{"id":"4169163ec9f2","type":"article","url":"https://hartvaat.nl/2026/05/11/invasieve-drukvolumelussen-onthullen-mechanisme-van-tricuspidalisinsufficientie-/","title":"Invasieve drukvolumelussen onthullen mechanisme van tricuspidalisinsufficiëntie bij HFrEF: RV-PA-ontkoppeling en sMR","title_en":"","category":"hartfalen","category_label":"Hartfalen","professions":["cardioloog"],"tags":["bloeddrukbehandeling","fractional-flow-reserve","hfpef","hfref","ouderen","rechterventrikelfalen","tricuspidalisinsufficiëntie","ventrikelfibrilleren"],"journal":"ESC heart failure","doi":"10.1093/eschf/xvag134","source_url":"https://doi.org/10.1093/eschf/xvag134","authors":["Alexander Schmeisser","Thomas Rauwolf","Thomas Groscheck","Tarek Bekfani","Katharina Fischbach","Blerim Luani","Ivan Tanev","Michael Hansen","Saskia Meißler","Paul Steendijk","Ruediger C Braun-Dullaeus"],"significance":6,"published":"2026-06-24","source_date":"2026-05-11","image":"","kennis":["https://hartvaat.nl/kennis/hartfalen/hfmref-hartfalen-met-matig-verminderde-ejectie/","https://hartvaat.nl/kennis/hartfalen/wat-is-hartfalen/"],"congress":"","summary_en":"Retrospective study integrating right ventricular pressure-volume loops and Swan-Ganz catheter data with RV/LV imaging in 134 patients with heart failure with reduced ejection fraction (HFrEF). Independent predictors of moderate-to-severe ventricular tricuspid regurgitation (vTR2/3) were: (1) presence of secondary mitral regurgitation (sMR; aOR 1.67), (2) elevated pulsatile RV loads with lower PA compliance (aOR 0.43; AUC 0.82; threshold <2.24 ml/mmHg), largely driven by sMR2/3 (aOR 4.56), and (3) progressive uncoupling of RV elastance/contractility relative to pulmonary elastance (Ees/Ea aOR 0.024; AUC 0.84; threshold <0.6). This RV-PA uncoupling occurred across the entire afterload range and was associated with higher all-cause mortality. The work identifies sMR and RV-PA uncoupling as core drivers of vTR in HFrEF — relevant for determining which patients may benefit from mechanical TR reduction.","created":"2026-07-03T10:33:06Z","updated":"2026-07-03T13:32:00Z","licence":"Citeer vrij, met bronvermelding en een link naar hartvaat.nl (de url van het record). Samenvattingen zijn redactioneel werk van HartVaat; de oorspronkelijke publicaties blijven van hun uitgevers (doi). Geen medisch advies.","body_markdown":"Retrospectieve studie waarbij rechter-ventriculaire druk-volumelussen (pressure-volume loops) en Swan-Ganz-data werden gekoppeld aan RV/LV-beeldvorming bij 134 patiënten met hartfalen met verminderde ejectiefractie (HFrEF). Onafhankelijke voorspellers van matige-tot-ernstige ventriculaire tricuspidalisinsufficiëntie (vTR2/3) waren: (1) aanwezigheid van secundaire mitralisinsufficiëntie (sMR; aOR 1,67), (2) verhoogde pulsatiele RV-belasting met lagere PA-compliance (aOR 0,43; AUC 0,82; drempel <2,24 ml/mmHg), grotendeels gedreven door sMR2/3 (aOR 4,56), en (3) progressieve ontkoppeling van RV-elastantie/contractiliteit ten opzichte van pulmonale elastantie (Ees/Ea-ratio aOR 0,024; AUC 0,84; drempel <0,6). Deze RV-PA-ontkoppeling trad op over het hele afterload-bereik en was geassocieerd met verhoogde totale sterfte. Het werk identificeert sMR en RV-PA-ontkoppeling als kerndrijvers van vTR bij HFrEF — relevant voor het bepalen van welke patiënten baat hebben bij mechanische TR-reductie.","abstract_original":"INTRODUCTION: 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 +/- secondary mitral regurgitation (sMR) on extent and severity of secondary vTR was investigated. METHODS: We integrated right ventricular (RV) pressure-volume loop and Swan-Ganz catheter data with RV/LV imaging findings in retrospective analysis of 134 HFREF patients. RESULTS: Parameters independently associated with the presence of vTR2/3 were (i) presence of sMR (adjusted odds-ratio: adOR=1.67, p=0.045), (ii) increased pulmonary vascular pulsatile RV loads (lower PA compliance, adOR=0.43, p=0.021; AUC=0.82, cut-off:<2.24 ml/mmHg, p<0.001), mainly due to concomitant moderate/severe sMR (sMR2/3) (adOR=4.56, p=0.012), and (iii) progressive un-coupling of RV elastance/contractility (Ees) to an increasing total afterload (pulmonary elastance, Ea) (Ees/Ea ratio: adOR=0.024, p=0.005; AUC=0.84, cut-off:<0.6, p<0.001). In addition, the RV-pulmonary artery (PA) un-coupling 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 to vTR0/1, independent of the afterload. RV-PA un-coupling and reduced PA-compliance were independently associated with all-cause mortality. DISCUSSION: The vTR2/3 in context of HFREF was independently associated with the presence of sMR, increased pulsatile loads, and a pronounced RV-PA un-coupling over almost entire afterload range. Future studies will need to determine under which haemodynamic conditions a mechanical TR reduction in HFREF patients is advisable."}