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Peer-reviewed veterinary case report

Atenolol effects on heart markers in cats with severe heart thickening

By Jung, S W & Kittleson, M D·Published in Journal of veterinary internal medicine·2011·William R. Pritchard Veterinary Medical Teaching Hospital, United States·View original on PubMed

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Original publication title: The effect of atenolol on NT-proBNP and troponin in asymptomatic cats with severe left ventricular hypertrophy because of hypertrophic cardiomyopathy: a pilot study.

Species:
cat

Plain-English summary

A group of six Maine Coon cats with severe heart thickening (hypertrophic cardiomyopathy) but no signs of heart failure were given atenolol, a medication often used to manage heart conditions. After 30 days of treatment, the levels of two important heart-related markers, NT-proBNP and cardiac troponin I, did not show any significant changes. This suggests that atenolol did not help reduce heart strain or damage in these cats. More research is needed to confirm these findings and explore better treatment options.

People also search for: cat hypertrophic cardiomyopathy treatment · Maine Coon heart disease · atenolol for cats heart condition

Abstract

BACKGROUND: Atenolol often is used empirically in cats with hypertrophic cardiomyopathy (HCM) before the onset of heart failure, although evidence of efficacy is lacking. Cardiac biomarkers play a critical role in the early detection of subclinical cardiac disease, in the prediction of long-term prognosis, and in monitoring the response to therapy in humans. HYPOTHESIS: Circulating concentrations of the biomarkers N-terminal pro-B type natriuretic peptide (NT-proBNP) and cardiac troponin I (cTnI) will decrease after chronic administration of atenolol PO to cats with severe HCM but no signs of heart failure. ANIMALS: Six Maine Coon or Maine Coon cross cats with severe HCM. METHODS: Cats were treated with atenolol (12.5 mg PO q12 h) for 30 days. No cat had left ventricular dynamic outflow tract obstruction caused by systolic anterior motion of the mitral valve. The concentrations of NT-proBNP and cTnI were assayed before and on the last day of drug administration. RESULTS: There was no statistically significant change in NT-proBNP (median before, 394 pmol/L; range, 71-1,500 pmol/L; median after, 439 pmol/L; range, 24-1,500 pmol/L; P = .63) or in cTnI (median before, 0.24 ng/mL; range, 0.10-0.97 ng/mL; median after, 0.28 ng/mL; range, 0.09-1.0 ng/mL; P = .69) after administration of atenolol. CONCLUSIONS: Atenolol administration did not decrease NT-proBNP or cTnI concentrations in cats with severe left ventricular hypertrophy caused by hypertrophic cardiomyopathy. These results suggest that atenolol did not decrease myocardial ischemia and myocyte death in these cats. A larger clinical trial is warranted to verify these findings.

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Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/21781160/