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Updated: Jan 14, 2026

Microfluidics in Assessing Platelet Function
Published on: November 8, 2024
Association Between Smoking and Thromboelastography With Platelet Mapping Parameters in Peripheral Artery Disease
Isabella Ferlini Cieri1, Adriana A Rodriguez Alvarez1, Mounika Naidu Boya1
1Division of Vascular and Endovascular Surgery, Massachusetts General Hospital, Boston, Massachusetts.
Introduction:
Peripheral artery disease (PAD) and smoking are intricately linked, yet the association between tobacco and coagulation dynamics in PAD patients remains incompletely understood. This study aims to compare thromboelastography parameters between smokers and nonsmokers with PAD undergoing revascularization.
Methods:
In this single-center, cross-sectional study, 174 PAD patients were stratified into three equal groups based on smoking status: nonsmokers (n = 58), former smokers (n = 58), and current smokers (n = 58). Comprehensive demographic data, medical history, and medication use were documented. Thromboelastography with platelet mapping was performed on all patients. Informed consent was obtained from all patients under institutional review board protocols 2022P001918 and 2022P002264. Statistical analysis included one-way analysis of variance for normally distributed variables, Kruskal-Wallis tests for non-normally distributed variables, and chi-square tests for categorical variables, with significance set at P < 0.05.
Results:
Significant differences in coagulation parameters were observed across smoking groups. Overall clot strength (citrated rapid thromboelastography maximum amplitude) progressively decreased from nonsmokers (67.90 mm) to former smokers (64.80 mm) to current smokers (62.50 mm) (P < 0.001). Fibrinogen contribution to clot formation (calculated functional fibrinogen maximum amplitude) showed similar decline (31.50 mm, 24.00 mm, 21.50 mm, respectively, P = 0.007). Clot formation kinetics (citrated kaolin kinetics time) was prolonged in current smokers (1.35 min) and former smokers (1.30 min) compared to nonsmokers (1.00 min) (P = 0.045). Notably, arachidonic acid-mediated platelet function was significantly impaired in current smokers, with increased arachidonic acid -pathway inhibition (66.5% versus 52.1% versus 25.3%, P = 0.043).
Conclusions:
Smoking is significantly associated with altered coagulation profiles in PAD patients, with implications for bleeding risk assessment and personalized antithrombotic therapy selection.
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