Search

Introduction: Optimal revascularization strategy and shorter duration of dual antiplatelet are required in patients with coronary artery disease concomitant with high bleeding risk (HBR). More complex percutaneous coronary intervention (PCI) and subsequent high thrombotic risk in patients with HBR have been also demonstrated. However, the characteristics of culprit plaque in patients with HBR remains to be elucidated. Hypothesis: HBR is associated with more complex plaque in culprit lesion in patients requiring PCI. Methods: A total of 362 consecutive patients with stable coronary disease, who underwent optical coherence tomography (OCT) imaging of the culprit lesion during PCI were included. The characteristics of culprit plaque assessed by OCT were compared between the HBR group (n=196) and the non-HBR group (n=166), which were classified based on the Academic Research Consortium for High Bleeding Risk (ARC-HBR). Results: The prevalence of severe calcified plaque (angle >180 degee, thickness >0.5mm and length >5mm) was significantly higher in the higher HBR group than in the non-HBR group (48 vs. 35%, p =0.016), although other characteristics were comparable (Panel A). Among patients with HBR, the incremental prevalence of severe calcified plaque according to the number of major ARC-HBR criteria met was observed ( p Conclusions: HBR was associated with a higher prevalence of severe calcified plaque in culprit lesion in patients with stable coronary disease requiring PCI. The greater number of major ARC-HBR criteria met was associated with a higher prevalence of severe calcified plaque among patients with HBR.

Introduction: The impact of high triglyceride (TG) level on the characteristics of coronary plaque remains to be elucidated. Hypothesis: Higher TG level is associated with higher prevalence of vulnerable coronary plaque in patients with coronary artery disease (CAD). Methods: A total of 865 consecutive patients who underwent optical coherence tomography (OCT) imaging of the culprit lesion were included. Patients were classified into either the higher TG group (non-fasting TG ≥ 200 mg/dL, n=150) or the lower TG group (non-fasting TG < 200 mg/dL, n=715). The morphologies of culprit plaque assessed by OCT were compared between the two groups. Results: The median (interquartile range) of TG in the 2 groups was 265.5 (221.5 – 314.8) mg/dL and 115.0 (84.0 – 152.0) mg/dL, respectively. The frequency of macrophage accumulation was significantly higher in the higher TG group than the lower TG group (41 vs. 33%, p=0.043) (Panel A), whereas the prevalence of other plaque components including thin-cap fibroatheroma (22 vs. 19%, p=0.386), microchannel (24 vs. 25%, p=0.907) and cholesterol crystal (23 vs. 23%, p=0.862) was comparable between the two groups. The incremental frequency of macrophage accumulation according to TG levels was observed (p=0.015, Panel B). Although the frequency of macrophage accumulation was comparable between the 2 groups among patients with a higher HDL cholesterol (HDL-C) level (>35 mg/dL), macrophage accumulation was significantly more frequent in the higher TG group than in the lower TG group (71 vs. 41%, p=0.032) among patients with a lower HDL-C level (≤35 mg/dL). Conclusions: Higher TG level was associated with higher frequency of macrophage accumulation in culprit plaques in patients with CAD. The present results may partly explain the role of TG on the development of culprit plaque in coronary artery.