Key result
Baseline aortic stenosis severity does not alter post-TAVI QFR changes across coronary territories.
Why the study?
TAVI significantly reduces transvalvular gradients, which may influence coronary hemodynamics, but whether the severity of aortic stenosis affects angiography-derived Quantitative Flow Ratio (QFR) measurements before and after TAVI remained uncertain.
Does transcatheter aortic valve implantation (TAVI) and baseline aortic stenosis severity alter angiography-derived Quantitative Flow Ratio (QFR) measurements in patients with severe aortic stenosis?
Observational (n=56)
No
Does transcatheter aortic valve implantation (TAVI) and baseline aortic stenosis severity alter angiography-derived Quantitative Flow Ratio (QFR) measurements in patients with severe aortic stenosis?
Angiography-derived coronary physiology assessed by QFR remains stable before and after TAVI regardless of baseline aortic stenosis severity, supporting the reliability of QFR for coronary lesion assessment prior to valve intervention.
Background Transcatheter aortic valve implantation (TAVI) results in a significant reduction of transvalvular gradients, which may influence coronary hemodynamics. Whether the severity of aortic stenosis affects angiography-derived coronary physiology remains uncertain. We investigated the impact of baseline aortic stenosis severity on paired Quantitative Flow Ratio (QFR) measurements obtained before and after TAVI. Methods This retrospective single-centre study included patients undergoing TAVI between October 2020 and September 2025 with available paired pre- and post-procedural invasive coronary angiographies. QFR was computed retrospectively using Medis QFR® 3.0. Only post-TAVI angiographies performed within six months were included. Vessel-level QFR values were compared before and after TAVI. Exploratory analyses were performed according to baseline hemodynamic severity. Results A total of 56 patients with paired pre- and post-TAVI coronary angiographies were included in the analysis. The median age at the time of TAVI was 82.0 [78.0 - 86.0] years. The median interval between baseline coronary angiography and TAVI was 4.0 [2.0 - 31.0] days, while the interval between TAVI and follow-up angiography was 57.0 [12.0 - 103.0] days. Baseline hemodynamic assessment revealed a median peak transvalvular gradient of 61.0 [40.0 - 79.3] mmHg and a median mean gradient of 36.0 [25.0-49.0] mmHg, reflecting a heterogeneous severe aortic stenosis population. Following valve implantation, gradients decreased substantially to 17.0 [11.0 - 23.0] mmHg and 9.0 [6.0 - 12.0] mmHg, respectively. (Table 1). Of 336 screened vessels, 81 (24.1%) were excluded due to overlap, tortuosity, occlusion, missing projections, or wire artefacts. Median ΔQFR values were comparable between groups, with no statistically significant differences in any coronary territory (left anterior descending artery p=0.314, left circumflex artery p=0.845, right coronary artery p=0.601) (Table 2). Conclusions Despite substantial reductions in transvalvular gradients, angiography-derived coronary physiology assessed by QFR remained stable across the TAVI timeline. Baseline severity of aortic stenosis did not translate into systematic changes in QFR following valve intervention. These findings suggest that coronary lesion assessment using QFR may be accurate and clinically applicable prior to valve intervention. Prospective studies are warranted to confirm these observations.
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Nela et al. (2026) conducted an observational in Severe aortic stenosis undergoing TAVI (n=56). Transcatheter aortic valve implantation (TAVI) / baseline aortic stenosis severity vs. Pre-TAVI vs post-TAVI paired measurements across baseline hemodynamic severity groups was evaluated on Change in vessel-level Quantitative Flow Ratio (ΔQFR) before and after TAVI across coronary territories (p=LAD 0.314, LCx 0.845, RCA 0.601). Baseline aortic stenosis severity did not significantly alter post-TAVI ΔQFR across coronary territories (LAD p=0.314, LCx p=0.845, RCA p=0.601).
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