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. 2024 May 6:17:2731-2744.
doi: 10.2147/JIR.S458950. eCollection 2024.

Impact of Platelet-to-HDL-Cholesterol Ratio on Long-Term Mortality in Coronary Artery Disease Patients with or Without Type 2 Diabetes: Insights from a Chinese Multicenter Cohort

Affiliations

Impact of Platelet-to-HDL-Cholesterol Ratio on Long-Term Mortality in Coronary Artery Disease Patients with or Without Type 2 Diabetes: Insights from a Chinese Multicenter Cohort

Wanying Wu et al. J Inflamm Res. .

Abstract

Background: Inflammation contributes to the initiation and advancement of both coronary atherosclerosis and type 2 diabetes mellitus (T2DM). Recent evidence has underscored the platelet-to-HDL-cholesterol ratio (PHR) as a promising inflammatory biomarker closely linked to the severity of coronary artery disease (CAD). Nevertheless, the risk of adverse clinical outcomes remains unclear among CAD patients with varying PHR levels and glycemic status.

Methods: A total of 56,316 CAD patients were enrolled, primarily focusing on mortality outcomes. Patients were categorized into four subgroups based on median baseline PHR values and glycemic status: lower PHR (PHR-L) and higher PHR (PHR-H) with or without T2DM. Cox proportional hazard model and subgroup analysis were employed to investigate the association between PHR and glycemic status with mortality.

Results: Over a median 5.32-year follow-up, 8909 (15.8%) patients experienced all-cause mortality, with 3873 (6.9%) deaths attributed to cardiovascular causes. Compared to individuals in PHR-L/non-DM, those in PHR-H/non-DM, PHR-L/DM and PHR-H/DM groups exhibited a higher risk of all-cause death [adjusted hazard ratio (HR) 1.12, 95% confidence interval (CI) 1.06-1.18; HR 1.21, 95% CI 1.14-1.29; HR 1.43, 95% CI 1.34-1.52, respectively], as well as cardiac mortality [HR 1.19, 95% CI 1.08-1.30; HR 1.58, 95% CI 1.44-1.74; HR 1.89, 95% CI 1.72-2.07, respectively]. Cox proportional hazard model also revealed the highest mortality risk among patients in PHR-H/DM compared to other groups (P <0.05). Restricted cubic spline regression analysis revealed a positive linear association between PHR and all-cause as well as cardiac mortality (P for non-linearity >0.05) after adjustment. Additionally, subgroup analysis indicated consistent effects on cardiac mortality within diverse subsets.

Conclusion: In this real-world observational cohort analysis, elevated PHR levels joint with T2DM were related to adverse long-term clinical outcomes in CAD patients. PHR levels may serve as a valuable tool for identifying high-risk individuals within this specific group.

Trial registration: The Cardiorenal ImprovemeNt II registry NCT05050877.

Keywords: all-cause mortality; cardiovascular mortality; coronary artery disease; diabetes; platelet-to-HDL-cholesterol ratio.

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Conflict of interest statement

The authors declare that they have no competing interests in this work.

Figures

Figure 1
Figure 1
Flow Chart of the Study.
Figure 2
Figure 2
Hazard ratios (95% CIs) for all-cause (A) and cardiovascular mortality (B) according to four subgroups. The analysis adjusted for age, sex, low-density lipoprotein, triglycerides, use of antiplatelets, use of statins, atrial fibrillation, anemia, chronic kidney disease, hypertension, congestive heart failure, stroke and percutaneous coronary intervention.
Figure 3
Figure 3
The association between PHR and glycemic metabolism status with all-cause (A) and cardiovascular mortality (B). Model adjusted for age, sex, low-density lipoprotein, triglycerides, use of antiplatelets, use of statins, atrial fibrillation, anemia, chronic kidney disease, hypertension, congestive heart failure, stroke and percutaneous coronary intervention.
Figure 4
Figure 4
Forest plot of cardiovascular mortality according to different subgroups. The analysis with adjustment for age, sex, low-density lipoprotein, triglycerides, use of antiplatelets, use of statins, atrial fibrillation, anemia, chronic kidney disease, hypertension, congestive heart failure, stroke and percutaneous coronary intervention.

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Associated data

Grants and funding

This research was supported by grants from Guangdong Provincial Science and Technology Project (2020B1111170011, KJ022021049); Guangdong Provincial Key Laboratory of Coronary Heart Disease Prevention (No. Y0120220151); and Guangdong Cardiovascular Institute (Z022017016; Y022017018).
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