI with DES in a porcine model.

Background and Objectives: Cigarette smoking is a major risk factor for atherosclerosis.Nicotine, a crucial constituent of tobacco, contributes to atherosclerosis development and progression. However, evidence of the association between nicotine and neointima formation is limited. We aimed to evaluate whether nicotine enhances neointimal hyperplasia in the native epicardial coronary arteries of pigs after percutaneous coronary intervention (PCI) with drug-eluting stents (DES). Methods: After coronary angiography (CAG) and quantitative coronary angiography (QCA), we implanted 20 DES into 20 pigs allocated to 2 groups: no-nicotine (n=10) and nicotine (n=10) groups. Post-PCI CAG and QCA were performed immediately. Follow-up CAG, QCA, optical coherence tomography (OCT), and histopathological analyses were performed 2 months post-PCI. Results: Despite intergroup similarities in the baseline QCA findings, OCT analysis showed that the nicotine group had a smaller mean stent and lumen areas, a larger mean neointimal area, greater percent area stenosis, and higher peri-strut fibrin and inflammation scores than the no-nicotine group. In immunofluorescence analysis, the nicotine group displayed higher expression of CD68 and α-smooth muscle actin but lower CD31 expression than the no-nicotine group. Conclusions Nicotine inhibited re-endothelialization and promoted inflammation and NIH after PCI with DES in a porcine model.

Background and Objectives: Cigarette smoking is a major risk factor for atherosclerosis.Nicotine, a crucial constituent of tobacco, contributes to atherosclerosis development and progression. However, evidence of the association between nicotine and neointima formation is limited. We aimed to evaluate whether nicotine enhances neointimal hyperplasia in the native epicardial coronary arteries of pigs after percutaneous coronary intervention (PCI) with drug-eluting stents (DES). Methods: After coronary angiography (CAG) and quantitative coronary angiography (QCA), we implanted 20 DES into 20 pigs allocated to 2 groups: no-nicotine (n=10) and nicotine (n=10) groups. Post-PCI CAG and QCA were performed immediately. Follow-up CAG, QCA, optical coherence tomography (OCT), and histopathological analyses were performed 2 months post-PCI. Results: Despite intergroup similarities in the baseline QCA findings, OCT analysis showed that the nicotine group had a smaller mean stent and lumen areas, a larger mean neointimal area, greater percent area stenosis, and higher peri-strut fibrin and inflammation scores than the no-nicotine group. In immunofluorescence analysis, the nicotine group displayed higher expression of CD68 and α-smooth muscle actin but lower CD31 expression than the no-nicotine group. Conclusions Nicotine inhibited re-endothelialization and promoted inflammation and NIH after PCI with DES in a porcine model.

The applicability of the Phoenix criteria and Phoenix Sepsis Score in higher-resource pediatric intensive care units (PICUs) outside the United States requires further validation. A retrospective cohort study analyzed electronic health records of 1,304 PICU admissions under 18 years old with suspected infection between February 2017 and December 2023. The score was calculated using two methods: 24-hour assessment, based on worst sub-scores within 24 hours of admission, and prompt assessment, using values closest to admission within 6 hours before or after. Based on the 24-hour assessment, in-hospital mortality was 8.3% for sepsis and 10.3% for septic shock. The score demonstrated an area under the precision-recall curve of 0.42 (95% confidence interval, 0.31–0.55) for in-hospital mortality. Results were consistent across both assessment methods. The Phoenix criteria and the Phoenix Sepsis Score are reliable predictors of mortality outcomes. Further investigation in diverse clinical settings is warranted.

The applicability of the Phoenix criteria and Phoenix Sepsis Score in higher-resource pediatric intensive care units (PICUs) outside the United States requires further validation. A retrospective cohort study analyzed electronic health records of 1,304 PICU admissions under 18 years old with suspected infection between February 2017 and December 2023. The score was calculated using two methods: 24-hour assessment, based on worst sub-scores within 24 hours of admission, and prompt assessment, using values closest to admission within 6 hours before or after. Based on the 24-hour assessment, in-hospital mortality was 8.3% for sepsis and 10.3% for septic shock. The score demonstrated an area under the precision-recall curve of 0.42 (95% confidence interval, 0.31–0.55) for in-hospital mortality. Results were consistent across both assessment methods. The Phoenix criteria and the Phoenix Sepsis Score are reliable predictors of mortality outcomes. Further investigation in diverse clinical settings is warranted.

The applicability of the Phoenix criteria and Phoenix Sepsis Score in higher-resource pediatric intensive care units (PICUs) outside the United States requires further validation. A retrospective cohort study analyzed electronic health records of 1,304 PICU admissions under 18 years old with suspected infection between February 2017 and December 2023. The score was calculated using two methods: 24-hour assessment, based on worst sub-scores within 24 hours of admission, and prompt assessment, using values closest to admission within 6 hours before or after. Based on the 24-hour assessment, in-hospital mortality was 8.3% for sepsis and 10.3% for septic shock. The score demonstrated an area under the precision-recall curve of 0.42 (95% confidence interval, 0.31–0.55) for in-hospital mortality. Results were consistent across both assessment methods. The Phoenix criteria and the Phoenix Sepsis Score are reliable predictors of mortality outcomes. Further investigation in diverse clinical settings is warranted.

The applicability of the Phoenix criteria and Phoenix Sepsis Score in higher-resource pediatric intensive care units (PICUs) outside the United States requires further validation. A retrospective cohort study analyzed electronic health records of 1,304 PICU admissions under 18 years old with suspected infection between February 2017 and December 2023. The score was calculated using two methods: 24-hour assessment, based on worst sub-scores within 24 hours of admission, and prompt assessment, using values closest to admission within 6 hours before or after. Based on the 24-hour assessment, in-hospital mortality was 8.3% for sepsis and 10.3% for septic shock. The score demonstrated an area under the precision-recall curve of 0.42 (95% confidence interval, 0.31–0.55) for in-hospital mortality. Results were consistent across both assessment methods. The Phoenix criteria and the Phoenix Sepsis Score are reliable predictors of mortality outcomes. Further investigation in diverse clinical settings is warranted.

Background and Objectives: Cigarette smoking is a major risk factor for atherosclerosis.Nicotine, a crucial constituent of tobacco, contributes to atherosclerosis development and progression. However, evidence of the association between nicotine and neointima formation is limited. We aimed to evaluate whether nicotine enhances neointimal hyperplasia in the native epicardial coronary arteries of pigs after percutaneous coronary intervention (PCI) with drug-eluting stents (DES). Methods: After coronary angiography (CAG) and quantitative coronary angiography (QCA), we implanted 20 DES into 20 pigs allocated to 2 groups: no-nicotine (n=10) and nicotine (n=10) groups. Post-PCI CAG and QCA were performed immediately. Follow-up CAG, QCA, optical coherence tomography (OCT), and histopathological analyses were performed 2 months post-PCI. Results: Despite intergroup similarities in the baseline QCA findings, OCT analysis showed that the nicotine group had a smaller mean stent and lumen areas, a larger mean neointimal area, greater percent area stenosis, and higher peri-strut fibrin and inflammation scores than the no-nicotine group. In immunofluorescence analysis, the nicotine group displayed higher expression of CD68 and α-smooth muscle actin but lower CD31 expression than the no-nicotine group. Conclusions Nicotine inhibited re-endothelialization and promoted inflammation and NIH after PCI with DES in a porcine model.

Background and Objectives: Real-world evidence on the relationship between delayed hospitalization and outcomes in myocardial infarction with nonobstructive coronary arteries (MINOCA) is lacking. Hence, we aimed to evaluate the clinical characteristics of patients with MINOCA and the 2-year mortality outcomes in this patient population according to the symptom-to-door time (SDT). Methods: Overall, 861 patients with MINOCA from 2 Korean nationwide observational registries (2011–2020) were included and categorized as early or late presenters. Late presentation was defined as SDT ≥12 hours in patients with ST-segment elevation myocardial infarction (STEMI) and SDT ≥24 hours in patients with non-STEMI. The primary outcome was 2-year all-cause mortality. Propensity score matching (PSM) and age-sex adjusted analysis were used to determine whether late presentation independently affected mortality.Multivariate logistic regression analysis was used to examine the independent factors correlated with late presentation. Results: In unadjusted data, late presenters had a notably higher risk of 2-year all-cause mortality than early presenters (hazard ratio [HR], 2.44; 95% confidence interval [CI], 1.47–4.08). This trend persisted in age-sex adjusted analysis (adjusted HR, 2.29; 95% CI, 1.36–3.84) and PSM-adjusted analysis (adjusted HR, 2.18; 95% CI, 1.05–4.53). The positive independent factors for late presentation included female sex, no emergency medical service use and high creatinine level, whereas the negative independent factor was a dyslipidemia. Conclusions Late presentation is associated with higher mortality in patients with MINOCA.Multidisciplinary efforts are needed to reduce pre-hospital delay, thereby improving the clinical outcomes in these patients.

Background: Atherogenic dyslipidemia, which is frequently associated with type 2 diabetes (T2D) and insulin resistance, contributes to the development of vascular complications. Statin therapy is the primary approach to dyslipidemia management in T2D, however, the role of non-statin therapy remains unclear. Ezetimibe reduces cholesterol burden by inhibiting intestinal cholesterol absorption. Fibrates lower triglyceride levels and increase high-density lipoprotein cholesterol (HDL-C) levels via peroxisome proliferator- activated receptor alpha agonism. Therefore, when combined, these drugs effectively lower non-HDL-C levels. Despite this, few clinical trials have specifically targeted non-HDL-C, and the efficacy of triple combination therapies, including statins, ezetimibe, and fibrates, has yet to be determined. Methods: This is a multicenter, prospective, randomized, open-label, active-comparator controlled trial involving 3,958 eligible participants with T2D, cardiovascular risk factors, and elevated non-HDL-C (≥100 mg/dL). Participants, already on moderate-intensity statins, will be randomly assigned to either Ezefeno (ezetimibe/fenofibrate) addition or statin dose-escalation. The primary end point is the development of a composite of major adverse cardiovascular and diabetic microvascular events over 48 months. Conclusion This trial aims to assess whether combining statins, ezetimibe, and fenofibrate is as effective as, or possibly superior to, statin monotherapy intensification in lowering cardiovascular and microvascular disease risk for patients with T2D. This could propose a novel therapeutic approach for managing dyslipidemia in T2D.