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1.
Reasons for performing study: To date, no information is available on the true biological elimination half‐life (T1/2) 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 T1/2 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 T1/2 of cTnI. Results: The average T1/2 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 T1/2 of troponin provides critical information in understanding the clinical application of this cardiac biomarker in equine practice.  相似文献   

2.
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.  相似文献   

3.
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4.
Background: Myocarditis is thought to occur secondary to equine influenza virus (EIV) infections in horses, but there is a lack of published evidence. Hypothesis/Objectives: We proposed that EIV challenge infection in ponies would cause myocardial damage, detectable by increases in plasma cardiac troponin I (cTnI) concentrations. Animals: Twenty‐nine influenza‐naïve yearling ponies: 23 were part of an influenza vaccine study (11 unvaccinated and 12 vaccinated), and were challenged with 108 EID50 EIV A/eq/Kentucky/91 6 months after vaccination. Six age‐matched healthy and unvaccinated ponies concurrently housed in a separate facility not exposed to influenza served as controls. Methods: Heparinized blood was collected before and over 28 days after infection and cTnI determined. Repeated measures analysis of variance, chi‐square, or clustered regression analyses were used to identify relationships between each group and cTnI. Results: All EIV‐infected ponies developed clinical signs and viral shedding, with the unvaccinated group displaying severe signs. One vaccinated pony and 2 unvaccinated ponies had cTnI greater than the reference range at 1 time point. At all other times, cTnI was <0.05 ng/mL. All control ponies had normal cTnI. There were no significant associations between cTnI and either clinical signs or experimental groups. When separated into abnormal versus normal cTnI, there were no significant differences among groups. Conclusions and Clinical Importance: This study demonstrated no evidence of severe myocardial necrosis secondary to EIV challenge with 108 EID50 EIV A/eq/Kentucky/91 in these sedentary ponies, but transient increases in cTnI suggest that mild myocardial damage may occur.  相似文献   

5.
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.  相似文献   

6.
Cardiac Troponin I (cTnI) is a polypeptide involved in myocardial contraction and has been shown to be a highly sensitive biomarker of myocardial injury in humans. Chronic myocardial ischemia was induced in eight adult sheep by anterior coronary artery legation. Forty-five days after coronary artery legation, sheep underwent autologous myoblasts implantation to the infarct area to improve local tissue regeneration. Blood samples were taken at regular intervals before and after the induced coronary ischemia and myoblast implantation and serum levels of cTnI were assessed with chemiluminescent immunodosage using a commercially available anti-human cTnI monoclonal antibody. cTnI levels began to increase the day after coronary legation and after myoblast implantation and gradually recovered to physiological levels in the next 14 days. Furthermore, the commercial anti-human antibody was shown to completely cross react with the ovine polypeptide as well as with canine, swine and equine sera.  相似文献   

7.
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.  相似文献   

8.
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.  相似文献   

9.
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.  相似文献   

10.
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.  相似文献   

11.

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.

Animals

Seventy-nine prospectively recruited dogs, grouped according to aetiology of collapse: generalized epileptic seizures (group E), cardiogenic syncope (group C), dogs with both epileptic seizures and cardiac disease (group B), vasovagal syncope (group V) or unclassified (group U).

Methods

Most patients had ECG (n = 78), echocardiography (n = 78) and BP measurement (n = 74) performed. Dogs with a history of intoxications, trauma, evidence of metabolic disorders or renal insufficiency (based on serum creatinine concentrations >150 μmol/L and urine specific gravity <1.030) were excluded. Serum cTnI concentrations were measured and compared between groups using non-parametric statistical methods. Multivariable regression analysis investigated factors associated with cTnI. Receiver operator characteristic curve analysis examined whether cTnI could identify cardiogenic syncope.

Results

Median cTnI concentrations were higher in group C than E (cTnI: 0.165 [0.02–27.41] vs. 0.03 [0.01–1.92] ng/mL; p<0.05). Regression analysis found that serum cTnI concentrations decreased with increasing time from collapse (p=0.015) and increased with increasing creatinine concentration (p=0.028). Serum cTnI diagnosed cardiogenic syncope with a sensitivity of 75% and specificity of 80%.

Conclusions

Serum cTnI concentrations were significantly different between groups C and E. However, due to the overlap in cTnI concentrations between groups cTnI, measurement in an individual is not optimally discriminatory to differentiate cardiogenic syncope from collapse with generalized epileptic seizures (both with and without cardiac disease) or vasovagal syncope.  相似文献   

12.
The purpose of this study was to develop prognostic models for heart failure in dogs with dilated cardiomyopathy (DCM). The prospective study included 26 dogs with DCM and 58 healthy dogs. The ervation time median was 250 days (1-600 days). All the dogs were clinically examined, had echocardiography, electrocardiography, and morphological and biochemical blood sampling. Twenty four deaths were found in the group of dogs with DCM and 1 demise in the healthy dog's group. There was a significant increase in the level of NT-pro-BNP and cTnI (p < 0.0005) in the group of dogs with DCM and a significant higher level of NT-pro-BNP and cTnI (p < 0.0005) in the dead dogs from group with DCM that died or were euthanized up to the 60th day of observation, compared to the animals that outlasted over 60 days of observation. The median level of NT-pro-BNP in the dogs which had short survival period (no more than 60 days) was 4865 pmol/L and the median level of cTnI in the same group of dogs was 0.63 ng/ml. The median level of NT-pro-BNP in the group of dogs with DCM, which lived longer than 60 days of observation was 978 pmol/l and the median level of cTnI in this group was 0.1 ng/ml. The level of NT-pro-BNP (r = 0.79) and cTnI (r = 0.4) correlated with the dogs' death. NT-pro-BNP and cTnI measurements could be useful to evaluate the survival the dogs with DCM. Increased level of NT-pro-BNP and cTnI is a bad prognosis. In the performed analysis of the Cox hazard regression it was found that cTnI level has a significant impact of the survival of the dogs (HR = 8.54; Cl 1.1-46.6; p = 0.02).  相似文献   

13.
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.  相似文献   

14.
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.  相似文献   

15.
A raised concentration of serum cardiac troponin I (cTnI) is a sensitive marker of cardiac myocyte injury in the cat and assays developed for its measurement in human patients have been validated in the cat. Raised levels have been associated with a number of cardiac insults including hypertrophic cardiomyopathy and trauma. Hyperthyroidism is a common disease of older cats and excess thyroid hormone is known to produce significant cardiovascular effects in this species. This study evaluated the effect of treatment for hyperthyroidism with radioactive iodine on cTnI concentration, assessed the association between thyroxin levels and glomerular filtration rate (GFR) and cTnI concentration in cats treated for hyperthyroidism and described changes in echocardiographic parameters following treatment. Prior to the treatment serum cTnI was measured and echocardiography performed, thyroxin, cTnI, and echocardiography were then repeated at various time points following radioisotope therapy. The results show that higher thyroxin levels were significantly (P=0.002) associated with a higher likelihood of the cat presenting with detectable levels of cTnI. No significant association was found between GFR and presence of detectable levels of cTnI. Furthermore the results indicate that the effects of hyperthyroidism on echocardiographic parameters appear considerably less in this study than in previous studies and that the main outcome of treatment on these parameters is a significant reduction in fractional shortening (P=0.006). These results suggest that chronic exposure to excess thyroid hormone may induce myocyte damage of sufficient severity to raise serum cTnI concentration in a proportion of cats that resolves following establishment of a euthyroid state.  相似文献   

16.
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.  相似文献   

17.
ObjectivesTo determine normal resting values for cardiac troponin I (cTnI) in healthy Standardbred, Thoroughbred and Warmblood horses and investigate if racing has an influence on cTnI concentrations.BackgroundMeasuring cTnI concentrations in plasma is the gold standard for detecting myocardial injury in humans. Cardiac troponin I is highly conserved between species and has gained interest as a marker for cardiac injury in horses. Increased levels of cTnI have been reported in association with endurance and short-term strenuous exercise on a treadmill in horses. However, the effect of true racing conditions has not yet been reported.Animals, materials and methodsBlood samples for analysis of cTnI concentrations in plasma were collected from 67 Standardbred racehorses, 34 Thoroughbred racehorses and 35 Warmblood dressage horses at rest. Blood samples were also collected prior to and after racing in 22 Standardbred racehorses and 6 Thoroughbred racehorses.ResultsAll horses except one had resting plasma cTnI concentrations <0.022 μg/L. Mild increases in cTnI concentrations were seen in some horses 1–2 h after the race (1/17 Standardbreds and 2/6 Thoroughbreds) as well as 10–14 h after the race (4/21 Standardbreds and 1/6 Thoroughbreds).ConclusionsResting cTnI concentrations in horses are low but mildly elevated cTnI concentrations may be detected in some horses 1–14 h after racing. These findings could be of importance when evaluating horses with suspected cardiac disease that recently have performed hard exercise.  相似文献   

18.
The current study was designed to determine the changes of the cardiac troponin I (cTnI) expression in blood and tissue during the myocardial degeneration in calves with foot-and-mouth disease (FMD). Seventeen crossbred calves presenting pathological signs for FMD confirmed by viral analysis were studied. A biochemistry panel and immunohistochemistry were performed on 17 diseased calves and 7 calves used as controls. Creatine kinase (CK), CK-myocardial band (CK-MB), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) activities were analyzed for both groups. Cardiac troponin I levels were measured by a commercially available enzyme-linked immunosorbent assay kit. Mean cTnI (14.8 +/- 1.9 ng/ml) concentration and CK (573 +/- 407 U/l), CK-MB (238 +/- 37 U/l), AST (84 +/- 7), and LDH (298 +/- 29 U/l) activities were higher in FMD cases compared with controls. Immunohistochemistry revealed loss or depletion of cTnI expression in myocardium of all cases. None of the 7 controls showed loss of cTnI expression. Increased serum cTnI concentration correlated with myocardial injury and loss of cTnI immunolabeling in cardiomyocytes of calves with FMD.  相似文献   

19.
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.  相似文献   

20.
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.  相似文献   

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