Cardiology Resident NC State University Cary, North Carolina, United States
Abstract:
Background: There are limited effective treatment options for subvalvular aortic stenosis (SAS) in dogs. The renin-angiotensin-aldosterone system (RAAS) is upregulated in cardiac conditions such as advanced myxomatous mitral valve disease and congestive heart failure. Modulation of RAAS improves outcomes in some cardiac conditions. Renin-angiotensin-aldosterone system profiles in dogs with SAS are unknown. Hypothesis/
Objectives: To determine if RAAS activation occurs in dogs with severe SAS and evaluate for progressive RAAS activation with increasing disease severity. We hypothesized that RAAS activation occurs in dogs with SAS. Animals: Twenty-two client-owned dogs with severe (maxPG >80mmHg) or very severe SAS (maxPG>130mmHg) and 22 age- and weight-matched healthy controls.
Methods: Prospective observational study. Dogs underwent echocardiographic examination and blood sample collection. Serum equilibrium concentrations of angiotensin II, 1-7, 1-10, III (2-8), 1-5, IV (3-8), aldosterone, PRA-S, ACE-S, and AA2 were evaluated using ultra-performance liquid chromatography-mass spectrometry. General linear models were used for each component of the RAAS profile to include an effect of group, sex, demeanor, and time since last meal as covariates. Type III tests were used to determine the significance of each variable.
Results: All RAAS components tested, aside from ACE-S, were significantly lower in the SAS groups than the healthy control group (all P < 0.039).
Conclusion: Differences in the classical and counter-regulatory arm of the RAAS are present in dogs with severe and very severe SAS. These results highlight a therapeutic target and a potential clinical benefit for the use of RAAS modulating drugs in dogs with severe SAS.
