A patient recently asked me about nicotine gum and cardiovascular disease risk. After all, everyone knows that smoking cigarettes is bad, but what about nicotine?
I didn’t have a good answer for him.
The following represents my research on the topic.
Acute Cardiovascular Effects of Nicotine
-Acutely increase heart rate up to 10 to 15 beats/min and increase blood pressure up to 5 to 10 mm Hg. These responses are similar to the effects of cigarette smoking.
-Increases cardiac output by increasing both heart rate and myocardial contractility.
-Gum chewing has been shown to aggravate regional myocardial hypoperfusion in patients with known coronary artery disease.
-Constricts some vascular beds, such as the skin. There is evidence that cutaneous vasoconstriction is modulated at least in part by release of vasopressin because the effect was inhibited by administration of a vasopressin antagonist.
-Dilates other vascular beds, such as skeletal muscle.
-Cause alpha-adrenergic vasoconstriction of coronary resistance vessels described previously, cigarette smoking may constrict coronary arteries, presumed due to nicotine-mediated catecholamine release. Of note, the chewing of 4 mg of nicotine gum by healthy nonsmokers has also been shown to blunt the increase in coronary blood flow that occurs with an increase in heart rate. This finding confirms that nicotine is capable of constricting coronary arteries even at low doses in humans.
-Does NOT cause platelet activation. Smoking tobacco does, but again, nicotine does not.
-Can inhibit the synthesis of prostacyclin in isolated blood vessels and isolated hearts. Prostacyclin is thought to be important in vascular homeostasis in that it is a local vasodilator and has antiplatelet aggregation effects. It has been speculated that nicotine could produce an imbalance between the vasodilating antiplatelet prostacyclin and the vasoconstricting platelet aggregation thromboxane A2, the latter of which is released from platelets. There is no convincing evidence that nicotine affects prostacyclin synthesis or release in people.
-Because of rapid delivery of high concentrations of nicotine, with minimal time for development of tolerance, cigarette smoking results in more intense acute cardiovascular effects than the same dose of nicotine absorbed from NRT.
-Cigarette smoking and transdermal nicotine appear to have similar overall hemodynamic effects; however, cigarette smoking activates coagulation and increases 24-h epinephrine excretion, whereas transdermal nicotine does not.
Chronic Cardiovascular Effects of Nicotine
An increased rate of development of aortic and carotid atherosclerosis during nicotine treatment of cholesterol-fed rabbits has been observed. Although these two studies suggest that nicotine may be atherogenic in the presence of hypercholesterolemia, the plasma concentrations of cholesterol produced were several fold greater than those usually seen in hypercholesterolemic humans. Another study used a lower dose of nicotine and a 2% cholesterol diet and failed to demonstrate increased atherosclerosis.
Oral nicotine administered to rats to achieve blood levels comparable to those in human smokers produced greater myointimal thickening of the aorta after experimental injury (denudation of the endothelium with a balloon catheter) than that in control animals. The excessive myointimal thickening in nicotine treated animals is consistent with a response to persistent injury to endothelial cells.
Nicotine and Lipids
Nicotine, by release of catecholamines, induces lipolysis and releases plasma free fatty acids. There is evidence that these free fatty acids are primarily taken up by the liver, which might be expected to increase the synthesis of VLDL, consistent with changes described in cigarette smokers.
Most studies in humans given nicotine preparations suggest that nicotine delivered in these forms does not have an adverse effect on lipid profiles. In one study, nicotine chewing gum (2 mg eight times a day) was given to healthy nonsmokers for 2 weeks. No changes in plasma concentrations of triglycerides; total, HDL or LDL cholesterol; or apolipoprotein A1 or B were noted.
In another study, 20 nonsmokers with ulcerative colitis received transdermal nicotine (15 mg/day) for 12 weeks. No changes in plasma lipids were found. Also, there were no changes in white cell count or platelet activation, and no evidence of endothelial damage was detected.
Data from smokers who stop smoking and use transdermal nicotine indicate that lipids change toward normal while taking nicotine.
Nicotine replacement is better than tobacco usage. Avoid both when possible.