01 March 2017 by Roberto Bernardo

Concentric RV remodeling represents an adaptive phenotype only in patients with advanced pulmonary arterial hypertension


Concentric right ventricular (RV) remodeling is thought an adaptive response in patients with pulmonary arterial hypertension (PAH). We sought to correlate markers of RV remodeling to afterload and performance in patients before and after treatment with parenteral treprostinil.


We prospectively analyzed 25 treatment-naive patients with advanced PAH before and after 3 months of monotherapy with parenteral treprostinil. Patients were divided into three subgroups based on two criteria including post-treatment cardiac MRI derived RV mass/volume (M/V) values above and below the median (≤0.4 eccentric and >0.4 concentric hypertrophy), as well as afterload (Ea, pulmonary artery elastance): Group 1 (M/V≤0.4, Ea≤0.8), Group 2 (M/V>0.4, Ea>0.8) and Group 3 (M/V≤0.4, Ea>0.8). The latter Ea was determined from a cut-off relative to its correlation to compliance estimates from mortality data previously published. Single-beat method RV-PA coupling was used for estimation of contractility (Ees, end-systolic elastance) to Ea ratio (Ees/Ea). MRI-derived RV ejection fraction (RVEF) was used as a surrogate for performance.


At baseline, Group 1 had lower pulmonary vascular resistance (PVR) than Groups 2 and 3 (see Table). RVEF was similar and Ees/Ea was preserved across all groups. After treatment, all groups demonstrated similar improvements in PVR and RVEF.  Ees/Ea was highest in Group 1 while lowest in Group 3 but RVEF similar between groups (see Table).  M/V slightly increased in Group 2 relative to Group 3 owing to increasing RV mass. After 22 ± 14.3 months follow-up, there were 1/11 (9%), 1/7 (14%) and 3/7 (43%) deaths in groups 1, 2, and 3, respectively.


Increased RV mass proportionate to chamber dilatation or concentric hypertrophy, represents a favorable adaptation to increased afterload. However, a low M/V or eccentric hypertrophy may be appropriate in cases of decreased afterload.

Key Contributors

1Bernardo R, 2Wickstrom K, 2Honkanen I, 3,4Desai AA, 4Vanderpool R and 4, 5Rischard F 1Department of Pulmonary and Critical Care Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, 2Department of Medicine, 3Department of Cardiology, 4Division of Translational and Regenerative Medicine, 5Department of Pulmonary, Critical Care, Sleep, and Allergy Medicine, , University of Arizona, Tucson, AZ 85721

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