Poster 118: Pulmonary Artery Pulsatility Index Predicts Long Term Kidney Function Outcomes in Heart Transplant Recipients Bridged With Short-Term Mechanical Circulatory Support

Background: Pulmonary artery pulsatility index (PAPi) reflects right ventricular–pulmonary vascular coupling and is commonly used to characterize right-sided shock physiology. Whether pre-transplant PAPi predicts post–heart transplant long term renal trajectory independent of short-term mechanical circulatory support (STMCS) strategy remains unclear.

Methods: We conducted a retrospective cohort analysis of 567 patients with four STMCS strategies: ECMO (n=53), Impella (n=116), intra-aortic balloon pump (IABP; n=87), and no MCS (n=311), excluding durable LVAD. Pre-transplant PAPi was categorized as low ( < 1), intermediate (1–2), or high (>2). Kidney outcomes included change in estimated glomerular filtration rate (ΔeGFR) at 1 month, 6 months, and 1 year post-transplant. Multivariable linear regression adjusted for baseline renal function and STMCS group. One-year mortality was assessed using logistic regression as a secondary outcome.

Outcome: Baseline eGFR was higher in patients with higher PAPi. Across all PAPi and MCS strata, renal function declined after transplant, with greater losses observed at 6 months and 1 year than at 1 month. Compared with low PAPi, intermediate and high PAPi were associated with significantly greater declines in eGFR at 6 months (β −11.2 and −7.7 mL/min/1.73 m², respectively; P< 0.01) and 1 year (β −9.6 and −8.6 mL/min/1.73 m², respectively; P≤0.01). Baseline eGFR was a strong inverse predictor of post-transplant renal change at all time points. MCS strategy was not independently associated with eGFR decline after adjustment. One-year mortality occurred in 34 patients (6.0%) and was not independently associated with PAPi group or MCS strategy after adjustment.

Conclusion: Pre-transplant PAPi independently predicts mid- and long-term renal outcomes after heart transplantation; STMCS strategy does not. Pre-transplant hemodynamic phenotype, rather than device selection, determines post-transplant renal vulnerability. We hypothesize PAPi captures a pre-transplant cardio-renal vulnerability from right-sided congestion, which persists beyond transplantation and manifests as accelerated post-transplant renal decline.