# Association of Remnant Cholesterol with Platelet Reactivity in Coronary Artery Disease Patients Receiving PCI

## TL;DR

This study shows that remnant cholesterol levels are linked to platelet reactivity in heart patients undergoing a common procedure, suggesting a possible connection between cholesterol and blood clotting risks.

## Contribution

The study is the first to report the relationship between remnant cholesterol and clopidogrel-related platelet reactivity in PCI patients on dual antiplatelet therapy.

## Key findings

- Higher remnant cholesterol levels were positively associated with high on-treatment platelet reactivity.
- Lower remnant cholesterol levels were negatively associated with low on-treatment platelet reactivity.
- The study suggests remnant cholesterol may be a potential marker for platelet reactivity in PCI patients.

## Abstract

Remnant cholesterol (RC) has received increasing attention and shown to be associated with bleeding and ischemic events in clinical research; however, the mechanisms remain incompletely understood.

To investigate the relationship between RC and platelet reactivity in patients with coronary artery disease (CAD) undergoing percutaneous coronary intervention (PCI) who received dual antiplatelet therapy with aspirin and clopidogrel.

A total of 10,724 consecutive PCI patients in China from January 2013 to December 2013 were enrolled. 6,633 patients had the results of thromborlastogram for analysis. Low on-treatment platelet reactivity (LTPR) and high on-treatment platelet reactivity (HTPR) were defined as adenosine diphosphate-induced platelet maximum amplitude of thromborlastogram <31 mm and >47 mm, respectively.

A total of 6,633 PCI patients (mean age, 58.20 ± 10.2 years; male, 77.5%) were finally enrolled. When RC was used as a continuous variable, the multivariate logistic regression showed that RC concentration was negatively associated with LTPR (OR: 0.761, 95% CI 0.609–0.950) and positively associated with HTPR (OR: 1.461, 95% CI 1.151–1.855). For RC quartiles, compared to the lowest quartile (Q1), quartiles 3 and 4 were negatively associated with LTPR (ORQ3: 0.853, 95% CI 0.735–0.990; ORQ4: 0.840, 95% CI 0.707–0.999). Meanwhile, higher quartiles of RC (Q2, Q3, Q4) were positively associated with HTPR (ORQ2: 1.193, 95% CI 1.015–1.402; ORQ3: 1.356, 95% CI 1.152–1.596; ORQ4: 1.404, 95% CI 1.164–1.694).

We reported that RC was associated with clopidogrel-related platelet reactivity in patients undergoing PCI received dual antiplatelet therapy. These results suggest an interaction between lipid and thrombosis, and remind us pay attention to RC levels in PCI patients.

In the large-scale (n = 6,633) and real-world study, we revealed that RC may modify the platelet reactivity to influence the risk of bleeding and ischemia in PCI patients. Our study firstly reported the relationship between RC and clopidogrel-related platelet reactivity in patients undergoing PCI received dual antiplatelet therapy. The findings may verify the complex interaction between lipid and thrombosis and suggest that RC may be a potential marker associated with platelet reactivity, which warrants further investigation in future studies.