Abstract

s S63 Results: Twenty-seven patients met inclusion criteria and had hemodynamic measures both preand post-LVAD. Results are outlined in the table below. All LVADs were implanted via median sternotomy. As expected, measures of RV load (pulmonary vascular resistance, pulmonary vascular compliance (CPA), and effective arterial elastance (Ea)) were lower on initial post-LVAD hemodynamic assessment (mean 67 days). Pulmonary capillary wedge pressure (PCWP) also significantly declined yet right atrial pressure (RAP) remained unchanged. Therefore, the RAP:PCWP ratio increased (0.52 vs. 0.86, p< 0.001). Two novel hemodynamic parameters that quantify RV adaptation to load conditions worsened after implant: CPA x RAP (22.6 vs 30.2, p= 0.04) and Ea/RAP (0.20 vs. 0.11, p< 0.001). At the 18-36 month hemodynamic assessment (mean 730 days), RA:PCWP ratio, CPA x RAP, and EA/ RAP significantly improved compared to the initial post-LVAD assessment suggesting improvement in RV function. Including only those patients with 18-36 month follow-up data (n= 9) yielded similar results. Conclusion: Although the RV is unloaded with LVAD implantation, RV function and its ability to accommodate afterload worsens during the perioperative time period. Over time, however, RV function appears to recover to near pre-LVAD baseline. Table 1. Hemodynamic measurements pre-LVAD, 0-6 months and 18-36 months postLVAD Pre-implant 0-6 months 18-36 months p value (pre vs 0-6 mo) p value (0-6 vs 18-36 mo) All Patients (N) 27 27 9 Right Atrial Pressure (RAP) (mmHg) 13 ± 8 11 ± 6 7 ± 4 0.61 0.09 Pulmonary Capillary Wedge Pressure (PCWP) (mmHg) 23 ± 10 13 ± 7 12 ± 6 < 0.001 0.73 RAP to PCWP Ratio 0.52 ± 0.17 0.86 ± 0.26 0.60 ± 0.21 < 0.001 0.01 Cardiac index (L/min/m2) 1.7 ± 0.4 2.4 ± 0.6 2.6 ± 0.2 < 0.001 0.47 Pulmonary Vascular Resistance (PVR) (Wood Units) 3.2 ± 1.8 2.4 ± 1.2 1.2 ± 0.3 0.07 0.002 Compliance (SV/PP) (mL/mmHg) 2.5 ± 1.7 3.1 ± 1.3 2.3 ± 1.1 0.03 0.13 Effective Arterial Elastance (Ea) (mmHg/mL) 1.2 ± 0.7 0.7 ± 0.3 0.9 ± 0.4 0.005 0.2 Compliance * RAP 22.6 ± 11.5 30.2 ± 14.3 15.0 ± 9.0 0.04 0.006 Ea/RAP 0.20 ± 0.24 0.11 ± 0.17 0.15 ± 0.05 < 0.001 0.002 Only subjects with data at 18-36 months (N) 9 9 9 Right Atrial Pressure (RAP) (mmHg) 11 ± 5 9 ± 5 7 ± 4 0.34 0.56 Pulmonary Capillary Wedge Pressure (PCWP) (mmHg) 22 ± 8 10 ± 6 12 ± 6 0.004 0.55 RAP to PCWP Ratio 0.49 ± 0.12 0.82 ± 0.26 0.60 ± 0.21 0.004 0.07 Pulmonary Vascular Resistance (PVR) (Wood Units) 2.3 ± 0.8 1.7 ± 0.8 1.2 ± 0.3 0.16 0.29 Compliance (SV/PP) (mL/ mmHg) 2.7 ± 1.3 4.1 ± 1.5 2.3 ± 1.1 0.04 0.01 Effective Arterial Elastance (Ea) (mmHg/mL) 0.9 ± 0.4 0.5 ± 0.3 0.9± 0.4 0.01 0.008 Compliance * RAP 25.1 ± 12.8 28.8 ± 14.4 15.0 ± 9.0 0.59 0.029 Ea/RAP 0.18 ± 0.11 0.08 ± 0.05 0.15 ± 0.05 0.02 0.02 responses to step changes (200-400 RPM) in CF-LVAD pump speed from a maximum of 10,580±60 RPM to a minimum of 8,580±440 RPM. Results: A representative tracing is displayed in Figure 1. Reductions in pump speed led to increases in pulsatility as determined by pulse pressure (high v. low speed: 17±7 v. 26±13 mmHg, P< 0.05) and pulsatility index (4.3±1.0 v. 6.1±0.7 units, P< 0.05). Both mean arterial pressure (MAP) and LVAD flow decreased during reductions in speed (MAP: 89±11 v. 75±13 mmHg; flow 5.8±1.1 v. 4.4±0.5 L/min, P< 0.05 for all comparisons). MSNA decreased during reductions in pump speed (45±17 v. 35±18 bursts/min, P< 0.05) despite the reduction in MAP. MSNA was inversely related to pulse pressure, even after adjustment for MAP (Figure 2). Conclusion: Restoration of pulsatile flow reduces the heightened SNA present in patients with CF-LVADs, likely through a baroreceptor-mediated pathway. Further study is needed to determine whether reduction of SNA in this setting leads to improved outcomes.

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