흡연자에서 관상동맥 내피세포 의존성 심근 혈류 예비능: H2(15)O PET 찬물자극 검사에 의한 평가 = Evaluation of Endothelium-dependent Myocardial Perfusion Reserve in Healthy Smokers; Cold Presser Test using H2(15)O PET

다국어 초록 (Multilingual Abstract)

Purpose: Much evidence suggests long-term cigarette smoking alters coronary vascular endothelial response. In this study, we applied nonnegative matrix factorization(NMF), and unsupervised learning algorithm, to CO-less H_(2)^(15)O-PET to investigate coronary endothlial dysfunction caused by smoking noninvasively. Materials and methods: This study enrolled eighteen young male volunteers consisting of 9 smokers (23.8±1.1 yr, 6.6±2.5 pack-years) and 9 nonsmokers (23.8±2.9 yr). They do not have any cardiovascular risk factor or disease history. Myocardial H_(2)^(15)O-PET was performed at rest, during cold (5°C) pressor stimulation and during adenosine infusion. Left ventricular blood pool and myocardium were segmented on dynamic PET data by NMF method. Myocardial blood flow (MBF) was calculated from input and tissue functions by a single compartmental model with correction of partial volume and spillover effects. Results: There were no significant difference in resting MBF between the two groups (Smokers: 1.43 0.41 ml/g/min and non-smikersL: 1.37±0.41 ml/g/min; p = NS). during cold pressor Stimulation, MBF in smokers was significantly lower than that in non-smokers (1.25±0.34 ml/g/min vs 1.59±0.29 ml/g/min ; p=0.019). The difference in the ratio of cold pressor MBF to resting MBF between the two groups was also significant )p=0.024; 90±24％ in smokers and 122±28％ in non-smokers.). During adenosine infusion, however, hyperemic MBF did not differ significantly between smokers and non-smokers (5.81±1.99 ml/g/min vs 5.11±1.31 ml/g/min ; p=NS). Conclusion: In smokers, MBF during cold pressor stimulation was significantly lower compared with nonsmokers, reflecting smoking-induced endothelial dysfunction. However, there was no significant difference in MBF during adenosine-induced hyperemia between the two groups.