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 arrhythmias and serum cardiac troponins in Vipera palaestinae envenomation in dogs

BACKGROUND: Vipera palaestinae is responsible for most poisonous envenomations in people and animals in Israel. Cardiac arrhythmias were reported in a retrospective study of V. palaestinae envenomations in dogs. HYPOTHESIS: Cardiac arrhythmias in V. palaestinae-envenomed dogs are associated with myocardial injury reflected by increased serum concentrations of cardiac troponins (cTns). ANIMALS: Forty-eight client-owned dogs envenomed by V. palaestinae. METHODS: Blood sampling (serum biochemistry and cTns, CBC, and coagulation tests) and electrocardiography were performed periodically up to 72 hours postenvenomation. Cardiac rhythm strips were assessed blindly for the presence and type of arrhythmias. RESULTS: Serum cTn-T and cTn-I concentrations were increased in 25% (n = 12) and 65% (n = 31) of the dogs at least once during hospitalization, respectively. Arrhythmias were identified in 29% (n = 14) of the dogs. Dogs with increased cTn-T had a significantly higher occurrence of arrhythmias (58 versus 19%), and higher resting heart rate upon admission and within the following 24 hours. Dogs with increased serum cTn-T concentrations were hospitalized for a significantly (P= .001) longer period compared to those with normal serum cTn-T concentrations. CONCLUSIONS AND CLINICAL RELEVANCE: Dogs envenomed by V. palaestinae appear to sustain some degree of myocardial injury, as reflected by increased serum cTn concentrations and by the occurrence of arrhythmias. The latter should alert clinicians to a potentially ongoing cardiac injury. An increase in cTn-T may be of clinical relevance and indicate a cardiac injury in V. palaestinae envenomations in dogs.     

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.     

Cardiac troponins I and T in dogs with pericardial effusion

Cardiac troponin I (cTnI) and cardiac troponin T (cTnT) are sensitive and specific markers for myocardial ischemia and necrosis. Dogs with pericardial effusion frequently have myocardial ischemia and necrosis, and these changes are more severe in dogs with hemangiosarcoma (HSA). We investigated the utility of using serum cTnI and cTnT concentrations to identify the idiopathic pericardial effusion from that associated with HSA. Blood samples for measurement of cTnI and cTnT concentrations were collected before pericardiocentesis in 37 dogs with pericardial effusion. Eighteen dogs had a mass consistent with HSA, 6 dogs had idiopathic pericardial effusion, 1 dog had mesothelioma, and 1 dog had a heart base tumor. No final diagnosis was achieved for 11 dogs. Dogs with pericardial effusion had significantly higher serum concentrations of cTnI (P < .001) but not cTnT (P = .16) than did normal dogs. Dogs with HSA had significantly higher concentrations of cTnI (2.77 ng/dL; range: 0.09-47.18 ng/dL) than did dogs with idiopathic pericardial effusion (0.05 ng/dL; range: 0.03-0.09 ng/dL) (P < .001). There was no difference in the concentration of cTnT between dogs with HSA and those with idiopathic pericardial effusion (P = .08). Measurement of cTnI may be useful in helping to distinguish between idiopathic pericardial effusion and pericardial effusion caused by HSA.     

Burn-induced subepicardial injury in frog heart: a simple model mimicking ST segment changes in ischemic heart disease

To mimic ischemic heart disease in humans, several animal models have been created, mainly in rodents bysurgically ligating their coronary arteries. In the present study, by simply inducing burn injuries on thebullfrog heart, we reproduced abnormal ST segment changes in the electrocardiogram (ECG), mimicking thoseobserved in ischemic heart disease, such as acute myocardial infarction and angina pectoris. The “currents ofinjury” created by a voltage gradient between the intact and damaged areas of the myocardium, negativelydeflected the ECG vector during the diastolic phase, making the ST segment appear elevated during the systolicphase. This frog model of heart injury would be suitable to explain the mechanisms of ST segment changesobserved in ischemic heart 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.     

Correlation of Serum Cardiac Troponin I and Myocardial Damage in Cattle with Monensin Toxicosis

Background: Cardiac troponin I (cTnI) is used as a biomarker of myocardial injury in people and small animals. Little is known about the diagnostic use of cTnI in cattle.
Hypothesis: Serum cTnI correlates to myocardial function and histopathologic lesions in cattle with monensin-induced myocardial injury.
Animals: Ten healthy cows.
Methods: Experimental study. Animals received 1 dose of monensin PO; 30 mg/kg (n = 1) or 40 mg/kg (n = 1) (Group A) or 50 mg/kg monensin (n = 8) (Group B) of body weight. Repeated measurements were performed of serum cTnI, biochemistry, and ECG and echocardiography until study termination at 80 (Group A) and 144 hours (Group B) after dosing. Semiquantitative histopathologic examinations of the heart were performed in each cow. A scoring system with regard to the magnitude of myocardial injury was established and a total heart score was compared with maximum cTnI concentration measured after monensin administration. Five hearts from healthy cows served as controls.
Results: Increased cTnI (>0.07 ng/mL) was found in 9/10 cows. cTnI was significantly associated with left ventricular shortening fraction ( r ²= 0.51; P = .02) and myocardial histopathologic lesion score ( r ²= 0.49; P = .021). All cows (n = 7) with evidence of myocardial necrosis had a cTnI concentration ≥ 1.04 ng/mL.
Conclusion and Clinical Importance: cTnI is related to myocardial necrosis and severity of myocardial damage in cattle with monensin toxicosis. cTnI could become a useful diagnostic tool in the noninvasive assessment of myocardial injury in cattle with naturally occurring cardiac disease.     

狐胆汁对蟾蜍离体心脏功能的影响

目的：研究狐胆汁对蟾蜍离体心脏的作用及对蟾蜍离体心脏细胞膜ATP酶活性的影响。方法：采用离体蛙心灌流法观察狐胆汁对离体蟾蜍心脏的收缩力、心率的影响,并通过定磷法检测狐胆汁对离体蟾蜍心肌细胞膜ATP酶活性的影响。结果：狐胆汁使蟾蜍离体心脏的收缩力加强,在0.3～4.0g/L浓度范围内,狐胆汁促进心肌收缩力的作用与剂量之间呈量效关系,最大效应可使心肌收缩力提高390%,心率减慢。随狐胆汁浓度提高,心肌细胞膜Ca^2＋-ATP酶活性提高,Na^＋K^＋-ATP酶、Mg^2＋-ATP酶、Ca^2＋Mg^2＋-ATP酶活性下降。结论：狐胆汁能提高蟾蜍离体心脏的功能,其作用机制有待进一步研究。     

Cardiac ganglioneuroma in a juvenile pig

A cardiac mass (3 × 5 × 3 cm) was detected at the base between the right auricular wall and right vena cava of a slaughtered 6-month-old female mixed-breed pig during a meat inspection. The tumor comprised infiltrative prominent interweaving fascicles of Schwann cells with Verocay bodies. Moreover, the ganglion cells were scattered or aggregated throughout the neoplastic tissue. The ganglion and Schwann cells had neither cellular atypism nor mitosis. On the basis of the bearing site as well as the morphological and immunohistochemical features, this is the first case of a cardiac ganglioneuroma in a pig.     

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.     

山羊心脏淋巴系的研究

在４０例山羊心外膜下多点注入３０％普鲁士蓝氯仿溶液，解剖观察心脏淋巴管及其淋巴流向；选择注射较好的心脏标本制成透明铺片，镜下观察测定淋巴管管径，并摄影记录。结果表明，山羊心脏的毛细淋巴管起自一盲端，并吻合成淋巴管丛，淋巴管有瓣膜，粗细不均。三级淋巴管汇入锥旁室间沟或冠状沟附近的四级淋巴管。四级淋巴管汇合成淋巴干，山羊心脏的淋巴干分２种类型，即双干型与单干型。淋巴干一般注入气管支气管左淋巴结，有时右淋巴干直接注入胸导管。心房壁薄，淋巴管比心室少而细     

Pathogenesis of single right coronary artery and pulmonic stenosis in English Bulldogs

English Bulldogs are the most common breed to have pulmonic stenosis. Previous studies showed that this congenital heart abnormality in Bulldogs frequently is caused by a circumpulmonary left coronary artery originating from a single right coronary artery. Fetal anasarca also occurs often in Bulldogs and might represent congestive heart failure, but the cause is unknown. To determine if fetal anasarca is associated with a coronary anomaly and pulmonic stenosis, major coronary arteries were studied in 6 bulldog puppies with fetal anasarca. Five of the puppies had normal coronary arteries, and this led to the conclusion that fetal anasarca usually is not associated with major coronary abnormalities or pulmonic stenosis. The 6th puppy had single right coronary artery with circumpulmonary left coronary artery and moderate subvalvular pulmonic stenosis. Serial section histology suggests that the underlying cause of this syndrome is malformation of the left aortic sinus (of Valsalva) and inversion of the proximal segment of the left main coronary artery.     

旋毛虫致小鼠心肌损伤的试验

本研究旨在对重度感染旋毛虫后小鼠心肌损伤的研究。通过对小鼠接种旋毛虫,1 000条/只,分别于不同时间对血清中心肌损伤标志物H-FABP、CK-MB和cTnT进行动态检测,以及心肌组织病理形态学变化进行观察。结果显示,H-FABP比CK-MB、cTnT敏感性高(P<0.05),出现及达到高峰的时间最早;感染旋毛虫后19d～24d,心肌组织损伤最为严重。H-FABP可用于早期旋毛虫病患者心肌损伤的诊断,具有较高的敏感性和特异性。     

Spontaneous Cardiac Hypertrophy in a Crl:CD(SD) Rat

Cardiac hypertrophy was observed in a 9-week-old Crl:CD(SD) rat that died unexpectedly. The animal was allocated to the control group of a toxicity study, and no abnormalities in its general conditions, body weight or food intake were observed. Necropsy revealed an increase in heart weight. Gross examination indicated cardiac enlargement with thickening of the right and left ventricular walls. Histopathological examination revealed hypertrophy of the cardiomyocytes in the right and left ventricular walls and the interventricular septum. Electron microscopic examination indicated bizarre nuclei and accumulation of an increased number of various sizes of mitochondria in the perinuclear region of the hypertrophied myocytes. Hypertrophied myocytes connected by intensely folded intercalated disks were also observed. Based on these findings, the animal was diagnosed with cardiac hypertrophy. This is the first case report of cardiac hypertrophy in this strain.