Associate Professor Nephrology-Urology North Carolina State University Raleigh, NC, United States
Background: The renin-angiotensin-aldosterone system (RAAS) is activated in congestive heart failure (CHF), but the relative contributions of advanced heart disease and diuretics are unknown. Additionally, the influence of parenteral furosemide and active CHF are unknown. Hypothesis/Objectives: Our objective was to evaluate RAAS metabolites and enzyme activities between dogs with active and stable naturally occurring CHF. Wee hypothesized that RAAS variables would be significantly higher in active CHF dogs. Animals: Forty active (pulmonary edema or effusions on exam requiring intravenous furosemide) CHF (38 degenerative valve disease (DVD), 1 dilated cardiomyopathy (DCM), 1 congenital heart disease), and 49 stable (receiving oral furosemide or torsemide without pulmonary edema or effusions on exam) CHF (33 DVD, 14 DCM, 2 congenital) dogs were included.
Methods: Prospective study. RAAS metabolites and enzyme activities were quantified by liquid chromatography-mass spectrometry/mass-spectroscopy using previously validated methods. Groups were compared using Wilcoxon rank sum test.
Results: Angiotensin II (P Conclusions and Clinical Importance: Most RAAS metabolites were higher in dogs with active CHF compared to dogs with stable CHF supporting global activation. Potential reasons include greater potency of intravenous furosemide compared to oral diuretics and sympathetic stimulation associated with active CHF. These results suggest that active and stable CHF populations should be considered separately when assessing the RAAS metabolites.
