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Effect of acute and long-term smoking on myocardial blood flow and flow reserve
1Department of Molecular and Medical Pharmacology, University of California School of Medicine, Los Angeles, USA.
Insights
Short-term smoking impairs coronary blood flow and reduces myocardial flow reserve. However, long-term smoking in young individuals does not affect coronary vasodilatory capacity.
Area of Science:
- Cardiology
- Cardiovascular Physiology
- Nuclear Cardiology
Background:
- Cigarette smoking is a significant risk factor for coronary artery disease and sudden cardiac death.
- The impact of acute and chronic smoking on coronary vasodilatory capacity and myocardial flow reserve in humans remains under-quantified.
Purpose of the Study:
- To investigate the effects of both short-term and long-term cigarette smoking on myocardial blood flow and coronary flow reserve.
- To quantify changes in coronary vasodilatory capacity in response to acute smoking.
Main Methods:
- Utilized positron emission tomography (PET) with 13N ammonia to measure myocardial blood flow at rest and during dipyridamole-induced hyperemia.
- Employed a two-compartment model for quantitative analysis.
- Compared 12 young long-term smokers with 12 age- and sex-matched healthy non-smokers.
Main Results:
- Short-term smoking significantly increased resting heart rate and blood pressure, leading to a rise in resting myocardial blood flow.
- Hyperemic myocardial blood flow decreased during short-term smoking.
- Myocardial flow reserve was significantly reduced during acute smoking compared to baseline.
- Long-term smoking in young individuals did not attenuate baseline myocardial blood flow or flow reserve compared to non-smokers.
Conclusions:
- Acute smoking acutely increases coronary vasomotor tone, significantly diminishing myocardial flow reserve.
- Long-term smoking in young individuals with a limited smoking history does not appear to impair coronary vasodilatory capacity.
- The acute reduction in myocardial flow reserve during smoking may lower the ischemic threshold in smokers with coronary artery disease, potentially increasing the risk of sudden cardiac death.
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 13N 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.