{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,23]],"date-time":"2026-08-23T18:16:34Z","timestamp":1787508994963,"version":"build-2736575974"},"reference-count":38,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"11","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2016,10,26]]},"abstract":"<jats:sec xml:lang=\"en\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p xml:lang=\"en\">Marfan syndrome (MFS) and familial non\u2013syndromal thoracic aortic aneurysm and dissection (ns\u2010TAAD) are genetic aortopathies causing aortic dilatation with increased aortic stiffness. Left ventricular (LV) contractility and ventricular\u2010vascular coupling index (VVI) were compared between MFS and ns\u2010TAAD and determinants of VVI were investigated.<\/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                      Patients with MFS (M 57, F 47) and ns\u2010TAAD (M 72, F 39) were studied by echocardiography and compared with controls (M 77, F 71). Aortic geometry, hemodynamics, LV work, LV contractility (end\u2010systolic elastance [E\n                      <jats:sub>es<\/jats:sub>\n                      ]), and VVI were documented. Aortic sinuses were equally dilated in MFS (19.7\u00b12.4) and ns\u2010TAAD (19.8\u00b11.8) compared to controls (16.2\u00b11.4\u00a0mm\u00b7m\n                      <jats:sup>\u22122<\/jats:sup>\n                      ,\n                      <jats:italic>P<\/jats:italic>\n                      &lt;0.001). Aortic stiffness index was increased in MFS (9.7\u00b15.1) and ns\u2010TAAD (10.8\u00b14.7) versus controls (5.4\u00b12.0,\n                      <jats:italic>P<\/jats:italic>\n                      &lt;0.01); LV stroke work was unchanged in MFS (436\u00b174) compared to controls (435\u00b160) but increased in ns\u2010TAAD (492\u00b1109\u00a0mJ\u00b7m\n                      <jats:sup>\u22122<\/jats:sup>\n                      <jats:italic>P<\/jats:italic>\n                      &lt;0.01). The LV E\n                      <jats:sub>es<\/jats:sub>\n                      was reduced in MFS (1.32\u00b10.19) compared to controls (1.65\u00b10.29\u00a0mm\u00a0Hg\u00b7mL\n                      <jats:sup>\u22121<\/jats:sup>\n                      ,\n                      <jats:italic>P<\/jats:italic>\n                      &lt;0.01) but increased in ns\u2010TAAD (1.83\u00b10.30,\n                      <jats:italic>P<\/jats:italic>\n                      &lt;0.01) and VVI was abnormal in MFS (0.71\u00b10.11) compared to controls (0.62\u00b10.07,\n                      <jats:italic>P<\/jats:italic>\n                      &lt;0.01) and ns\u2010TAAD (0.62\u00b10.09). Treatment with \u03b2\u2010blockers was associated with partial normalization of VVI in MFS. A VVI \u22650.8 was associated with increased risk of death and heart failure in MFS.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p xml:lang=\"en\">Left ventricular contractility and ventricular\u2010vascular coupling are abnormal in MFS but preserved in ns\u2010TAAD, and are independent of aortic stiffness, consistent with intrinsic impairment of myocardial contractility in MFS.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/jaha.116.003705","type":"journal-article","created":{"date-parts":[[2016,11,16]],"date-time":"2016-11-16T22:55:23Z","timestamp":1479336923000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":18,"title":["Ventricular\u2010Vascular Coupling in Marfan and Non\u2010Marfan Aortopathies"],"prefix":"10.1161","volume":"5","author":[{"given":"Farina","family":"Loeper","sequence":"first","affiliation":[{"name":"Charite Hospital, Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jantine","family":"Oosterhof","sequence":"additional","affiliation":[{"name":"Erasmus University, Rotterdam, Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark","family":"van den Dorpel","sequence":"additional","affiliation":[{"name":"Erasmus University, Rotterdam, Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Denise","family":"van der Linde","sequence":"additional","affiliation":[{"name":"Sydney Medical School, University of Sydney, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yaxin","family":"Lu","sequence":"additional","affiliation":[{"name":"Sydney Medical School, University of Sydney, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elizabeth","family":"Robertson","sequence":"additional","affiliation":[{"name":"Sydney Medical School, University of Sydney, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brett","family":"Hambly","sequence":"additional","affiliation":[{"name":"Sydney Medical School, University of Sydney, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Richmond","family":"Jeremy","sequence":"additional","affiliation":[{"name":"Sydney Medical School, University of Sydney, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCULATIONAHA.105.541078"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.0000164580.39991.3d"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1161\/CIRCHEARTFAILURE.113.000383"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2005.07.037"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jtcvs.2006.07.001"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.hlc.2012.08.049"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1016\/j.jacc.2011.12.052"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1007\/s003800200003"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.36.4.489"},{"key":"e_1_3_2_11_2","first-page":"1329","article-title":"Abnormal muscle mechanosignaling triggers cardiomyopathy in mice with Marfan syndrome","volume":"124","author":"Cook JR","year":"2014","unstructured":"Cook JR, Carta L, Benard L, Chemaly ER, Chiu E, Rao SK, Hampton TG, Yurchenco P; GenTAC Registry Consortium , Costa KD, Hajjar RJ, Ramirez F. 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