Present a case of migrainous thoracalgia with unique features.

Migrainous thoracalgia (MT) refers to chest pain that may arise from a neurologic etiology, potentially linking migraine and cardiovascular conditions. While migraine itself has not been consistently associated with increased acute coronary syndrome (ACS) risk, MT remains a diagnosis of exclusion that requires a full cardiologic workup. The pathophysiology remains unclear, and no definitive treatment protocol exists.

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A 57-year-old woman with a history of chronic migraine since her 20s began experiencing new episodes of severe, transient chest pain (CP) in 2018, typically following migraine attacks. Initial cardiologic evaluation, including electrocardiograms and troponin levels, was unremarkable, but persistent symptoms led to further testing. She was diagnosed with fibromuscular dysplasia and a spontaneous coronary artery dissection (SCAD) in a distal artery, and she was treated for non-ST segment elevation myocardial infarction (NSTEMI). Despite appropriate management, the CP continued, occurring weekly and often following migraine headaches, prompting repeated emergency department visits. Further workup, including echocardiograms, cardiac MRI, catheterizations, and PET scans, revealed microvascular disease without atherosclerosis. Her CP consistently responded to nitroglycerin. Improved migraine control, especially with Ubrogepant and calcium channel blockers, also correlated with fewer CP episodes. The patient was later admitted to the Jefferson Headache Center for management of her refractory migraine. Treatment with IV lidocaine, magnesium, ketorolac, and neuroleptics, without nitroglycerin, provided several days of relief from migraine but several months of relief from CP. 

This case represents a severe form of MT with microvascular coronary artery disease and SCAD, underscoring the importance of cardiologic evaluation. The overlap in response to cardiac and migraine therapies, particularly nitroglycerin and lidocaine, suggests a shared vascular mechanism between migraine and CA. Further studies are warranted to explore the pathophysiology of MT and its optimal treatment strategies.