Cardiac Troponin I in Calves with Congenital Heart Disease
Article first published online: 11 JUN 2012
Copyright © 2012 by the American College of Veterinary Internal Medicine
Journal of Veterinary Internal Medicine
Volume 26, Issue 4, pages 1056–1060, July-August 2012
How to Cite
Suzuki, K., Uchida, E., Schober, K. E., Niehaus, A., Rings, M. D. and Lakritz, J. (2012), Cardiac Troponin I in Calves with Congenital Heart Disease. Journal of Veterinary Internal Medicine, 26: 1056–1060. doi: 10.1111/j.1939-1676.2012.00953.x
- Issue published online: 13 JUL 2012
- Article first published online: 11 JUN 2012
- Manuscript Accepted: 2 MAY 2012
- Manuscript Revised: 12 APR 2012
- Manuscript Received: 19 DEC 2011
- Ministry of Education, Culture and Sciences of Japan. Grant Number: 21580393
- Congenital heart disease;
- Vertebral heart score
The association between plasma cardiac troponin I (cTnI) and the magnitude of cardiac enlargement in calves with congenital heart disease (CHD) are not well defined.
To investigate the relationship between plasma cTnI concentrations and cardiac size in healthy calves and calves with CHD.
A total of 19 healthy calves (control) and 12 Holstein calves with CHD (patent ductus arteriosus, ventricular septal defect, tetralogy of Fallot or double outlet right ventricle).
Case control study. All animals underwent a comprehensive transthoracic echocardiographic study to document cardiac health or presence of CHD. The vertebral heart score (VHS) was determined in each animal using right lateral survey radiographic images. Blood samples were collected via jugular venipuncture and plasma cTnI concentration and creatine kinase (CK) activity were determined by a 3rd generation immunoassay and an automatic biochemical analyzer, respectively. Groups were compared using Mann-Whitney U-test and receiver-operating characteristics (ROC) curve analysis.
Calves with CHD had significantly larger VHS values and higher plasma cTnI concentrations (P < .001) compared to control. Creatine kinase activity was not different between the control and CHD groups of calves. Diagnostic cutoffs of VHS and plasma cTnI for discrimination of groups were 8.9 vertebrae and 0.035 ng/mL, respectively. The cTnI concentration in plasma was significantly correlated with VHS (r 2=0.512, P < .001).
Conclusion and Clinical Relevance
Our results suggest that determination of plasma cTnI concentrations in calves with clinical signs compatible with CHD might prove useful as a guide to quantify cardiac remodeling associated with increased cardiac size.