AIM Controversial results for the effect of chronic smoking on platelet aggregation response were found in different studies. In this study, the effect of chronic smoking on in-vitro pl atelet aggregation induced by various agonists were investigated in coronary artery disease patients. Methods and results: 121 patients (Group 1: 53 chronic smokers and Group II: 68 non-smbkers) who had elinical and Iaboratuary data of stable angina pectoris and contro lled unstable angina pectoris were included in the study. Platelet rich plasm of the patients was obtained before coronary angiography and in vitro treated seperately with adenosine diphosphate (10 ı.ım ol/L) , collagen (0.6 ı.ıgm/ml) and epinephrine (20 ı.ımoi/L) . Activation and duration of platelet aggregation slopes were measured and calculated for each agonist by Turbodimetric Method of Bohr. Activation ratios and duration of ADP, collagen, and epineprine induced in-vitro platelet aggregation response were s ignificantly more in Group I (p<0.05, <0.001 , <0.0001 for ratio of activation and p<0.05, p<0.05, p <0.00 I fo r d uration of activation respectively).
CONCLUSION Clinical studies investigaling effects of more potent antiaggregant drugs added to aspirin are needed in chron ic smoking coronary artery disease patients.
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