Key result
Feline cardiomyopathy linked to significantly higher RAAS peptides and aldosterone vs healthy controls.
Why the study?
Circulating RAAS activity has not been comprehensively characterized in cats with systemic hypertension or cardiomyopathy, and the effects of furosemide or amlodipine treatment on the RAAS remain incompletely evaluated.
Does systemic hypertension, cardiomyopathy, and their associated medical treatments alter circulating RAAS biomarker concentrations in cats?
Observational (n=66)
No
Does systemic hypertension, cardiomyopathy, and their associated medical treatments alter circulating RAAS biomarker concentrations in cats?
Feline cardiomyopathy is associated with significant baseline RAAS activation which is further stimulated by furosemide therapy, underscoring a pathophysiologic rationale for RAAS-mitigating treatments.
Answers are grounded in this paper and cite their sources.
Hypothesis-generating for RAAS inhibition in feline cardiomyopathy; prospective trials needed before clinical adoption.
BACKGROUND: Activity of the circulating renin-angiotensin-aldosterone system (RAAS) has not been comprehensively characterized in cats with systemic hypertension (SH) or cardiomyopathy (CM), and the effects of furosemide or amlodipine treatment on the RAAS have not been fully evaluated in cats. HYPOTHESIS/OBJECTIVES: To document RAAS activity in cats with SH or CM compared to healthy cats and determine how RAAS profiles change with furosemide or amlodipine treatment. ANIMALS: Sixty-six client-owned cats: 15 with SH (7 amlodipine-treated, 8 untreated), 17 with advanced CM (7 furosemide-treated, 10 not furosemide-treated), and 34 healthy cats. METHODS: Equilibrium concentrations of RAAS peptides and aldosterone were quantified in serum samples by liquid chromatography-mass spectrometry. Variables were compared between groups using Kruskal-Wallis analysis with post hoc Holms-corrected Dunn's testing. RESULTS: Compared with healthy cats, cats with CM had higher concentrations of angiotensin I, aldosterone, and plasma renin activity (all P < .01), and these differences remained significant (P < .03) after considering subgroups of untreated or furosemide-treated cats. Compared with healthy cats, untreated cats with SH showed no differences in RAAS biomarkers, whereas amlodipine-treated cats had higher concentrations of angiotensins I, II, III, IV, and 1-7, aldosterone, and plasma renin activity (all P < .03). Multivariable analysis determined that furosemide and amlodipine treatments were independent predictors of increased RAAS biomarker concentrations. CONCLUSIONS AND CLINICAL IMPORTANCE: Cats with CM had increased RAAS activity, whereas cats with untreated SH did not. Furosemide and amlodipine both led to nonspecific activation of both classical and alternative RAAS pathways in cats.
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Ward et al. (2022) conducted an observational in Cardiomyopathy or Systemic Hypertension in cats (n=66). Cardiomyopathy (CM) and Systemic Hypertension (SH) vs. Healthy matched cats was evaluated on Equilibrium concentrations of RAAS peptides and aldosterone (p=<0.01). Cats with cardiomyopathy had significantly increased concentrations of angiotensin I, aldosterone, and plasma renin activity compared to healthy cats.
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