Abstract 18384: Hispanic Disparities in PAH: Multi-Modality Validation of Increased Susceptibility to Right Ventricular Dysfunction
Introduction: Hispanics are known to have increased baseline right ventricular (RV) wall thickness and cardiovascular risk factors compared to non-Hispanics. We, therefore, hypothesized that Hispanics have reduced RV function in response to increased pulmonary afterload compared to non-Hispanics.
Methods: A total of 127 WHO Groups I and IV pulmonary arterial hypertension (PAH) patients were prospectively enrolled and underwent echocardiography and right heart catheterization (RHC) within 4 months, with a subset also performing six-minute walk test (6MWT, n=86). After comparing baseline characteristics between self-reported Hispanics (n=28) and non-Hispanics (n=99), ethnicity effects were assessed using hierarchical linear regression models adjusted for age, gender, indexed pulmonary vascular resistance (PVRi), PAH medication use, and days from echo to RHC.
Results: Baseline characteristics between the two groups were not significantly different except for age, which was higher in non-Hispanics (60.9+13.7 yrs) compared to Hispanics (51.9+12.2 yrs, P<0.01). In fully adjusted models, Hispanics exhibited significantly greater RV remodeling and dysfunction compared to non-Hispanics as evidenced (Table I) by echocardiography (Tricuspid annular plane systolic excursion, TAPSE, and RV wall thickness) and RHC (mean right atrial pressure, RAP). Hispanics also exhibited greater effective arterial elastance (Ea) and increased pulmonary arterial occlusion (wedge) pressure compared to non-Hispanics. 6MWT also revealed trends toward lower average distances in Hispanics versus non-Hispanics.
Conclusions: Hispanics with PAH exhibit increased pathological RV remodeling and systolic dysfunction validated by both echo and RHC with decreased trends in functional capacity (6MWT) compared to non-Hispanics. This susceptibility may be influenced, in part, by increased pulmonary artery elastance and relatively higher but “normal” wedge pressures.
Author Disclosures: B. Natarajan: None. V. Nair: None. P. Dherange: None. M. Whitaker: None. I. Riaz: None. A. Shewale: None. V. Yarlagadda: None. K. Patel: None. K. Knox: None. Z. Khalpey: None. P. Suryanarayana: None. S.M. Black: None. J.G. Garcia: None. F. Rischard: None. J.X. Yuan: Consultant/Advisory Board; Modest; Actelion Sterring Committee for Young Investigator Program, Bayer HealthCare US Medical Affairs Cardiopulmonary Franchise Scientific Advisory Council. Research Grant; Significant; NIH grant. A.A. Desai: None.
- © 2016 by American Heart Association, Inc.