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Smoking Cessation Normalizes Coronary Endothelial Vasomotor Response Assessed with ¹⁵O-Water and PET in Healthy Young Smokers

¹ Department of Nuclear Medicine, Hokkaido University Graduate School of Medicine, Sapporo, Japan; ² Department of Cardiovascular Medicine, Hokkaido University Graduate School of Medicine, Sapporo, Japan; ³ Department of Molecular Imaging, Hokkaido University Graduate School of Medicine, Sapporo, Japan; and ⁴ Department of Health Sciences, Hokkaido University, Sapporo, Japan

Correspondence: For correspondence or reprints contact: Nagara Tamaki, MD, PhD, Department of Nuclear Medicine, Hokkaido University School of Medicine, Kita-15, Nishi-7, Kita-ku, Sapporo-city, 060-8638, Japan. E-mail: natamaki{at}med.hokudai.ac.jp

Cigarette smoking is one of the risk factors of cardiovascular diseases and is related to abnormal peripheral and coronary vascular vasomotion. Coronary vascular endothelial dysfunction is caused by chronic smoking in smokers without epicardial coronary artery stenosis. The coronary endothelial vasomotion abnormality is restored by interventions such as L-arginine or vitamin C infusion. However, to our knowledge, the effect of smoking cessation on coronary vasomotor response has not been elucidated. Therefore, the aim of this study was to assess the effect of smoking cessation on coronary vasomotor response by quantitative myocardial blood flow (MBF) measurement using ¹⁵O-water and PET. Methods: Fifteen young smokers (Brinkman index > 100; mean age ± SD, 26 ± 4 y) with no evidence of heart disease or cardiovascular risk factors, except for smoking, and age-matched nonsmokers (n = 12) were enrolled in this study. MBF was measured at rest, during the cold pressor test (CPT), before and at 1 and 6 mo after smoking cessation. In addition, MBF measurement during adenosine triphosphate (ATP) infusion was performed before and at 6 mo after smoking cessation. In nonsmokers, MBF was measured at rest, during ATP infusion, and during the CPT. Results: MBF at rest and during ATP infusion did not differ between smokers and nonsmokers (0.73 ± 0.12 vs. 0.80 ± 0.15 mL/g/min and 3.15 ± 1.43 vs. 3.69 ± 0.76 mL/g/min, respectively; P = not significant). In contrast, MBF during the CPT in smokers was lower than that in nonsmokers (0.90 ± 0.19 vs. 1.12 ± 0.28 mL/g/min; P < 0.05). There was no significant difference in MBF either at rest or during ATP infusion between before and after smoking cessation, but MBF during the CPT increased at 1 mo in comparison with before cessation of smoking (0.90 ± 0.19 vs. 1.02 ± 0.22 mL/g/min; P < 0.01). An improvement of MBF response to the CPT was preserved at 6 mo after smoking cessation. Conclusion: Coronary vasomotor abnormality assessed by MBF response to the CPT was improved at 1 mo after smoking cessation. These findings indicate that coronary endothelial dysfunction may be reversible within 1 mo after smoking cessation in healthy young smokers.

Key Words: myocardial blood flow • cigarette smoking • cold pressor test • coronary vascular endothelium • PET • ¹⁵O-water • cardiovascular disease

COPYRIGHT © 2006 by the Society of Nuclear Medicine, Inc.

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