Fibrosis 4 Index After Left Ventricular Assist Device Implantation: Right Congestion or Device Shear?

Kurihara et al report that a post-operative FIB4 1.45 predicts haemocompatibility-related adverse events after left-ventricular-assist-device implantation. 1They 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. 4aken 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.