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Background: Cigarette smoking may increase platelet aggregation and cause atherothrombotic cardiovascular events. We aimed to investigate the impact of cigarette smoking on platelet function in patients with ischemic coronary heart disease (CHD)., Methods: Twenty patients with ischemic stable CHD under aspirin therapy (300 mg/d), who continue to smoking despite all warnings, and 20 nonsmokers with CHD are enrolled in the study. Platelet function is studied at the morning, before and 15 minutes after the first cigarette, by the Platelet Function Analyzer (PFA)-100, with collagen and epinephrine and collagen and adenosine diphosphate cartridges. Post aspirin platelet hyperactivity is defined as having a closure time (CT) shorter than 186 seconds despite regular aspirin intake. Serial CT measurements are analyzed by paired samples t test., Results: Persistent platelet activity was present in 4 smoker (20%) and 3 nonsmoker (15%) patients at the beginning. Platelet activity measured by the PFA-100 is been increased significantly after cigarette smoking (P = .004). Shorter CTs were determined after smoking in all patients with and without baseline persistent platelet activity, and 4 more participants became aspirin nonresponder (P = .004). No significant differences in demographic, hematological, and biochemical parameters were determined between aspirin responders and nonresponders., Conclusions: We determined that cigarette smoking may increase platelet aggregation in patients with ischemic CHD in an aspirin nonresponsive manner. Our results emphasize the importance of quitting cigarette smoking in patients with CHD.

Interleukin-15 (IL-15) is a potent proinflammatory cytokine that is now considered a key component of atherosclerosis. Proinflammatory gene polymorphisms lead to variations in the production and level of the proteins. In light of these findings, we hypothesized that variations in the gene coding for IL-15 influence the risk of coronary heart disease (CHD) by modulating the IL-15 levels. To test this hypothesis, we examined 5 single nucleotide polymorphisms (SNPs) in IL-15 gene and IL-15 levels in 102 patients with acute coronary syndrome (ACS), 102 patients with chronic ischemic stable CHD and 162 healthy control subjects. This study is the first report showing the influences of IL-15 gene variants and IL-15 levels on CHD. The five single nucleotide polymorphisms (SNPs) within the IL-15 gene, G367A, C267T, A14035T, C13687A, and A10504G were carried out by polymerase chain reaction/restriction fragment length polymorphism (PCR/RFLP). Serum IL-15 levels were significantly higher in both acute and chronic patients than in controls. Genetic variants of IL-15 gene and IL-15 levels were associated with CHD. In conclusion, our study supports the hypothesis that genetic variation in IL-15 gene and IL-15 levels influence the risk of CHD. Further studies are needed to confirm our hypothesis., (Copyright 2009 Elsevier Ltd. All rights reserved.)

Background: Current evidence supports the preventive role of statins on platelet aggregation in patients with coronary heart disease., Aim: Our aim was to determine the effects of aggressive statin therapy on platelet function in patients with coronary heart disease., Material and Methods: A total of 178 consecutive patients (37-68 years old, 35.9% women) with stable coronary artery disease (CAD) was enrolled in the study. Platelet function assays were realized by the Platelet Function Analyzer (PFA)-100 with collagen and epinephrine (Col/Epi) and collagen and ADP (Col/ADP) cartridges. Aspirin resistance was defined as having a closure time (CT) of <186 s with Col/Epi cartridges despite regular aspirin therapy. A statin therapy protocol applied to the patients with aspirin resistance for 3 months., Results: We determined that 20 (11.2%) of patients had aspirin resistance by the PFA-100. Mean closure time measured with the Col/ADP cartridges was 83 +/- 18 s (53-162 s). Of the patients 12 were not on a statin therapy and eight were taking 10 mg daily atorvastatin. After 3 months of 40 mg daily atorvastatin therapy 13 subjects with aspirin resistance became aspirin sensitive by PFA-100 (P < 0.0001). There was also a significant decrease in total and LDL cholesterol levels and an increase in HDL cholesterol at the third month of statin therapy (P < 0.0001 for all)., Conclusion: Statin therapy reduced the in vitro aspirin resistance in 65% of the patients after a therapy of 3 months. Further studies are needed to elucidate the mechanism of statins' effects on platelet reactivity.

Objectives: The aim of our study was to determine the relation between exercise stress test and aspirin resistance in patients with stable coronary artery disease., Background: Clinically aspirin resistance is defined as having thrombotic and embolic cardiovascular events despite regular aspirin therapy., Methods: We studied platelet functions of 62 patients with stable coronary artery disease and 20 subjects with normal coronary arteries by Platelet Function Analyzer (PFA-100, Dade Behring, Germany) at rest and after exertion with collagen and/or epinephrine (Col/Epi) and collagen and/or ADP cartridges. Closure time (CT)<186 seconds was defined as aspirin resistance with Col/Epi cartridges of PFA-100. Symptom limited treadmill stress test (protocol of Bruce) was performed with Oxford Streslink TD-1 system., Results: 8 (12.9%) patients were aspirin resistant by PFA-100 (CT<186s despite regular aspirin therapy) at rest. At the first minute of the recovery period of exercise stress test 14 (22.5%) patients were aspirin resistant by PFA-100. CTs with Col/ADP were respectively 89+/-6 s (83--100s) and 89+/-5 s (82--104s) at rest and after exercise (p=0.107). 20.3% (11/54) of patients known as in vitro aspirin sensitives at rest had shorter CTs and 11.1% (6/54) had aspirin resistance after exercise (p=0.004). There was no statistically significiant difference in platelet functions in the control group after exertion., Conclusion: We conclude that 11.1% of in vitro aspirin sensitive subjects at rest had aspirin resistance after exercise by PFA-100. In some individuals, exercise induced platelet activation is aspirin insensitive at usual antiplatelet doses. We need further clinical trials to optimize antiplatelet therapy in patients with coronary artery disease.