Long-term smoking causes more advanced coronary endothelial dysfunction in middle-aged smokers compared to young smokers.
OBJECTIVE
Smoking cessation has been shown to normalize the coronary endothelial dysfunction in healthy young smokers. However, its effect has not been explored in middle-aged smokers with a longer history of smoking. Therefore, we compared the effects of smoking cessation on coronary vasomotor response between both young and middle-aged smokers and identified the predictor for its improvement.


METHODS
This study investigated 14 young healthy smokers (age 25.2 ± 2.3 years), 13 middle-aged smokers (age 42.0 ± 6.5 years) and 10 non-smokers. Myocardial blood flow (MBF) was measured by using (15)O-water positron emission tomography (PET).


RESULTS
At baseline, the ratio of MBF during the cold pressor test (CPT) to that at rest (MBF(CPT/rest)), the index of coronary endothelial function, was significantly decreased in both young and middle-aged smokers compared to non-smokers (1.24 ± 0.20 and 1.10 ± 0.39 vs 1.53 ± 0.18, p < 0.05 and p < 0.001, respectively). The ratio of MBF during adenosine triphosphate infusion to that at rest was significantly decreased in middle-aged smokers compared to young smokers and non-smokers (3.34 ± 1.52 vs 4.43 ± 0.92 and 4.69 ± 1.25, p < 0.05, respectively). MBF(CPT/rest) at 1 month after smoking cessation significantly increased in young smokers, but not in middle-aged smokers. By multivariate analysis, baseline serum malondialdehyde-modified low-density lipoprotein (MDA-LDL) was an independent predictor for the changes in MBF(CPT/rest) after smoking cessation (β = -0.45, p < 0.05).


CONCLUSIONS
Coronary endothelial dysfunction was reversible by short-term smoking cessation in young smokers, but not in middle-aged smokers, which was associated with serum MDA-LDL levels. Long-term smoking exposure could lead to more advanced coronary endothelial dysfunction and atherosclerosis possibly via oxidative stress.
Department of Cardiovascular Medicine, Hokkaido University Graduate School of Medicine, Kita-ku, Sapporo, Japan. naya@med.hokudai.ac.jp
Masanao
M
Naya
Koichi
K
Morita
Keiichiro
K
Yoshinaga
Osamu
O
Manabe
Daisuke
D
Goto
Kenji
K
Hirata
Chietsugu
C
Katoh
Nagara
N
Tamaki
Hiroyuki
H
Tsutsui
D000328:Adult; D000368:Aged; D000375:Aging / Q000097:blood / Q000473:pathology* / Q000502:physiology*; D016022:Case-Control Studies; D003324:Coronary Artery Disease / Q000097:blood / Q000473:pathology / Q000503:physiopathology; D003331:Coronary Vessels / Q000503:physiopathology*; D004730:Endothelium, Vascular / Q000473:pathology*; D006439:Hemodynamics; D006801:Humans; D007053:Ice; D008077:Lipoproteins, LDL / Q000097:blood; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008875:Middle Aged; D012039:Regional Blood Flow; D012907:Smoking / Q000097:blood / Q000473:pathology* / Q000503:physiopathology*; D016540:Smoking Cessation; D013997:Time Factors; D014666:Vasomotor System / Q000503:physiopathology; D055815:Young Adult
D007053:Ice; D008077:Lipoproteins, LDL; D008315:Malondialdehyde