Low-grade inflammation, thrombogenicity, and atherogenic lipid profile in cigarette smokers

Cigarette smoking is one of the major risk factors for atherosclerotic coronary disease, but the precise mechanism(s) by which cigarette smoking promotes atherosclerosis remains unknown. As there is now increasing evidence that atherosclerosis is an inflammatory condition, the present study investigated whether inflammation exists in smokers.

The inflammatory markers and lipid profiles were compared among a current-smoker group (210 patients, mean age 61.8 +/- 11.0 years), past-smoker group (115 patients, 67.1 +/- 9.0 years) and never-smoked group (113 patients, 68.2 +/- 10.7 years), all of whom had no apparent signs of inflammation. The respective levels of blood leukocytes, platelets, C-reactive protein and fibrinogen were significantly higher in current-smokers than in the never-smoked group (6,600 +/- 1,723 /microl vs 5,638 +/- 1,313 /microl p<0.01; 22.7 +/- 6.8 x 10(4) /microl vs 18.7 +/- 7.4 x 10(4) /microl, p<0.01; 3.50+/-4.91 mg/L vs 1.92+/-3.02 mg/L, p<0.01; 334.2 +/- 90.9 mg/dl vs 314.7 +/- 80.2 mg/dl, p<0.05). The respective levels of plasma triglycerides, remnant-like particle cholesterol and apolipoprotein-B were significantly higher and that of high-density lipoprotein cholesterol significantly lower in the current-smokers than in the never-smoked group (152.4 +/- 96.2 mg/dl vs 120.5 +/- 58.1 mg/dl, p<0.01; 5.4+/-6.3 mg/dl vs 3.8 +/- 2.0 mg/dl, p<0.05; 101.6 +/- 23.7 mg/dl vs 95.0 +/- 21.2 mg/dl, p<0.05; 45.2 +/- 12.3 mg/dl vs 50.6 +/- 15.6 mg/dl, p<0.01). Past smokers had intermediate values between those of current-smokers and never-smoked.

Low-grade inflammation, atherogenic dyslipidemia, and hypercoagulability are present in smokers compared with those who have never smoked among subjects without apparent inflammation who underwent coronary angiography on suspicion of coronary artery disease.