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. 2024 Nov 29;14(1):29699.
doi: 10.1038/s41598-024-81537-1.

Impact of haemoglobinA1c on platelet reactivity and cardiovascular outcomes in patients undergoing drug-eluting stent implantation

Yilin Wu #  1 , Xuan Jiang #  2 , Lijuan Jiang  3 , Hongyu Ji  3 , Min Liu  4 , Weizhen Li  5   6
Affiliations

Impact of haemoglobinA1c on platelet reactivity and cardiovascular outcomes in patients undergoing drug-eluting stent implantation

Yilin Wu et al. Sci Rep. .

Abstract

This study investigates the impact of hemoglobin A1c on platelet reactivity and cardiovascular outcomes in patients undergoing drug-eluting stent implantation. HbA1c levels were categorized into 3 groups: < 6.5%, 6.5-8.5%, and > 8.5%. ROC (resistance to clopidogrel) and ROA (resistance to aspirin) were calculated. The primary endpoint was a composite of MACE, including all-cause mortality, nonfatal MI, and ischemia-driven revascularization. The secondary endpoints comprised individual MACE components. The incidence of ROC was 9.3% (151 of 1621), whereas that of ROA was 16.5% (268 of 1621). The ROC for each of the 3 groups significantly increased with increasing HbA1c levels [4.3% vs. 7.1% vs. 10.1%, p = 0.006]; however, the ROA did not [16.4% vs. 17.7% vs. 14.3%, P = 0.694]. HbA1c > 8.5 was significantly associated with ROC (3.356 [1.231, 9.234], p = 0.009). Compared with the HbA1c < 6.5 subgroup, the HbA1c˃8.5 subgroup was significantly associated with MACE (3.142 [2.346, 4.206], < 0.001), nonfatal MI (2.297 [1.275, 4.137], P = 0.006) and ischemia-driven revascularization (3.845 [2.082, 7.101], p < 0.001), but not all-cause mortality (2.371 [0.551, 10.190], 0.246) at the 36-month follow-up. HbA1c levels were positively correlated with ROC, but the adverse cardiovascular events were driven by elevated HbA1c, constituting an argument to intensify glycemic control in subjects with diabetes after intracoronary stent placement.

Keywords: Atherosclerosis; Glycated hemoglobin; Percutaneous coronary intervention; Platelet reactivity.

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Conflict of interest statement

Declarations. Competing interests: The authors declare no competing interests. Ethics approval and consent to participate: The study protocols were approval by the Ethics Committee of Jiading Branch of Shanghai General Hospital and performed in accordance with the Declaration of Helsinki. All participants provided written informed consent to participate in the study.

Figures

Fig. 1
Fig. 1
Prevalence of ROC, ROA by HbA1C category. (a) The prevalence of ROC. ROC is defined as ADP inhibition rate of less than 30%. (b) The prevalence of ROA. ROA is defined as AA inhibition rate of less than 50% assessed by TEG. ROC resistance to clopidogrel, ADP adenosine diphosphate, ROA resistance to aspirin, AA arachidonic acid, TEG thromboelastographic.
Fig. 2
Fig. 2
Kaplan–Meier curves showing the association between HBIaC groups and clinical outcomes. (A) Kaplan–Meier curves showing the association between MACE and HBIaC groups. (B) Kaplan–Meier curves showing the association between Non-fatal MI and HBIaC groups. (C) Kaplan–Meier curves showing the association between all-cause mortality and HBIaC groups. (D) Kaplan–Meier curves showing the association between ischemia-driven revascularization and HBIaC groups. MACE major adverse cardiovascular event, MI myocardial infarction.
Fig. 3
Fig. 3
RCS model showing the association between HB1aC and MACE. RCS restricted cubic spline, MACE major adverse cardiovascular event, HR hazard ratio.
Fig. 4
Fig. 4
ROC curve for prediction of MACE. MACE major adverse cardiovascular even, ROC receiver operating characteristic, AUC area under curve, CI confidential interval.
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