Abstract 10940: Distensibility of the Pulmonary Circulation During Exercise in Heart Failure
Background: Pulmonary vascular distensibility (PVD) permits the pulmonary arteries to increase in size to accommodate increased blood flow and is measured as the percent increase in pulmonary vessel diameter per mmHg increase in pressure. We hypothesized that impaired PVD is related to reduced functional capacity in patients with heart failure (HF) or pulmonary arterial hypertension (PAH).
Methods and Results: Patients with HF and preserved ejection fraction (HFpEF, n=48), HF and reduced ejection fraction (HFrEF, n=55), PAH (n=18), and age matched controls (n=30) underwent cardiopulmonary exercise testing with invasive hemodynamic monitoring and first-pass radionuclide ventriculography. PVD was lowest in the PAH group (mean±SD 0.36±0.25% per mmHg) and intermediate in the HFpEF and HFrEF groups (0.92±0.39 and 0.84±0.33% per mmHg, respectively) compared to controls (1.39±0.32, P<0.0001 for all three, Fig. 1A). PVD was strongly associated with measurements of right ventricular-pulmonary vascular function during exercise including change in RVEF (ρ=0.39, P<0.0001, Fig. 1B) and change in pulmonary vascular resistance (ρ=-0.51, P<0.0001) with exercise. PVD was an independent predictor of peak VO2 in a multivariate model that included age, gender, hemoglobin, resting cardiac index, resting LVEF, and resting mean pulmonary artery pressure. 14 out of 26 HFrEF patients who were treated with sildenafil (25-75 mg orally TID) for 12 weeks demonstrated a 24.6% increase in PVD (p=0.015) compared to no change in PVD in those treated with placebo (n=12).
Conclusions: Pulmonary vascular distensibility is reduced in patients with HF and PAH and is closely related to functional capacity and RV systolic function during exercise. Furthermore, distensibility was modifiable with selective pulmonary vasodilator therapy, suggesting that distensibility of the pulmonary vessels may be an important therapeutic target in the treatment of HF and pulmonary hypertension.
Author Disclosures: B.P. Dhakal: None. R. Malhotra: None. P.P. Pappagianopoulos: None. A.S. Eisman: None. G.D. Lewis: None.
- © 2015 by American Heart Association, Inc.