{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,29]],"date-time":"2026-05-29T19:05:09Z","timestamp":1780081509941,"version":"3.54.0"},"reference-count":36,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2026,5,11]],"date-time":"2026-05-11T00:00:00Z","timestamp":1778457600000},"content-version":"vor","delay-in-days":6,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100016242","name":"Boston Scientific","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100016242","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,5,5]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Introduction<\/jats:title>\n                    <jats:p>Heart failure with reduced ejection fraction (HFrEF) accompanied by moderate or severe ventricular tricuspid-valve leaflet regurgitation (vTR2\/3) is prognostically unfavourable; however, the underlying pathophysiology has not yet been sufficiently clarified. The hypothesis of a causative role of left ventricular (LV) dysfunction +\/\u2212 secondary mitral regurgitation (sMR) on the extent and severity of secondary vTR was investigated.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We integrated right ventricular (RV) pressure\u2013volume loop and Swan-Ganz catheter data with RV\/LV imaging findings in a retrospective analysis of 134 HFrEF patients.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>Parameters independently associated with the presence of vTR2\/3 were (i) presence of sMR (adjusted odds-ratio [aOR] = 1.67, P = .045), (ii) increased pulmonary vascular pulsatile RV loads (lower pulmonary artery [PA] compliance, aOR = 0.43, P = .021; area under the curve [AUC] = 0.82, cut-off &amp;lt;2.24\u2005ml\/mmHg, P &amp;lt; .001), mainly due to concomitant moderate\/severe sMR (sMR2\/3) (aOR = 4.56, P = .012), and (iii) progressive uncoupling of RV elastance\/contractility (Ees) to an increasing total afterload (pulmonary elastance, Ea) (Ees\/Ea ratio: aOR = 0.024, P = .005; AUC = 0.84, cut-off &amp;lt;0.6, P &amp;lt; .001). In addition, the RV-PA uncoupling was not only determined by the higher afterload in vTR2\/3, but was also observed across the entire total afterload range (Ea tertile). This resulted in a larger and more dysfunctional RV in vTR2\/3 compared with vTR0\/1, independent of the afterload. RV-PA uncoupling and reduced PA compliance were independently associated with all-cause mortality.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>The vTR2\/3 in context of HFrEF was independently associated with the presence of sMR, increased pulsatile loads, and a pronounced RV-PA uncoupling over almost the entire afterload range. Future studies will need to determine under which haemodynamic conditions a mechanical tricuspid regurgitation reduction in HFrEF patients is advisable.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1093\/eschf\/xvag134","type":"journal-article","created":{"date-parts":[[2026,5,7]],"date-time":"2026-05-07T11:43:08Z","timestamp":1778154188000},"source":"Crossref","is-referenced-by-count":0,"title":["Interaction of secondary ventricular tricuspid regurgitation with RV in HFREF: an invasive pressure-volume loop study"],"prefix":"10.1093","volume":"13","author":[{"given":"Alexander","family":"Schmeisser","sequence":"first","affiliation":[{"name":"Division of Cardiology and Angiology, Department of Internal Medicine, Magdeburg University , Leipziger Str. 44, Magdeburg D-39120 ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-5542-8539","authenticated-orcid":false,"given":"Thomas","family":"Rauwolf","sequence":"additional","affiliation":[{"name":"Division of Cardiology and Angiology, Department of Internal Medicine, Magdeburg University , Leipziger Str. 44, Magdeburg D-39120 ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"Groscheck","sequence":"additional","affiliation":[{"name":"Division of Cardiology and Angiology, Department of Internal Medicine, Magdeburg University , Leipziger Str. 44, Magdeburg D-39120 ,","place":["Germany"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tarek","family":"Bekfani","sequence":"additional","affiliation":[{"name":"Division of Cardiology and Angiology, Department of Internal Medicine, Magdeburg University , Leipziger Str. 44, Magdeburg D-39120 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