Short-term cigarette smoking markedly reduced myocardial flow reserve from 3.36 at baseline to 2.28 (P<0.0001), whereas long-term smoking did not attenuate coronary vasodilatory capacity.
Observational (n=24)
Does acute and long-term cigarette smoking reduce myocardial blood flow and flow reserve in young adults?
Acute cigarette smoking markedly reduces myocardial flow reserve during hyperemia, which may lower the ischemic threshold, although long-term smoking in young individuals with a short smoking history does not attenuate baseline coronary vasodilatory capacity.
Absolute Event Rate: 2.28% vs 3.36%
p-value: p=<.0001
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.
Czernin et al. (Thu,) conducted a observational in Healthy (smokers and nonsmokers) (n=24). Short-term cigarette smoking vs. Baseline (no acute smoking) was evaluated on Myocardial flow reserve (p=<.0001). Short-term cigarette smoking markedly reduced myocardial flow reserve from 3.36 at baseline to 2.28 (P<0.0001), whereas long-term smoking did not attenuate coronary vasodilatory capacity.