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LETTER

Myocardial Infarction in a Patient Who Smoked while Wearing a Nicotine Patch

right arrow James G. Warner, Jr., MD, EdD, and William C. Little, MD

15 April 1994 | Volume 120 Issue 8 | Page 695


TO THE EDITOR:

Transdermal nicotine was introduced in 1992 to treat tobacco dependence. Although the use of nicotine patches in patients with coronary artery disease is appealing, its safety is unclear. We recently treated a patient who, while wearing a nicotine patch, had an acute myocardial infarction soon after starting to smoke a cigarette.

Our patient, a 47-year-old male smoker, suffered an inferior myocardial infarction in December 1991. Coronary arteriography at another institution showed a subtotal stenosis of the mid-right coronary artery and only a 50% stenosis of the left anterior descending artery. He stopped smoking and began wearing a 21-mg nicotine patch. One week later, while continuing to wear the patch, he smoked a cigarette for approximately 5 minutes and developed severe chest pain radiating to his left arm and jaw. Thirty minutes later, an electrocardiogram showed ST elevation in the anterolateral leads, and thrombolytic therapy was administered. He was transferred to our institution for cardiac catheterization, which showed that the infarction was caused by a new subtotal occlusion of the proximal left anterior descending artery.

Nicotine increases blood pressure and heart rate both directly and through activation of the sympathetic nervous system, thus increasing myocardial oxygen consumption [1]. Nicotine can provoke angina in patients with coronary artery disease and can also trigger infarction. Muller and colleagues [2] hypothesized that activities associated with increased catecholamine levels can both trigger plaque rupture and promote the occlusive thrombus formation that can result in myocardial infarction or sudden cardiac death. Nicotine, by evoking the release of catecholamines [1], stimulating platelet aggregation [3], and increasing platelet-vessel wall interactions [3], may be a potent trigger of myocardial infarction.

During cigarette smoking, nicotine is rapidly absorbed, producing peak blood levels of about 15 ng/mL within the first few minutes [1], whereas a 21-mg transdermal nicotine patch produces peak blood levels of about 18 ng/mL between 5 to 6 hours after application [4]. Thus, nicotine levels would be markedly elevated when the patch and smoking are combined, especially within the early minutes of smoking. We postulate that high plasma nicotine concentrations produced by the combination of smoking and nicotine patch use triggered the acute infarction in our patient.

Just as it is important for these patients not to smoke after presenting with an ischemic event, it is also unwise to start them on nicotine patches once discharged because of potential adverse cardiovascular effects of nicotine [5]. Furthermore, patients with coronary artery disease should be advised that the high nicotine levels produced when smoking is combined with nicotine patch use may trigger myocardial infarction.


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Bowman Gray School of Medicine; Winston-Salem, NC 27157


References
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1. Benowitz NL. Pharmacologic aspects of cigarette smoking and nicotine addiction. N Engl J Med. 1988; 319:1318-30.

2. Muller JE, Tofler GH, Stone PH. Circadian variation and triggers of onset of acute cardiovascular disease. Circulation. 1989; 79:733-43.

3. Folts JD, Gering SA, Laibly SW, Bertha BG, Bonebrake FC, Keller JW. Effects of cigarette smoke and nicotine on platelets and experimental coronary artery thrombosis. Adv Exp Med Biol. 1990; 273: 339-58.

4. Gorsline J, Gupta SK, Dye D, Rolf CN. Steady-state pharmacokinetics and dose relationship of nicotine delivered from Nicoderm (Nicotine Transdermal System). J Clin Pharmacol. 1993; 33:161-8.

5. Orleans CT, Ockene JK. Routine hospital-based quit-smoking treatment for the postmyocardial infarction patient: an idea whose time has come. J Am Coll Cardiol. 1993; 22:1703-5.

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