Abstract
Smoking is known to affect microcirculatory function in a middle-aged population. However, the effects of smoking on myocardial perfusion in young smokers have not been studied. Myocardial perfusion was measured in 15 smokers (24 ± 2 years) and 15 nonsmokers (24 ± 3 years) using positron emission tomography. Myocardial perfusion was measured at rest, during cold stress and during dipyridamole. Resting myocardial blood flow was similar in the two groups. The well-described correlation between rate-pressure product and myocardial blood flow was present only in the nonsmokers (r<sup>2</sup> = 0.61, p < 0.001). Myocardial blood flow corrected for the rate-pressure product declined during cold by 20% in the smokers [1.11 ± 0.28 vs. 0.92 ± 0.20 ml·g<sup>–1</sup>·min<sup>–1</sup> (p = 0.012)], but remained unchanged in nonsmokers [1.11 ± 0.25 vs. 1.09 ± 0.30 ml·g<sup>–1</sup>·min<sup>–1</sup> (p = NS)]. Dipyridamole-induced hyperemia was similar in the two groups [2.23 ± 0.78 vs. 2.42 ± 0.65 ml·g<sup>–1</sup>·min<sup>–1</sup> (p = NS)]. In conclusion, smoking induces abnormalities in myocardial microcirculatory regulation in young otherwise healthy smokers. The coronary flow reserve, however, is not significantly altered.
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