(P175) PATIENTS WITH LEFT VENTRICULAR ASSIST DEVICES EXHIBIT PERSISTENT RESISTIVE AND PULSATILE PULMONARY VASCULAR ABNORMALITIES

Background: Pulmonary hypertension and pulmonary vascular remodeling are common amongst patients with advanced heart failure and are associated with increased mortality. Unfortunately, severe pulmonary hypertension is a contraindication to heart transplant, due to early post-operative graft dysfunction and right ventricular failure. Left ventricular assist device (LVAD) implantation is a strategy to decrease pulmonary venous pressures thus reversing pulmonary hypertension; however these patients continue to experience graft dysfunction after heart transplantation. The objective of our study was therefore to assess residual abnormalities of pulmonary vascular function in the context of pulmonary venous pressure in LVAD recipients compared to healthy controls.

METHODS AND RESULTS: A retrospective analysis of invasive hemodynamics as measured by right heart catheterization was conducted from 2 hemodynamic databases including patients with LVADs (n=96, age 53±13 years, BMI 26.5±5.9 kg/m2) and otherwise healthy men and women (n=36, age 56±7 years, BMI 25.4±3.0 kg/m2). Measurements included pulmonary artery wedge pressure (PAWP) as an estimate of pulmonary venous pressure, mean pulmonary artery pressure (mPAP), PA pulse pressure (PA PP), cardiac output (CO) and stroke volume (SV), which were also indexed to body surface area (BSA). Calculated estimates of pulmonary total pulmonary resistance (TPulmR) [mPAP/CO], pulmonary vascular resistance (PVR) [(mPAP-PAWP)/CO] and pulsatile loading (pulmonary compliance, PulmCp [SV/PA PP]) (Table 1). To understand the relative contributions of resistive and pulsatile pulmonary vascular loading the relationships between PVR and PulmCp were calculated (RC-time) and compared between groups. LVAD patients demonstrated significantly lower PAWP (7.6±4.7 mmHg vs. 9.6±3.0mmHg, p=0.02) and lower SV index (32.5±8.4mL/m2 vs. 41.7±7.6mL/m2, p< 0.01) compared to healthy controls. Despite lower PAWP, LVAD patients demonstrated higher PVR and lower PulmCp, reflecting augmented pulsatile loading. LVAD patients were located on the horizontal limb of the RC-time relationship (Figure 1). Additionally LVAD patients with residual higher PAWP 10mmHg had the most impaired compliance compared to LVAD patients with PAWP 10mmHg (3.05 vs. 4.34 mL/mmHg, p< 0.01). In healthy controls, compliance was higher regardless of mPAWP (5.79 vs. 5.40 mL/mmHg, p=0.5) (Figure 1).

Conclusion: In a group of age and BMI matched individuals these data demonstrate that the use of LVADs are very effective at reducing pulmonary venous pressure, resulting in ‘supranormal’ PAWP. Despite lower PAWP and normal mPAP, patients with LVADs exhibited persistent resistive and pulsatile pulmonary vascular hemodynamic abnormalities compared to healthy control. Determining whether such hemodynamic abnormalities are associated with evidence of RV dysfunction or graft failure after transplant will help clarify their importance.