New study in rats suggests that nicotine at concentrations found in the blood of smokers may increase atrial vulnerability to inducible atrial tachycardia and atrial fibrillation in normal adult atria with no atrial disease.
Large numbers of Americans still smoke cigarettes or use over-the-counter nicotine products such as patches and gums to satisfy their craving for nicotine. However, serious and sometime fatal cases of atrial fibrillation (AF) have been reported in patients who use a nicotine product. This is particularly true when the individual has smoked while using a nicotine patch. AF is the most common type of disturbance of the normal rhythm of the heart and affects some two million people annually. At its most devastating, AF results in stroke (brain attack) and congestive heart failure. Previous studies have concluded that transdermal nicotine patches should be used cautiously because of the high risk of AF they carry for patients with heart disease.
How specific atrial substrates control and modulate atrial vulnerability, which can induce atrial tachycardia (AT) and AF (AT/AF) in response to acute doses of nicotine, is poorly understood. One substrate known to modulate atrial vulnerability to inducible AT/AF is enhanced atrial interstitial fibrosis, commonly found among the aging. Against this backdrop a team of researchers has hypothesized that nicotine concentrations found in the blood of certain smokers exerts a differential influence on the atria and on different substrates for AT/AF. They tested their hypothesis by determining atrial sensitivity to nicotine by inducible AT/AF in young and old rats.
Conclusions and Discussion
The results of this study show that atrial sensitivity to nicotine for inducible AT/AF is different in young vs. old rats. Nicotine significantly increased atrial vulnerability to inducible AT/AF in the young rats while suppressing AT/AF induction in the old rats, causing complete prevention of inducible AT/AF and high degrees of interartrial conduction block. These results also suggest that nicotine at concentrations found in the blood of smokers (30-85 ng/ml) might increase atrial vulnerability to inducible AT/AF in normal adult atria with no atrial disease.
Limitations of the Study
This study was done using Landendorff-perfused normal young and aged hearts with no other detectable confounding atrial disease. Applicability of these findings to human clinical settings may not be possible – particularly the potential use of nicotine as an anti- AT/AF agent in the aged population -- because of the detrimental effects of nicotine in causing high degrees of interatrial conduction block.
Source: November 2003 edition of the American Journal of Physiology—Heart and Circulatory Physiology.
Donna Krupa | APS
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