{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,17]],"date-time":"2026-09-17T08:36:49Z","timestamp":1789634209935,"version":"build-2803163510"},"reference-count":33,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2012,4,5]],"date-time":"2012-04-05T00:00:00Z","timestamp":1333584000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Headache"],"published-print":{"date-parts":[[2012,6]]},"abstract":"<jats:p>\n                    <jats:bold>Background.\u2014<\/jats:bold>\n                    New\u2010onset migraine headache attacks (MHAs) can occur after atrial septal device implantation in patients without previous migraine. Plasma calcitonin gene\u2010related peptide (CGRP), which plays a crucial role in migraine pathophysiology, has shown to be released from specific cardiac tissues.\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Methods and Results.\u2014<\/jats:bold>\n                    We prospectively collected patients before and after closure and measured plasma CGRP levels using enzyme\u2010linked 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\u2010onset MHAs. The patients with MHAs had bigger ASD size (20\u2003\u00b1\u20030.9 vs 16\u2003\u00b1\u20031\u2003mm,\n                    <jats:italic>P<\/jats:italic>\n                    \u2003=\u2003.009) and lower CGRP levels before closure (21.1\u2003\u00b1\u20033.9 vs 90.1\u2003\u00b1\u200327.1\u2003pg\/mL,\n                    <jats:italic>P<\/jats:italic>\n                    \u2003=\u2003.042) 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\u2003\u00b1\u200345.5 vs 45.6\u2003\u00b1\u200325.5\u2003pg\/mL,\n                    <jats:italic>P<\/jats:italic>\n                    \u2003=\u2003.03).\n                  <\/jats:p>\n                  <jats:p>\n                    <jats:bold>Conclusion.\u2014<\/jats:bold>\n                    Bigger ASD size and lower plasma CGRP levels before closure can be a potential predictor of new\u2010onset MHAs. Furthermore, a significant increase of CGRP levels during migraine attack implies that the occurrences of new\u2010onset 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\u2010onset MHAs after ASD closure.\n                  <\/jats:p>","DOI":"10.1111\/j.1526-4610.2012.02152.x","type":"journal-article","created":{"date-parts":[[2012,4,5]],"date-time":"2012-04-05T18:47:28Z","timestamp":1333651648000},"page":"985-992","source":"Crossref","is-referenced-by-count":10,"title":["Calcitonin Gene\u2010Related Peptide and Size of the Atrial Septal Defect in New\u2010Onset Migraine After Transcatheter Closure: Results of a Preliminary 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