Key result
Moderate-to-severe vTR in HFrEF is linked to RV-PA uncoupling and ~67% greater odds of secondary MR.
Why the study?
Moderate or severe ventricular tricuspid regurgitation in HFREF carries a poor prognosis, but its underlying pathophysiology and the role of left ventricular dysfunction with or without secondary mitral regurgitation remain unclear.
What hemodynamic and imaging parameters are associated with moderate or severe secondary ventricular tricuspid regurgitation in patients with HFrEF?
Observational (n=134)
What hemodynamic and imaging parameters are associated with moderate or severe secondary ventricular tricuspid regurgitation in patients with HFrEF?
In HFrEF patients, moderate-to-severe secondary tricuspid regurgitation is independently associated with secondary mitral regurgitation, increased pulsatile loads, and pronounced RV-PA uncoupling.
Moderate/severe sMR and low PA compliance associate with vTR2/3 in HFrEF; leaves open whether sMR correction alters tricuspid progression.
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.
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Schmeisser et al. (2026) conducted an observational in Heart failure with reduced ejection fraction (HFREF) (n=134). Secondary mitral regurgitation (sMR) and RV-PA uncoupling was evaluated on Presence of moderate or severe ventricular tricuspid regurgitation (vTR2/3) (adOR 1.67, p=0.045). Moderate or severe ventricular tricuspid regurgitation in HFREF was independently associated with secondary mitral regurgitation (adOR 1.67, p=0.045) and RV-PA uncoupling (adOR 0.024, p=0.005).
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