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<p>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, <i>p</i> &lt; 0.001; RV: 0.5 [0.4, 0.6] to 0.4 [0.3, 0.4] mmHg/mL, <i>p</i> = 0.006). Despite an acute decline in LV contractility, measured by end-systolic elastance (<i>p</i> = 0.021), there was a significant net improvement in ventriculo-arterial coupling in both the LV (<i>p</i> = 0.003) and RV (<i>p</i> = 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, <i>p</i> &lt; 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, <i>p</i> = 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, <i>p</i> &lt; 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, <i>p</i> = 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.</p> Graphical abstract <p></p>

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Acute bi-ventricular haemodynamic changes after transcatheter aortic valve implantation for severe aortic stenosis assessed using invasive pressure-volume loops

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  • 发表日期：

    2026年5月23日

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  • Vitaliy Androshchuk,
  • Edouard Long,
  • Omar Chehab,
  • Joshua Wilcox,
  • Benedict McDonaugh,
  • Ronak Rajani,
  • Bernard Prendergast,
  • Tiffany Patterson,
  • Simon Redwood

摘要

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.

Graphical abstract