Arterial blood nicotine concentration and coronary vasoconstrictive effect of low-nicotine cigarette smoking

Abstract

Low-nicotine cigarettes have been advertised to the public as less harmful to the cardiovascular system. We studied the effects of smoking two low-nicotine cigarettes on arterial and venous blood nicotine levels, hemodynamics, and coronary vascular tone in 12 patients referred for diagnostic coronary arteriography. All were chronic smokers as evidenced by their elevated baseline arterial and venous cotinine blood levels (139 ± 30 ng/ml and 155 ± 34 ng/ml, respectively). High-resolution coronary angiograms were evaluated “blindly” before and after smoking. An electronic caliper was used to measure the diameter of disease-free coronary segments of the left anterior descending and circumflex arteries. Arterial nicotine levels rose from 5 ± 1 ng/ml at baseline to 37 ± 7 ng/ml (p < 0.01) after the first cigarette was smoked and to 45 ± 8 ng/ml (p < 0.01) after the second cigarette. Venous nicotine levels rose from 8 ± 2 ng at baseline to 15 ± 3 ng/ml (p < 0.05) after the first cigarette and to 20 ± 3 ng/ml (p < 0.01) after the second cigarette. After the first cigarette heart rate increased 8 ± 2 beats/min (p < 0.003) and double product 1229 ± 400 beats/min × mm Hg (p < 0.02). Compared to baseline values, after the second cigarette heart rate increased 9 ± 1 beats/min (p < 0.001) and double product 1767 ± 486 beats/min × mm Hg (p < 0.01). Systolic, diastolic, and mean blood presure did not change significantly after either the first or second cigarette. The left anterior descending artery diameter changed from 2.31 ± 0.2 mm before smoking to 2.03 ± 0.2 mm after the first cigarette was smoked (p < 0.01) and 2.10 ± 0.2 mm after the second cigarette (p < 0.01). The circumflex artery diameter changed from 2.49 ± 0.2 mm before smoking to 2.19 ± 0.1 mm after the first cigarette (p < 0.01) and to 2.21 ± 0.2 mm after the second cigarette (p < 0.01). Correlation of changes in coronary diameter (constriction) with increments in arterial nicotine levels showed a borderline correlation with the first cigarette (r = 0.46, p = 0.049) and a significant correlation with the second cigarette (r = 0.61, p = 0.003). No correlation was found with venous nicotine levels. We conclude that smoking low-nicotine cigarettes evokes significant increases in arterial blood nicotine concentrations, which substantially exceed venous levels, increases heart rate and double product, and induces significant coronary vasoconstriction. Therefore smoking low-nicotine cigarettes produces adverse effects on the cardiovascular system.