Elimination half‐life of intravenously administered equine cardiac troponin I in healthy ponies

Reasons for performing study: To date, no information is available on the true biological elimination half‐life (T_1/2) of cardiac troponin I (cTnI) in the equine species. Such data are required to better evaluate the optimal time to acquire the cTnI sample following acute myocardial injury. Objective: To determine the T_1/2 of equine cTnI. Methods: Four healthy ponies received i.v. injections of recombinant equine cTnI. Plasma cTnI concentrations were measured with a point‐of‐care cTnI analyser at multiple time points after injection. Standard pharmacokinetic analysis was performed to establish the T_1/2 of cTnI. Results: The average T_1/2 of cTnI was determined to be 0.47 h using a single rate elimination model. Conclusion: The elimination of recombinant equine cTnI following i.v. administration is very rapid. Establishing the T_1/2 of troponin provides critical information in understanding the clinical application of this cardiac biomarker in equine practice.     

Cardiac troponin I concentrations following medetomidine‐butorphanol sedation in dogs

ObjectiveTo evaluate the effect of medetomidine–butorphanol sedation on serum cardiac troponin I (cTnI) concentration, a marker of myocardial ischemia and injury, in healthy dogs undergoing pre–surgical radiographs for orthopedic procedures.Study designProspective clinical study.AnimalsTwenty client–owned dogs with no history of cardiac disease.MethodsDogs were evaluated for pre–existing cardiac disease with electrocardiogram (ECG), noninvasive blood pressure and echocardiogram. Sedation was achieved using a combination of medetomidine (10 μg kg^?1) and butorphanol (0.2 mg kg^?1) intravenously. Blood pressure, heart rate and ECG were serially recorded throughout the duration of sedation. Serum cTnI concentration was measured at baseline and 6, 18, and 24–hours post–sedation.ResultsFollowing administration of medetomidine and butorphanol, all dogs were adequately sedated for radiographs and had a decreased heart rate and increased diastolic blood pressure. Arrhythmias associated with increased parasympathetic tone occurred, including a sinus arrhythmia further characterized as a sinus bigeminy in 17 of the dogs. Serum cTnI was undetectable at all time points in all but three dogs. Two of the three dogs had a detectable concentration of cTnI at all time points measured, including prior to sedation. Only one of the two dogs had a cTnI concentration above the normal reference interval. The dogs that exhibited detectable cTnI had no significant difference in signalment, heart rate, blood pressure, or lactate concentration as compared to those with undetectable cTnI.Conclusions and clinical relevanceSedation with medetomidine and butorphanol had predictable cardiovascular effects including bradycardia, an increase in arterial blood pressure, and arrhythmias in apparently healthy dogs requiring radiographs for orthopedic injuries, but did not induce significant increases in serum cTnI concentration following the drug doses used in this study.     

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.     

Cardiac troponin I in cats with hypertrophic cardiomyopathy

The molecular structure of cardiac troponin I (cTnI) is highly conserved across mammalian species and assays developed for its measurement in human patients have been validated in a number of veterinary species. A raised concentration of circulating cTnI is a sensitive and specific marker of cardiac myocyte injury. Raised levels have been documented in a variety of cardiac diseases in both human and veterinary patients. This study compared serum cTnI concentrations between 16 cats diagnosed with hypertrophic cardiomyopathy (HCM) using echocardiography and 18 control cats. The results show that cats with HCM have significantly higher concentration of serum cTnI (median 0.95 ng/ml, range 0.2-4.1 ng/ml) than control cats (median <0.2 ng/ml, range <0.2-0.25 ng/ml) [P<0.0001]. Furthermore in cats with cardiomyopathy a weak correlation was found between the thickness of the left ventricular freewall in diastole measured by ultrasound and serum cTnI concentration (r(2)=0.28;P=0.036). These results suggest that measurement of serum cTnI concentration may enable cats with cardiomyopathy to be distinguished from normal cats using the assay described here.     

Cardiac troponin I in feline hypertrophic cardiomyopathy

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.     

High serum troponin I concentration as a marker of severe myocardial damage in a case of suspected exertional heatstroke in a dog

A young, overweight dog presented with sudden onset lethargy and collapse following exercise in warm environmental conditions. Investigations revealed systolic hypotension, multiform ventricular premature complexes, irregular myocardial echogenicity with poor left ventricular systolic function and a markedly elevated troponin cTnI (180 ng/mL, reference range <0.3 ng/mL) consistent with severe myocyte damage. Infectious causes of myocarditis were ruled out on the basis of serological and polymerase chain reaction blood tests. Exercise-induced malignant hyperthermia was excluded from the history, an exercise tolerance test and genetic testing for the RYR1 V547A mutation. The diagnosis was myocardial damage secondary to suspected exertional heatstroke, from which the dog recovered uneventfully over a number of weeks and serum troponin normalised. This is the first case report in any species including man, documenting high troponin as a marker of severe myocardial damage following suspected heatstroke.     

Cardiac troponin I and C-reactive protein concentrations in dogs with severe pulmonic stenosis before and after balloon valvuloplasty

Objective

To report cardiac troponin I (cTnI) and C-reactive protein (CRP) concentrations in dogs with severe pulmonic stenosis (PS) before and after balloon valvuloplasty (BV).

Background

Increased morbidity and mortality have been reported with severe PS and histopathologic evidence of myocardial damage is demonstrated with BV. Severity of myocardial injury and inflammation associated with severe PS and BV, as assessed by cTnI and CRP, is unknown.

Animals, materials and methods

Serum cTnI and CRP concentrations were measured in dogs with severe PS (n = 23) and following BV (n = 16).

Results

Baseline cTnI and CRP were elevated in 7/23 (30.4%) and 8/23 (34.8%) dogs. Median cTnI at baseline and post-BV were 0.20 ng/mL (range, 0.20-1.29 ng/mL) and 2.85 ng/mL (range, 0.21-55.40 ng/mL), respectively. Median CRP at baseline and post-BV were 3.40 μg/mL (range, 0-14.70 μg/mL) and 11.70 μg/mL (range, 4.20-120 μg/mL), respectively. Post-BV concentrations were significantly increased compared to baseline for cTnI (p < 0.001) and CRP (p = 0.001).

Conclusions

Serum cTnI and CRP are increased in dogs with severe PS and following BV. Future studies should evaluate whether biomarkers correlate with severity and prognosis of PS or can be used to guide therapy.     

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.