The Influence of High‐Intensity Moderate Duration Exercise on Cardiac Troponin I and C‐Reactive Protein in Sled Dogs

Background: C‐reactive protein (CRP) and cardiac troponin I (cTnI) are biomarkers of systemic inflammation and cardiac damage, respectively. Objective: To investigate the effects of short‐duration high‐intensity exercise on plasma cTnI and serum CRP concentrations in sprint racing sled dogs. Animals: Twenty‐two Alaskan sled dogs of 2 different teams participating in a 2‐day racing event. Methods: In this prospective field study, cephalic venipuncture was performed on all dogs before racing and immediately after racing on 2 consecutive days. Plasma cTnI and serum CRP concentrations were evaluated at each time point. Results: There was a mild, significant rise (P < .01) in median cTnI concentrations from resting (0.02 ng/mL; 0.0–0.12 ng/mL) on both days after racing (day 1 = 0.06, 0.02–0.2 ng/mL; day 2 = 0.07, 0.02–0.21 ng/mL). Serum CRP concentrations showed a mild significant increase (P < .01) on day 2 after racing mean (9.2 ± 4.6 μg/mL) as compared with resting (6.5 + 4.3 μg/mL) and day 1 after racing (5.0 + 2.9 μg/mL). Neither cTnI or CRP concentrations exceeded the upper reference range for healthy dogs. Conclusions and Clinical Relevance: Strenuous exercise of short duration did not result in cTnI concentrations above the reference range for healthy dogs. Although increased after 2 days of short‐duration strenuous exercise, CRP did not reach concentrations suggestive of inflammation, as reported previously in the endurance sled dogs. Therefore, we surmise that moderate exercise does not present a confounding variable in the interpretation of cTnI and CRP concentrations in normal dogs.     

Cardiac troponin-I concentration in dogs with cardiac disease

Cardiac troponin-I (cTnI) is a highly sensitive and specific marker of myocardial injury and can be detected in plasma by immunoassay techniques. The purpose of this study was to establish a reference range for plasma cTnI in a population of healthy dogs using a human immunoassay system and to determine whether plasma cTnI concentrations were high in dogs with acquired or congenital heart disease, specifically cardiomyopathy (CM), degenerative mitral valve disease (MVD), and subvalvular aortic stenosis (SAS). In total, 269 dogs were examined by physical examination, electrocardiography, echocardiography, and plasma cTnI assay. In 176 healthy dogs, median cTnI was 0.03 ng/mL (upper 95th percentile = 0.11 ng/mL). Compared with the healthy population, median plasma cTnI was increased in dogs with CM (0.14 ng/mL; range, 0.03-1.88 ng/mL; P < .001; n = 26), in dogs with MVD (0.11 ng/mL; range, 0.01-9.53 ng/mL; P < .001; n = 37), and in dogs with SAS (0.08 ng/mL; range, 0.01-0.94 ng/mL; P < .001; n = 30). In dogs with CM and MVD, plasma cTnI was correlated with left ventricular and left atrial size. In dogs with SAS, cTnI demonstrated a modest correlation with ventricular wall thickness. In dogs with CM, the median survival time of those with cTnI >0.20 ng/mL was significantly shorter than median survival time of those with cTnI <0.20 ng/mL (112 days versus 357 days; P = .006). Plasma cTnI is high in dogs with cardiac disease, correlates with heart size and survival, and can be used as a blood-based biomarker of cardiac disease.     

Serum cardiac troponin I in canine syncope and seizures

Objective

To determine if serum cardiac troponin I (cTnI) concentration distinguishes between cardiogenic syncope and collapsing dogs presenting with either generalized epileptic seizures (both with and without cardiac disease) or vasovagal syncope.

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%).     

Cardiac troponin I in the normal dog and cat

Cardiac troponin I (cTnI) has proven to be a highly specific and sensitive marker for myocardial cellular damage in many mammalian species. The structure of cTnI is highly conserved across species, and assays for human cTnI (including the one used in the current study) have been validated in the dog. Blood concentrations of cTnI rise rapidly after cardiomyocyte damage, and assay of cTnI potentially may be valuable in many clinical diseases. The purpose of this study was to establish the normal range of cTnI in heparinized plasma of dogs and cats. Forty one clinically normal dogs and 21 cats were included in the study. One to 3 milliliters of blood were collected by venipuncture into lithium heparin vacutainers for analysis of cTnI (Stratusz CS). The range of plasma cTnI concentrations in dogs was <0.03 to 0.07 ng/mL with a mean of 0.02 ng/mL, with the upper tolerance limit (0.07 ng/mL) at the 90th percentile with 95% confidence. In cats, the range was <0.03 to 0.16 ng/mL with a mean of 0.04 ng/mL, and the upper tolerance limit (0.16 ng/mL) at the 90th percentile as well with 90% confidence. This study establishes preliminary normal ranges of plasma cTnI in normal dogs and cats for comparison to dogs and cats with myocardial injury or disease.     

Serum concentrations of cardiac troponin I and cardiac troponin T in dogs with class IV congestive heart failure due to mitral valve disease

Objective: The objective of this study was to evaluate the incidence of circulating detectable serum levels of cardiac troponin I (CTnI) and circulating detectable serum levels of cardiac troponin T (CTnT) in dogs with class IV congestive heart failure (CHF) due to mitral valve disease (MVD) at admission. An additional study aim was to determine if detectable troponin levels correlated with the magnitude of several clinical parameters. Design: Prospective clinical investigation. Setting: Small animal emergency and critical care referral hospital. Interventions: Blood was collected before emergency treatment from 15 dogs presenting in class IV CHF due to MVD. Measurements: Serum concentrations of CTnI, CTnT at presentation. Main results: Six dogs (40%) had a detectable CTnI (median 0.24, range 0.12–0.31 ng/mL), and the remainder were less than 0.1 ng/mL and deemed non‐detectable. The one dog (7%) that had a detectable CTnT (0.02 ng/mL) also had a detectable CTnI (0.23 ng/mL). There was no statistical difference in survival to discharge between dogs with non‐detectable troponin levels and those with detectable troponin levels; however, dogs with detectable troponin levels had shorter overall survival times. Dogs with a detectable level of CTnI had a median survival of 67.5 days (range 1–390 days), and dogs with a non‐detectable level of CTnI had a median survival time of 390 days (range 20–912 days) (P=0.02). Conclusion: This study suggests that CTnI can be detected at admission in the blood of 40% of dogs with class IV CHF due to MVD. Dogs with non‐detectable levels of cardiac troponins had a significantly longer overall survival time. The encouraging results of this small pilot study warrant further investigation.     

RESEARCH PAPER: Incidence of elevation of cardiac troponin I prior to and following routine general anaesthesia in dogs

ObjectiveTo estimate the incidence of raised cTnI after general anaesthesia in dogs and to explore major risk factors influencing this.Study designProspective clinical study.AnimalsA total of 107 (ASA physical status 1?2) dogs, 63% male and 37% female, median age 5 years (range 0.3–13.4), median weight 24.4 kg (range 4.2–66.5 kg) undergoing anaesthesia for clinical purposes.MethodsVenous blood samples were taken within 24 hours prior to induction and 24 hours after the termination of anaesthesia. Serum concentrations of cardiac troponin I were measured using a chemiluminescent enzyme immunometric assay with a lower level of detection of 0.20 ng mL^?1 (below this level <0.20 ng mL^?1). Continuous data were assessed graphically for normality and paired and unpaired data compared with the Wilcoxon signed ranks and Mann–Whitney U‐tests respectively. Categorical data were compared with the Chi squared or Fisher’s exact test as appropriate (p < 0.05).ResultsOf the 107 dogs recruited, 100 had pre‐ and post‐anaesthetic cTnI measured. The median pre‐anaesthesia cTnI was ‘<0.20’ ng mL^?1 (range ‘<0.20’–0.43 ng mL^?1) and the median increase from pre‐anaesthesia level was 0.00 ng mL^?1 (range ?0.12 to 0.61 ng mL^?1). Fourteen dogs had increased cTnI after anaesthesia relative to pre‐anaesthesia (14%, 95% CI 7.2–20.8%, range of increase 0.03–0.61 ng mL^?1). Six animals had cTnI levels that decreased (range 0.02–0.12 ng mL^?1). Older dogs were more likely to have increased cTnI prior to anaesthesia (OR = 5.32, 95% CI 1.35–21.0, p = 0.007) and dogs 8 years and over were 3.6 times as likely to have an increased cTnI after anaesthesia (95% CI 1.1–12.4, p = 0.028).Conclusion and clinical relevanceIncreased cTnI after anaesthesia relative to pre‐anaesthesia levels was observed in a number of apparently healthy dogs undergoing routine anaesthesia.     

Effect of racing on the serum concentrations of cardiac troponin I and creatine kinase myocardial band in racing camels (Camelus dromedarius)

This study was designed to investigate the effect of racing on the serum concentrations of cardiac troponin I (cTnI) and creatine kinase myocardial (CK-MB) in healthy racing camels (Camelus dromedarius). Twenty-three racing camels scheduled for a 5 km race were investigated in this study. From each camel, 3 blood samples were collected: 24 h before racing (T0), within 2 h after the race (T1) and 24 h post-race (T2). Following the 5 km race, 91.3 % of the racing camels had increases in serum cTnI concentrations, while concentrations remained unchanged in 8.7 %. The cTnI concentration (median 0.06 ng/mL; range, 0.03–0.15 ng/mL) was significantly higher (P?<?0.001) than the pre-race values (median 0.04 ng/mL; range, 0.01–0.07 ng/mL). Twenty-four hours post-race, the cTnI concentrations had returned very nearly to their pre-race values (median 0.04 ng/mL; range, 0.00–0.09 ng/mL) and were not significantly different (P?=?0.35) from the pre-race values. Following the 5 km race, increases in CK-MB mass were seen in 17.4 % of the camels, with no changes in 4.3 % and decreases in 78.3 %. The CK-MB mass (median 0.41 ng/mL; range, 0.19–0.60 ng/mL) did not differ significantly (P?=?0.84) when compared to the pre-race values (median 0.42 ng/mL; range, 0.32–0.55 ng/mL). Twenty-four hours post-race, the CK-MB mass concentrations (median 0.41 ng/mL; range, 0.15–0.55 ng/mL) did not differ significantly (P?>?0.05) compared to pre-race or immediate post-race values. Resting cTnI concentrations in the racing camels were initially low, but increased above the baseline level in most of the camels immediately after racing, and returned to pre-race values within the 24-h post-race period. CK-MB is a less sensitive biomarker for myocardial activity as compared with cTnI. These findings could be of importance when evaluating racing camels with suspected cardiac disease after recent hard exercise.     

Cardiac Troponin I Is Associated with Severity of Myxomatous Mitral Valve Disease, Age, and C-Reactive Protein in Dogs

Background: Concentrations of cardiac troponin I (cTnI) and C-reactive protein (CRP) might be associated with cardiac remodeling in dogs with myxomatous mitral valve disease (MMVD). Age- and sex-dependent variations in cTnI concentration have been described.
Objective: To investigate whether plasma concentrations of cTnI and CRP are associated with severity of MMVD, and investigate potential associations of dog characteristics on cTnI and CRP concentrations.
Animals: Eighty-one client-owned dogs with MMVD of varying severity.
Methods: Dogs were prospectively recruited for the study. Dogs were classified according to severity of MMVD. Plasma cTnI was analyzed by a high sensitivity cTnI assay with a lower limit of detection of 0.001 ng/mL, and plasma CRP was analyzed by a canine-specific CRP ELISA.
Results: Higher cTnI concentrations were detected in dogs with moderate (0.014 [interquartile range 0.008–0.029] ng/mL, P = .0011) and severe (0.043 [0.031–0.087] ng/mL, P < .0001) MMVD, compared with healthy dogs (0.001 [0.001–0.004] ng/mL). Dogs with severe MMVD also had higher cTnI concentrations than dogs with mild (0.003 [0.001–0.024] ng/mL, P < .0001) and moderate ( P = .0019) MMVD. There were significant associations of age, CRP, heart rate, and left ventricular end-diastolic diameter, on cTnI concentration C-reactive protein did not differ among severity groups, but was significantly associated with cTnI, breed, and systolic blood pressure on CRP concentration.
Conclusions and Clinical Importance: Analysis of cTnI concentration has potential to increase knowledge of overall cardiac remodeling in dogs with MMVD. However, effect of age on cTnI needs consideration when assessing cTnI.     

Cardiac troponin I in pastured and race-training Thoroughbred horses

Cardiac troponin I (cTnI), a myocardial polypeptide, is a highly sensitive and specific biomarker of myocardial injury in people and dogs. The structure of cTnI is highly conserved across species, and equine myocardium has high reactivity with human immunoassays. The purpose of this study was to describe cTnI concentrations in normal pastured and race-training Thoroughbred horses. Ten horses on pasture and 10 horses in race training were studied. Horses were considered normal on the basis of physical examination, training performance, electrocardiography (ECG), and echocardiography. Serum cTnI concentrations were determined with a colorimetric immunoassay. The assay has an analytical sensitivity of 0.04 ng/mL. Serum cTnI concentrations in race-training horses were not significantly different from those of pastured horses. When groups were combined, mean cTnI concentration (+/- SD) was 0.047 +/- 0.085 ng/mL. and the median was 0 (range, 0-0.35 ng/mL). The 90th percentile for both groups combined was 0.11 ng/mL. This study establishes a preliminary reference range for serum cTnI in normal Thoroughbred horses.     

The effect of atenolol on NT-proBNP and troponin in asymptomatic cats with severe left ventricular hypertrophy because of hypertrophic cardiomyopathy: a pilot study

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. Hypothesis: 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. Animals: 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.     

Serum concentrations of monocyte chemoattractant protein‐1 in healthy and critically ill dogs

Background: The chemokine monocyte chemoattractant protein‐1 (MCP‐1) is a primary regulator of monocyte mobilization from bone marrow, and increased concentrations of MCP‐1 have been associated with sepsis and other inflammatory disorders in critically ill people. The relationship between MCP‐1 and disease in dogs has not been evaluated previously. Objective: The purpose of this study was to assess serum concentrations of MCP‐1 in healthy dogs, dogs in the postoperative period, and critically ill dogs. We hypothesized that MCP‐1 concentrations would be significantly increased in critically ill dogs compared with postoperative or healthy dogs. Methods: Serum concentrations of MCP‐1 were measured in 26 healthy control dogs, 35 postoperative dogs, and 26 critically ill dogs. Critically ill dogs were further subgrouped into dogs with sepsis, parvovirus gastroenteritis, immune‐mediated hemolytic anemia, and severe trauma (n=26). MCP‐1 concentrations were determined using a commercial canine MCP‐1 ELISA. Associations between MCP‐1 concentrations and disease status were evaluated statistically. Results: MCP‐1 concentration was significantly higher in critically ill dogs (median 578 pg/mL, range 144.7–1723 pg/mL) compared with healthy dogs (median 144 pg/mL, range 4.2–266.8 pg/mL) and postoperative dogs (median 160 pg/mL, range 12.6–560.4 pg/mL) (P<.001). All subgroups of critically ill dogs had increased MCP‐1 concentrations with the highest concentrations occurring in dogs with sepsis. However, differences among the 4 subgroups were not statistically significant. Conclusion: Critically ill dogs had markedly increased serum concentrations of MCP‐1 compared with postoperative and healthy dogs. These results indicate that surgery alone is not sufficient to increase MCP‐1 concentrations; thus, measurement of MCP‐1 may be useful in assessing disease severity in critically ill dogs.     

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.     

Comparison of canine cardiac troponin I concentrations as determined by 3 analyzers

BACKGROUND: Recent interest in cardiac biomarkers has led to the validation of several commercial analyzers for cardiac troponin I (cTnI) evaluation in dogs; however, these analyzers have not been standardized. HYPOTHESIS: It was hypothesized that canine plasma cTnI concentrations as determined by 3 different analyzers would be similar. ANIMALS: Twenty-three dogs with cardiac disease were studied. METHODS: Reconstituted purified canine free cTnI was diluted with canine plasma to 8 concentrations (0.01, 0.1, 0.78, 1.56, 3.13, 6.25, 12.5, and 25 ng/mL), for analysis by 3 analyzers, the Biosite Triage Meter, the Dade-Behring Stratus, and the Beckman-Coulter Access AccuTnI. Plasma samples from 23 dogs with cardiac disease were also analyzed for cTnI concentrations on all analyzers. RESULTS: Troponin I concentrations in sick dogs were <0.05-5.72 ng/mL (Biosite), 0.02-11.1 ng/mL (Access), and 0.02-9.73 ng/mL (Stratus). Analyzer results were highly correlated with each other (r = 0.97 to 1.0 for purified dilutions, r = 0.61 to 0.89 for samples from dogs); however, the limits of agreement were wide for both purified dilutions and clinical samples. Recovery was highest for the Access (334-1467%) and lowest for the Biosite (38-60%); Stratus 52-233%. Analyzer variability was lowest for the Access (1.2-10.4%) and highest for the Stratus (4.8-33.6%); Biosite 2.8-16.5%. CONCLUSIONS AND CLINICAL IMPORTANCE: Results from this study suggest that although canine cTnI values obtained from the Biosite, Stratus, and Access analyzers are closely correlated, they cannot be directly compared with each other. In the absence of a gold standard none of the analyzers can be considered more correct than the others.     

Retrospective evaluation of postoperative nasotracheal tubes for oxygen supplementation in dogs following surgery for brachycephalic syndrome: 36 cases (2003–2007)

Objective – To assess the utility of nasotracheal tubes in postoperative oxygen supplementation in dogs following corrective surgery for brachycephalic syndrome. Design – Retrospective study 2003–2007. Setting – University teaching hospital. Animals – Thirty‐six client‐owned dogs that underwent corrective surgery for brachycephalic syndrome. Interventions – None. Measurements and Main Results – Medical records were reviewed for animals that underwent surgical interventions for brachycephalic syndrome including palatoplasty, ventriculectomy, and rhinoplasty. Data collected included signalment, presenting complaints, analgesic and surgical interventions, type of supplemental oxygen therapy, complications and mortality occurring during hospitalization. A nasotracheal tube (NTT) was placed in 20 dogs at the end of surgery; 16 dogs received other forms of oxygen supplementation (8) or no oxygen supplementation (8) during recovery. The total number of postoperative complications was similar in both groups (8/20 dogs with NTTs and 7/16 in those without NTTs). However, respiratory distress was observed in 5 dogs without NTTs but was not observed in any dog while an NTT was in place. One dog in each group died postoperatively. Conclusion – Placement of an NTT was found to be easy and may offer benefit in dogs with brachycephalic syndrome as a noninvasive means of delivering oxygen. The use of NTT may minimize severe postoperative morbidity, in particular by reducing postoperative respiratory distress.     

Long‐term survival with stereotactic radiotherapy for imaging‐diagnosed pituitary tumors in dogs

Published studies on the use of stereotactic radiotherapy for dogs with pituitary tumors are limited. This retrospective observational study describes results of stereotactic radiotherapy for 45 dogs with imaging‐diagnosed pituitary tumors. All dogs were treated at a single hospital during the period of December 2009–2015. The stereotactic radiotherapy was delivered in one 15 Gray (Gy) fraction or in three 8 Gy fractions. At the time of analysis, 41 dogs were deceased. Four were alive and censored from all survival analyses; one dog received 8 Gy every other day and was removed from protocol analyses. The median overall survival from first treatment was 311 days (95% confidence interval 226–410 days [range 1–2134 days]). Thirty‐two dogs received 15 Gy (median overall survival 311 days; 95% confidence interval [range 221–427 days]), and 12 received 24 Gy on three consecutive days (median overall survival 245 days, 95% confidence interval [range 2–626 days]). Twenty‐nine dogs had hyperadrenocorticism (median overall survival 245 days), while 16 had nonfunctional masses (median overall survival 626 days). Clinical improvement was reported in 37/45 cases. Presumptive signs of acute adverse effects within 4 months of stereotactic radiotherapy were noted in 10/45, and most had improvement spontaneously or with steroids. Late effects versus tumor progression were not discernable, but posttreatment blindness (2), hypernatremia (2), and progressive neurological signs (31) were reported. There was no statistical difference in median overall survival for different protocols. Patients with nonfunctional masses had longer median overall survival than those with hyperadrenocorticism (P = 0.0003). Survival outcomes with stereotactic radiotherapy were shorter than those previously reported with definitive radiation, especially for dogs with hyperadrenocorticism.     

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.     

Cerebrospinal Fluid Myelin Basic Protein as a Prognostic Biomarker in Dogs with Thoracolumbar Intervertebral Disk Herniation

Background: Release of myelin basic protein (MBP) into the cerebrospinal fluid (CSF) is associated with active demyelination and correlates with outcome in various neurological diseases. Hypothesis/Objectives: To describe associations among CSF MBP concentration, initial neurological dysfunction, and long‐term ambulatory outcome in dogs with acute thoracolumbar intervertebral disk herniation (IVDH). Animals: Five hundred and seventy‐four dogs with acute thoracolumbar IVDH and 16 clinically normal dogs. Methods: Prospective case series clinical study. Signalment, initial neurological dysfunction as determined by a modified Frankel score (MFS), and ambulatory outcome at >3‐month follow‐up were recorded. Cisternal CSF MBP concentration was determined by an ELISA. Associations were estimated between CSF MBP concentration and various clinical parameters. Results: Dogs with thoracolumbar IVDH that did not ambulate at follow‐up had a higher CSF MBP concentration (median, 3.56 ng/mL; range, 0.59–51.2 ng/mL) compared with control dogs (median, 2.22 ng/mL; range, 0–3.82 ng/mL) (P= .032). A CSF MBP concentration of ≥3 ng/mL had a sensitivity of 78% and specificity of 76% to predict an unsuccessful outcome based on receiver‐operating characteristics curve analysis (area under the curve =0.688, P= .079). Affected dogs with a CSF MBP concentration ≥3 ng/mL had 0.09 times the odds of ambulation at follow‐up compared with affected dogs with CSF MBP concentration <3 ng/mL when adjusted for initial MFS (95% confidence interval 0.01–0.66, P= .018). Conclusions and Clinical Importance: These results would suggest that CSF MBP concentration may be useful as an independent prognostic indicator in dogs with thoracolumbar IVDH.     

Pharmacokinetics of a controlled‐release liposome‐encapsulated hydromorphone administered to healthy dogs

The purpose of the study was to assess the pharmacokinetics of liposome‐encapsulated (DPPC‐C) hydromorphone administered intravenously (IV) or subcutaneously (SC) to dogs. A total of eight healthy Beagles aged 12.13 ± 1.2 months and weighing 11.72 ± 1.10 kg were used. Dogs randomly received liposome encapsulated hydromorphone, 0.5 mg/kg IV (n = 6), 1.0 mg/kg (n = 6), 2.0 mg/kg (n = 6), or 3.0 mg/kg (n = 7) SC with a 14–28 day washout between trials. Blood was sampled at serial intervals after drug administration. Serum hydromorphone concentrations were measured using liquid chromatography with mass spectrometry. Serum concentrations of hydromorphone decreased rapidly after IV administration of the DPPC‐C formulation (half‐life = 0.52 h, volume of distribution = 12.47 L/kg, serum clearance = 128.97 mL/min/kg). The half‐life of hydromorphone after SC administration of DPPC‐C formulation at 1.0, 2.0, and 3.0 mg/kg was 5.22, 31.48, and 24.05 h, respectively. The maximum serum concentration normalized for dose (C_MAX/D) ranged between 19.41–24.96 ng/mL occurring at 0.18–0.27 h. Serum hydromorphone concentrations fluctuated around 4.0 ng/mL from 6–72 h after 2.0 mg/kg and mean concentrations remained above 4 ng/mL for 96 h after 3.0 mg/kg DPPC‐C hydromorphone. Liposome‐encapsulated hydromorphone (DPPC‐C) administered SC to healthy dogs provided a sustained duration of serum hydromorphone concentrations.     

Serum Cardiac Troponin I Concentration in Dogs with Precapillary and Postcapillary Pulmonary Hypertension

Background: Pulmonary hypertension (PH) is a disease condition leading to right-sided cardiac hypertrophy and, eventually, right-sided heart failure. Cardiac troponin I (cTnI) is a circulating biomarker of cardiac damage.
Hypothesis: Myocardial damage can occur in dogs with precapillary and postcapillary PH.
Animals: One hundred and thirty-three dogs were examined: 26 healthy controls, 42 dogs with mitral valve disease (MVD) without PH, 48 dogs with pulmonary hypertension associated with mitral valve disease (PH-MVD), and 17 dogs with precapillary PH.
Methods: Prospective, observational study. Serum cTnI concentration was measured with a commercially available immunoassay and results were compared between groups.
Results: Median cTnI was 0.10 ng/mL (range 0.10–0.17 ng/mL) in healthy dogs. Compared with the healthy population, median serum cTnI concentration was increased in dogs with precapillary PH (0.25 ng/mL; range 0.10–1.9 ng/mL; P < .001) and in dogs with PH-MVD (0.21 ng/mL; range 0.10–2.10 ng/mL; P < .001). Median serum cTnI concentration of dogs with MVD (0.12 ng/mL; range 0.10–1.00 ng/mL) was not significantly different compared with control group and dogs with PH-MVD. In dogs with MVD and PH-MVD, only the subgroup with decompensated PH-MVD had significantly higher cTnI concentration compared with dogs with compensated MVD and PH-MVD. Serum cTnI concentration showed significant modest positive correlations with the calculated pulmonary artery systolic pressure in dogs with PH and some echocardiographic indices in dogs with MVD and PH-MVD.
Conclusions and Clinical Importance: Serum cTnI is high in dogs with either precapillary and postcapillary PH. Myocardial damage in dogs with postcapillary PH is likely the consequence of increased severity of MVD.