BackgroundIn previous studies, the TyG index (triglyceride-glucose index) has been proven to be closely associated with the prognosis of cardiovascular disease. However, the impact of TyG index on the prognosis of patients with ischemic HF (heart failure) undergoing PCI (percutaneous coronary intervention) is still unclear.MethodIn this study, 2055 patients with ischemic HF were retrospectively enrolled and classified into four groups based on quartiles of the TyG index. The primary endpoint was MACE (major adverse cardiovascular events) consisting of all-cause mortality, non-fatal MI (myocardial infarction), and any revascularization. The incidence of the endpoints among the four groups was assessed through Kaplan-Meier survival analysis. The independent correlation between TyG index and endpoints was analyzed with multivariate Cox regression models. Besides, the RCS (restricted cubic spline) analysis was performed to examine the nonlinear relationship between TyG index and MACE.ResultThe incidence of MACE was significantly higher in participants with a higher TyG index. The positive association between the TyG index and MACE was also confirmed in the Kaplan–Meier survival analyses. Multivariate cox proportional hazards analysis indicated that the TyG index was independently associated with the increased risk of MACE, regardless of whether TyG was a continuous [TyG, per 1−unit increase, HR (hazard ratio) 1.41, 95% CI (confidence interval) 1.22-1.62, P < 0.001] or categorical variable [quartile of TyG, the HR (95% CI) values for quartile 4 was 1.92 (1.48-2.49), with quartile 1 as a reference]. In addition, the nonlinear association of TyG index with MACE was shown through RCS model and the risk of MACE increased as the TyG index increased in general (Nonlinear p=0.0215). Besides, no obvious interaction was found in the association of TyG with MACE between the DM (diabetes mellitus) group and the no-DM group.ConclusionAmong patients with ischemic HF undergoing PCI, the TyG index was correlated with MACE independently and positively.

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BackgroundInflammation increases the risk of thrombosis in coronary artery disease (CAD) patients and affects the antiplatelet efficacy of clopidogrel. C1q interacts with platelets to activate platelets and induce thrombosis by participating in and regulating the inflammatory response. Whether C1q affects adenosine diphosphate (ADP)-induced platelet reactivity during clopidogrel therapy was unclear and our study aimed to explore the issue.MethodWe enrolled 1,334 CAD patients receiving clopidogrel therapy and evaluated the association between C1q level and high residual platelet reactivity (HRPR) using logistic regression and restricted cubic spline (RCS). HRPR was defined as ADP-induced maximum amplitude (MAADP) > 47 mm plus ADP-induced platelet aggregation (ADPi) < 50%.ResultsA total of 516 patients (38.7%) performed HRPR. The frequency of HRPR increases with the increase in C1q level (26.3%, 38.4%, 43.2%, and 46.7% for the 1st to 4th quartile of C1q). The result of multivariate logistic regression demonstrated elevated C1q as an independent predictor for HRPR (2nd quartile: OR = 1.722, 95% CI 1.215–2.440; 3rd quartile: OR = 2.015, 95% CI 1.413–2.874; 4th quartile: OR = 2.362, 95% CI 1.631–3.421, compared to the 1st quartile). RCS depicted the nonlinear relationship between C1q and HRPR risk (p for non-linear < 0.05).ConclusionThe current research is the first to explore the association of C1q and ADP-induced platelet reactivity and to demonstrate elevated C1q as an independent risk factor for HRPR in CAD patients during clopidogrel therapy.

Background: It has been demonstrated in previous studies that red blood cell distribution width (RDW) is correlated with the severity and prognosis of cardiovascular disease. The target of our study was to assess the relationship between RDW and the prognosis of ischemic cardiomyopathy (ICM) patients undergoing percutaneous coronary intervention (PCI). Methods: The study retrospectively enrolled 1986 ICM patients undergoing PCI. The patients were divided into three groups by RDW tertiles. The primary endpoint was major adverse cardiovascular events (MACE) and the secondary endpoints were each of the components of MACE (all-cause mortality, nonfatal myocardial infarction (MI) and any revascularization). Kaplan–Meier survival analyses were conducted to show the association between RDW and the incidence of adverse outcomes. The independent effect of RDW on adverse outcomes was determined by multivariate Cox proportional hazard regression analysis. In addition, the nonlinear relationship between RDW values and MACE was explored using restricted cubic spline (RCS) analysis. The relationship between RDW and MACE in different subgroups was determined using subgroup analysis. Results: As RDW tertiles increased, the incidences of MACE (Tertile 3 vs. Tertile 1: 42.6 vs. 23.7, p < 0.001), all-cause death (Tertile 3 vs. Tertile 1: 19.3 vs. 11.4, p < 0.001) and any revascularization (Tertile 3 vs. Tertile 1: 20.1 vs. 14.1, p < 0.001) increased significantly. The K–M curves showed that higher RDW tertiles were related to increased incidences of MACE (log-rank, p < 0.001), all-cause death (log-rank, p < 0.001) and any revascularization (log-rank, p < 0.001). After adjusting for confounding variables, RDW was proved to be independently associated with increased risks of MACE (Tertile 3 vs. Tertile 1: HR, 95% CI: 1.75, 1.43–2.15; p for trend < 0.001), all-cause mortality (Tertile 3 vs. Tertile 1: HR, 95% CI: 1.58, 1.17–2.13; p for trend < 0.001) and any revascularization (Tertile 3 vs. Tertile 1: HR, 95% CI: 2.10, 1.54–2.88; p for trend < 0.001). In addition, the RCS analysis suggested nonlinear association between RDW values and MACE. The subgroup analysis revealed that elderly patients or patients with angiotensin receptor blockers (ARBs) had a higher risk of MACE with higher RDW. Patients with hypercholesterolemia or without anemia also had a higher risk of MACE. Conclusions: RDW was significantly related to the increased risk of MACE among ICM patients undergoing PCI.