INTRANASAL NICOTINE SPRAY DOES NOT AUGMENT THE ADVERSE-EFFECTS OF CIGARETTE-SMOKING ON MYOCARDIAL OXYGEN-DEMAND OR CORONARY ARTERIAL DIMENSIONS

PURPOSE: Nicotine replacement therapy has become a popular therapy for smokers attempting to stop smoking. Unfortunately, some subjects cont inue to smoke while receiving it. Since nicotine is believed to be the primary constituent of cigarette smoke responsible for its acute adve rse effects on myocardial oxygen supply and demand, concomitant nicoti ne replacement therapy and smoking theoretically could provoke a marke d decrease in myocardial oxygen supply and increase in demand. This st udy was performed to assess the effects of cigarette smoking with and without concomitant intranasal nicotine spray on: (a) myocardial oxyge n demand, (b) coronary arterial dimensions, and (c) the development of acute cardiovascular tolerance. PATIENTS AND METHODS: In 19 smokers r eferred for cardiac catheterization for the evaluation of chest pain, we assessed the effects of cigarette smoking with and without concomit ant intranasal nicotine spray on: (a) heart rate-systolic arterial pre ssure product (an estimate of myocardial oxygen demand), (b) coronary arterial dimensions (measured with computer-assisted quantitative arte riography), and (c) the development of acute cardiovascular tolerance. RESULTS: Smoking a first cigarette increased rate pressure product (P <0.001) and decreased coronary arterial dimensions (P <0.0001). Subse quently, neither variable was altered by intranasal nicotine spray or a second cigarette. Despite a substantial increase in serum nicotine c oncentration with nicotine spray and smoking, acute cardiovascular tol erance appears to develop. CONCLUSIONS: Cigarette smoking causes an in crease in myocardial oxygen demand and concomitant coronary arterial v asoconstriction. However, further increases in the serum nicotine conc entration do not cause a greater increase in demand or decrease in cor onary arterial dimensions. These data suggest that humans acutely deve lop tolerance to an increasing nicotine concentration, thereby helping to explain the apparent lack of a potential synergistic adverse effec t associated with continued smoking during nicotine replacement therap y.