https://doi.org/10.1007/s00392-025-02625-4
1Herz- und Diabeteszentrum NRW Klinik für Kardiologie Bad Oeynhausen, Deutschland; 2Herz- und Diabeteszentrum NRW Allgemeine und Interventionelle Kardiologie/Angiologie Bad Oeynhausen, Deutschland; 3Herzzentrum der Universität zu Köln Klinik III für Innere Medizin Köln, Deutschland
Objective
Current data indicates that both surgical and interventional treatment of aortic regurgitation (AR) result in an initial deterioration of left ventricular ejection fraction despite improvement of symptoms. However, further data analysing underlying hemodynamic mechanisms of this finding is limited.
Methods
We analysed 58 patients with isolated AR who underwent transfemoral TAVR with a dedicated TAVR system to treat AR (Trilogy JenaValve) at two centres in Germany from April 2019 to May 2024. Using non-invasive, echocardiography-supported volume measurements and (non-invasive) blood pressure measurements via an arm cuff, pressure-volume (PV) diagrams were reconstructed in these patients. The end-systolic elastance served as a load-independent contractility marker, while load dependent markers of systolic function like left ventricular ejection fraction (LVEF), and global longitudinal strain (GLS) were additionally calculated at baseline and before discharge.
Results
LVEF and GLS significantly decreased immediately after intervention compared to baseline (LVEF 50.1 ± 10.1% at baseline vs. 44.5 ± 9.8% at discharge; p < 0.001); GLS -14.3 ± 3.4% at baseline vs. -10.9 ± 3.4% at discharge [p < 0.001]). End-diastolic volume (EDV), on the other hand, showed significant decline after intervention (151,2 ± 54,5 ml at baseline vs. 121 ± 42,7 ml at discharge [p < 0.001]) indicating an immediate reduction of preload. Pressure-volume analyses revealed that end-systolic elastance did not significantly change after intervention (2.8 ± 0.9 mmHg/ml [n=22] at baseline vs. 2.4 ± 1.1 mmHg/ml at discharge; p = 0.15).
Conclusions
While LVEF and GLS as preload-dependent markers of left-ventricular systolic function significantly deteriorate immediately after TAVR in patients with severe aortic regurgitation, end-systolic elastance as a preload-independent marker of left-ventricular contractility shows no significant change. We therefore hypothesize that LVEF and GLS overestimate left-ventricular contractility in aortic regurgitation and that increased preload might disguise already existing impairment of left-ventricular contractility in patients with aortic regurgitation. Our findings could explain limited prognosis of patients with severe aortic regurgitation and preserved LVEF and GLS and reinforce the importance of early intervention to improve prognosis.