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Objective: To evaluate the effects of noncardiac disease on c-terminal brain natriuretic peptide (cBNP) concentrations in dogs., Design: Prospective observational study., Setting: Urban university veterinary hospital., Animals: Thirty-eight apparently healthy dogs, 28 dogs with cardiac disease (14 CHF, 14 non-CHF), and 81 dogs with primary noncardiac diseases., Interventions: none., Materials and Methods: Plasma was collected from each dog and analyzed for active (cBNP) B-type natriuretic peptide using an assay that is being investigated for commercial use (Biosite)., Measurements and Main Results: Dogs with CHF had significantly higher plasma cBNP concentrations than dogs with subclinical cardiac disease, apparently healthy dogs, or dogs with primary noncardiac disease. However, 21% (28/133) of dogs without CHF (including healthy dogs, dogs with primary noncardiac disease, and dogs with subclinical cardiac disease) had cBNP concentrations above previously identified diagnostic thresholds for CHF, reiterating the importance of reestablishing new diagnostic cutoffs when considering comorbidities affecting B-type natriuretic peptide levels., Conclusions: A clinically relevant proportion of nondyspneic dogs with primary noncardiac diseases have increased cBNP concentrations that exceed previously identified diagnostic thresholds, potentially limiting the ability of this test to identify CHF when noncardiac comorbidities exist. Interpretation of increased cBNP concentrations in such cases must be appropriately interpreted with further diagnostic investigation., (© Veterinary Emergency and Critical Care Society 2011.)

Objective: To determine whether plasma cardiac troponin I (cTnI) concentrations can be used to discriminate cardiac from noncardiac causes of dyspnea in cats., Design: Prospective, multicenter study., Animals: Client-owned cats with dyspnea attributable to congestive heart failure (D-CHF; n=31) or to noncardiac causes (D-NCC; n=12)., Procedures: For each cat, plasma cTnI concentration was analyzed by use of a solid-phase radial partition immunoassay; values in cats with D-CHF and D-NCC were compared. A receiver operating characteristic curve was analyzed to determine the accuracy of plasma cTnI concentration for diagnosis of D-CHF., Results: Median plasma concentration of cTnI in cats with D-CHF (1.59 ng/mL; range, 0.20 to 30.24 ng/mL) was significantly higher than in cats with D-NCC (0.165 ng/mL; range, 0.01 to 1.42 ng/mL). With regard to the accuracy of plasma cTnI concentration for diagnosis of D-CHF, the area under the receiver operating characteristic curve was 0.84. At plasma concentrations > or = 0.2 ng/mL, cTnI had 100% sensitivity but only 58% specificity for identification of CHF as the cause of dyspnea. At plasma concentrations > or = 1.43 ng/mL, cTnI had 100% specificity and 58% sensitivity for identification of CHF as the cause of dyspnea., Conclusions and Clinical Relevance: On the basis of the derived diagnostic limits, CHF as the cause of dyspnea could be ruled in or ruled out without additional diagnostic testing in > 50% of the study cats. Measurement of plasma cTnI concentration may be clinically useful for differentiation of cardiac from noncardiac causes of dyspnea in cats. (J Am Vet

Measurement of plasma cardiac troponin I concentration ([cTnI]) is a sensitive and specific means for detecting myocardial damage in many mammalian species. Studies have shown that [cTnI] increases rapidly after cardiomyocyte injury. The molecular structure of cTnl is highly conserved across species, and current assays developed for its detection in humans have been validated in many species. In this study, [cTnI] was quantified using a 2-site sandwich assay in plasma of healthy control cats (n = 33) and cats with moderate to severe hypertrophic cardiomyopathy (HCM) (n = 20). [cTnI] was significantly higher in cats with HCM (median, 0.66 ng/mL; range, 0.05-10.93 ng/mL) as compared with normal cats (median, <0.03 ng/mL; range, <0.03-0.16 ng/mL) (P < .0001). An increase in [cTnI] was also highly sensitive (sensitivity = 85%) and specific (specificity = 97%) for differentiating cats with moderate to severe HCM from normal cats. [cTnI] was weakly correlated with diastolic thickness of the left ventricular free wall (r2 = .354; P = .009) but not with the diastolic thickness of the interventricular septum (P = .8467) or the left atrium: aorta ratio (P = .0652). Furthermore, cats with congestive heart failure at the time of cTnI analysis had a significantly higher [cTnI] than did cats that had never had heart failure and those whose heart failure was controlled at the time of analysis (P = .0095 and P = .0201, respectively). These data indicate that cats with HCM have ongoing myocardial damage. Although the origin of this damage is unknown, it most likely explains the replacement fibrosis that is consistently identified in cats with moderate to severe HCM.