From Ahmanson Biological Imaging Clinic/Nuclear Medicine, Department of
Molecular and Medical Pharmacology and Department of Physiology (F.D.M.), UCLA
School of Medicine and Laboratory of Structural Biology & Molecular
Medicine, University of California, Los Angeles.
Correspondence to Johannes Czernin, MD, Ahmanson Biological Imaging Clinic/Nuclear Medicine, Department of Molecular and Medical Pharmacology, UCLA School of Medicine, AR-259 CHS, Los Angeles, CA 90095-6948. E-mail jczernin{at}mail.nuc.ucla.edu
Background—The effect of long-term
smoking on coronary vasomotion and vasodilator capacity in
healthy smokers is unknown.
Methods and Results—Myocardial blood flow (MBF) was quantified
with [13N]ammonia and positron emission tomography (PET)
at rest, during cold pressor testing
(endothelium-dependent vasomotion), and during
dipyridamole-induced hyperemia in 16 long-term
smokers and 17 nonsmokers. MBF at rest did not differ between the 2
groups. Cold induced similar increases in rate-pressure product
(RPP) in smokers and nonsmokers. However, MBF increased only in
nonsmokers and was, during cold, higher than in smokers (0.91±0.18
versus 0.78±0.14 mL · g-1 ·
min-1, P<0.05). MBF normalized to the RPP
(derived from the ratio of MBF ([milliliters per gram per minute] to
RPP [beats per minute times millimeters of mercury] times 10 000)
declined in smokers but remained unchanged in nonsmokers (0.86±0.10
versus 0.72±0.11, P=0.0006, and 0.99±0.25 versus
0.96±0.27, P=NS). The hyperemic response to
dipyridamole and the myocardial flow reserve did not
differ between the 2 groups. In a multiple regression model adjusted
for age, sex, serum lipid levels, years of smoking, and pack-years,
years of smoking was the strongest predictor of the normalized blood
flow response to cold (P<0.001), followed by the
HDL/LDL ratio.
Conclusions—The normal hyperemic response to
dipyridamole in long-term smokers indicates a preserved
endothelium-independent coronary vascular
smooth muscle relaxation, whereas the abnormal response to cold
suggests a defect in coronary vasomotion likely located at the
level of the coronary endothelium. Its severity
depends on the total exposure time to smoking.
© 1998 American Heart Association, Inc.
Clinical Investigation and Reports
Effects of Long-term Smoking on Myocardial Blood Flow, Coronary Vasomotion, and Vasodilator Capacity
Key Words: blood flow • smoking • tomography • cold pressor test
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