Asians have a much lower incidence of adverse coronary events than Caucasians. We sought to evaluate the characteristics of coronary lipid-rich plaques (LRP) in Asian patients with acute coronary syndrome (ACS) and stable angina (SA). We also aimed to identify surrogate markers for the extent of LRP. We evaluated 207 patients (ACS, n = 75; SA, n = 132) who underwent percutaneous coronary intervention under near infrared spectroscopy intravascular ultrasound (NIRS-IVUS). Plaque characteristics and the extent of LRP [defined as a long segment with a 4-mm maximum lipid-core burden index (maxLCBI4mm)] on NIRS in de-novo culprit and non-culprit segments were analyzed. The ACS culprit lesions had a significantly higher maxLCBI4mm (median [interquartile range (IQR)]: 533 [385–745] vs. 361 [174–527], p < 0.001) than the SA culprit lesions. On multivariate logistic analysis, a large LRP (defined as maxLCBI4mm ≥ 400) was the strongest independent predictor of the ACS culprit segment (odds ratio, 3.87; 95% confidence interval, 1.95–8.02). In non-culprit segments, 19.8% of patients had at least one large LRP without a small lumen. No significant correlation was found between the extent of LRP and systematic biomarkers (hs-CRP, IL-6, TNF-α), whereas the extent of LRP was positively correlated with IVUS plaque burden (r = 0.24, p < 0.001). We confirmed that NIRS-IVUS plaque assessment could be useful to differentiate ACS from SA culprit lesions, and that a threshold maxLCBI4mm ≥ 400 was clinically suitable in Japanese patients. No surrogate maker for a high-risk LRP was found; consequently, direct intravascular evaluation of plaque characteristics remains important.

Background:Cerebrovascular disease often coexists with coronary artery disease (CAD), and it has been associated with worse clinical outcomes in CAD patients. However, the prognostic effect of prior stroke on long-term outcomes in patients with acute coronary syndrome (ACS) is still unclear.Methods and Results:An observational cohort study of ACS patients who underwent emergency percutaneous coronary intervention (PCI) between January 1999 and May 2015 was conducted. Patients were divided into 2 groups according to their history of stroke. We evaluated both all-cause death and cardiac death. Of the 2,548 consecutive ACS patients in the current cohort, 268 (10.5%) had a history of stroke at the onset of ACS. Patients with a history of stroke were older and had a higher prevalence of comorbidities such as hypertension or renal deficiency. The cumulative incidences of all-cause death and cardiac death were significantly higher in patients with a history of stroke (both log-rank P<0.0001). Multivariate Cox hazard regression analysis showed that a history of stroke was significantly associated with the incidences of all-cause death (hazard ratio [HR] 1.49, 95% confidence interval [CI] 1.20–1.85, P=0.0004) and cardiac death (HR 1.41, 95% CI 1.03–1.93, P=0.03).Conclusions:About 10% of the ACS patients had a history of stroke and had worse clinical outcomes.

Background: In‐stent restenosis, especially for neoatherosclerosis, is a major concern following percutaneous coronary intervention. This study aimed to elucidate the association of features of in‐stent restenosis lesions revealed by optical coherence tomography (OCT)/optical frequency domain imaging (OFDI) and the extent of lipid‐rich neointima (LRN) assessed by near‐infrared spectroscopy (NIRS) and intravascular ultrasound, especially for neoatherosclerosis. Methods and Results: We analyzed patients undergoing percutaneous coronary intervention for in‐stent restenosis lesions using both OCT/OFDI and NIRS–intravascular ultrasound. OCT/OFDI‐derived neoatherosclerosis was defined as lipid neointima. The existence of large LRN (defined as a long segment with 4‐mm maximum lipid core burden index ≥400) was evaluated by NIRS. In 59 patients with 64 lesions, neoatherosclerosis and large LRN were observed in 17 (26.6%) and 21 lesions (32.8%), respectively. Naturally, large LRN showed higher 4‐mm maximum lipid core burden index (median [interquartile range], 623 [518–805] versus 176 [0–524]; P <0.001). In OCT/OFDI findings, large LRN displayed lower minimal lumen area (0.9±0.4 versus 1.3±0.6 mm ² ; P =0.02) and greater max lipid arc (median [interquartile range], 272° [220°–360°] versus 193° [132°–247°]; P =0.004). In the receiver operating characteristic curve analysis, 4‐mm maximum lipid core burden index was the best predictor for neoatherosclerosis, with a cutoff value of 405 (area under curve, 0.92 [95% CI, 0.83–1.00]). In multivariable logistic analysis, only low‐density lipoprotein cholesterol (odds ratio, 1.52 [95% CI, 1.11–2.08]) was an independent predictor for large LRNs. Conclusions: NIRS‐derived large LRN was significantly associated with neoatherosclerosis by OCT/OFDI. The neointimal characterization by NIRS–intravascular ultrasound has potential as an alternative method of OCT/OFDI for in‐stent restenosis lesions.

Purpose Asians often face the problems of clopidogrel resistance and East Asian paradox. This study aimed to evaluate the effects of P2Y₁₂ inhibitors, including low-dose prasugrel 2.5 mg, on the P2Y₁₂ reaction unit (PRU) in the chronic phase after percutaneous coronary intervention (PCI). Methods A total of 348 patients were studied. PRU was measured 6–12 months after PCI and subsequently, 6 months later using a P2Y₁₂ assay, respectively. This study evaluated the proportion of bleeding risk (PRU ≤ 85) and ischemic risk (PRU ≥ 239) as primary endpoints, and the prediction of bleeding risk and ischemic risk using multivariable logistic regression analysis. Results At baseline, 136 patients (39%) received prasugrel 3.75 mg, 48 patients (14%) received prasugrel 2.5 mg, and 164 patients (47%) received clopidogrel 75 mg. Clopidogrel 75 mg had a significantly higher proportion of ischemic risk within one year after PCI than the other groups, and was an independent predictor for ischemic risk with reference of prasugrel 3.75 mg. In addition, switching from clopidogrel 75 mg to prasugrel 2.5 mg significantly lowered and aggregated the PRU value. Whereas, dose reduction of prasugrel had a significantly lower proportion of bleeding risk over one year after PCI than the continuation of prasugrel 3.75 mg, and was an independent predictor for bleeding risk with reference of continuation of prasugrel 3.75 mg. Conclusions Prasugrel 2.5 mg has a lower ischemic risk and a more stable PRU value compared with clopidogrel treatment. Prasugrel also contributes to a decline in bleeding risk with concomitant dose reduction. Trial Registration University Hospital Medical Information Network (UMIN), ID: UMIN000029541, Date: October 16, 2017 (https://center6.umin.ac.jp/cgi-open-bin/ctr_e/ctr_view.cgi?recptno=R000033395).

Introduction: The long-term impact of renin-angiotensin system (RAS) inhibitors for secondary prevention in patients with chronic kidney disease (CKD) and coexisting coronary artery disease remains unclear. Methods: Altogether, 1,160 consecutive patients with CKD (mean age, 70 ± 9 years; 78% men) who underwent their first percutaneous coronary intervention (PCI) between 2000 and 2018 were included and analyzed. Based on their RAS inhibitor use, 674 patients (58%) were allocated to the RAS inhibitor group, and 486 patients (42%) were allocated to the non-RAS inhibitor group. This study evaluated the incidence of 3-point major adverse cardiovascular events (3P-MACE), including cardiovascular death, nonfatal acute coronary syndrome and nonfatal stroke, admission for heart failure (HF), target vessel revascularization (TVR), and all-cause death. Results: During a median follow-up duration of 7.8 years, 280 patients (24.1%) developed 3P-MACE, 134 patients (11.6%) were hospitalized for HF, 171 patients (14.7%) underwent TVR, and 348 patients (30.0%) died of any causes. The cumulative incidence rate of 3P-MACE in the RAS inhibitor group was significantly lower than in the non-RAS inhibitor group (31.7% vs. 39.0%, log-rank test, p = 0.034); however, that of admission for HF in the RAS inhibitor group was significantly higher than in the non-RAS inhibitor group (28.1% vs. 13.3%, log-rank test, p < 0.001). The subgroup of preserved ejection fraction, non-acute myocardial infarction, and non-proteinuria tended to promote the onset of HF rather than cardiovascular prevention by RAS inhibitors. Conclusion: The long-term RAS inhibitor use for patients with CKD after PCI might prevent cardiovascular events but increase the risk of HF.