Case Report
Acute Myocardial Infarction Following the Use of Antimigraine Therapy
October 2004
Case Report. This is the case of a 50-year-old woman who presented to hospital with an anterior myocardial infarction. She was treated with thrombolysis, with front loaded r-tPA, within 2 hours of onset of symptoms. She had previously been fit and well with no known risk factors for cardiovascular disease. She had no history of illicit drug use. She had been taking zolmitriptan (2.5 mg o.d.) for migraine for 6 months. Two days prior to her myocardial infarction, she increased the dose of zolmitriptan to 2.5 mg b.d. She had recurrence of chest pain with further ST elevation anteriorly (Figure 1) over the following 2 days and subsequently underwent urgent coronary angiography which showed normal coronary arteries. Left ventriculography showed antero-apical akinesia with an estimated ejection fraction of 45% (Figure 2). Over the ensuing few days, she developed further chest pain associated with ST-elevation in the same territory. Both her symptoms and ECG changes reverted spontaneously within 15 minutes. She was subsequently treated with diltiazem 360 mg p.o. daily. She was then discharged home on daily aspirin 100 mg as well as diltiazem. Zolmitriptan was discontinued at that time.
During the subsequent 2 months, the patient experienced infrequent atypical chest pain. At this stage she was transferred to our tertiary center where she underwent repeat coronary angiography with ergotamine provocative test. During the same procedure which showed normal coronaries, she was investigated with intravascular ultrasound (ClearView 40 MHz Ultra, Boston Scientific, Natick, Massachusetts) of the left anterior descending artery which failed to reveal any evidence of intracoronary plaques. She also underwent vasoconstricter provocation testing with escalating doses of intracoronary ergotamine (8, 16, 32 and 50 mg). Each dose was administered in the left coronary artery via a 6 French left Judkins diagnostic catheter for a period of 5 minutes with repeat contrast injection following each dose. With intracoronary ergotamine, she did not experience any chest pain, ECG changes or a reduction in coronary caliber. In addition, the cold pressor test was performed with hand insertion in ice water for 2 minutes. This did not induce any chest pain or ischemic ECG changes. The patient was reassured and was advised not to restart zolmitriptan for her migraines.
Discussion. Several reports have documented a relationship between antimigraine drugs and cardiac effects. Sumatriptan has been associated with cardiac symptoms such as chest pain,1–3 myocardial infarction4,5 and even cardiac arrest.6 Zolmitriptan is a 5-hydroxytryptamine (5-HT) derivative and has agonist activity at the 5-HT 1B/1D receptor. Antimigraine drugs such as sumatriptan are thought to cause cardiac symptoms by coronary vasoconstriction, and this has been demonstrated both in vivo7 and in vitro studies.8–10 In a recent study a comparison was made between a number of “first generation” antimigraine drugs (like sumatriptan) and the newer “second generation” drugs (such as zolmitriptan) that are thought to cause less coronary vasoconstriction.11 This was an in vitro study that compared the effect of the various antimigraine drugs in human isolated coronary artery.
It demonstrated that all current antimigraine drugs, including zolmitriptan, cause coronary vasoconstriction in vitro.11 These findings were also confirmed by a further study using zolmitriptan.12 By measuring the maximum contractile response (E max) in human isolated coronary artery segments, the concentration eliciting 50% of E max (EC 50), and the maximum plasma concentrations (C max), the ratio of C max/EC 50 was calculated. This ratio was indicative of coronary vasoconstriction occurring in vivo.11 This ratio was indicative of coronary vasoconstriction occurring in vivo.11 This study showed that the C max of zolmitriptan and sumitriptan were Conclusion. We can conclude from this case that zolmitriptan was the most likely cause of coronary vasoconstriction which resulted in myocardial infarction. Although antimigraine drugs are contraindicated in patients with coronary artery disease, caution needs to be taken in those individuals with no risk factors for coronary heart disease and who complain of chest pain. In such cases, the drug should be discontinued and should not be restarted.
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