Immediate reduction in stressed blood volume after percutaneous ventricular assist device implantation in cardiogenic shock: Reverse translational study suggesting baroreflex-mediated redistribution

Background

The percutaneous ventricular assist device (PVAD) is an established mechanical circulatory support modality for cardiogenic shock (CS). While its primary effect is left ventricular unloading, venous return remains a fundamental determinant of systemic hemodynamics. Venous return is governed by stressed blood volume (SBV), yet the impact of PVAD support on SBV has never been systematically evaluated.

Purpose

To determine whether PVAD modifies SBV in patients with CS and to validate the physiological reproducibility of clinically observed SBV changes in an experimental model using a reverse translational approach.

Methods

Clinical study: We organized a prospective multicenter registry of patients with CS supported by PVAD therapy (UNLOADERS-PVAD registry, N = 189). SBV was estimated from right atrial pressure (RAP), left atrial pressure (LAP), and CO using a generalized circulatory equilibrium model (Fig. 1A). SBV trends were analyzed at four points: pre-PVAD, just after PVAD, 24-hrs after PVAD, and before PVAD weaning. Temporal changes were assessed using a linear mixed-effects model.

Experimental study: Acute heart failure was induced in four anesthetized canines (Beagles, 10.40.3 kg) by coronary microembolization. We implanted PVAD under fluoroscopic guidance. SBV was calculated using the same generalized circulatory equilibrium model as human. Hemodynamic measurements were obtained at minimum support (P1), maximum support (P3–7)), and after returning to minimum support for 30-min at each stage.

Results

In UNLOADERS-PVAD registry, compared with pre-PVAD, SBV showed significant reduction just after PVAD initiation (p < 0.001) and PVAD achieved a 16.5 mL/kg decrease in SBV from pre-PVAD implantation to before PVAD weaning (p < 0.001) (Fig. 1B). In the canine model, the increase of PVAD support immediately reduced SBV, which returned to baseline after minimum PVAD support, reproducing the clinical findings. In a representative case, plasma epinephrine levels varied inversely with changes in PVAD flow, paralleling SBV dynamics (Fig. 2A). SBV decreased at maximum support and returned to baseline levels upon returning to minimum support in all four animals, demonstrating a consistent directional response. Additionally, SBV demonstrated an inverse relationship with PVAD-induced increases in arterial pressure (r = −0.51) (Fig. 2B), suggesting baroreflex-mediated sympathetic withdrawal and redistribution of venous blood volume.

Conclusion

PVAD support induces immediate SBV reduction in CS in both clinical and experimental settings. These findings suggest that PVAD therapy not only unloads the left ventricle but also modulates autonomic tone and systemic venous return through baroreflex-mediated mechanisms.Fig.1FIg.2