Hemodynamic and microcirculatory early adaptations following transcatheter aortic valve implantation (TAVI): A physiological pilot study.

BACKGROUND: Transcatheter aortic valve implantation (TAVI) abruptly relieves aortic stenosis. The consequences for the peripheral vascular network, organ perfusion and postoperative organ dysfunction remain unclear. This study assessed hemodynamic and microcirculatory changes after TAVI, and their association with postoperative organ dysfunction. METHODS: This prospective, single-center physiological study included 20 patients with severe aortic stenosis undergoing transfemoral TAVI at Geneva University Hospitals (January-June 2024). Hemodynamic and microcirculatory assessment included arterial stiffness (tonometry), temperature gradients (T grad), reactive hyperemia (near-infrared spectroscopy and photoplethysmography) and plasma vascular endothelium growth factor (VEGF) concentrations before and after TAVI. The primary outcome was perioperative changes in macro- and microcirculatory parameters; secondary outcomes were organ dysfunction within 7 days. RESULTS: TAVI immediately increased aortic pressures and amplified pressure waves. By day 1, central-peripheral T grad decreased, perfusion index rose (from 2.5 [0.9-4.2] to 3.9 [1.9-5.5]; p < 0.05), and tissue oxygen re-saturation slope increased (from 2.6 [1.5-3.4] to 3.9 [2.8-4.7] %/s; p < 0.05), independent of macrocirculatory parameters. Large artery stiffness decreased, despite a reduction in the total arterial compliance, without changes in small-vessel resistance. Cardiac index changes showed wide interindividual variability and correlated with vascular and VEGF dynamics. Patients with postoperative organ dysfunction had higher baseline VEGF (52.9 vs. 28.7 pg/mL, p = 0.033) and greater postoperative increases. CONCLUSION: TAVI induces rapid macro- and microcirculatory changes, with early tissue perfusion improvement despite transient microcirculatory reserve impairment. VEGF dynamics were associated with postoperative complications, suggesting endothelial activation as a marker of vulnerability and linking baseline endothelial status to vascular adaptation and outcomes.