Abstract 14059: Low Systemic Arterial Pressure and Greater Vascular Stiffness after Transcatheter Aortic Valve Replacement are Independently Associated with Mortality in the PARTNER I Trial and Registry
Introduction: Residual left ventricular afterload after aortic valve replacement (AVR) for aortic stenosis (AS) is usually determined by assessing the transvalvular pressure gradient, effective orifice area and prosthesis-patient mismatch.
Hypothesis: We hypothesized that the afterload contribution of the systemic vasculature may impact clinical outcomes after valve replacement.
Methods: Of patients with symptomatic AS at high or prohibitive surgical risk receiving transcatheter AVR (TAVR) in the PARTNER I trial or registry, 2140 patients with echocardiograms performed and systolic blood pressure (SBP) measured at 30 days after TAVR between 100-170mmHg were included. Systemic arterial compliance (SAC) at 30 days was calculated as stroke volume index / arterial pulse pressure. A multivariable Cox PH model evaluated the relationship between SBP (100-129 vs. 130-170mmHg) or SAC (dichotomized by median) at 30 days and all-cause death (30 days to 1 year). The model adjusted for 13 clinical and echocardiographic variables.
Results: Compared to patients (n=1131) with SBP 130-170, patients (n=1009) with SBP 100-129 had a higher rate of all-cause death (20.1% vs. 12.1%, p<0.001). Patients with low SAC (n=953) had a higher rate of all-cause death compared to those with high SAC (n=954) (17.3% vs. 12.4%, p=0.002). Four groups based on SBP and SAC had different rates of all-cause death (Figure). After multivariable adjustment, both SBP 100-129 (adjusted HR 1.83, 95% CI 1.42-2.38, p<0.001) and low SAC (adjusted HR 1.83, 95% CI 1.38-2.42, p<0.001) were associated with increased mortality.
Conclusions: Lower SBP and low SAC (greater stiffness) after TAVR are each associated with increased mortality and when both were present the impact was additive. While the role of the systemic vasculature in survival after TAVR has not been emphasized, these findings suggest that blood pressure targets and adjunctive medical therapy to decrease vascular stiffness may improve outcomes.
Author Disclosures: B.R. Lindman: Consultant/Advisory Board; Modest; Roche Diagnostics. Research Grant; Significant; Young Investigator Award from Gilead. Other Research Support; Significant; Assay support from Roche Diagnostics and BG-Medicine. P.S. Douglas: None. R.T. Hahn: Research Grant; Significant; Philips Healthcare. Honoraria; Modest; St. Jude Medical. Consultant/Advisory Board; Modest; Edwards Lifesciences. N.J. Weissman: None. W.J. Stewart: None. H. Jilaihawi: Consultant/Advisory Board; Modest; Edwards Lifesciences, St. Jude Medical, Venus MedTech. C.M. Otto: None. K. Xu: None. A. Zajarias: Consultant/Advisory Board; Modest; Edwards Lifesciences. H.S. Maniar: None. E. Tuzcu: Other; Modest; Travel reimbursement for PARTNER Executive Committee activities. M.B. Leon: Other; Modest; Travel reimbursement for PARTNER Executive Committee activities. P. Pibarot: Research Grant; Significant; Canada research Chair in Valvular Heart Diseases, Canadian Institutes of Health research, Ottawa, Ontario, Canada. Consultant/Advisory Board; Modest; Edwards Lifesciences.
- © 2014 by American Heart Association, Inc.