An unusual cause of chest pain: Acute coronary syndrome following administration of ergotamine tartrate

Abstract

For many years, ergotamine has been used for the acute treatment of migraine. Ergotamine may produce coronary vasospasm, which is often associated with ischemic electrocardiography changes and angina pectoris. A 62-year-old woman who was admitted to the emergency department because of chest pain is described. She had a history of severe migraine attacks and started to use ergotamine tartrate 0.75 mg daily the day before. Electrocardiography revealed sinus tachycardia with left anterior hemiblock and T wave inversion in the precordial leads. Cardiac biomarker levels were elevated. After discontinuation of the drug and initiation of vasodilator treatment, her chest pain resolved. Patients with migraine may have an underlying vasospastic disorder predisposing them to coronary artery spasm. Physicians should be alerted to potential cardiac vasospastic effects of low-dose ergotamine in the treatment of migraine.

Ergotamine is a widely used drug in the management of acute migraine (1). In most patients, ergotamine is well tolerated; however, it has been reported that ergot alkaloids can provoke coronary artery spasm in patients with variant angina (2). In the present report, we describe a case involving a woman with migraine who experienced acute coronary syndrome following therapy with low-dose ergotamine.

CASE PRESENTATION

A 62-year-old woman was admitted to the emergency department (ED) due to chest pain described as a squeezing retrosternal pain radiating to the left arm. She had a history of severe migraine attacks and started to use ergotamine tartrate 0.75 mg daily the day before. She had no history of Raynaud’s phenomenon. On arrival to the ED, she had a blood pressure of 128/78 mmHg, a pulse of 104 beats/min, a respiratory rate of 20 breaths/min, an oral temperature of 36.7°C and oxygen saturation of 99% on room air. Her physical examination was normal. Electrocardiography revealed sinus tachycardia with left anterior hemiblock and T wave inversion in the precordial leads (Figure 1). A complete blood count and serum biochemistry were normal. Cardiac biomarkers were elevated (creatine kinase/MB 954 U/L [normal range 30 U/L to 170 U/L]; myoglobin 6.84 nmol/L, [normal range 1.42 nmol/L to 2.91 nmol/L]; and troponin T 0.564 μg/L, [normal range 0 μg/L to 0.1 μg/L]). Transthoracic echocardiography revealed hypokinesia at the interventricular septum. Her chest pain was believed to be related to coronary vasospasm associated with ergotamine tartrate; ergotamine was discontinued. Treatment consisting of acetylsalicylic acid 300 mg/day, a 300 mg loading dose of clopidogrel, low-molecular-weight heparin, diltiazem slow release 120 mg twice daily and oral isosorbide mononitrate 40 mg twice daily was started. After initiation of therapy, her chest pain resolved. Six hours after symptom onset, she underwent urgent coronary angiography, which revealed normal coronary arteries (Figure 2). Her subsequent course was uneventful, and she was advised to avoid medications containing ergotamine in the future.

Figure 1).

Electrocardiogram showing T wave inversions in the precordial leads

Figure 2).

Coronary angiography revealing normal coronary arteries. Left panel Normal left coronary arteries in left anterior oblique view. Right panel Normal right coronary artery

DISCUSSION

Myocardial infarction (MI) is a major cause of death and disability worldwide (3). The most common etiology is atherothrombosis, but other causes such as coronary artery spasm, coronary embolism, anemia, dysrhythmias, hypertension or hypotension may also cause MI (3). Vasospastic angina, often referred to as ‘variant’ angina, is a temporary increase in coronary vascular tone causing a marked but transient reduction in luminal diameter (4). This coronary vasospastic state is usually focal at a single site and can occur in either a normal or diseased vessel. Patients are predominantly younger women who may not have the classical cardiovascular risk factors. It has been associated with vasospastic disorders such as Raynaud’s phenomenon and migraine headaches (5).

Ergotamine is a well-known ergot alkaloid used for the treatment of migraine. It acts as an α-adrenergic, serotoninergic and dopamine-receptor agonist (1,6). It may cause side effects such as weakness, nausea, vomiting and uterine contractions (1). Ergotamine may produce coronary vasospasm, which is often associated with ischemic electrocardiographic changes and angina pectoris (7). The vasoconstrictor effect of ergotamine in isolated human coronary artery is long-lasting and persists even after repeated washings (8). Similarly, intravenous administration of ergotamine (0.25 mg) caused a reduction in coronary microcirculatory blood flow as measured by positron emission tomography (9); it may also cause sudden cardiac death and arrhythmias (7). In our patient, coronary vasospasm developed with a 0.75 mg tablet of ergotamine tartrate. Treatment of ergotamine-induced coronary vasospasm consists mainly of discontinuation of ergot alkaloid and administration of vasodilator therapy (1,2,6). The clinical course is usually self-limited and patients should be advised to avoid medications containing ergot alkaloids.

CONCLUSION

Some patients with migraine have an underlying vasospastic disorder predisposing them to coronary artery spasm. Physicians should be alerted to potential cardiac vasospastic effects of low-dose ergotamine in the treatment of migraine.