It is widely known that chronic cigarette smoking alters coronary vascular endothelial response, but studies such as this indicate that damage begins much earlier in the smoker's life than previously believed. The risk of death from coronary artery disease is up to six times higher in smokers than in nonsmokers, and a decline in responsiveness to vasodilators is one of the factors that leads directly to narrowing of arteries and subsequent heart attack and stroke.
Cigarette smoking is the leading cause of preventable premature death in the United States and accounts for more than 400,000 deaths annually. PET is a diagnostic imaging test that measures metabolic activity and generates images of organ or tissue function.
The presentation by Dr. Iwado and colleagues is one of many at the SNM meeting that look at the ability of PET to predict future illness and provide valuable information for proactive treatment planning.
The Society of Nuclear Medicine Annual Meeting is being held June 15-19 at the Los Angeles Convention Center, Los Angeles, CA. In addition to educational sessions, the meeting will focus on leading medical developments in the field of nuclear medicine, including radioimmunotherapy with a new class of drugs that target cancer, diagnostic breakthroughs with PET, and other topics. More than 5,000 specialists in the field of nuclear medicine, including scientists, technologists, researchers, and representatives from the medical industry, are expected to attend. The Society of Nuclear Medicine is an international scientific and professional organization with more than 13,000 members dedicated to promoting the science, technology, and practical applications of nuclear medicine. The SNM is based in Reston, VA.
For late-breaking news about the world of nuclear medicine and events at the 49th Annual Society of Nuclear Medicine meeting, visit www.snm.org
Abstract 185. Monday, June 17, 4:39-4:51 p.m. Room 410
Diminished Endothelium-Dependent Coronary Artery Vasodilator Function in Smokers in Health Young Adults Evaluated by 15O-Labeled Water PET
Y. Iwado*, K. Yoshinaga, H. Furuyama, Y. Ito, K. Noriyasu, C. Katoh, Y. Kuge, E. Tsukamoto, and N. Tamaki
Hokkaido University Graduate School of Medicine
Abstract No. 185
DIMINISHED ENDOTHELIUM-DEPENDENT CORONARY ARTERY VASODILATOR FUNCTION IN SMOKERS IN HEALTHY YOUNG ADULTS EVALUATED BY 15O-LABELED WATER POSITRON EMISSION TOMOGRAPHY.Y. Iwado*, K. Yoshinaga, H. Furuyama, Y. Ito, K. Noriyasu, C. Katoh, Y. Kuge, E. Tsukamoto, N. Tamaki, Hokkaido University Graduate School of Medicine, Sapporo, Japan. (200095) Objectives: Chronic cigarette smoking alters coronary vascular endothelial response. To determine if altered response also occurs in young individuals without manifest coronary disease, we quantified coronary blood flow at rest, following adenosine vasodilator stress and during the cold pressor test in healthy young smokers. Methods: Myocardial blood flow (MBF) was quantified by 15O-labeled water positron emission tomography in healthy men with age ranging from 20 to 35 (smokers: 18, non-smokers: 12, age 27.4 ± 4.4 vs. 26.3 ± 3.3). The smokers had been smoking cigarettes for 9.4 ± 4.9 pack-years. MBF was measured at rest, during intravenous adenosine-triphosphate (ATP: 0.16 mg/kg/min) infusion (hyperemic response), and during cold pressor test (CPT) (endothelial vasodilator response). Results: Rest-MBF and hyperemic-MBF did not differ between the smokers and the non-smokers (rest: 0.86 ± 0.11 vs. 0.92 ± 0.14 and ATP: 3.20 ± 1.12 vs. 3.69 ± 0.76 ml/g/min; P = ns). Coronary flow reserve was similar between the two groups (the smokers: 3.78 ± 1.83, the non-smokers: 4.03 ± 0.68; P = ns). Although CPT induced a similar increase of rate-pressure product in the smokers and the non-smokers (10430 ± 1820 vs. 9236 ± 1356 beats/min/mmHg), CPT-MBF was significantly decreased in the smokers (0.65±0.12 mL/g/min) compared with the non-smokers (0.87 ± 0.12 ml/g/min)(P < 0.05). In addition, the ratio of CPT-MBF to resting MBF was inversely correlated with pack-years (r = -0.57; P = 0.014). Conclusion: Endothelium-dependent coronary artery vasodilator function is impaired in apparently healthy young smokers.