Higher remnant cholesterol-inflammatory index (RCII) quartiles independently predicted high on-treatment platelet reactivity and increased 5-year ischemic risk (HRQ4:1.411).
Does higher remnant cholesterol inflammatory index (RCII) predict high on-treatment platelet reactivity and ischemic events in post-PCI patients on DAPT?
The remnant cholesterol inflammatory index (RCII) is a novel biomarker that independently predicts high on-treatment platelet reactivity and 5-year ischemic risk in post-PCI patients on DAPT.
Tasa de eventos absoluta: 0% vs 0%
Abstract Background In recent years, remnant cholesterol (RC) and high-sensitivity C-reactive protein (hs-CRP) have garnered increasing attention due to their association with ischemic events in coronary clinical research. However, the combined effect of these two factors remains not fully understood. Aim This study aimed to assess the relationship between the remnant cholesterol inflammatory index (RCII), high-on-treatment platelet reactivity (HTPR), and ischemic events in patients with coronary artery disease undergoing percutaneous coronary intervention (PCI) while receiving dual antiplatelet therapy (DAPT). Methods A total of 10,724 consecutive PCI patients in China from January 2013 to December 2013 were enrolled, among whom 6,555 patients had the results of thromborlastogram (TEG) with DAPT for analysis. RCII was calculated using the formula: RCII = RC (mg/dL) × hs-CRP(mg/L)/10. High on-treatment platelet reactivity (HTPR) was defined as adenosine diphosphate-induced platelet maximum amplitude of TEG47mm, respectively. Logistic regression was used to assess the relationship between the RCII and HTPR. In further analysis, Cox regression was applied to evaluate the association between the RCII and ischemic events during the five-year follow-up. The ischaemic endpoints included all-cause death, myocardial infarction, revascularization or stroke. Results After a 5-year follow-up, 6,555 patients (age,58.25±10.28; male,77.6%) were finally analyzed and a total of 1,354 (20.70%) patients experienced ischemic events. The multivariate logistic regression showed that RCII was independently and positively associated with HTPR (OR: 1.088, 95%CI 1.026-1.154, p=0.005). For quartiles of RCII, compared with the lowest quartile (Q1), the higher quartile of RCII (Q2, Q4) was also associated with HTPR (ORQ2: 1.277, 95%CI 1.072-1.523, p=0.006; ORQ4: 1.482, 95%CI 1.238-1.773, p0.001) (Figure 1). Because HTPR was thought to be related to higher risk of ischemic events, in subsequent analysis, we validated the relationship between RCII and ischemic events. After adjusting for confounders, compared with patients with the Q1 of RCII, patients with Q2 and Q4 of RCII had the highest risk of ischemic events (HRQ2: 1.235, 95%CI 1.056-1.444, p=0.008; HRQ4: 1.411, 95%CI 1.203-1.655, p0.001) (Figure 2). Conclusions In this large sample real-world study, we first reported that the RCII as a novel composite biomarker was not only an independent risk factor for HTPR, but also representing a higher risk of ischemic events. Clinically, the integration of RCII may enhance the risk stratification ability, thereby identifying high-risk patients who may benefit from intensified antithrombotic therapy or lipid-lowering treatment.
Liu et al. (Sat,) reported a other. Higher remnant cholesterol-inflammatory index (RCII) quartiles independently predicted high on-treatment platelet reactivity and increased 5-year ischemic risk (HRQ4:1.411).