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Calcitonin Gene‐Related Peptide and Size of the Atrial Septal Defect in New‐Onset Migraine After Transcatheter Closure: Results of a Preliminary Study
Author(s) -
Wei ShuHao,
Fan PiChuan,
Kuo PingHung,
Chiou LihChu,
Wang JouKou
Publication year - 2012
Publication title -
headache: the journal of head and face pain
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.14
H-Index - 119
eISSN - 1526-4610
pISSN - 0017-8748
DOI - 10.1111/j.1526-4610.2012.02152.x
Subject(s) - calcitonin gene related peptide , migraine , medicine , calcitonin , anesthesia , endocrinology , cardiology , neuropeptide , receptor
Background.— New‐onset migraine headache attacks (MHAs) can occur after atrial septal device implantation in patients without previous migraine. Plasma calcitonin gene‐related peptide (CGRP), which plays a crucial role in migraine pathophysiology, has shown to be released from specific cardiac tissues. Methods and Results.— We prospectively collected patients before and after closure and measured plasma CGRP levels using enzyme‐linked immunosorbent assay. Forty atrial septal defect (ASD) patients who had no migraine previously were enrolled. Four (23.5%) of the 17 consecutive patients whose CGRP levels were checked before ASD closure had new‐onset MHAs. The patients with MHAs had bigger ASD size (20 ± 0.9 vs 16 ± 1 mm, P = .009) and lower CGRP levels before closure (21.1 ± 3.9 vs 90.1 ± 27.1 pg/mL, P = .042) than those without. Among the 5 patients with blood samplings both during and between attacks, a paired comparison revealed a significantly increased level during attack (257.2 ± 45.5 vs 45.6 ± 25.5 pg/mL, P = .03). Conclusion.— Bigger ASD size and lower plasma CGRP levels before closure can be a potential predictor of new‐onset MHAs. Furthermore, a significant increase of CGRP levels during migraine attack implies that the occurrences of new‐onset MHAs after ASD closure correlate with the release of CGRP. This suggests CGRP sensitization from a lower baseline may be involved in the occurrence of new‐onset MHAs after ASD closure.