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Cigarette smoking is associated with increased circulating proinflammatory and procoagulant markers in patients with chronic coronary artery disease : effects of aspirin treatment . BACKGROUND Smoking is associated with endothelial dysfunction . Cytokines released by injured endothelium promote vascular interactions with leukocytes and platelets . We investigated whether ( a ) cigarette smoking is linked to increased cytokine production , which may mediate platelet activation and thrombin generation in chronic coronary artery disease ( CAD ) , and ( b ) aspirin treatment inhibits smoking-related changes on cytokines , platelets , and thrombin . METHODS AND RESULTS Plasma macrophage-colony-stimulating factor ( M-CSF ) and C-reactive protein ( CRP ) were measured in 100 patients with chronic CAD , 60 of whom were chronic smokers . Prothrombin fragments 1+2 and urinary 11-dehydro-thromboxane B2 ( TXB2 ) were additionally measured in 60 of 100 patients ( 30 of whom were smokers ) and in 24 healthy controls . Smokers ( n = 20 ) matched for age , myocardial ischemia , and other risk factors with 20 nonsmokers entered a double-blind crossover trial of aspirin ( 300 mg/d for 3 weeks ) versus placebo . Blood and urine measurements were repeated after each treatment . Compared with nonsmokers , smokers had 3-fold median M-CSF ( 1499 vs 476 pg/mL ) , 2-fold CRP ( 1.5 vs 0.8 mg/L ) , and higher 11-dehydro-TXB 2 ( 3.6 vs 2.1 ng/mg creatinine , P < .01 for all comparisons ) . After aspirin treatment , M-CSF , CRP , 11-dehydro-TXB 2 , and prothrombin fragments 1+2 remained higher in smokers compared with nonsmokers despite a significant reduction of these markers by aspirin ( P < .05 ) . M-CSF remained related to 11-dehydro-TXB 2 excretion during both treatment phases ( P < .01 ) suggesting that cytokine-mediated thromboxane A 2 production was not altered by aspirin . CONCLUSIONS Smoking is associated with increased M-CSF , CRP , and platelet activity . Although aspirin treatment reduces the proinflammatory and procoagulant markers in smokers , it does not abolish the proinflammatory effects of smoking in patients with chronic CAD .
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Intervention_Pharmacological
aspirin
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Intervention_Pharmacological
aspirin
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Intervention_Control
placebo .
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Intervention_Pharmacological
aspirin
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Outcome_Physical
3-fold median M-CSF
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Outcome_Physical
2-fold CRP
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Outcome_Physical
11-dehydro-TXB
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Outcome_Physical
M-CSF
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Outcome_Physical
CRP
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Outcome_Physical
11-dehydro-TXB 2
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Outcome_Physical
prothrombin fragments 1+2 remained higher
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Participant_Condition
chronic coronary artery disease
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Participant_Sample-size
100
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Participant_Condition
chronic CAD
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Participant_Sample-size
60
21754
Participant_Condition
chronic smokers
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Participant_Sample-size
60
21756
Participant_Condition
smokers
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Participant_Sample-size
24
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Participant_Condition
Smokers
21759
Participant_Sample-size
20
21760
Participant_Sample-size
20
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Participant_Condition
nonsmokers
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Participant_Condition
chronic CAD