Pulmonary Artery Pulsatility Index After Pediatric Heart Transplant

Abstract

Background: Pulmonary Artery Pulsatility index (PAPi) is calculated by pulmonary artery pulse pressure divided by central venous pressure and is directly proportional to right ventricular contractility and stroke volume, and inversely related to pulmonary artery afterload and filling pressures. While PAPi as a prognostic hemodynamic measure has been studied in various adult populations, including to predict right ventricular (RV) failure following left ventricular assist device (LVAD) implantation and to predict renal outcomes following heart transplant (HTx), it has not been evaluated in children post HTx. We hypothesize that PAPi will correlate with known hemodynamic parameters and predict acute kidney injury (AKI) following pediatric HTx. Methods: Medical records and hemodynamic data were retrospectively reviewed for patients ≤18 years old undergoing HTx at a single center between 1/2007-9/2021. Subgroups by HTx indication were myopathy or congenital heart disease (CHD). PAPi was calculated at routine cardiac catheterizations initially following HTx, and at 6 months, 1 year, and 5 years post HTx, with normal being PAPi ≥2.0. Correlations between PAPi and established hemodynamic measures collected at post HTx catheterizations including right ventricular end diastolic pressure (RVEDp), thermodilution cardiac index (TDCI), and central venous pressure to pulmonary capillary wedge pressure ratio (CVP-to-PCWP ratio) were analyzed using linear regressions. Correlation between PAPi and AKI was analyzed using a Fischer’s Exact test. Results: Fifty-three children underwent HTx in myopathy (n=27) or CHD (n=26) subgroups. PAPi correlated with RVEDp (p<0.001), TDCI (p=0.004), and CVP-to-PCWP ratio (p<0.001). At 6 months post HTx, PAPi <2.0 was associated with increased incidence of AKI (n=12/53, p=0.047). In analyzing 5-year trends, the myopathy subgroup had a normal early PAPi with no significant change at any time point. However, the CHD subgroup had a normal early (2.12 ± 0.18) and 6 month (2.45 ± 0.25) PAPi, but had a decline to an abnormal PAPi at 1 year (1.98 ± 0.13) and 5 years post HTx (1.67 ± 0.16). This decline between the 6 month and 5-year catheterizations was statistically significant (p=0.048). Conclusions: PAPi in children post HTx correlates with established hemodynamic parameters routinely collected post HTx and may serve as a marker predicting renal dysfunction 6 months post HTx. Following HTx, PAPi declined significantly for the CHD subgroup. These findings suggest that incorporating PAPi into existing risk models may substantially improve earlier implementation for advanced therapies, thus improving clinical outcomes. PAPi as a comprehensive prognostic hemodynamic measure post pediatric HTx should be investigated in a larger multi-center study.