Calcitonin Gene‐Related Peptide and Size of the Atrial Septal Defect in New‐Onset Migraine After Transcatheter Closure: Results of a Preliminary Study

Abstract

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. 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). 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.