Comparison of Whole Blood Impedance Platelet Aggregation Using Adenosine Diphosphate and Arachidonic Acid Between Smokers and Non-Smokers: Whole Blood Impedance Platelet Aggregation Between Smokers and Non-Smokers

Riffat Sultana; Farhana Naz; Maryam Afzal; Yusra Rashid; Nazish Saqlain

doi:10.54393/pjhs.v7i9.3714

Authors

Riffat Sultana Department of Pathology, Lahore General Hospital, Lahore, Pakistan
Farhana Naz Department of Pathology, Lahore General Hospital, Lahore, Pakistan
Maryam Afzal Department of Pathology, University College of Medicine and Dentistry, The University of Lahore, Lahore, Pakistan
Yusra Rashid Department of Pathology, Lahore General Hospital, Lahore, Pakistan
Nazish Saqlain Department of Pathology, Lahore General Hospital, Lahore, Pakistan

DOI:

https://doi.org/10.54393/pjhs.v7i9.3714

Keywords:

Whole Blood Aggregometry, Impedance Aggregometry, Platelet Aggregation, Arachidonic Acid, Adenosine Diphosphate, Cigarette Smoking

Abstract

Smoking enhances platelet aggregability and related ischemic and vascular events. However, data on whole blood impedance platelet aggregation in relation to both smoking duration and daily cigarette consumption separately in apparently healthy Pakistani adults are limited. Objective: To assess the association of smoking duration and number of cigarettes smoked daily with increased platelet aggregation and find out factors independently predicts increased aggregation. Methods: A comparative cross-sectional study was done at the Department of Pathology, Lahore General Hospital. Sixty-five smokers and non-smokers each (a total of 130) were enrolled using non-probability convenience sampling. History and venous samples were taken, and whole blood platelet aggregometry was performed using Arachidonic Acid and Adenosine diphosphate. Chi-Square and Logistic Regression tests were applied, p-value<0.050 was considered significant. Results: 84.6% of non-smokers had normal aggregation with both agonists. The percentage of individuals with enhanced aggregation increased as the duration of smoking and the number of daily cigarettes increased. Analysis showed a statistically significant association between abnormal aggregation and increased duration of smoking and number of daily cigarettes. Logistic Regression showed duration of smoking as an independent predictor of increased aggregation with ADP only (p-value=0.006, Exp(B)=15). The number of cigarettes smoked daily was not an independent predictor after adjusting for confounders. Results for age and hematocrit were not significant. Conclusions: Cigarette smoking is associated with increased platelet aggregation. Longer duration of smoking independently predicts high ADP-induced platelet aggregation after adjusting for age and hematocrit. The number of cigarettes smoked daily is not an independent predictor of increased aggregation.

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