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Early von Willebrand Factor Dynamics and Subclinical Hemolysis After TAVI
Session:
Sessão de Posters 26 - Implantação transcateter da válvula aórtica (TAVI): desfechos, complicações e biomarcadores
Speaker:
Erivaldo Figueiredo Pires Andrade
Congress:
CPC 2026
Topic:
F. Valvular, Myocardial, Pericardial, Pulmonary, Congenital Heart Disease
Theme:
15. Valvular Heart Disease
Subtheme:
15.7 Valvular Heart Disease - Other
Session Type:
Posters Eletrónicos
FP Number:
---
Authors:
Erivaldo Figueiredo; Luana Alves; Emanuel Oliveira; Catarina Amaral Marques; Catarina Faria; Isabel Miranda; Francisca Saraiva; Fábio Trindade; Marta Tavares Silva; Adelino Leite Moreira; Rui André Rodrigues; Carla Sousa
Abstract
<p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"><strong><span style="font-size:11.0pt">Background:</span></strong><br /> <span style="font-size:11.0pt">Severe aortic stenosis induces high shear forces leading to loss of high–molecular-weight von Willebrand factor (vWF) multimers. Although transcatheter aortic valve implantation (TAVI) rapidly normalizes shear, the relationship between early peri-procedural changes in vWF and biochemical evidence of hemolysis remains unclear. Understanding this interaction may refine the interpretation of early post-procedural laboratory abnormalities and identify a shear-related hemostatic phenotype.</span></span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"><strong><span style="font-size:11.0pt">Objectives:</span></strong><br /> <span style="font-size:11.0pt">To evaluate the association between early peri-procedural vWF variation and biochemical markers of subclinical hemolysis following TAVI.</span></span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"><strong><span style="font-size:11.0pt">Methods:</span></strong><br /> <span style="font-size:11.0pt">We retrospectively analyzed TAVI patients with paired pre-procedural and 48-hour vWF measurements. Total vWF was analyzed as percentage change from baseline (</span><span style="font-size:11.0pt">Δ</span><span style="font-size:11.0pt">vWF%). Patients were classified as vWF-recoverers with ≥10% increase at 48 hours. Hemolysis markers included hemoglobin (Hb), haptoglobin, reticulocyte count, and lactate dehydrogenase (LDH). Subclinical hemolysis was defined as </span><span style="font-size:11.0pt">Δ</span><span style="font-size:11.0pt">Hb ≤ −1.5 g/dL plus </span><span style="font-size:11.0pt">Δ</span><span style="font-size:11.0pt">reticulocytes ≥ +0.2%. Group comparisons used the Mann–Whitney U test, and correlations were assessed with Spearman’s rho.</span></span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"><strong><span style="font-size:11.0pt">Results:</span></strong><br /> <span style="font-size:11.0pt">Ninety-eight patients were included (mean age 78.9 ± 17.1 years, 68.2% women). Among 47 patients with paired measurements, median </span><span style="font-size:11.0pt">Δ</span><span style="font-size:11.0pt">vWF% was +3.3%, with 42.6% classified as recoverers. Subclinical hemolysis occurred exclusively among non-recoverers, affecting 16.7% of this subgroup (3/18), while no events were observed in recoverers (0/13; Fisher p=0.245). Among 17 patients with paired LDH data, LDH increased modestly overall (+24 U/L), yet the rise was markedly greater in non-recoverers (+43 U/L) compared with recoverers (−6 U/L), although not statistically significant (p=0.088). A consistent pattern emerged whereby impaired vWF recovery aligned with higher hemolytic activity: </span><span style="font-size:11.0pt">Δ</span><span style="font-size:11.0pt">vWF% correlated inversely with </span><span style="font-size:11.0pt">Δ</span><span style="font-size:11.0pt">LDH (</span><span style="font-size:11.0pt">ρ</span><span style="font-size:11.0pt">=−0.41; p=0.18), and LDH demonstrated a borderline significant inverse correlation with haptoglobin decline (</span><span style="font-size:11.0pt">ρ</span><span style="font-size:11.0pt">=−0.49; p=0.075). Reticulocyte response was also numerically higher in non-recoverers, reinforcing the coherence of the hemolytic profile.</span></span></span></p> <p style="text-align:justify"><span style="font-size:12pt"><span style="font-family:Aptos,sans-serif"><strong><span style="font-size:11.0pt">Conclusion:</span></strong><br /> <span style="font-size:11.0pt">Impaired early recovery of vWF after TAVI is associated with a biochemical pattern consistent with subclinical hemolysis, despite limited statistical power. These findings suggest that early vWF dynamics may reflect residual shear or prosthesis-related biomechanical stress and impaired early vWF recovery after TAVI may serve as a relevant marker to identify patients at increased risk of subclinical hemolysis, supporting closer post-procedural monitoring and potentially guiding early management strategies.</span></span></span></p>
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