LONG-TERM CIGARETTE-SMOKING IS ASSOCIATED WITH INCREASED MYOCARDIAL PERFUSION HETEROGENEITY ASSESSED BY POSITRON EMISSION TOMOGRAPHY

The pathophysiology of smoking-related coronary events in patients wit h normal coronary arteries is incompletely understood. This study was conducted to explore, in subjects without symptoms of cardiovascular d isease, the long-term effects of smoking on regional. coronary artery vasoactivity, especially during sympathetic stimulation. In ten smokin g and ten non-smoking sex- and age-matched healthy volunteers, segment al myocardial perfusion was studied using dynamic parametric nitrogen- 13 ammonia positron emission tomography at rest and during sympathetic stimulation evoked by the cold Dresser stimulation, Smokers demonstra ted a higher myocardial perfusion at rest (116+/-17 ml/min/100 g vs 96 +/-20 ml/min/100 g, P <0.01) and an impaired myocardial perfusion incr ease during cold presser stimulation (1.02+/-0.15 vs 1.18+/-0.17, P <0 .05). The heterogeneity of perfusion. expressed as coefficient of vari ation, was significantly different between the smoking and the non-smo king group, The coefficient of variation of segmental myocardial perfu sion was higher in smelters at rest (17.5%+/-4.2% vs 13.5%+/-1.9%, P < 0.05) and during cold presser stimulation (17.0%+/-3.2% vis 13.9%+/-1. 8%, P <0.05), We conclude that the long-term effects of smoking in hea lthy volunteers are associated with (1) increased myocardial perfusion at rest, (2) impaired myocardial perfusion response to cold presser s timulation, and (3) increased myocardial perfusion heterogeneity both at rest and during cold presser stimulation. These results may suggest that in healthy subjects the longterm effect of smoking is related to abnormal coronary artery vasoactivity, presumably induced by an inter play of regional endothelial dysfunction and autonomic dysregulation.