Abate, Ornella

Borgarelli, Michele

Borrelli, Antonio

Cagnasso, Aurelio

Tarducci, Alberto

Zanatta, Renato

English

Institutional Research Information System University of Turin

Veterinary Research Communications, 28 (2004) 385–388© 2004 Kluwer Academic Publishers. Printed in the NetherlandsSerum Values of Cardiac Troponin-T in Normal andCardiomyopathic DogsA. Tarducci*, O. Abate, M. Borgarelli, A. Borrelli, R. Zanatta and A. CagnassoDepartment of Animal Pathology, Faculty of Veterinary Medicine, University of T orino,Grugliasco (T o), Italy*Correspondence: Dipartimento di Patologia Animale – Facolta` di MedicinaVeterinaria, V ia L . da V inci, 44 – 10095 Grugliasco (T orino) – ItalyE-mail: alberto.tarducci@unito.itKeywords: troponin T, dog, heart, dilated cardiomyopathy, ventricular hypokinesisINTRODUCTIONTogether with tropomyosin, the troponin complex participates in the contraction ofskeletal and cardiac muscles. Troponin is composed of three subunits, namely tro-ponin C (TnC), troponin I (TnI), and troponin T (TnT), which binds tropomyosin.There are three different isoforms of TnT and TnI, two of which are specific forskeletal muscle, while the third is specific for the myocardium (cTnT and cTnI). Asthe homology between troponins is about 95% among mammals, commercial diag-nostic kits designed for use in humans also provide excellent results in other animals.(O’Brien et al., 1997).In human medicine, the measurement of cTnT or cTnI levels is now used togetherwith measurement of the levels of creatine kinase (CK) and lactate dehydrogenase(LDH) and their isozymes for assessment of myocardial damage. For diagnosticpurposes, one advantage is that these proteins are normally absent in blood in sub-jects without myocardial damage. Even minimal increases in the serum levels of theseproteins are indicative of myocardial damage and, in the case of cTnT, it is detectablein serum from 2 h to 14 days following the onset of myocardial damage. Moreover, incontrast to the isozymes of CK and LDH, the results are not influenced by use ofdifferent clinical samples (hemolytic, lipemic, bile samples). The degree of increase inthe level of cTnT is relatively proportional to the degree of myocardial damage, withprognostic implications as well. At the same time, the extreme sensitivity of thistechnique also allows for its use in other nonischemic pathologies including chroniccardiac insufficiency, pulmonary emboli, acute myocarditis, systemic hypertension,arrhythmias, and toxicity from doxorubicin (De Francesco, 2002). In veterinary medi-cine, O’Brien et al. (1997) have demonstrated the utility of measuring the levels ofcTnT in the diagnosis of experimentally induced myocardial damage.MATERIALS ANDMETHODScTnT levels were determined using an immunochemical test developed for humansusing whole, heparinized venal blood (Cardiac Reader, Roche) within 2 h of blood385386collection. Values of cTnT less than 0.05 were considered negative (expressedin ng/ml). Values of cTnT between 0.05–0.1, 0.1–2, and >2 were considered as low,intermediate, and high, respectively. The cTnT levels were measured for a controlgroup of 20 dogs that were judged as healthy on the basis of history and objectiveclinical examination with particular attention to the cardiovascular system. Thisgroup of animals comprised subjects with different races and gender with an agebetween 1 to 12 years (mean 6.1). Another group of 30 animals was defined ascardiomyopathic on the basis of clinical and instrumental examination (e.g., echocar-diograph and ecoDoppler, radiography and EKG). These all had cardiac insuffi-ciencies between 1b and 3a, according to the ISACHC classification. On the basis ofechocardiographic examination, the myocardiopathic group was further divided intotwo subgroups: non-hypokinetic myocardiopathic (12 dogs aged between 3 monthsand 16 years, mean 7.5) and hypokinetic myocardiopathic (global or segmental hypo-kinetic; 18 dogs aged between 7 months and 15 years, mean 6.0). Statistical analysisusing Fisher’s test was employed to evaluate the correlation between a positive cTnTtest and cardiac insufficiency, as well as ventricular kinetics. The aim of the presentwork was to determine the value of cTnT for healthy dogs and for dogs affected withdifferent cardiac pathologies, evaluating eventual correlations between cTnT levels,the ISACHC classification for cardiac insufficiency, the index of systolic volume(ESV-I), and ventricular kinetics.RESULTSThe control group of healthy dogs had values of serum cTnT that were below detect-able levels (i.e., <0.05 ng/ml). Ten of the 30 myocardiopathic dogs (33%) testedpositive for cTnT. However, there was no significant correlation between a positiveresult in the cTnT assay and the type of cardiac insufficiency or with the ESV-I. Inthe non-hypokinetic group, only one of the 12 dogs (8.3%) which had an intermediatelevel of cTnT was positive. In the hypokinetic myocardiopathic group, 9 out of 18animals tested positive, three with low levels of cTnT, four with intermediate levels,and two with high levels. The probability of a positive cTnT value was significantlyhigher for hypokinetic animals with respect to non-hypokinetic dogs (Fisher’s exacttest, OR=10, p<0.05).It was possible to carry out a second examination for 4 out of 10 dogs at follow-upvisits during the course of therapy. In three animals, the cTnT level was belowdetectable levels by the second control visit and was associated with an improvementin general clinical conditions in all cases. The remaining dog, diagnosed with dilativemyocardiopathy, had levels of cTnT that had increased over a two week interval,although they still fell in the intermediate value category. During this period, thedog’s conditions progressively worsened in spite of therapy and the animal died threedays after the last visit. For the three dogs with dilative myocardiopathy, the value ofcTnT was below detection limits.387DISCUSSIONThe absence of detectable cTnT (>0.05 ng/ml) in healthy dogs confirms the utility ofthis assay in assessing acute myocardial damage, similar to that reported both forboth human and veterinary subjects (De Francesco, 2002). The results of the presentwork indicate the usefulness of the cTnT test for the identification of cardiopathicsubjects for whom disease is associated with myocardial damage. Furthermore, ourdata are also interesting in relation to the lack of correlation between a positive cTnTresult and the degree of systolic insufficiency. In addition, the observation that only50% of the hypokinetic group was positive for cTnT suggests that the assay may haveparticular utility in discriminating animals with myocardial damage in course fromthose in which hypokinesis is most likely indicative of a previous injury. On the otherhand, the positive test results observed in non-hypokinetic, myocardiopathic subjectsimplies that the measurement of cTnT is a diagnostic tool that is valuable for theidentification of myocardial damage, even in animals that would not otherwise besuspected to have myocardial damage on the basis of clinical and instrumentalexamination.The determination of cTNT during the follow-up period may also have prognosticimplications. During this period, clinical improvement was seen in all three 3 caseswith negative cTnT, while in the subject for whom increased levels of cTnT wereobserved, clinical deterioration was noted and resulted in sudden death. Lastly, forthe three dogs with dilative myocardiopathy serum cTnT was not detected. This maybe explained by the low concentrations of troponin T at the myocardial level, asreported by O’Brien (1997) for Dobermans affected with idiopathic dilative myocar-diopathy. Our results are in contrast to those found for humans, in which a relativelyhigh percentage of patients were found to be positive for cTnT during the course ofdilative myocardiopathy. It has been reported that the return to normal levels ofcTnT following therapy also has a beneficial impact on prognosis, with survival timesthat are significantly higher (Sato et al., 2001). However, in the present study thenumber of animals with dilative myocardiopathy, all with negative cTnT, is too smallto make any conclusions in this regard.ACKNOWLEDGEMENTSThis work was supported by grants from Italian MURST.REFERENCESDe Francesco, T.C., Atkins, C.E., Keene, B.W., Coats, J.R. and Hauck, M.L., 2002. Prospective clinicalevaluation of serum cardiac troponin T in dogs admitted to a veterinary teaching hospital. Journal ofVeterinary Internal Medicine, 16, 553–557O’Brien, P.J., 1997. Deficiencies of myocardial troponin-T and creatine kinase MB isoenzyme in dogs withidiopathic dilated cardiomyopathy. American Journal Veterinary Research, 58, 11–16388O’Brien P.J. Dameron, G.W., Beck, M.L., Kang, Y.J., Erickson, B.K., Di Battista, T.H., Miller, K.E.,Jackson, K.N. and Mittelstadt, S., 1997. Cardiac troponin T is a sensitive, specific biomarker of cardiacinjury in laboratory animals. L aboratory Animal Science, 47, 486–495Sato, Y., Yamada, T., Taniguchi, R., Nagai, K., Makiyama, T., Okada, H., Kataoka, K., Ito, H.,Matsumori, A., Sasayama, S. and Takatsu, Y., 2001. Persistently increased serum concentrations ofcardiac Troponin T in patients with idiopathic dilated cardiomyopathy are predictive of adverseoutcomes. Circulation, 103, 369–374

Serum values of cardiac Troponin -T in normal and cardiomyopathic dogs

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Serum values of cardiac Troponin -T in normal and cardiomyopathic dogs

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