Dissociation between platelet decline and von willebrand factor profiles after TAVI: implications for acute kidney injury

Background

Platelet decline is a frequent early finding after transcatheter aortic valve implantation (TAVI) and may reflect procedural trauma, inflammatory activation, or microvascular stress. von Willebrand factor (vWF) is a key endothelial-derived glycoprotein involved in platelet adhesion under high shear stress and plays a central role in primary hemostasis and microvascular integrity. The relationship between early post-TAVI platelet decline and acute kidney injury (AKI) remains poorly defined, and its potential link to vWF-related mechanisms is unknown.

Purpose

To assess the association between early post-TAVI platelet decline and AKI, and to evaluate whether platelet dynamics are related to changes in vWF antigen levels or high-molecular-weight multimer (HMWM) ratios.

Methods

We retrospectively analyzed TAVI patients with paired baseline and 48-hour platelet counts. Platelet decline was expressed as percentage change from baseline (Δplatelets%), with a ≥30% reduction defined as clinically relevant. AKI was defined according to KDIGO criteria based on post-procedural creatinine changes. Hemostatic assessment included vWF antigen and HMWM ratios measured before TAVI and at 48 hours. Continuous variables were compared using independent-samples t-tests, categorical associations using chi-square testing, and correlations using Pearson’s coefficients. Odds ratios were estimated with Haldane–Anscombe correction when required.

Results

Among 98 patients undergoing TAVI (mean age 78.9 ± 17.1 years; 68.2% women), 85 had complete platelet, renal, and vWF data. Mean platelet decline at 48 hours was –29.8 ± 14.4%. AKI occurred in 6/85 patients (7.1%).

Patients who developed AKI experienced a significantly greater platelet decline compared with those without AKI (–47.7 ± 6.5% vs –28.5 ± 13.9%; p = 0.00016). A ≥30% platelet reduction was observed in 41/85 patients (48.2%) and was associated with a higher incidence of AKI (14.6% vs 0%; χ² = 4.88; p = 0.027). Using Haldane–Anscombe correction, the estimated odds ratio for AKI associated with ≥30% platelet decline was 16.3.

In contrast, platelet decline showed no significant correlation with vWF antigen levels or HMWM ratios at baseline or 48 hours (all r ≈ 0.16; p > 0.12). vWF parameters did not differ between patients with and without AKI (all p > 0.29), and multimeric profiles evolved similarly across platelet-decline strata.

Conclusions

Early platelet decline after TAVI is strongly associated with AKI but appears independent of vWF antigen levels or multimeric alterations. Platelet reduction may represent an early, readily available marker of post-procedural renal stress, reflecting mechanisms distinct from vWF-mediated endothelial dysfunction.