1Herzzentrum Leipzig - Universität Leipzig Klinik für Innere Medizin/Kardiologie Leipzig, Deutschland; 2Helios Park-Klinikum Leipzig Klinik für Innere Medizin I - Kardiologie, Angiologie Leipzig, Deutschland; 3Herzzentrum Leipzig - Universität Leipzig Diagnostische und Interventionelle Radiologie Leipzig, Deutschland; 4Universitätsmedizin der Johannes Gutenberg-Universität Mainz Kardiologie 1, Zentrum für Kardiologie Mainz, Deutschland
Background: The aim of this study was to analyze the pathophysiological implications of severe tricuspid regurgitation (TR) in patients with heart failure with preserved ejection fraction (HFpEF) by using transcatheter edge-to-edge tricuspid valve repair (T-TEER) as a model of right ventricular (RV) volume overload relief.
Methods: This prospective interventional single arm trial (NCT04782908) included patients with invasively diagnosed HFpEF (i.e. left-ventricular enddiastolic pressure [LVEDP] >15 mmHg and preserved ejection fraction i.e. LVEF ≥50%). All patients received transthoracic echocardiography and cardiac magnetic resonance imaging (MRI) immediately before and 1-month after TV-TEER. During T-TEER LV pressure-volume loops were recorded by using a conductance catheter (). The primary outcome was the periprocedural change in the ratio of LVEDP to left-ventricular end-diastolic volume (LVEDV) as surrogate for preload independent diastolic function. The secondary outcomes included single-beat estimated end-diastolic pressure volume-relationships (EDPVRs), and LV distending pressure (calculated as LVEDP-mean right atrial pressure) as well as changes at 1-month in LVEDV and right ventricular EDV (RVEDV) as surrogates for ventricular interdependence.
Results: Overall, 20 patients (median age 78, interquartile range [IQR] 72 to 83 years, 65% female) were included. T-TEER reduced TR by a median of 2 (of 5) grades (IQR 2 to 1). T-TEER increased the LV stroke volume (LVSV) and enddiastolic volume (LVEDV) (p<0.001), without increasing LV end diastolic pressure (LVEDP) (p=0.094), consequently diastolic function improved with a reduction in LVEDP/LVEDV (p=0.001) and a rightward shift of the end-diastolic pressure-volume relationship (Figure 1B).
The increase in LVEDV correlated with a decrease in RV end-diastolic volume (RVEDV) (p<0.001) implying more favourable LV to RV interaction as a possible cause for improved filling. Further LV transmural pressure increased (p=0.028), mainly driven by a reduction in right atrial pressure (r=0.69, p<0.001) implying stronger LV distension in the restricted pericardial space caused by a relief of pericardial pressure. Further, secondary to a decrease in early RV filling, improvements in early LV filling were observed, correlating with an alleviation of leftwards bowing of the septum (r=0.60, p<0.001, Figure 1C and 1D, p<0.01, respectively).
Conclusion: The specific pathophysiology of HFpEF and TR is characterized by ventricular interaction driven by unfavourable septal motion and pericardial restraints. This pathophysiological state appears to be at least partially reversible following the reduction of TR and RV volume overload through T-TEER. Both the reduction in early and end-diastolic RV filling enables the LV to distend more effectively within the restricted pericardial space. This, in turn, results in the interventricular septum bowing less towards the LV during early diastole, allowing for increased filling volume while concurrently reducing filling pressures.