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Peer-reviewed veterinary case report

Plasma growth differentiation factors 8 and 11 levels in cats with congestive heart failure secondary to hypertrophic cardiomyopathy.

Journal:
Journal of veterinary cardiology : the official journal of the European Society of Veterinary Cardiology
Year:
2019
Authors:
Yang, V K et al.
Affiliation:
Department of Clinical Sciences · United States

Abstract

OBJECTIVES: Growth differentiation factor (GDF) 11 has been shown to reduce cardiac hypertrophy in mice. Low levels of GDF-11 are associated with cardiac hypertrophy in humans. The authors hypothesized that plasma GDF-11 level is decreased in cats with hypertrophic cardiomyopathy (HCM). Given the close homology between GDF-11 and myostatin/GDF-8, GDF-8 levels were also assessed. ANIMALS: Thirty-seven client-owned cats were enrolled, including cats with normal cardiac structure (n = 16), cats with HCM or hypertrophic obstructive cardiomyopathy (HOCM; n = 14), and cats with HCM and congestive heart failure (CHF; n = 7). METHODS: Plasma samples were analyzed for GDF-8 and GDF-11 using liquid chromatography tandem-mass spectrometry. Levels of GDF-8 and GDF-11 were compared between cats with normal cardiac structure, HCM or HOCM, and CHF. RESULTS: No differences in GDF-11 concentrations were found between cats with normal cardiac structure and cats with HCM/HOCM, with or without history of CHF. Decreased GDF-8 concentrations were detected in cats with CHF compared to cats with HCM/HOCM without history of CHF (p=0.031) and cats with normal cardiac structure (p=0.027). Growth differentiation factor 8 was higher in cats with HOCM compared to those with CHF (p=0.002). No statistical difference was noted in GDF-8 level as a function of age, weight, or body condition score. CONCLUSIONS: Plasma GDF-11 was not different between cats with HCM/HOCM and cats with normal cardiac structure regardless of age. Plasma GDF-8 was decreased in cats with CHF compared to cats with normal cardiac structure and cats with asymptomatic HCM/HOCM, suggesting a possible role in CHF development.

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Original publication: https://pubmed.ncbi.nlm.nih.gov/31568985/