Affiliation:
1. From the Department of Molecular and Medical Pharmacology, Division of Nuclear Medicine and Biophysics, University of California School of Medicine, and the Laboratory of Structural Biology and Molecular Medicine, University of California, Los Angeles.
Abstract
Background
Cigarette smoking is a major preventable risk factor for coronary artery disease and sudden cardiac death. However, the effect of acute and long-term cigarette smoking on coronary vasodilatory capacity and myocardial flow reserve has not been quantified in humans.
Methods and Results
To examine the effect of short-term and long-term smoking, myocardial blood flow was quantified at rest and during dipyridamole-induced hyperemia (0.56 mg/kg) in 12 smokers (10 males and 2 females; mean age, 27±4 years) under baseline conditions (reflecting the effect of long-term smoking) and during short-term cigarette smoking with
13
N ammonia, positron emission tomography, and a two-compartment model. Twelve sex- and age-matched nonsmokers served as control subjects. Smoking significantly increased the rate-pressure product at rest from 7525±1290 to 9160±1125 (
P
<.001 versus baseline), which was paralleled by a proportional increase in myocardial blood flow at rest (0.70±0.17 versus 0.88±0.17 mL · g
−1
· min
−1
;
P
<.05 versus baseline). In contrast, hyperemic blood flow declined from 2.23±0.35 at baseline (
P
=NS versus control) to 1.98±0.32 mL · g
−1
· min
−1
during smoking (
P
<.01 versus baseline). Accordingly, the myocardial flow reserve declined from 3.36±0.83 in smokers at baseline to only 2.28±0.28 during smoking (
P
<.0001 versus baseline). Thus, myocardial blood flow and flow reserve were similar in young, long-term smokers and young, healthy nonsmokers.
Conclusions
Short-term smoking increases the coronary vasomotor tone during dipyridamole-induced hyperemia and markedly reduces the myocardial flow reserve. In contrast, long-term smoking does not attenuate the coronary vasodilatory capacity in young individuals with a relatively short smoking history. It might be speculated that the short-term reduction in the coronary vasodilatory capacity during smoking could lower the ischemic threshold in smokers with coronary artery disease and contribute to the increased risk for sudden cardiac death.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Subject
Physiology (medical),Cardiology and Cardiovascular Medicine
Reference39 articles.
1. Contributions of the framingham study to the conquest of coronary artery disease
2. Kannel WB Higgins M. Smoking and hypertension as predictors of cardiovascular risk in population studies. J Hypertens . 1990;8(suppl 5):S3-S8.
3. Pharmacologic Aspects of Cigarette Smoking and Nicotine Addiction
4. Norepinephrine and Epinephrine Release and Adrenergic Mediation of Smoking-Associated Hemodynamic and Metabolic Events
5. Groppelli A Omboni S Parati G Mancia G. Blood pressure and heart rate response to repeated smoking before and after beta-blockade and selective alpha 1 inhibition. J Hypertens . 1990;8(suppl 5):S35-S40.
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