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젊은 흡연자 및 비흡연자에서 찬물자극 후 심근혈류 예비능을 H215O PET을 이용하여 측정한 후 비교함으로써 흡연에 의한 관상동맥 내피세포의 기능저하를 평가하고자 하였다.젊은 흡연자 9명(23.8±1.1 세; 6.6±2.5 pack-years) 및 비흡연자 9명(23.8±2.9 세)에 대하여 안정상태 및 찬물자극 후, 그리고 아데노신 주입 중에 H215O를 순간주사하고 동적 PET영상을 획득한 뒤, NMF 방법으로 입력 방사능곡선 및 조직 방사능곡선을 처리하여 심근혈류량을 산출하였다. 흡연자군 및 비흡연자군 사이에 심박수혈압곱 및 안정시 혈류량에는 유의한 차이가 없었다. 그러나, 찬물자극 자극 후에는 심근혈류가 흡연자군에서 비흡연자군에 비하여 유의하게 낮았으며(흡연자군 심근혈류 = 1.25±0.34 ml/g/min, 비흡연자군 심근혈류=1.59±0.29 ml/g/min ;p=0.019), 특히 안정시 심근혈류에 대한 찬물자극 후의 심근혈류의 비(내피세포 기능에 의한 심근혈류의 예비능)도 흡연자에서 유의하게 낮았다(흡연자군 = 90±24%, 비흡연자군 = 122±28% ; p=0.024). 한편, 아데노신 주입시의 심근혈류는 두 군 간에 유의한 차이가 관찰되지 않았다(흡연자군 심근혈류 = 5.81±1.99 ml/g/min, 비흡연자군 심근혈류 = 5.11±1.31 ml/g/min ; p=NS). 결론: 젊은 흡연자에서 찬물자극 후에 H215O PET을 이용하여 측정하여 산출한 심근혈류의 예비능이 젊은 비흡연자에 비하여 감소되어 있어서 흡연에 의한 관상동맥 내피세포의 기능장애를 확인할 수 있었다.


Purpose: Much evidence suggests long-term cigarette smoking alters coronary vascular endothelial response. In this study, we applied nonnegative matrix factorization (NMF), an unsupervised learning algorithm, to CO-less H215O-PET to investigate coronary endothelial 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 H215O-PET was performed at rest, during cold (5℃) 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-smokers: 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.