Nicotine does not compromise resting myocardial blood flow autoregulation in smokers at high cardiovascular risk

Nicotine has been recognized for years as being pharmacologically responsible for the sympathoexcitatory effects of smoking. The effects of nicotine supplementation on myocardial blood flow as assessed by positron emission tomography are, however, unknown. We tested the hypothesis that nicotine substitution could interfere with myocardial blood flow autoregulation at rest in habitual smokers at risk of coronary artery disease. The short-term effect of a 4-mg nicotine tablet on myocardial blood flow was quantified with 13N ammonia positron emission tomography in 12 smokers with high cardiovascular risk (10 males and 2 females; mean age = 58+/-8 years; SCORE risk >5%). Nicotine increased systolic blood pressure from 129+/-7 to 134+/-7 mmHg (p = .03) and heart rate from 67+/-2 to 69+/-2 bpm (p = .04). As a result, nicotine raised the rate-pressure product from 8618+/-622 to 9285+/-627 bpm mmHg (p = .02). Nicotine tended to increase myocardial blood flow in the circumflex artery territory, but this effect failed to reach the level of statistical significance (from 0.56+/-0.06 to 0.63+/-0.03 ml/min/g; p>.15). This trend disappeared when myocardial blood flow was normalized for the rise in the rate-pressure product. Global myocardial perfusion, normalized for the changes in rate-pressure product, remained unchanged from 0.70+/-0.06 at baseline to 0.71+/-0.03 (ml/min/g)/(bpm mmHg) after nicotine. Nicotine supplementation in habitual smokers with high cardiovascular risk increased myocardial work without compromising resting myocardial blood flow autoregulation.