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.     

Influence of Transportation on the Serum Concentrations of the Cardiac Biomarkers Troponin I and Creatine Kinase-myocardial Band (CK-MB) and on Cortisol and Lactate in Horses

The objective of this study was to determine the influence of transportation on the serum concentrations of the cardiac biomarkers troponin I (cTnI) and creatine kinase-myocardial band (CK-MB) and on cortisol and lactate in horses. For this purpose, 10 horses were transported for 300 km. Blood samples were collected 24 hours before transport (T0), just before transport (T1), during transport at 50 km (T2), 100 km (T3), 200 km (T4), and 300 km (T5). An additional blood sample (T6) was collected 24 hours after transport. The median resting basal cTnI values in the horses were at T0, 0.000 ± 0.007 ng/mL and at T1, 0.01 ± 0.007 ng/mL. The median resting basal CK-MB values in the horses were at T0, 0.19 ± 0.05 ng/mL and at T1, 0.16 ± 0.05 ng/mL. Statistical analyses showed no significant differences of cTnI and CK-MB among the measured values (T0–T6). On the other side, the cortisol and lactate concentrations increased significantly (P < .01) at T2, T3, T3, and T4 compared with the resting values at T0. At T6, cortisol and lactate concentrations had returned to pretransport values, with no statistically significant differences compared with pretransport concentrations. In conclusion, the 300-km transportation of the horses did not influence the levels of the cardiac biomarkers, cTnI and CK-MB. The serum concentrations of cortisol and lactate, on the other side, increased significantly. The possible influence of transportation for longer distances or under more stressful conditions (higher temperature or in horses not used for transportation) on cTnI and CK-MB concentrations needs to be further investigated.     

Atrial natriuretic peptide and cardiac troponin I concentrations in healthy Warmblood horses and in Warmblood horses with mitral regurgitation at rest and after exercise

ObjectiveAtrial natriuretic peptide (ANP) and cardiac troponin I (cTnI) serve as biomarkers for increased cardiac pressure/volume loading and for myocardial stress or damage. The objective was to describe the time course of plasma ANP concentrations (Cp_ANP) and plasma cTnI concentrations (Cp_cTnI) in horses with mitral regurgitation (MR) compared to healthy horses at rest and after exercise, and to describe the relationship of Cp_ANP with cardiac dimensions and intracardiac pressures.Animals15 healthy Warmblood horses and 7 Warmblood horses with MR.MethodsCardiac dimensions at rest were measured using echocardiography. All horses underwent standardized treadmill exercise. Biomarker concentrations and intracardiac pressures were measured at rest and after exercise. Hypotheses were tested using statistical methods. The level of significance was P < 0.05.ResultsHorses with MR showed increased left atrial (LA) and left ventricular (LV) dimensions but similar exercise capacity compared to healthy horses. Pulmonary capillary wedge pressures (PCWP) and Cp_ANP increased with exercise. Horses with MR had higher PCWP and higher Cp_ANP at rest and after exercise compared to healthy horses, with the maximum difference in Cp_ANP reached 10 min after exercise. Cp_ANP was significantly related to PCWP and – although inconsistently and only in healthy horses – to echocardiographic indices of LA and LV size and function. Cp_cTnI was low throughout the study in both groups.ConclusionsCp_ANP is increased in horses with MR and is related to LA pressures and to left heart dimensions. MR is not necessarily associated with exercise intolerance and exercise-induced myocardial stress or damage.     

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.     

Biochemical markers of cardiac injury in normal, surviving septic, or nonsurviving septic neonatal foals

The cardiac biomarkers cardiac troponin T (cTnT) and I (cTnI) and the cardiac isoenzyme of creatine kinase (CKMB) are used extensively in human medicine to diagnose and provide valuable prognostic information in patients with ischemic, traumatic, and septic myocardial injury. We designed a study to establish normal values for these markers in healthy, neonatal foals and to compare them with values obtained from septic neonates in a referral hospital population. The 25th, 50th, 75th, and 95th percentiles for cTnI and CKMB in the healthy-foal population were 0.08, 0.14, 0.25, 0.49 ng/mL and 1.4, 2.3, 4.0, 7.4 ng/mL, respectively. The values obtained for cTnT were frequently (43/52 foals; 83%) below the lower limit of detection of the assay (0.009 ng/mL), but the median and range were 0.009 and 0.009-0.041 ng/mL, respectively. In the septic foal population, the 25th, 50th, 75th, and 95th percentile values for cTnI and CKMB were 0.05, 0.12, 0.22, and 1.10 ng/mL and 2.0, 4.4, 7.8, and 24 ng/mL, respectively. The values obtained for cTnT were less frequently below the lower limit of detection (23/38 foals; 60%) compared with the healthy foal population, and the median and range were 0.009 and 0.009-0.20 ng/mL, respectively. Significantly higher values were observed for cTnT and CKMB in septic foals compared with the healthy neonatal foal population, but there were no differences among septic foals in survivors compared with nonsurvivors. These findings suggest that myocardial injury occurs during septicemia in neonatal foals but that the injury is not associated with survival among septic foals.     

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.     

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.     

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.

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.     

Cardiac troponin I is elevated in dogs and cats with azotaemia renal failure and in dogs with non-cardiac systemic disease

OBJECTIVE: To determine if dogs and cats with renal failure, or other severe non-cardiac disease, and no antemortem evidence of cardiac disease on basic clinical evaluation, have elevated levels of cardiac troponin I (cTnI). DESIGN: Cross-sectional study using 56 dogs and 14 cats with primary non-cardiac disease (39 dogs with azotaemic renal failure, 14 cats with azotaemic renal failure, 17 dogs with non-cardiac systemic disease); 7/25 dogs and 6/14 cats had murmurs detected on physical examination. Serum or heparinised plasma was collected and analysed for cTnI. RESULTS: Cardiac troponin I concentrations were elevated above reference intervals in 70% of dogs and 70% of cats with azotaemic renal failure and in 70% of dogs with a variety of systemic non-cardiac diseases. Cardiac troponin I concentrations did not correlate with the degree of azotaemia, presence of murmurs, hypertension or type of non-cardiac illness. CONCLUSIONS: Cardiac troponin I concentration is often elevated in dogs and cats with azotaemic renal failure and in dogs with other systemic non-cardiac illness, suggesting that these conditions often result in clinically inapparent myocardial injury or possibly altered elimination of cTnI.     

Evaluation of assays for troponin I in healthy horses and horses with cardiac disease

Cardiac troponin I (cTnI) is a marker for detection of myocardial damage in horses. Many cTnI assays exist and medical studies have shown that the clinical performance of assays differs. The aim of this study was to compare two different cTnI assays in horses. Serum samples were taken from 23 healthy horses (group 1) and 72 horses with cardiac disease (group 2). Cardiac troponin I was determined using assay 1 in laboratory A (limit of detection, LOD, 0.03 ng/mL) and assay 2 in laboratories B and C (LOD 0.01 ng/mL). In group 1, a median cTnI concentration of <0.03 (<0.03–0.04) ng/mL and <0.01 (<0.01–0.15) ng/mL was found with assays 1 and 2, respectively. A higher median value was demonstrated in group 2 for both assays (assay 1: 0.11 ng/mL, range 0.03–58.27 ng/mL, P < 0.001; assay 2: 0.02 ng/mL, range 0.01–22.87 ng/mL, P = 0.044). Although a significant correlation between assays existed, large mean differences that could be important for clinical interpretation of test results were found. A small mean difference was found between laboratories B and C. A significant optimal (P < 0.001) cut-off value for detection of cardiac disease could only be determined for assay 1 (0.035 ng/mL, sensitivity 70%, specificity 91%). Assay 1 performed better for detection of cardiac disease in horses in this study.     

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.