Czernin J, Sun K, Brunken R, Böttcher M, Phelps M, Schelbert H
Department of Molecular and Medical Pharmacology, University of California School of Medicine, Los Angeles, USA.
Circulation. 1995 Jun 15;91(12):2891-7. doi: 10.1161/01.cir.91.12.2891.
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.
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.
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.
吸烟是冠状动脉疾病和心源性猝死的主要可预防风险因素。然而，急性和长期吸烟对冠状动脉舒张能力和心肌血流储备的影响尚未在人体中得到量化。
为了研究短期和长期吸烟的影响，在基线条件下（反映长期吸烟的影响）以及在短期吸烟期间，使用13N氨、正电子发射断层扫描和双室模型，对12名吸烟者（10名男性和2名女性；平均年龄，27±4岁）静息及双嘧达莫诱发充血（0.56mg/kg）时的心肌血流进行了量化。12名年龄和性别匹配的非吸烟者作为对照。吸烟使静息时的心率血压乘积从7525±1290显著增加至9160±1125（与基线相比，P<.001），同时静息时心肌血流也相应增加（0.70±0.17对0.88±0.17mL·g-1·min-1；与基线相比，P<.05）。相比之下，充血血流从基线时的2.23±0.35（与对照相比，P=无显著差异）降至吸烟期间的1.98±0.32mL·g-1·min-1（与基线相比，P<.01）。因此，吸烟者的心肌血流储备从基线时的3.36±0.83降至吸烟期间的仅2.28±0.28（与基线相比，P<.0001）。因此，年轻的长期吸烟者和年轻健康的非吸烟者的心肌血流和血流储备相似。
短期吸烟会增加双嘧达莫诱发充血时的冠状动脉血管运动张力，并显著降低心肌血流储备。相比之下，长期吸烟不会削弱吸烟史相对较短的年轻人的冠状动脉舒张能力。可以推测，吸烟期间冠状动脉舒张能力的短期降低可能会降低冠心病吸烟者的缺血阈值，并增加心源性猝死的风险。
