Acute myocardial infarction soon after nicotine replacement therapy

Sir, Cigarette smoking is a major risk factor for vascular disease. Fifty percent of smokers die of smoking‐related causes, and continuing to smoke doubles the risk of death for patients with coronary artery disease. Hence smoking cessation is the most effective intervention available to patients with heart disease. Nicotine replacement therapy (NRT) is an effective smoking cessation intervention. A systematic review of 47 trials showed that smoking cessation rates were doubled by NRT over a period of 6–12 months.1 These studies also concluded that NRT does not contribute substantially to acute cardiovascular events, and hence can be prescribed safely in patients with coronary artery disease.2,3 In recent months, there have been major efforts to expand the prescription of NRT to smokers.4,5 We describe acute myocardial infarction (MI) developing within days of initiation of NRT, shortly after a first clinical presentation with angina pectoris, in an attempt to draw attention to potential risks of NRT in patients who have had recent coronary plaque rupture. A 47‐year‐old man with no previous medical history was admitted with new‐onset exertional angina over 3 days. There was no rest pain. Initial and serial 12‐lead electrocardiograms showed no ischaemic changes. Cardiac enzyme and troponin I levels (12 h from admission) stayed within the normal ranges. During an exercise stress test, he managed a high workload (12.4 metabolic equivalents), although ischaemic ST segment depression developed in the second stage of the Bruce protocol. He remained angina‐free, and was discharged on aspirin, atenolol, isosorbide mononitrate and atorvastatin. He was also commenced on nicotine patches (Nicorette, Pharmacia & Upjohn, 15 mg for 16 h/day) to help quit smoking. Three days later he presented with acute central chest pain. He had not smoked a cigarette since discharge. An electrocardiogram confirmed inferior myocardial infarction with ST segment elevation, and reteplase was administered with prompt ST segment resolution. The clinical course was uncomplicated. Coronary angiography revealed a discrete stenosis of the right coronary artery which was successfully stented. Anecdotal cases of acute cardiovascular events in people using NRT have been reported, although such reports do not establish causality.6 Smokers have a higher risk of cardiac events even after they stop smoking, and hence it is difficult to ascribe such events specifically to NRT as opposed to the underlying disease or the delayed effects of smoking. However, most evidence of safety of NRT in patients with coronary artery disease comes from patients with stable IHD kept under close surveillance.2,3,7 Safety of NRT in patients with unstable coronary syndromes (UCS) has never been established, despite the fact that this is the commonest manifestation of coronary artery disease in hospital practice. While coincidence cannot be excluded in the patient described, there is a clear temporal relationship between initiation of NRT and acute MI in a patient whose expected risk of MI is of the order of 1:600 over 30 days.8 A variety of mechanisms explain why NRT might predispose to MI in a patient with coronary artery disease, especially in the setting of recent plaque rupture; these include coronary vasoconstriction and increased heart work due to tachycardia and hypertension.9 While the pharmacokinetics of NRT suggest that nicotine acquired in this way is less harmful than the bolus effect of cigarette smoking, we would highlight the paucity of safety data for NRT in patients with UCS. We also suggest that NRT be formally contra‐indicated in UCS, pending prospective safety studies in this group of patients.