The Effect of Atenolol on NT-proBNP and Troponin in Asymptomatic Cats with Severe Left Ventricular Hypertrophy because of Hypertrophic Cardiomyopathy

A Pilot Study

S. W. Jung, Mark D Kittleson

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

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 (12.5mg PO q12h) 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, 394pmol/L; range, 71-1,500pmol/L; median after, 439pmol/L; range, 24-1,500pmol/L; P = .63) or in cTnI (median before, 0.24ng/mL; range, 0.10-0.97ng/mL; median after, 0.28ng/mL; range, 0.09-1.0ng/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.

Original languageEnglish (US)
Pages (from-to)1044-1049
Number of pages6
JournalJournal of Veterinary Internal Medicine
Volume25
Issue number5
DOIs
StatePublished - Sep 2011

Fingerprint

natriuretic peptides
troponins
Troponin
Atenolol
Brain Natriuretic Peptide
Hypertrophic Cardiomyopathy
cardiomyopathy
Left Ventricular Hypertrophy
hypertrophy
Cats
cats
Troponin I
heart failure
biomarkers
Heart Failure
Biomarkers
heart diseases
myocardial ischemia
Mitral Valve
myocytes

Keywords

  • Beta blocker
  • Biomarker
  • Drug therapy
  • Myocardial ischemia

ASJC Scopus subject areas

  • veterinary(all)

Cite this

@article{c6204464e56a4d648cb8c16951be5388,
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",
abstract = "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 (12.5mg PO q12h) 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, 394pmol/L; range, 71-1,500pmol/L; median after, 439pmol/L; range, 24-1,500pmol/L; P = .63) or in cTnI (median before, 0.24ng/mL; range, 0.10-0.97ng/mL; median after, 0.28ng/mL; range, 0.09-1.0ng/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.",
keywords = "Beta blocker, Biomarker, Drug therapy, Myocardial ischemia",
author = "Jung, {S. W.} and Kittleson, {Mark D}",
year = "2011",
month = "9",
doi = "10.1111/j.1939-1676.2011.0754.x",
language = "English (US)",
volume = "25",
pages = "1044--1049",
journal = "Journal of Veterinary Internal Medicine",
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T1 - The Effect of Atenolol on NT-proBNP and Troponin in Asymptomatic Cats with Severe Left Ventricular Hypertrophy because of Hypertrophic Cardiomyopathy

T2 - A Pilot Study

AU - Jung, S. W.

AU - Kittleson, Mark D

PY - 2011/9

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N2 - 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 (12.5mg PO q12h) 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, 394pmol/L; range, 71-1,500pmol/L; median after, 439pmol/L; range, 24-1,500pmol/L; P = .63) or in cTnI (median before, 0.24ng/mL; range, 0.10-0.97ng/mL; median after, 0.28ng/mL; range, 0.09-1.0ng/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.

AB - 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 (12.5mg PO q12h) 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, 394pmol/L; range, 71-1,500pmol/L; median after, 439pmol/L; range, 24-1,500pmol/L; P = .63) or in cTnI (median before, 0.24ng/mL; range, 0.10-0.97ng/mL; median after, 0.28ng/mL; range, 0.09-1.0ng/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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KW - Drug therapy

KW - Myocardial ischemia

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