{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T19:32:08Z","timestamp":1790105528847,"version":"4.0.1"},"reference-count":43,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"10","license":[{"start":{"date-parts":[[2023,10,1]],"date-time":"2023-10-01T00:00:00Z","timestamp":1696118400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc-nd\/4.0\/"}],"content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circ: Heart Failure"],"published-print":{"date-parts":[[2023,10]]},"abstract":"<jats:sec>\n            <jats:title>BACKGROUND:<\/jats:title>\n            <jats:p>Surgical removal of thromboembolic material by pulmonary endarterectomy (PEA) leads within months to the improvement of right ventricular (RV) function in the majority of patients with chronic thromboembolic pulmonary hypertension. However, RV mass does not always normalize. It is unknown whether incomplete reversal of RV remodeling results from extracellular matrix expansion (diffuse interstitial fibrosis) or cellular hypertrophy, and whether residual RV remodeling relates to altered diastolic function.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>METHODS:<\/jats:title>\n            <jats:p>We prospectively included 25 patients with chronic thromboembolic pulmonary hypertension treated with PEA. Structured follow-up measurements were performed before, and 6 and 18 months after PEA. With single beat pressure-volume loop analyses, we determined RV end-systolic elastance (Ees), arterial elastance (Ea), RV\u2013arterial coupling (Ees\/Ea), and RV end-diastolic elastance (stiffness, Eed). The extracellular volume fraction of the RV free wall was measured by cardiac magnetic resonance imaging and used to separate the myocardium into cellular and matrix volume. Circulating collagen biomarkers were analyzed to determine the contribution of collagen metabolism.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>RESULTS:<\/jats:title>\n            <jats:p>\n              RV mass significantly decreased from 43\u00b115 to 27\u00b111g\/m\n              <jats:sup>2<\/jats:sup>\n              (\u221215.9 g\/m\n              <jats:sup>2<\/jats:sup>\n              [95% CI, \u221221.4 to \u201310.5];\n              <jats:italic toggle=\"yes\">P<\/jats:italic>\n              &lt;0.0001) 6 months after PEA but did not normalize (28\u00b19 versus 22\u00b16 g\/m\n              <jats:sup>2<\/jats:sup>\n              in healthy controls [95% CI, 2.1 to 9.8];\n              <jats:italic toggle=\"yes\">P<\/jats:italic>\n              &lt;0.01). On the contrary, Eed normalized after PEA. Extracellular volume fraction in the right ventricular free wall increased after PEA from 31.0\u00b13.8 to 33.6\u00b13.5% (3.6% [95% CI, 1.2\u20136.1];\n              <jats:italic toggle=\"yes\">P<\/jats:italic>\n              =0.013) as a result of a larger reduction in cellular volume than in matrix volume (\n              <jats:italic toggle=\"yes\">P<\/jats:italic>\n              <jats:sub>interaction<\/jats:sub>\n              =0.0013). Levels of MMP-1 (matrix metalloproteinase-1), TIMP-1 (tissue inhibitor of metalloproteinase-1), and TGF-\u03b2 (transforming growth factor-\u03b2) were elevated at baseline and remained elevated post-PEA.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>CONCLUSIONS:<\/jats:title>\n            <jats:p>Although cellular hypertrophy regresses and diastolic stiffness normalizes after PEA, a relative increase in extracellular volume remains. Incomplete regression of diffuse RV interstitial fibrosis after PEA is accompanied by elevated levels of circulating collagen biomarkers, suggestive of active collagen turnover.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/circheartfailure.122.010336","type":"journal-article","created":{"date-parts":[[2023,9,7]],"date-time":"2023-09-07T09:00:49Z","timestamp":1694077249000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":19,"title":["Long-Term Effects of Pulmonary Endarterectomy on Right Ventricular Stiffness and Fibrosis in Chronic Thromboembolic Pulmonary Hypertension"],"prefix":"10.1161","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8541-6088","authenticated-orcid":true,"given":"Natalia J.","family":"Braams","sequence":"first","affiliation":[{"name":"Amsterdam UMC location Vrije Universiteit Amsterdam, PHEniX Laboratory, Department of Pulmonary Medicine, the Netherlands (N.J.B., A.K., J.v.W., J.N.W., S.M.A.J., A.B., E.J.N., A.V.N., F.S.d.M., H.J.B.)."},{"name":"Amsterdam Cardiovascular Sciences, Pulmonary Hypertension and Thrombosis, the Netherlands (N.J.B., A.K., J.v.W., J.N.W., S.M.A.J., E.J.N., J.T.M., A.V.N., F.S.d.M., H.J.B., L.J.M.)."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1238-4139","authenticated-orcid":true,"given":"Azar","family":"Kianzad","sequence":"additional","affiliation":[{"name":"Amsterdam UMC location Vrije Universiteit Amsterdam, PHEniX Laboratory, Department of Pulmonary Medicine, the Netherlands (N.J.B., A.K., J.v.W., J.N.W., S.M.A.J., A.B., E.J.N., A.V.N., F.S.d.M., H.J.B.)."},{"name":"Amsterdam Cardiovascular Sciences, Pulmonary Hypertension and Thrombosis, the Netherlands (N.J.B., A.K., J.v.W., J.N.W., S.M.A.J., E.J.N., J.T.M., A.V.N., F.S.d.M., H.J.B., 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