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Vol. 65. Issue 2.
Pages 191-193 (February 2012)
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Vol. 65. Issue 2.
Pages 191-193 (February 2012)
DOI: 10.1016/j.rec.2011.04.009
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Prinzmetal Angina in the Migraine's Aura Resolving With Headache
Angina de Prinzmetal en el aura de la migraña que se resuelve con la cefalea
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Vincent Roulea,
Corresponding author
v.roule@hotmail.fr

Corresponding author: v.roule@hotmail.fr
, Adrien Lemaitrea, Ziad Dahdouha, Mathieu Bignona, Gilles Grolliera
a Service de Cardiologie, Centre Hospitalier Universitaire de Caen, Caen, France
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To the Editor,

We report the case of a 28-year-old woman referred to our hospital for constrictive chest pain with a left hemiparesis. She reported using oral contraceptive but had no cardiovascular risk factors. She had a history of unusual migraine with aura (left hemiparesis) since the age of 17 but had never been medicated and specifically not by ergotamine tartrate or triptan. Clinical examination showed left hemiparesis with a normal blood pressure of 132/76mmHg. The electrocardiogram (ECG) revealed a sinus rhythm with ST-segment elevation in the inferior leads with mirror image in the anterior leads suggestive of an acute inferior myocardial infarction (Figure 1A). Per-critical acute transthoracic echocardiography revealed a mild hypokinesis of the inferior wall. The ascending aorta was normal without obvious criteria for aortic dissection. The neurologic signs led us to perform a computed tomography (Figure 1B) that ruled out an intracerebral hemorrhage. The patient received treatment for acute coronary syndrome: sublingual nitrates, intravenous acetylsalicylic acid, loading dose of clopidogrel, and curative dose of enoxaparin. She was transferred without delay to the catheterization laboratory for primary percutaneous intervention. On her way to the catheterization laboratory, the chest pain and the hemiparesis disappeared but she complained of an intense headache. The coronary angiography demonstrated smooth coronary arteries with normal blood flow and no obstructive lesion (Figure 1C). The postangiography ECG was normal (Figure 1D). The 6-h troponin T rose to 11.6 ng/ml. The migraine headaches were treated by analgesics and her acute coronary syndrome was treated by acetylsalicylic acid and verapamil. The echocardiogram at day 5 was normal and the patient was discharged. She remained event-free at 1 year.

Figure 1. A, Per-critical ST-segment elevation in the electrocardiogram inferior leads. B, Normal cerebral computed tomography. C, Normal coronary angiogram with a smooth right coronary artery. D, Post-critical normal electrocardiogram.

The migraine headache is a common disease affecting approximately 13% of the population.1 For 25% of these patients, migraine is associated with aura characterized by neurological symptoms and signs preceding or accompanying the headaches. In the literature, migraine with aura but not the migraine without aura was associated with an increased risk of myocardial infarction and ischemic stroke.2

The underlying pathophysiology of migraine is not fully understood. The condition is viewed as an inherited brain disorder but the vascular mechanisms are clearly implicated. Indeed, altered vascular reactivity has been found in patients with migraine.3 In our patient, we think that the aura was associated with a coronary spasm, most probably of the right coronary artery at the origin of the ST-segment elevation in the inferior leads. It remains possible that a coronary thrombosis with spontaneous thrombolysis or mediated by antiplatelet and anticoagulant therapy or a coronary microvascular dysfunction or a stress cardiac disease could explain the ECG changes. Indeed, no provocation test was done in our patient during the coronary angiogram but the ECG modifications and the early normal coronary angiogram suggested Prinzmetal angina. Then, during the migraine headache which is associated with a cerebral vessel vasodilation, the coronary vasospasm disappeared and the ECG normalized. It should be noted that our patient took no chronic therapy for her migraine such as triptan or ergotamine tartrate, both known to provoke coronary vasospasm.4 The mechanisms that link migraine to the vascular events remained under discussion but are independent of many cardiovascular risk factors.2 Several pathomechanisms have been proposed, such as an increase of the prothrombotic or vasoactive factors, decreased endothelium-dependent relaxation, and increased oxidative stress and inflammation of the vessel wall.5 Moreover, epidemiological data suggest a strong association between the migraine and acquired vascular disorders such as Raynaud phenomenon.6

Our case, with its 2-step evolution, lends support to the idea that the migraine with aura might be the manifestation of a general vasospastic disorder making the patients with migraine prone to a coronary artery spasm.

Corresponding author: v.roule@hotmail.fr

Bibliography
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The epidemiology of migraine..
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Kurth T, Gaziano JM, Cook NR, Logroscino G, Diener HC, Buring JE..
Migraine and risk of cardiovascular disease in women..
JAMA. , 296 (2006), pp. 283-291
[3]
Vanmolkot FH, Van Bortel LM, De Hoon JN..
Altered arterial function in migraine of recent onset..
Neurology. , 68 (2007), pp. 1563-1570
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Mueller L, Gallagher RM, Ciervo CA..
Vasospasm-induced myocardial infarction with sumatriptan..
Headache. , 36 (1996), pp. 329-331
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Dalkara T, Nozari A, Moskowitz MA..
Migraine aura pathophysiology: the role of blood vessels and microembolisation..
Lancet Neurol. , 9 (2010), pp. 309-317
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Increased prevalence of migraine and chest pain in patients with primary Raynaud disease..
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Revista Española de Cardiología (English Edition)

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