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: 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.
  
  
  OBJECTIVE
  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.
  
  
  METHODS
  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.
authors.affiliation: William R. Pritchard Veterinary Medical Teaching Hospital, University of California, Davis, CA, USA.
authors.forename: S W
authors.initials: SW
authors.lastname: Jung
authors.forename: M D
authors.initials: MD
authors.lastname: Kittleson
mesh_terms: D058671:Adrenergic beta-1 Receptor Antagonists / Q000494:pharmacology / Q000627:therapeutic use*; D000818:Animals; D001262:Atenolol / Q000494:pharmacology / Q000627:therapeutic use*; D015415:Biomarkers / Q000097:blood; D002312:Cardiomyopathy, Hypertrophic / Q000097:blood / Q000150:complications / Q000188:drug therapy / Q000662:veterinary*; D002371:Cat Diseases / Q000097:blood* / Q000188:drug therapy; D002415:Cats; D005260:Female; D017379:Hypertrophy, Left Ventricular / Q000097:blood / Q000188:drug therapy / Q000209:etiology / Q000662:veterinary*; D008297:Male; D020097:Natriuretic Peptide, Brain / Q000097:blood*; D010446:Peptide Fragments / Q000097:blood*; D010865:Pilot Projects; D019209:Troponin C / Q000097:blood*
chemical_list: D058671:Adrenergic beta-1 Receptor Antagonists; D015415:Biomarkers; D010446:Peptide Fragments; D019209:Troponin C; C109794:pro-brain natriuretic peptide (1-76); D020097:Natriuretic Peptide, Brain; D001262:Atenolol