Data Management And Sharing System of China National Clinical Research Center for Neurological Diseases

Smokers with Elevated Glycated Albumin Could Not Benefit from Dual Antiplatelet Therapy After Minor Stroke or Transient Ischemic Attack

First author:Hongyu Zhou

Corresponding author:Yongjun Wang

Minor stroke Transient ischemic attack Antiplatelet therapy Smoke Glycated albumin Prognosis

essential_information

  • Person in charge:Hongyu Zhou
  • Data Sources: CHANCE
  • Number of papers:CHANCE20200155
  • Published time:2023-06-01

2023-06-01

Published articles

Journal:Cerebrovascular Diseases

Publication type: Original Contributions

IF(IF): 3.104

PMID: 37263240 Link To Pubmed Full text Download

Background And Purpose

Recent studies identified the smoking‒clopidogrel paradox among patients with a recent minor stroke or transient ischemic attack (TIA), that is, current smokers had a greater benefit in stroke prevention at 90 days from clopidogrel.1 It may be attributed to the increase in cytochrome P450 1A2 activity by smoking, which promotes the production of clopidogrel active metabolite and leads to stronger platelet inhibition.2 Elevated glycated albumin (GA) levels reflect poor glycemic control for at least 2 to 4 weeks before the stroke. Previous studies figured out that the protective effect of dual antiplatelet therapy is not apparent in minor stroke or TIA patients with elevated GA level, which may be related to hyperglycemia decreased the formation of clopidogrel active metabolite.3-5 However, it is still unknown whether smoking could counteract the inhibition of hyperglycemia on clopidogrel. Therefore, we aimed to investigate the impact of smoking on clopidogrel efficacy in patients with minor ischemic stroke or transient ischemic attack under different GA level.

Method

We analyzed data from the Clopidogrel in High-risk patients with Acute Nondisabling Cerebrovascular Events (CHANCE) trial. A subgroup of 3044 patients with baseline GA levels was included and categorized by smoking status and GA levels. The primary efficacy outcome was a new stroke within 90 days. The safety outcome was any bleeding event at 90 days. The interaction of smoking status with antiplatelet therapy was calculated by Cox proportional hazards regression model.

Conclusion

Smokers with elevated GA levels could not benefit from dual antiplatelet therapy after minor stroke or TIA.

Main results

In patients with GA levels ≤15.5%, the proportion of smokers was 37.7% (719/1908), while in patients with GA levels >15.5% was 51.6% (586/1136). During the 3-mo follow-up period, 299 (9.9%) patients had a new stroke occurrence. In patients with elevated GA levels, both smokers and non-smokers could not benefit from dual antiplatelet therapy (smokers, adjusted HR 0.70, 95%CI 0.42-1.17; non-smokers, adjusted HR 0.82, 95%CI 0.57-1.18). In patients with normal GA levels, dual antiplatelet therapy reduced the risk of stroke recurrence in smokers by 72% (adjusted HR 0.28, 95%CI 0.14-0.56), and in non-smokers by 53% (adjusted HR 0.47, 95%CI 0.26-0.86). However, whether the GA level was elevated or normal, there was no significant interaction between smoking status and antiplatelet therapy.