Clopidogrel use and smoking cessation result in lower coated-platelet levels after stroke

Abstract

Coated-platelets are a subset of highly procoagulant platelets elevated in patients with non-lacunar ischemic stroke and associated with stroke recurrence. Cross-sectional studies in controls have shown that smoking is associated with higher coated-platelet levels while chronic use of serotonin reuptake inhibitors (SSRIs), statins or aspirin is associated with lower coated-platelet levels. We now investigate if initiation of treatment with SSRIs, statins, clopidogrel, aspirin or oral anticoagulants and smoking cessation impacts coated-platelet levels at 90 days after ischemic stroke. Coated-platelet levels, reported as percent of cells converted to coated-platelets, were measured in 87 consecutive patients with stroke at baseline and repeated at 90 days. Repeated-measure ANOVA was used to determine if initiation of treatment with individual medications or smoking cessation impacted coated-platelet levels. Decreased coated-platelets levels at 90 days as compared to baseline were observed after initiation of treatment with clopidogrel (p = .0001, partial η² = 0.17) and smoking cessation (p = .014, partial η² = 0.10). Initiation of treatment with SSRIs, statins, aspirin or oral anticoagulants did not result in significant changes in coated-platelet potential. These novel longitudinal data suggest that clopidogrel therapy and smoking cessation attenuate coated-platelet potential at 90 days after ischemic stroke.

Keywords:

• Clopidogrel
• Platelets
• smoking
• stroke

Acknowledgments

We thank Leslie Guthery and Eleanor Mathews for assistance with data collection and David L. Gordon for thoughtful comments on the manuscript.

Declaration of interest statement

The authors have no conflicts of interests to report.

Statement of contribution

Contributions: A.C.K. provided patient recruitment and participated in study design, data collection, and classification. A.S.V. was involved in study design, epidemiological analyses, and data presentation. G.L.D. participated in study design and performed coated-platelet measurements. C.I.P. provided patient recruitment and participated in study design, data collection, and classification. All authors participated in the interpretation of results and manuscript preparation.

Additional information

Funding

The work was supported by grants from the United States Department of Veterans Affairs (Award Number 1I01CX000340) and the American Heart Association (15GRNT25270010). These funding sources had no involvement in study design, collection, analysis and interpretation of data, writing of the manuscript or the decision to submit the article for publication.