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 troponins as indicators of acute myocardial damage in dogs

Cardiac troponin I (cTnI) and T (cTnT) have a high sequence homology across phyla and are sensitive and specific markers of myocardial damage. The purpose of this study was to evaluate the Cardiac Reader, a human point-of-care system for the determination of cTnT and myoglobin, and the Abbott Axsym System for the determination of cTnI and creatine kinase isoenzyme MB (CK-MB) in healthy dogs and in dogs at risk for acute myocardial damage because of gastric dilatation-volvulus (GDV) and blunt chest trauma (BCT). In healthy dogs (n = 56), cTnI was below detection limits (<0.1 microg/L) in 35 of 56 dogs (reference range 0-0.7 microg/L), and cTnT was not measurable (<0.05 ng/mL) in all but 1 dog. At presentation, cTnI, CK-MB, myoglobin, and lactic acid were all significantly higher in dogs with GDV (n = 28) and BCT (n = 8) than in control dogs (P < .001), but cTnT was significantly higher only in dogs with BCT (P = .033). Increased cTnI or cTnT values were found in 26 of 28 (highest values 1.1-369 microg/L) and 16 of 28 dogs (0.1-1.7 ng/mL) with GDV, and in 6 of 8 (2.3-82.4 microg/L) and 3 of 8 dogs (0.1-0.29 ng/mL) with BCT, respectively. In dogs suffering from GDV, cTnI and cTnT increased further within the first 48 hours (P < .001). Increased cardiac troponins suggestive of myocardial damage occurred in 93% of dogs with GDV and 75% with BCT. cTnI appeared more sensitive, but cTnT may be a negative prognostic indicator in GDV. Both systems tested seemed applicable for the measurement of canine cardiac troponins, with the Cardiac Reader particularly suitable for use in emergency settings.     

Serum cardiac troponin I concentration in dogs with ehrlichiosis

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

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 troponins in canine babesiosis

This study compared the sensitivity of ECG and cardiac troponins to predict cardiac histopathological changes, clinical severity, and survival in canine babesiosis. One control group (n = 9) and 4 groups of dogs with mild uncomplicated babesiosis (n = 8), severe uncomplicated babesiosis (n = 9), complicated babesiosis (n = 8), and babesiosis and concurrent immune-mediated hemolytic anemia (IMHA) (n = 9) were studied. A 1-minute lead II ECG was recorded, and cardiac troponin I (cTnI) and T (cTnT) concentrations in plasma were measured. cTnI concentrations were significantly higher in the complicated (mean, 9.9; SE, +/-5.76) and concurrent IMHA (mean, 6.53; SE, +/-4.32) groups and in the 3 dogs that died of the disease (mean, 22.17; SE, +/-12.85) than in the control dogs (concentration below detection limit of test, -0.3 ng/mL). The 3 nonsurvivors had the most severe cardiac histopathological changes, but no arrhythmia and minimal other ECG changes. Dogs with babesiosis developed a variety of ECG abnormalities, but the abnormalities were not associated with disease severity, outcome, or plasma cardiac troponin concentrations. The exception was the presence of ventricular premature complexes (VPCs), which were associated with high cardiac troponin concentrations. This study showed an association between cTnI concentration and histological changes, clinical severity, and survival and no correlation between ECG abnormalities and histological changes or biochemical evidence of myocardial damage as reflected by cTnI concentrations. From this study, it was concluded that the analysis of plasma cTnI is a feasible and sensitive test and is superior to cTnT in diagnosing cardiac involvement in dogs with babesiosis.     

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.     

Plasma vascular endothelial growth factor concentrations in healthy dogs and dogs with hemangiosarcoma

Vascular endothelial growth factor (VEGF) is a dimeric glycosylated polypeptide growth factor with potent angiogenic, mitogenic, and vascular permeability-enhancing properties specific for endothelial cells. In humans, VEGF seems to play a major role in tumor growth, and plasma concentrations correlate with tumor burden, response to therapy, and disease progression. This study compared plasma VEGF concentrations in healthy client-owned dogs (n = 17) to dogs with hemangiosarcoma (HSA; n 16). Dogs with HSA were significantly more likely to have detectable concentrations of plasma VEGF (13/17) compared to healthy dogs (1/17; P < .001). The median plasma VEGF concentration for dogs with HSA was 17.2 pg/mL (range, < 1.0-66.7 pg/mL). Plasma VEGF concentrations in dogs with HSA did not correlate with stage of disease or tumor burden, but 1 dog had undetectable VEGF during chemotherapy that subsequently increased with disease progression.     

Concentrations of cardiac Troponin I before and after ovariohysterectomy in 46 female dogs with pyometra

Background

Canine pyometra is a common disease in countries where routine spaying of young dogs is not common practice. This disease is known to lead to systemic inflammation potentially affecting multiple organs in the body, including the heart. Cardiac-specific Troponin I (cTnI) is a sensitive marker of myocardial cell damage, which can result from ischemia, trauma, toxins or inflammation. Dogs with pyometra are also exposed to anaesthesia which can potentially result in myocardial cell damage. The aims of the study were 1) to evaluate the occurrence of myocardial cell damage as indicated by increased serum concentrations of cTnI in dogs with pyometra and relate these to presence of systemic inflammation and 2) to evaluate the change in cTnI-concentrations after anaesthesia and surgery.

Methods

Serum cTnI concentration was measured preoperatively and one day after surgery in 46 female dogs with pyometra and 15 female dogs that underwent surgery for other reasons (ovariohysterectomy and mammary tumours).

Results

Forty-six female dogs of different breeds diagnosed with pyometra were included. The dogs had a median age of 8.5 years (IQR 7.5–10) and a median weight of 29 kg (IQR 9–32). Of the 46 dogs, 37 (80%) fulfilled the chosen criteria for systemic inflammatory response syndrome (SIRS) at inclusion. Thirteen (28%) of the dogs had increased cTnI concentrations (> 0.2 μg/l) before surgery and 18 (39%) had increased cTnI-concentrations the day after surgery. The cTnI concentrations in the 13 dogs with increased preoperative cTnI concentrations decreased in 8 dogs, increased in 4 dogs, and was unchanged in one dog. Seven dogs with nondetectable preoperative cTnI concentrations had increased postoperative concentrations. The only significant association between the studied laboratory or clinical variables (including SIRS) and cTnI concentration was preoperative percentage band neutrophils (PBN) and postoperative cTnI concentration (P = 0.016). In total, 20 dogs (43%) had increased pre- or postoperative cTnI concentrations. Seven dogs (15%) had pre-or postoperative concentrations of cTnI of 1.0 μg/l or higher.

Conclusion

Mild to moderate increases in cTnI appears to be common in dogs with pyometra before and after surgery, but the clinical importance of this finding is uncertain. None of the studied clinical variables were found to reliably predict increased preoperative cTnI concentrations. Because of the pre- and postoperative variation in cTnI concentrations, it was not possible to identify a negative effect of anaesthesia and surgery on myocardial cell integrity.     

Thoracoscopic partial pericardiectomy in 13 dogs

Thirteen dogs with cardiac tamponade resulting from pericardial effusion were prospectively evaluated to determine feasibility and outcome of thoracoscopic partial pericardiectomy. A lateral thoracoscopic approach allowed adequate exposure to remove a 4- to 5-cm-diameter section of pericardium in all dogs. Complete resolution of cardiac tamponade occurred in all dogs for which there was follow-up (11 dogs). Ten of 13 dogs (76.9%) had neoplastic pericardial effusion. One of these dogs remains alive at 220 days postoperatively and is asymptomatic. The mean survival of the remaining 9 patents with neoplastic effusion was 128 days (range, 14-544 days; median, 38 days). Three of 13 patients (23.1%) had idiopathic pericardial effusion. Two of these dogs remain alive at 585 and 1,250 days postoperatively. One dog with idiopathic pericardial effusion developed cardiomyopathy and was euthanized 18 days after the procedure. Results indicate that the procedure was technically successful in all dogs. No anesthetic complications occurred. Procedural complications included phrenic nerve transection (1 dog), lung laceration (1 dog), and moderate intraoperative bleeding (1 dog). No adverse clinical manifestations of the complications were apparent. We conclude that thoracoscopic partial pericardiectomy is technically feasible and offers several advantages over conventional open thoracic surgical pericardiectomy.     

Evaluation of the presence of selected viral and bacterial nucleic acids in pericardial samples from dogs with or without idiopathic pericardial effusion

Many viruses have been identified in pericardial fluid and in tissue samples from humans with pericarditis by means of molecular diagnostics. In canine idiopathic pericardial effusion there is as yet no conclusive evidence to support the involvement of an infectious agent. This study was designed to investigate a possible relationship between idiopathic pericardial effusion in dogs and viruses most commonly encountered in humans affected with viral pericarditis. Coxsackievirus B3 RNA, influenza virus type A RNA, human adenovirus type 2 DNA, human cytomegalovirus DNA, and parvovirus B19 DNA were investigated using PCR on pericardial effusion samples and pericardial tissue specimens collected from 14 dogs with idiopathic pericardial effusion. PCR was also used to test for two bacteria, Borrelia burgdorferi and Chlamydia pneumoniae. The same microorganisms were also looked for in pericardial effusions or pericardial washes from 10 dogs with neoplastic pericardial effusion, and in samples collected from 10 dogs which died of a non-cardiac disease. One pericardial effusion sample from a dog with the idiopathic form of the disease tested positive for influenza virus type A and sequencing of the amplicon confirmed the PCR result. In another dog from the same group a cytomegalovirus was detected by PCR in the effusion, but sequencing showed this to be a false-positive result. The genomes of the microorganisms investigated were not detected in neoplastic effusions or pericardial washes. The results indicate that viral and bacterial DNA/RNA of relevance for human pericarditis is rare in pericardial samples from dogs with idiopathic pericardial effusion. The finding of influenza type A viral RNA in pericardial fluid from one dog with the idiopathic form of the disease warrants further investigation.     

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.     

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.     

Intracranial Lesions in Dogs With Hemangiosarcoma

A retrospective analysis of 85 dogs with hemangiosarcoma (HSA) that underwent complete necropsy, including gross examination of the brain, was conducted. Grossly identifiable intracranial lesions were present in 17 dogs. Twelve of 85 dogs (14.2%) had brain metastases. Four of 85 dogs (4.7%) had hemorrhagic lesions and/or ischemic necrosis without identifiable tumor. One dog had a primary central nervous system tumor. Signs of intracranial disease were present in six of 85 dogs (7.1%) with HSA; four had brain metastases and two had nonneoplastic lesions. Metastases had a propensity for cerebrum and gray matter. Dogs with brain metastases had more widely disseminated disease than dogs without brain metastases (P less than 0.001). Dogs with pulmonary metastases were at greater risk for developing brain metastases than dogs without pulmonary metastases (odds ratio = 8.31). Although thoracic radiography accurately identified ten of 12 dogs (83%) with pulmonary metastases, too few cases were available to assess the applicability/accuracy of thoracic radiography in predicting the presence or absence of brain metastases in dogs with malignancy and signs of intracranial disease.     

Concurrent splenic and right atrial mass at presentation in dogs with HSA: a retrospective study

The objective of this retrospective study was to evaluate the presence of concurrent splenic and cardiac hemangiosarcoma (HSA). Dogs were divided into two groups: group 1 included 23 dogs with splenic HSA, and group 2 included 31 dogs with a cardiac HSA. All dogs were fully assessed for metastasis with thoracic radiography, abdominal and/or cardiac ultrasound, and/or postmortem examination. Two dogs (8.7%) in group 1 had a concurrent cardiac mass. Neither of these dogs had pericardial effusion, and both were golden retrievers. Thirteen of the dogs in group 1 presented with a hemoabdomen. Concurrent intra-abdominal metastasis was noted in seven dogs. In group 2, 9/31 (29%) of the dogs had a concurrent splenic HSA, and 13/31 (42%) of the dogs had evidence of metastasis to another site. There was a significant association between age and the presence of nonsplenic metastasis (odds ratio, 0.457). The rate of concurrent right atrial mass detected by cardiac ultrasound in dogs with splenic HSA was 8.7%, which is less than previously reported. For dogs with right atrial HSA, the risk of metastasis to nonsplenic sites decreases with age.     

Serum Cardiac Troponin I Concentration in Retired Racing Greyhounds

Background: Cardiac troponin I (cTnI) is a polypeptide found specifically in cardiac muscle tissue that has been used as a diagnostic and prognostic indicator of cardiomyopathy. Increases in cTnI are associated with myocardial pathologic processes. However, high serum cTnI concentrations have been observed in normal Greyhounds.
Hypothesis: We hypothesized that Greyhounds have cTnI concentrations higher than non-Greyhound dogs, and that a separate reference range should be established for Greyhounds.
Animals: Blood samples were collected from the jugular vein from a group of 20 healthy Greyhound blood donors.
Methods: Analysis of serum cTnI was performed with an immunoassay system with a detection level of 0.01 ng/mL, as described previously. The Greyhound values were compared with 2 groups of Boxers with and without arrhythmogenic right ventricular cardiomyopathy (ARVC), and to a group of non-Boxer control dogs from a previous study.
Results: The mean cTnI concentration in Greyhounds was significantly higher ( P < .0001) than that in non-Greyhound control dogs, although not significantly different from normal Boxers ( P = .50), or Boxers with ARVC ( P = .58). Greyhound serum cTnI concentrations were in the range found in Boxers with ARVC. The proposed reference range for cTnI in Greyhounds is 0.05–0.16 ng/mL.
Conclusions and Clinical Importance: Greyhounds have a reference range for serum cTnI concentrations that differs from that of other previously published reference ranges for dogs of other breeds. Until a broader database and more precise reference range can be established, caution should be exercised in interpreting serum cTnI concentrations in Greyhounds with suspected cardiac 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.     

Idiopathic pericarditis in dogs: no evidence for an immune-mediated aetiology

OBJECTIVE: To ascertain whether specific immunological changes are associated with canine pericardial effusion due to idiopathic pericarditis. METHODS: In this prospective study, serum antinuclear antibody and serum and pericardial fluid immunoglobulin (Ig) G, Ig M and Ig A concentrations were measured in dogs with pericardial effusion due to idiopathic pericarditis or pericardial neoplasia. The secretory index relative to albumin concentration was calculated in order to distinguish between Ig actively secreted into the pericardial fluid and that derived from the blood accumulating within the pericardial sac. Statistical analysis was performed comparing the results obtained between the two groups of dogs. RESULTS: Only three dogs were antinuclear antibody positive; two of these dogs had idiopathic pericarditis and one had neoplasia. Mean serum Ig M and Ig A concentrations were lower than the reference values in both groups, and the secretory indices for Ig M and Ig A were greater than 1.0. However, there was no significant difference with respect to any Ig measurement between the two groups of dogs (P>0.1). CLINICAL SIGNIFICANCE: The results of the present study do not support the hypothesis that canine idiopathic pericarditis has a significant 'immune-mediated' aetiology or immunological features that distinguish it from the pericardial changes associated with local neoplastic disease.     

Cardiac Troponin‐I Concentration,Myocardial Arteriosclerosis,and Fibrosis in Dogs with Congestive Heart Failure because of Myxomatous Mitral Valve Disease

Background

Few previous studies have investigated the association between biomarkers and cardiac disease findings in dogs with naturally occurring myxomatous mitral valve disease (MMVD).

Aim

To investigate if histopathological changes at necropsy could be reflected by in vivo circulating concentrations of cTnI and aldosterone, and renin activity, in dogs with naturally occurring congestive heart failure because of MMVD.

Animals

Fifty privately owned dogs with MMVD and heart failure.

Methods

Longitudinal Study. Dogs were prospectively recruited and examined by clinical and echocardiographical examination twice yearly until time of death. Blood was stored for batched analysis of concentrations of cTnI and aldosterone, and renin activity. All dogs underwent a standardized necropsy protocol.

Results

cTnI were associated with echocardiographic left ventricular end‐diastolic dimension (P < .0001) and proximal isovolumetric surface area radius (P < .004). Furthermore, in vivo cTnI concentrations reflected postmortem findings of global myocardial fibrosis (P < .001), fibrosis in the papillary muscles (P < .001), and degree of arterial luminal narrowing (P < .001) Aldosterone or renin activity did not reflect any of the cardiac disease variables investigated.

Conclusion and clinical importance

Cardiac fibrosis and arteriosclerosis in dogs with MMVD are reflected by circulating cTnI concentration, but not by aldosterone concentration or renin activity. Cardiac troponin I could be a valuable biomarker for myocardial fibrosis in dogs with chronic cardiac diseases.     

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.     

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

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