Assessment of a point‐of‐care cardiac troponin I test to differentiate cardiac from noncardiac causes of respiratory distress in dogs

Objectives – To (1) determine a reference interval for cardiac troponin I (cTnI) using a point‐of‐care device in normal dogs and compare the results with those published by the manufacturer and (2) determine if cTnI differs among dogs with cardiogenic and noncardiogenic respiratory distress. Design – Prospective observational study. Setting – Emergency and referral veterinary hospital. Animals – Twenty‐six clinically normal dogs and 67 dogs in respiratory distress. Interventions – All dogs underwent whole blood sampling for cTnI concentrations. Measurements and Results – Normal dogs had a median cTnI concentration of 0.03 ng/mL (range 0–0.11 ng/mL). Thirty‐six dogs were diagnosed with noncardiogenic respiratory distress with a median cTnI concentration of 0.14 ng/mL (range 0.01–4.31 ng/mL). Thirty‐one dogs were diagnosed with cardiogenic respiratory distress with a median cTnI concentration of 1.74 ng/mL (range 0.05–17.1 ng/mL). A significant difference between cTnI concentrations in normal dogs and dogs with noncardiogenic respiratory distress was not detected. Significant differences in cTnI concentrations were found between normals versus cardiogenic and cardiogenic versus noncardiogenic respiratory distress groups. Significant differences in cTnI concentrations were identified in >10 when compared with the <5 and the 5–10 years of age groups. Receiver operating curve analysis identified cTnI concentrations >1.5 ng/mL as the optimal “cut‐off point” having a sensitivity of 78% and specificity of 51.5%. The area under the receiver operating curve was 0.72. Overall test accuracy was 65%. Conclusions – cTnI concentrations were significantly increased in dogs with cardiogenic respiratory distress versus dogs with noncardiogenic respiratory distress and normal dogs. A significant difference between normal dogs and dogs with noncardiogenic causes of respiratory distress was detected. Although highly sensitive when cTnI concentrations exceed 1.5 ng/mL, the test has low specificity. Assessment of cTnI by the methodology used cannot be recommended as the sole diagnostic modality for evaluating the cause of respiratory distress in dogs.     

High cardiac troponin I plasma concentration in a calf with myocarditis

A 15-day-old Brown Swiss calf, whose dam had suffered from foot-and-mouth disease, was presented with a history of depression and failure to suckle. The calf had an irregular cardiac rhythm and increased plasma cardiac troponin I (cTnI) detected with a commercial human immunoassay. The calf died the following day and myocarditis was detected. The cTnI assay may be useful in diagnosis of myocarditis in cattle.     

Assessment of the diagnostic accuracy of circulating cardiac troponin I concentration to distinguish between cats with cardiac and non-cardiac causes of respiratory distress

Objective

To determine if serum cardiac troponin I (cTnI) concentrations can distinguish cardiac from non-cardiac causes of respiratory distress (RD) in cats.

Animals, materials and methods

53 cats. cTnI concentrations were measured in 30 cats with non-cardiac respiratory distress (RD-NC) and compared to 23 cats with RD due to congestive heart failure (RD + CHF).

Results

The RD + CHF group had higher median cTnI concentration (0.94 ng/ml interquartile range IQR 0.54-4.00, range <0.20 - 90.14) than the RD-NC group (<0.2 ng/ml IQR < 0.2-0.33, range <0.20-41.1, p < 0.001). The area under the curve (AUC) was 0.842 (95% CI 0.728-0.955) for the receiver operator curve (ROC) analysis of the accuracy of cTnI concentrations to discriminate RD + CHF from RD-NC cats. A cut-off of ≥ 0.81 ng/ml discriminated RD + CHF from RD-NC cats with a sensitivity and specificity of 65.2% and 90.0% respectively. However considerable overlap in cTnI concentrations between the 2 groups was identified.

Conclusions

Serum cTnI concentrations were different in RD + CHF compared to RD-NC cats. However the overlap in cTnI concentrations between the 2 groups reduced the clinical efficacy of the assay which therefore should not be used as a stand-alone test but in combination with other diagnostics such as echocardiography and radiography.     

Serum cardiac troponin I concentration in dogs with ehrlichiosis

Background: Ehrlichiosis is a multisystemic disease with the potential to cause cardiomyocyte injury in naturally infected dogs.
Hypothesis: Myocardial injury occurs in dogs infected with Ehrlichia canis .
Animals: One-hundred and ninety-four dogs from Brazil with clinical and laboratory abnormalities indicative of ehrlichiosis. Sixteen healthy dogs served as controls.
Methods: Electrocardiogram, echocardiogram, noninvasive blood pressure measurement, and serum cardiac troponin I (cTnI) concentrations were evaluated. Serologic assays and PCR determined the exposure and infection status for E. canis, Anaplasma spp., Babesia canis vogeli, Bartonella spp., Borrelia burgdorferi, Dirofilaria immitis, Ehrlichia chaffeensis, Ehrlichia ewingii, Leishmania chagasi , and spotted-fever group Rickettsia . Dogs were assigned to groups according to PCR status: E. canis infected, infected with other vector-borne organisms, sick dogs lacking PCR evidence for infection, and healthy controls.
Results: E. canis -infected dogs had higher serum cTnI concentrations than controls (median: 0.04 ng/dL; range 0.04–9.12 ng/dL; control median: 0.04 ng/dL; range: 0.04–0.10 ng/dL; P = .012), and acute E. canis infection was associated with myocardial injury (odds ratio [OR]: 2.67, confidence interval [CI] 95%: 1.12–6.40, P = .027). Severity of anemia was correlated with increased risk of cardiomyocyte damage ( r = 0.84, P < .001). Dogs with clinical signs of systemic inflammatory response syndrome (SIRS) were at higher risk for myocardial injury than were other sick dogs (OR: 2.55, CI 95%: 1.31–4.95, P = .005).
Conclusions and Clinical Importance: Acute infection with E. canis is a risk factor for myocardial injury in naturally infected Brazilian dogs. Severity of anemia and SIRS might contribute to the pathophysiology of myocardial damage.     

Effect of routine cardiovascular catheterization on cardiac troponin I concentration in dogs

ObjectiveTo determine changes in cardiac troponin I concentration (cTnI) associated with cardiovascular catheterization in dogs.Animals, materials and methodscTnI was measured after transarterial coil embolization of patent ductus arteriosus (PDA), balloon valvuloplasty (BV), and pacemaker implantation (PACE). Dogs undergoing ovariohysterectomy (OHE) were used as a control, with 15 animals in each group. Blood for the cTnI assay was collected at baseline (T0), at 5 h (T5), 24 h (T24) and 10 days (T240) post-procedure. The effects of age, duration and difficulty of the procedure were evaluated.ResultsThere was no difference in cTnI concentration at T0 for any of the groups. There was a significant increase in cTnI concentration for BV and PACE, but not PDA at T5 and T24. PACE at T24 and T240 also had higher cTnI than control. Dogs with longer procedure times had significantly higher concentration of cTnI. There was no correlation between the difficulty of the procedure or peri-procedure complications and cTnI.ConclusioncTnI increased during some cardiovascular catheterization procedures, but returned to normal values at 24–240 h. Patients undergoing long catheterization procedures have increased risk for myocardial injury, but this was not related to short-term prognosis.     

Distinguishing cardiac and noncardiac dyspnea in 48 dogs using plasma atrial natriuretic factor, B-type natriuretic factor, endothelin, and cardiac troponin-I

BACKGROUND: It is challenging to differentiate congestive heart failure (CHF) from noncardiac cause of dyspnea. HYPOTHESIS: Circulating concentrations of atrial natriuretic peptide (NT-proANP), B-type natriuretic peptide (BNP), endothelin-I (ET-1), and cardiac troponin-I (cTnI) can be used to help distinguish between cardiac and noncardiac causes of dyspnea in dogs. ANIMALS: Forty-eight client-owned dogs admitted to a veterinary teaching hospital for respiratory distress. METHODS: Blood samples from patients were prospectively obtained. The etiology of dyspnea was determined by using physical examination, thoracic radiographs, and echocardiography. RESULTS: CHF was diagnosed in 22 dogs, and dyspnea of noncardiac origin (noHD group) was diagnosed in 26 dogs. Analyses revealed significant difference between groups for NT-proANP (geometric mean, 95% confidence [CI]; no HD: 0.26 nmol/mL, 95% CI 0.17-1.09; CHF: 1.38 nmol/mL, 95% CI 1.09-1.74 nmol/mL; P < .0001), BNP (noHD: 12.18 pg/mL, 95% CI 10.91-16.17 pg/mL; CHF: 34.97 pg/mL, 95% CI 23.51-52.02 pg/mL; P < .0001), and ET-1 (noHD: 0.32 fmol/mL, 95% CI 0.23-0.46 fmol/mL; CHF: 1.26 fmol/mL, 95% CI 0.83-1.91 fmol/mL; P < .0001). Plasma cTnI concentrations were not significantly different between groups (noHD: 0.29 ng/mL, 95% CI 0.12-0.72 ng/mL; CHF: 0.42 ng/mL, 95% CI 0.18-0.97, P = .53). Receiver operating curves indicated areas under the curve for NT-proANP, BNP, and ET-1 of 0.946, 0.886, and 0.849, respectively. CONCLUSIONS AND CLINICAL IMPORTANCE: Plasma NT-proANP, BNP, and ET-1, but not cTnI, appear useful for distinguishing between dogs with cardiac and noncardiac causes of dyspnea, with plasma NT-proANP having the highest sensitivity (95.5%) and specificity (84.6%).     

Serum cardiac troponin I and cardiac troponin T concentrations in dogs with gastric dilatation-volvulus

OBJECTIVE: To determine whether serum concentrations of cardiac troponin I (cTnI) and cardiac troponin T (cTnT) are increased in dogs with gastric dilatationvolvulus (GDV) and whether concentrations correlate with severity of ECG abnormalities or outcome. DESIGN: Prospective case series. ANIMALS: 85 dogs with GDV. PROCEDURE: Serum cTnl and cTnT concentrations were measured 12 to 24, 48, 72, and 96 hours after surgery. Dogs were grouped on the basis of severity of ECG abnormalities and outcome. RESULTS: cTnl and cTnT were detected in serum from 74 (87%) and 43 (51%) dogs, respectively. Concentrations were significantly different among groups when dogs were grouped on the basis of severity of ECG abnormalities (none or mild vs moderate vs severe). Dogs that died (n = 16) had significantly higher serum cTnI (24.9 ng/ml) and cTnT (0.18 ng/ml) concentrations than did dogs that survived (2.05 and < 0.01 ng/ml, respectively). Myocardial cell injury was confirmed at necropsy in 4 dogs with high serum cardiac troponin concentrations. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicate that concentrations of cTnI and cTnT suggestive of myocardial cell injury can commonly be found in serum from dogs with GDV and that serum cardiac troponin concentrations are associated with severity of ECG abnormalities and outcome.     

Effect of general anesthesia on plasma cardiac troponin I concentrations in healthy horses

Objective

To evaluate the effect of general anesthesia on plasma cTnI concentrations in horses.

Animals, materials and methods

Thirty-two horses undergoing general anesthesia and either elective surgery or MRI without surgery were prospectively studied. Twenty-nine horses (22 surgical, 7 imaging) completed the study. Plasma cTnI concentrations were determined prior to anesthesia and at 6, 12 and 24 h following discontinuation of the inhalant anesthetic.

Results

All horses had cTnI values within the reference range at all time points. Six horses (21%) developed detectable cTnI 6 or 12 h following anesthesia. Risk factors for detectable cTnI include increasing age and dorsal recumbency. Horses with detectable cTnI had significantly lower mean and diastolic arterial blood pressures than those without detectable cTnI.

Conclusion

Uncomplicated general anesthesia with or without surgery does not result in cardiac troponin I elevations above the reference range in the first 24 h postoperatively.     

Evaluation of serum cardiac troponin I concentration in Boxers with arrhythmogenic right ventricular cardiomyopathy

OBJECTIVE: To evaluate serum cardiac troponin I (cTnI) concentrations in Boxers with arrhythmogenic right ventricular cardiomyopathy (ARVC), unaffected (control) Boxers, and control non-Boxers. ANIMALS: 10 Boxers with a clinical diagnosis of ARVC defined by > or = 1,000 ventricular premature complexes (VPCs)/24 h on an ambulatory ECG, 10 control Boxers assessed as normal by the presence of < 5 VPCs/24h, and 10 control non-Boxers. PROCEDURES: Serum was extracted from a blood sample from each dog. Analysis of serum cTnI concentrations was performed. RESULTS: Mean +/- SD serum cTnI concentration was 0.142 +/- 0.05 ng/mL for Boxers with ARVC, 0.079 +/- 0.03 ng/mL for control Boxers, and 0.023 +/- 0.01 ng/mL for control non-Boxers. A significant difference in serum cTnI concentrations was observed among the 3 groups. In the combined Boxer population (ie, Boxers with ARVC and control Boxers), a significant correlation was found between serum cTnI concentration and number of VPCs/24 h (r = 0.78) and between serum cTnI concentration and grade of ventricular arrhythmia (r = 0.77). CONCLUSIONS AND CLINICAL RELEVANCE: Compared with clinically normal dogs, Boxers with ARVC had a significant increase in serum cTnI concentration. For Boxers, correlations were found between serum cTnI concentration and number of VPCs/24 h and between concentration and the grade of arrhythmia. Because of the overlap in serum cTnI concentrations in control Boxers and Boxers with ARVC, future studies should evaluate the correlation of serum cTnI concentration with severity of disease in terms of degree of myocardial fibrofatty changes.     

Cloning and sequencing of equine cardiac troponin I and confirmation of its usefulness as a target analyte for commercial troponin I analyzers.

The analysis of cardiac troponin I (cTnI) in the diagnosis of myocardial injury in domestic animals is gaining popularity. In this study, equine cTnI was sequenced and compared with previously characterized cTnI from other species. A 6-amino-acid N-terminal deletion unique to the horse was identified. This deletion was outside the epitope region of cTnI recognized by most commercial immunoassays and did not affect the ability of a commercial analyzer system to detect recombinant equine cTnI. No function could be ascribed to the deleted portion. These data support the use of commercial analyzers in measuring equine cTnI.     

Serum and plasma cardiac troponin I concentrations in clinically normal Thoroughbreds in training in Australia

Cardiac troponin I is a potentially useful test to identify cardiac muscle damage in the horse. Measurements of cardiac troponin I from serum or heparinised plasma samples from 23 clinically normal Thoroughbred horses in race training were analysed through a standard Australian commercial laboratory using the ADVIA Centaur Assay. The cardiac troponin I concentrations were < 0.15 microg/L from all samples. The test was then validated using macerated equine myocardium. Cardiac troponin I concentration may be useful in determining whether poor performance in Thoroughbred horses is related to active myocardial disease.     

Utility of plasma N-terminal pro-brain natriuretic peptide (NT-proBNP) to distinguish between congestive heart failure and non-cardiac causes of acute dyspnea in cats

BackgroundCirculating plasma N-terminal pro-brain natriuretic peptide (NT-proBNP) concentration facilitates emergency diagnosis of congestive heart failure (CHF) in people. Its utility to discriminate between dyspneic cats with CHF vs. primary respiratory disease requires further assessment. Our objectives were to determine if NT-proBNP (1) differentiates dyspneic cats with CHF vs. primary respiratory disease; (2) increases with renal insufficiency; (3) correlates with left atrial dimension, radiographic cardiomegaly, and estimated left ventricular filling pressure (E/E_a).MethodsNT-proBNP was measured in 167 dyspneic cats (66 primary respiratory disease, 101 CHF) to evaluate (1) relationship with clinical parameters; (2) ability to distinguish CHF from primary respiratory disease; (3) optimal cut-off values using receiver operating characteristic (ROC) curve analysis.ResultsNT-proBNP (1) was higher (median and inter-quartile [25th–75th] percentile) in CHF (754 pmol/L; 437, 1035 pmol/L) vs. primary respiratory disease (76.5 pmol/L; 24, 180 pmol/L) cohorts (P < 0.001); (2) positively correlated in CHF cats with increased inter-ventricular septal end-diastolic thickness (ρ = 0.266; P = 0.007) and LV free wall thickness (ρ = 0.218; P = 0.027), but not with radiographic heart size, left atrial size, left ventricular dimensions, E/E_a ratio, BUN, creatinine, or thyroxine; (3) distinguished dyspneic CHF cats from primary respiratory disease at 265 pmol/L cut-off value with 90.2% sensitivity, 87.9% specificity, 92% positive predictive value, and 85.3% negative predictive value (area under ROC curve, 0.94).ConclusionsNT-proBNP accurately discriminated CHF from respiratory disease causes of dyspnea.