EFFECT OF ACUTE AND LONG-TERM SMOKING ON MYOCARDIAL BLOOD-FLOW AND FLOW RESERVE

Citation
J. Czernin et al., EFFECT OF ACUTE AND LONG-TERM SMOKING ON MYOCARDIAL BLOOD-FLOW AND FLOW RESERVE, Circulation, 91(12), 1995, pp. 2891-2897
Citations number
39
Categorie Soggetti
Cardiac & Cardiovascular System",Hematology
Journal title
ISSN journal
00097322
Volume
91
Issue
12
Year of publication
1995
Pages
2891 - 2897
Database
ISI
SICI code
0009-7322(1995)91:12<2891:EOAALS>2.0.ZU;2-E
Abstract
Background Cigarette smoking is a major preventable risk factor for co ronary artery disease and sudden cardiac death. However, the effect of acute and long-term cigarette smoking on coronary vasodilatory capaci ty and myocardial flow reserve has not been quantified in humans. Meth ods and Results To examine the effect of short-term and long-term smok ing, myocardial blood flow was quantified at rest and during dipyridam ole-induced hyperemia (0.56 mg/kg) in 12 smokers (10 males and 2 femal es; mean age, 27 +/- 4 years) under baseline conditions (reflecting th e effect of longterm smoking) and during short-term cigarette smoking with N-13 ammonia, positron emission tomography, and a two-compartment model. Twelve sex- and age-matched nonsmokers served as control subje cts. Smoking significantly increased the rate-pressure product at rest from 7525 +/- 1290 to 9160 +/- 1125 (P<.001 versus baseline), which w as paralleled by a proportional increase in myocardial blood flow at r est (0.70 +/- 0.17 versus 0.88 +/- 0.17 mL . g(-1).(-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 myocardia l flow reserve declined from 3.36 +/- 0.83 in smokers at baseline to o nly 2.28 +/- 0.28 during smoking (P<.0001 versus baseline). Thus, myoc ardial blood flow and flow reserve were similar in young, long-term sm okers and young, healthy nonsmokers. Conclusions Short-term smoking in creases the coronary vasomotor tone during dipyridamole-induced hypere mia and markedly reduces the myocardial flow reserve. In contrast, lon g-term smoking does not attenuate the coronary vasodilatory capacity i n young individuals with a relatively short smoking history. It might be speculated that the short-term reduction in the coronary vasodilato ry capacity during smoking could lower the ischemic threshold in smoke rs with coronary artery disease and contribute to the increased risk f or sudden cardiac death.