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Migrainous Thoracalgia in a Patient with Chronic Migraine and Coronary Vasospasm: A Case Report
Dean Zeldich1, Victor S Wang1,2, Cyril David1
1Department of Neurology, Jefferson Headache Center, Thomas Jefferson University Hospital, Philadelphia, PA, USA.
Migrainous thoracalgia (MT) refers to chest pain (CP) potentially arising from a neurologic etiology, often temporally linked to migraine. We present a 57-year-old woman with chronic migraine who developed recurrent CP typically following migraine attacks. Despite multiple cardiac evaluations, including cardiac MRI and catheterizations, she was diagnosed with fibromuscular dysplasia, spontaneous coronary artery dissection, and coronary microvascular disease. Her CP partially responded to nitroglycerin and improved modestly with migraine control using ubrogepant and calcium channel blockers. During admission for refractory migraine, she received intravenous lidocaine, magnesium, ketorolac, and neuroleptics, resulting in several months of CP remission despite brief migraine relief. Longitudinal follow-up demonstrated that eptinezumab was associated with improvement in both migraine and CP symptoms. This case highlights the diagnostic challenge of MT and the overlap between migraine and coronary vasospastic or microvascular processes. The observed improvement in CP following migraine-directed therapies raises the possibility of a shared neurovascular mechanism, although causality cannot be established. Greater awareness of MT and interdisciplinary management may improve outcomes in similar patients.
Migrainous thoracalgia (MT) refers to chest pain (CP) potentially arising from a neurologic etiology, often temporally linked to migraine. We present a 57-year-old woman with chronic migraine who developed recurrent CP typically following migraine attacks. Despite multiple cardiac evaluations, including cardiac MRI and catheterizations, she was diagnosed with fibromuscular dysplasia, spontaneous coronary artery dissection, and coronary microvascular disease. Her CP partially responded to nitroglycerin and improved modestly with migraine control using ubrogepant and calcium channel blockers. During admission for refractory migraine, she received intravenous lidocaine, magnesium, ketorolac, and neuroleptics, resulting in several months of CP remission despite brief migraine relief. Longitudinal follow-up demonstrated that eptinezumab was associated with improvement in both migraine and CP symptoms. This case highlights the diagnostic challenge of MT and the overlap between migraine and coronary vasospastic or microvascular processes. The observed improvement in CP following migraine-directed therapies raises the possibility of a shared neurovascular mechanism, although causality cannot be established. Greater awareness of MT and interdisciplinary management may improve outcomes in similar patients.
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