Fibrosis 4 Index After Left Ventricular Assist Device Implantation: Right Congestion or Device Shear?
Year: 2025
Type: article
Abstract: Kurihara et al report that a post-operative FIB4 ≥ 1.45 predicts haemocompatibility-related adverse events after left-ventricular-assist-device implantation.1 They interpret the index as a marker of liver fibrosis; we suggest 2 additional, non-exclusive drivers that deserve scrutiny. First, the cohort pools 6 distinct pumps whose shear-stress profiles differ markedly. HeartMate II axial flow, HVAD centrifugal, Jarvik 2000, EVAHEART, DuraHeart, and HeartMate 3 were analysed together, yet current registry data show that pump thrombosis and stroke rates vary from 2% with full-magnetic levitation to 12% with older axial designs.2 Device-specific shear stress degrades von-Willebrand-factor multimers and activates platelets independently of hepatic status.3 In the Tokyo series, vWF activity was 25% higher in the elevated-FIB4 group, but this association may be differentially driven by pump type rather than by liver injury itself. Re-analysing the data with device—FIB4 interaction terms, or stratifying by pump class, would clarify whether the prognostic value of FIB4 is uniform across technologies. Second, right-sided congestion remains a plausible biological pathway. Patients with FIB4 ≥ 1.45 entered the study with higher right-atrial and wedge pressures, and 1 month after surgery, their central venous pressure was still 1.5 mmHg above the low-FIB4 group.1 Persistent venous hypertension reduces portal flow, raises sinusoidal AST/ALT, and lowers platelets, thereby inflating FIB4 without requiring true fibrosis. The haemostatic abnormalities seen in right heart failure—namely, elevated vWF antigen and shortened platelet survival—are mechanistically congruent with the well-characterized acquired von Willebrand syndrome driven by the high-shear environment of continuous-flow LVADs.4 Taken together, pump-specific shear and right-heart overload offer mechanistic explanations that do not rely on hepatic scar tissue. If either pathway dominates, clinicians can intervene early: selecting low-shear devices for patients with borderline FIB4, intensifying diuretics, or considering tricuspid repair when central venous pressure remains >12 mmHg. We encourage the authors to re-examine their cohort. Adding device—FIB4 interaction coefficients, or repeating the Cox model within homogeneous pump subgroups, would reveal whether the hazard ratio for HRAEs is consistent. Likewise, entering post-operative right-atrial pressure as a time-varying covariate would test whether congestion mediates the FIB4 signal. A prospective registry that records central venous pressure, pump type, and contemporaneous FIB4 could validate these alternatives within 12 months. We congratulate Kurihara and colleagues for spotlighting a routinely available index that forecasts device-related complications. Dissecting the relative contributions of pump shear, right-heart load, and genuine liver fibrosis will transform FIB4 from a passive marker into an actionable target. None declared. B.X. conceived the letter; G.W. and Y.L. drafted and revised the manuscript. Not applicable.
Authors: Bin Xiong, Guowei Wei, Youqin Li
Institution: Guangdong Medical College
Language: English
Subfield: Biomedical Engineering
Field: Engineering
Domain: Physical Sciences
Open Access status: bronze
OpenAlex ID: W4415764276