Background: Pulmonary hypertension is common amongst patients with advanced heart failure and is a contraindication to transplantation due to high early morbidity and mortality. Implantation of left ventricular assist devices (LVADs) is a strategy to reduce filling pressures and improve pulmonary pressures. We hypothesized that residual abnormalities of pulmonary vascular function after apparent normalization of pulmonary pressures may persist, but have not been previously described. Therefore, our objective was to measure pulmonary vascular hemodynamics in LVAD recipients, and evaluate associations between the resistive and pulsatile components of the vascular hemodynamic load with mortality after cardiac transplantation.
METHODS AND RESULTS: This study is a retrospective analysis comparing hemodynamic variables, using analysis of variance, in LVAD patients (n=101) undergoing surveillance right heart catheterization (RHC) in comparison to healthy volunteers (n=36). LVAD patients had ‘supranormal’ (e.g. lower) pulmonary artery wedge pressures (PAWP) (8±5mmHg vs. 10±3mmHg in healthy individuals, p=0.03) and normal mean pulmonary artery pressures (17±6mmHg vs. 15±3mmHg, p=0.03). Despite lower PAWP, LVAD patients demonstrated higher pulmonary vascular resistance (PVR) (171±85 dynesseccm-5 vs. 110±41 dynesseccm-5, p< 0.01) and impaired pulmonary compliance (PulmCp) (4±2mL/mmHg vs. 6±2mL/mmHg, p< 0.01) vs. healthy individuals. Vital status was obtained and analyzed with Kaplan-Meier curves and Log-Rank (Mantel-Cox) regression from the time of patients last RHC to death or last contact. Among patients supported with an LVAD: 19 died on support, 63 underwent heart transplant, and 10 died within 30-days post-transplant. Lower right atrial pressure, pulmonary artery pulse pressure, and greater PulmCp (Table 1) was observed among patients who were survivors at 30-days post-transplant. When time to death during LVAD support was stratified by PulmCp (above and below the median) there was significantly higher survival in those with greater PulmCp (84±7 months vs. 74±10 months, (χ²(1) = 4.827, p = 0.03) (Figure 1A). Among LVAD patients (n=63) undergoing heart transplant, patients with greater PulmCp had significantly higher survival at 30-days (χ²(1) = 4.559, p = 0.03) (Figure 1C) and during long-term follow-up (90±8 months vs. 78±13 months, χ²(1) = 4.567, p = 0.03) (Figure 1B).
Conclusion: Abnormalities in pulmonary vascular resistive and pulsatile afterload persist post-LVAD implantation and are associated with decreased survival during LVAD support and post-transplant. Further research is required to determine the mechanism of death and how LVADs may lead to remodelling of the pulmonary vasculature over time.
