ArticleCardiovascular intervention and therapeutics2026
Acute bi-ventricular haemodynamic changes after transcatheter aortic valve implantation for severe aortic stenosis assessed using invasive pressure-volume loops.
Article in Cardiovascular intervention and therapeutics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
Abstract
Transcatheter aortic valve implantation (TAVI) aims to relieve the increased left ventricular (LV) afterload imposed by aortic stenosis (AS). However, the early haemodynamic impact of TAVI on bi-ventricular performance remains poorly characterised. This prospective study quantified the acute bi-ventricular response following TAVI for severe symptomatic AS using gold-standard invasive pressure-volume loop (PVL) assessment. Left and right ventricular (RV) PVLs were recorded using a conductance catheter pre- and immediately post-TAVI. Indices of contractile function, ventriculo-arterial coupling and energetics were derived. In total, 12 patients (84.1 years [interquartile range: 77.1, 87.2]; female 25%) were included. TAVI resulted in significant bi-ventricular reductions in afterload, measured by effective arterial elastance (LV: 2.1 [1.8, 2.3] to 1.4 [1.3, 1.7] mmHg/mL, p < 0.001; RV: 0.5 [0.4, 0.6] to 0.4 [0.3, 0.4] mmHg/mL, p = 0.006). Despite an acute decline in LV contractility, measured by end-systolic elastance (p = 0.021), there was a significant net improvement in ventriculo-arterial coupling in both the LV (p = 0.003) and RV (p = 0.006). Both the LV and RV demonstrated significant reductions in stroke work (SW) (LV-SW: 11,915.0 [9,727.5, 15,288.7] to 7,360.5 [6,937.0, 9,113.1] mmHg/mL, p < 0.001; RV-SW: 1,506.9 [1,420.5, 1,676.2] to 1,418.1 [1,250.8, 1,510.3] mmHg/mL, p = 0.020) and pressure volume area (PVA) (LV-PVA: 16,188.5 [13,171.5, 18,726.5] to 9,674.2 [9,185.9, 11,872.2] mmHg/mL, p < 0.001; RV-PVA 2,176.1 [2,046.3, 2,885.1] to 1,960.2 [1,835.6, 2,269.0] mmHg/mL, p = 0.002), with stable SW/PVA ratios. The acute haemodynamic effects of TAVI for severe symptomatic AS extend beyond the LV. Patients experienced bi-ventricular unloading, improved ventriculo-arterial coupling and reduced myocardial metabolic demand.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.