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Published on: December 7, 2012
Clopidogrel use and smoking cessation result in lower coated-platelet levels after stroke
Angelia C Kirkpatrick1,2, Andrea S Vincent3, George L Dale1
1Department of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK, USA.
Insights
Clopidogrel and smoking cessation significantly reduced coated-platelet levels in stroke patients. These findings highlight potential therapeutic strategies for managing procoagulant platelets after ischemic stroke.
Area of Science:
- Cardiovascular Medicine
- Hematology
- Neuroscience
Background:
- Coated-platelets are highly procoagulant cells linked to ischemic stroke and recurrence.
- Elevated coated-platelets are observed in non-lacunar ischemic stroke patients.
- Previous studies suggest smoking increases, while SSRIs, statins, and aspirin decrease coated-platelet levels.
Purpose of the Study:
- To investigate the longitudinal impact of initiating specific treatments and smoking cessation on coated-platelet levels 90 days post-ischemic stroke.
Main Methods:
- A cohort of 87 ischemic stroke patients had coated-platelet levels measured at baseline and 90 days.
- Repeated-measure ANOVA analyzed the effect of initiating SSRIs, statins, clopidogrel, aspirin, oral anticoagulants, or smoking cessation.
Main Results:
- Initiation of clopidogrel therapy significantly decreased coated-platelet levels (p = .0001, partial η² = 0.17).
- Smoking cessation also led to a significant reduction in coated-platelet levels (p = .014, partial η² = 0.10).
- No significant changes in coated-platelet levels were observed with SSRIs, statins, aspirin, or oral anticoagulants.
Conclusions:
- Clopidogrel therapy and smoking cessation effectively attenuate coated-platelet potential within 90 days after ischemic stroke.
- These interventions may offer novel therapeutic avenues for reducing thrombotic risk in stroke patients.
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.
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