{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,13]],"date-time":"2026-10-13T06:35:47Z","timestamp":1791873347597,"version":"4.3.4"},"reference-count":32,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"21","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2024,11,5]]},"abstract":"<jats:sec xml:lang=\"en\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p xml:lang=\"en\">Mitral annular disjunction (MAD), posterior displacement of the mitral valve leaflet hinge point, predisposes to arrhythmias or sudden cardiac death. We evaluated the burden of MAD, mitral valve prolapse (MVP), and mitral regurgitation (MR) by heritable thoracic aortic disease gene in a cross\u2010sectional analysis of 2014\u20132023 data in the Montalcino Aortic Consortium registry.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Methods and Results<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      MAD was determined by direct measurement of echocardiographic images. MR and MVP were defined according to current clinical guidelines. Associations were evaluated using \u03c7\n                      <jats:sup>2<\/jats:sup>\n                      or Fisher exact tests. MR and MVP were enriched in Montalcino Aortic Consortium participants (672) with pathogenic variants (PV) in transforming growth factor\u2010\u03b2 pathway genes. The combination of MR and MVP was associated with mitral surgery and arrhythmias. In the subgroup with available images, MAD was enriched in\n                      <jats:italic toggle=\"no\">SMAD3<\/jats:italic>\n                      PV compared with other transforming growth factor\u2010\u03b2 PV (prevalence ratio 1.8 [1.1\u20132.8],\n                      <jats:italic toggle=\"no\">P<\/jats:italic>\n                      &lt;0.02). Severe disjunction (&gt;10\u2009mm) was only observed in the transforming growth factor\u2010\u03b2 subgroup and was further enriched in participants with\n                      <jats:italic toggle=\"no\">SMAD3<\/jats:italic>\n                      PV (prevalence ratio 3.1 [1.1\u20138.6]). MVP (prevalence ratio 5.2 [3.0\u20139.0]) and MR (PR 2.7 [1.8\u20133.9]) were increased in participants with MAD, but MAD was not independently associated with adverse cardiac or aortic events.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      Pathological mitral valve phenotypes are more prevalent in individuals with PV in transforming growth factor\u2010\u03b2 pathway genes, particularly\n                      <jats:italic toggle=\"no\">SMAD3<\/jats:italic>\n                      . MR and MVP but not MAD are associated with adverse aortic and cardiac events. Because congenital mitral disease may be the primary presenting feature of SMAD3 PV, genetic testing for heritable thoracic aortic disease should be considered for such individuals, especially if they also have a family history of heritable thoracic aortic disease.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/jaha.124.036274","type":"journal-article","created":{"date-parts":[[2026,7,15]],"date-time":"2026-07-15T11:03:20Z","timestamp":1784113400000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":6,"title":["Mitral Annular Disjunction in Heritable Thoracic Aortic Disease: Insights From the Montalcino Aortic Consortium"],"prefix":"10.1161","volume":"13","author":[{"ORCID":"https:\/\/orcid.org\/0009-0007-7214-2939","authenticated-orcid":false,"given":"Kishan L.","family":"Asokan","sequence":"first","affiliation":[{"name":"University of Texas Health Science Center at 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