Abstract: SA-PO1099

Aldosterone Breakthough Does Not Affect Central Hemodynamics

Session Information

  • Salt and Hypertension
    November 04, 2017 | Location: Hall H, Morial Convention Center
    Abstract Time: 10:00 AM - 10:00 AM

Category: Hypertension

  • 1104 Hypertension: Clinical and Translational - Salt and Hypertension

Authors

  • Beenken, Andrew, New York Presbyterian/Columbia University, New York CIty, New York, United States
  • Bomback, Andrew S., Columbia University, New York, New York, United States
Background

Angiotensin converting enzyme inhibitors (ACEi) and angiotensin receptor blockers (ARB) are widely used in patients with congestive heart failure (CHF) and chronic kidney disease (CKD), but up to 40% of patients on these agents experience aldosterone breakthrough, with aldosterone levels rising above pre-treatment levels after 6-12 months of RAAS blockade. Aldosterone breakthrough has been associated with worsening CHF and CKD, yet the pathophysiology remains unclear. While aldosterone breakthrough has not been associated with elevated peripheral blood pressure (PBP), no studies have yet evaluated the effect of breakthrough on central blood pressure (CBP).

Methods

In this cross-sectional study, 19 subjects with well-controlled PBP (<140/90), on stable doses of ACEi/ARB for >1 year, had aldosterone levels checked and CBP parameters measured using the SphygmoCor® system. The CBP parameters of subjects with or without breakthrough, defined as serum aldosterone >15 ng/dL, were compared.

Results

Of 19 subjects, 6 had breakthrough with a mean aldosterone level of 33.8 ng/dL, and 13 were without breakthrough with a mean level of 7.1 ng/dL. There was no significant difference between subjects with and without breakthrough in any of the CBP parameters (mmHg), including CBP (92 ± 16 vs. 95 ± 8, p=0.5), central pulse pressure (40 ± 10 vs. 34 ± 11, p=0.2), augmentation pressure (10 ± 5 vs. 7 ± 6, p=0.3), and augmentation index (16 ± 8 vs. 16 ± 12, p=0.4).

Conclusion

We found no correlation between aldosterone breakthrough and CBP. Accordingly, the clinical impact of aldosterone breakthrough on CKD and CHF likely depends on its non-genomic, pro-fibrotic, and pro-inflammatory effects rather than its regulation of extracellular volume.