Catecholamine-associated left ventricular hypertrophy in dogs with hyperadrenocorticism and myxomatous mitral valve disease: a prospective pilot study.

IMPORTANCE: Endogenous Cushing's syndrome increases the risk of cardiac hypertrophy, dysfunction, and cardiovascular mortality. Given the high prevalence of hyperadrenocorticism (HAC) and myxomatous mitral valve disease (MMVD) in dogs, endocrine-cardiac interactions may influence disease progression but remain poorly characterized. OBJECTIVE: To evaluate the effects of concurrent HAC on cardiac remodeling and function in dogs with subclinical MMVD and identify metabolic and neurohormonal markers, particularly catecholamine metabolites, associated with left ventricular hypertrophy and dysfunction. METHODS: Twenty-one client-owned dogs (HAC + MMVD, MMVD-only controls, and healthy controls [each n = 7]) were prospectively enrolled. Echocardiographic variables, including speckle-tracking echocardiography, hematologic and biochemical parameters, and urinary normetanephrine: creatinine ratios, were evaluated at baseline and follow-up. RESULTS: The HAC + MMVD group showed significantly increased urinary normetanephrine: creatinine ratios than both healthy control group and MMVD-only control group (p = 0.011 and p = 0.007, respectively). Urinary normetanephrine: creatinine ratio was independently associated with interventricular septum wall thickness in diastole (IVSdN, B = 0.000222, 95% confidence interval [CI] 0.000050 to 0.000393, p = 0.026). Δ Urinary normetanephrine: creatinine was positively associated with Δ IVSdN after adjusting for Δ days (B = 0.000308, 95% CI 0.000108 to 0.000507, p = 0.016). Global longitudinal strain (GLS) was lower in the HAC + MMVD group than both the healthy control group and the MMVD-only control group (p = 0.001 and p = 0.002, respectively). However, GLS was not associated with normetanephrine levels (r = 0.179, 95% CI -0.698 to 1.000, p = 0.720). CONCLUSIONS AND RELEVANCE: This exploratory pilot study is the first suggesting a potential neuroendocrine mechanism underlying endocrine-cardiac remodeling in dogs with concurrent HAC and MMVD, whereby increased catecholamine activity may be associated with left ventricular hypertrophy.