Reduction of diameter of the left ventricle of dogs by plication of the left ventricular free wall

OBJECTIVE: To determine effects of reducing the diameter of the left ventricle of dogs by plication of the left ventricular free wall. ANIMALS: 8 healthy adult mixed-breed dogs. PROCEDURE: Left lateral thoracotomy and a T-shaped pericardiotomy were performed. The free wall of the left ventricle was imbricated with 3 interrupted transfixing sutures applied in a horizontal mattress pattern, using 3-0 polypropylene suture assembled on a straight cutting needle. Surgeons were careful to avoid the coronary vessels. Echocardiography was performed 24 hours before and 48 hours after surgery. Electrocardiography was performed before and 1, 2, 7, 15, 21, 30, and 60 days after surgery. RESULTS: Echocardiographic measurements revealed that the diameter of the left ventricle was reduced by a mean of 23.5%. Electrocardiography revealed ventricular premature complexes 24 hours after surgery that regressed without treatment during the first week after surgery. CONCLUSIONS AND CLINICAL RELEVANCE: Plication of the left ventricular free wall of dogs can reduce end-diastolic and end-systolic dimensions of the left ventricle. The technique is simple and does not require cardiopulmonary bypass. According to Laplace's law, the reduction of cardiac diameter leads to reduction on free-wall tension and may improve left ventricular function in dilatated hearts. Thus, additional studies involving dogs with dilated cardiomyopathy should be conducted.     

Primary left ventricular hemangiosarcoma diagnosed by endomyocardial biopsy in a dog

An 8-year-old spayed Golden Retriever was examined because of recent onset of congestive heart failure complicated by ventricular arrhythmias. Echocardiography revealed a thickened, hypokinetic region of the left ventricular free wall. Fluoroscopically guided transarterial endomyocardial biopsy of the hypokinetic region of the left ventricle revealed infiltration of the endocradium by neoplastic cells consistent with hemangiosarcoma. The dog's clinical condition deteriorated 7 weeks later, and necropsy confirmed the diagnosis and primary site of origin of the tumor. This report describes the clinical use of an endomyocardial biopsy technique to diagnose an infiltrating myocardial tumor that was associated with signs mimicking canine dilated cardiomyopathy.     

Use of western immunoblot for evaluation of myocardial dystrophin, alpha-sarcoglycan, and beta-dystroglycan in dogs with idiopathic dilated cardiomyopathy

OBJECTIVE: To evaluate the potential importance of dystrophin, alpha-sarcoglycan (adhalin), and beta-dystroglycan, by use of western blot analysis, in several breeds of dogs with dilated cardiomyopathy. SAMPLE POPULATION: Myocardial samples obtained from 12 dogs were evaluated, including tissues from 7 dogs affected with dilated cardiomyopathy, 4 control dogs with no identifiable heart disease (positive control), and 1 dog affected with Duchenne muscular dystrophy (negative control for dystrophin). Of the affected dogs, 4 breeds were represented (Doberman Pinscher, Dalmatian, Bullmastiff, and Irish Wolfhound). PROCEDURE: Western blot analysis was used for evaluation of myocardial samples obtained from dogs with and without dilated cardiomyopathy for the presence of dystrophin and 2 of its associated glycoproteins, alpha-sarcoglycan and beta-dystroglycan. RESULTS: Detectable differences were not identified between dogs with and without myocardial disease in any of the proteins evaluated. CONCLUSIONS AND CLINICAL RELEVANCE: Abnormalities in dystrophin, alpha-sarcoglycan, and beta-dystroglycan proteins were not associated with the development of dilated cardiomyopathy in the dogs evaluated in this study. In humans, the development of molecular biological techniques has allowed for the identification of specific causes of dilated cardiomyopathy that were once considered to be idiopathic. The use of similar techniques in veterinary medicine may aid in the identification of the cause of idiopathic dilated cardiomyopathy in dogs, and may offer new avenues for therapeutic intervention.     

Permanent Transvenous Pacemaker Implantation in Forty Dogs

Permanent transvenous cardiac pacemakers were implanted in 40 dogs. Electrocardiographic diagnoses included persistent atrial standstill (3 dogs), sick sinus syndrome (8 dogs), and high-grade second-degree or third-degree atrioventricular (AV) block (29 dogs). Thirteen dogs were alive and well 4 to 42 months after pacemaker implantation (mean, 16.9 months). The mean and median survival times of the 26 dogs that died or were euthanatized during the study were 17.9 months and 13 months, respectively. Most of these dogs succumbed to problems unrelated to the arrhythmia and pacemaker implant. One dog was lost to follow-up. Complications associated with permanent transvenous pacemaker implantation included lead dislodgement, infection, hematoma formation, skeletal muscle stimulation, ventricular arrhythmia, migration of the pulse generator, and skin erosion. Lead dislodgement was the most common complication, occurring in 7 of 9 dogs paced using untined electrode leads and in 6 of 30 dogs paced using tined leads. Lead dislodgement did not occur in the only dog paced using an actively fixed endocardial lead. It was concluded that permanent transvenous cardiac pacing is a feasible, less traumatic alternative to epimyocardial pacing in dogs, but that successful use of this technique requires careful implantation technique and anticipation of the potential complications.     

Transvenous cardiac pacing in 19 dogs and one cat

Eighteen dogs and one cat with symptomatic bradycardias were equipped with cardiac pacemakers. One further dog died during anaesthesia for pacemaker placement. Each animal was sedated, and a ‘tined’ transvenous pacing lead was passed to the apex of the right ventricle from the jugular vein. Following temporary pacing and general anaesthesia, the permanent pacemaker was placed subcutaneously at the neck in the dogs and at the abdominal wall in the cat. In 11 dogs and the cat, the pacemaker was implanted in a dacron pouch. Complications (mainly serous reaction to the pacemaker) developed in four out of seven dogs in which no pouch had been employed. The pacing lead was retained after discharge from hospital in all except one dog. Pacing successfully relieved clinical signs in all cases. Fifteen out of 18 dogs and the cat survived one year after pacing and the mean survival time was greater than 18 months. Transvenous pacing is a simple and reliable technique that avoids transthoracic or transabdominal surgery for pacemaker lead placement.     

Magnetic Resonance Imaging of Right Ventricular Morphology and Function in Boxer Dogs with Arrhythmogenic Right Ventricular Cardiomyopathy

Background: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a myocardial disease characterized by fibrofatty replacement of the right ventricle and ventricular tachyarrhythmias, reported most commonly in the Boxer dog. Although ARVC is characterized as a myocardial disease, the impact of the disease on the function of the right ventricle has not been well studied.
Objective: To noninvasively evaluate the function and anatomy of the right ventricle in Boxer dogs with ARVC.
Animals: Five adult Boxer dogs with ARVC and 5 healthy size-matched hound dogs.
Methods: Magnetic resonance imaging was performed on an ECG-gated conventional 1.5-T scanner using dark blood imaging and cine acquisitions. Images were evaluated by delineation of endocardial right and left ventricular contours in the end-diastolic and end-systolic phases of each slice. Right and left end-systolic and end-diastolic volumes were generated using Simpson's rule and ejection fraction was calculated. Images were evaluated for right ventricular (RV) aneurysms and wall motion abnormalities. Spin echo images were reviewed for the presence of RV myocardial fatty replacement or scar.
Results: RV ejection fraction was significantly lower in Boxers with ARVC compared with the controls (ARVC 34%± 11 control 53%± 10, P < .01). There was an RV aneurysm in 1 dog with ARVC but not in any of the controls. RV myocardial gross fatty changes were not observed in dogs of either group.
Conclusions and Clinical Importance: These findings could be interpreted to suggest that arrhythmias and myocardial dysfunction precede the development of morphological abnormalities in dogs with ARVC.     

Association between results of ambulatory electrocardiography and development of cardiomyopathy during long-term follow-up of Doberman pinschers

OBJECTIVE: To characterize ambulatory electrocardiographic results of overtly healthy Doberman Pinschers and determine associations between those results and development of dilated cardiomyopathy. DESIGN: Cohort study. ANIMALS: 114 (58 male, 56 female) overtly healthy Doberman Pinschers without echocardiographic evidence of cardiac disease on initial examination. PROCEDURE: Echocardiograms and 24-hour ambulatory electrocardiograms (Holter recordings) were obtained initially and at variable intervals. The status (live vs dead) of all dogs was known at least 2 years and as long as 10 years after initial examination (mean [+/- SD] follow-up time, 4.33 +/- 1.84 years). Associations between development of dilated cardiomyopathy and number of ventricular premature contractions (VPC), age, and sex were determined. RESULTS: 55 dogs (48%) did not have VPC on initial Holter recordings, and only 8 dogs had > 50 VPC/24 hours. The likelihood that a dog would have VPC was associated with increasing age and being male. At least 1 VPC/24 hours, and in particular, > 50 VPC/24 hours or > or = 1 couplet or triplet of VPC/24 hours, were predictive of subsequent development of dilated cardiomyopathy. Fifty-four dogs (47%) developed dilated cardiomyopathy; 12 were still alive at the end of the study, and 42 had died. Twenty-five of these 42 dogs died after the onset of congestive heart failure (CHF), 15 died suddenly before the onset of overt CHF, and 2 died of noncardiac causes. More males developed dilated cardiomyopathy than females, and dogs that died suddenly were approximately 1 year younger than those that developed CHF. CONCLUSIONS AND CLINICAL RELEVANCE: Results of high-quality Holter recordings may be used to identify overtly healthy Doberman Pinschers that are at a high risk for dilated cardiomyopathy.     

Use of tissue Doppler imaging to confirm the diagnosis of dilated cardiomyopathy in a dog with equivocal echocardiographic findings

A 1-year-old healthy female Great Dane was referred for an echocardiographic examination prior to anesthesia and surgical correction of prolapse of the right third eyelid gland. Findings of a physical examination were normal. Conventional 2-dimensional and M-mode echocardiography revealed equivocal findings of dilated cardiomyopathy (DCM). Conversely, tissue Doppler imaging revealed a dramatic decrease in systolic and early diastolic radial myocardial velocity gradients, which were related to a decrease in endocardial velocities. Four months later, the diagnosis of DCM was confirmed via conventional echocardiography. In dogs with equivocal conventional echocardiographic findings of DCM, severe myocardial alterations may be detected via tissue Doppler imaging and this technique may enable early diagnosis of radial myocardial dysfunction.     

Cranial vena caval syndrome secondary to transvenous pacemaker implantation in two dogs

Superior vena caval syndrome is a rare, but reported complication of transvenous pacemaker implantation in humans. This syndrome can occur secondary to fibrotic and/or thrombotic obstruction of venous blood flow into the right atrium. The therapeutic approach depends on the suspicion of the presence of an active thrombus and may include antithrombotics, angioplasty and/or surgical venoplasty. We describe two dogs that developed severe pleural effusion secondary to stricture formation in the cranial vena cava 4 years after dual chamber transvenous pacemaker implantation. The stenosis was most likely due to fibrosis secondary to the transvenous pacemaker leads. Balloon angioplasty of the lesion resulted in resolution of the pleural effusion in both patients. Balloon angioplasty appears to be a viable therapeutic approach in dogs with cranial vena caval syndrome caused by focal stenotic lesions.     

Prospective clinical evaluation of serum cardiac troponin T in dogs admitted to a veterinary teaching hospital

The purpose of this study was to measure serum cardiac troponin T (cTnT) with a commercially available human enzyme-linked immunoassay (ELISA) test in various groups of dogs, including those undergoing doxorubicin chemotherapy. Serum samples were obtained from 6 groups of dogs: (1) normal adult dogs (n = 15); (2) dogs with asymptomatic dilated cardiomyopathy (n = 5); (3) dogs with congestive heart failure (n = 10); (4) dogs with untreated neoplasia (n = 20); (5) dogs with skeletal muscle trauma (n = 10); and (6) dogs with neoplasia receiving doxorubicin chemotherapy (n = 4). One serum sample was obtained from each of the normal dogs, those with asymptomatic cardiomyopathy, those with congestive heart failure, and those with untreated neoplasia. Serum samples were obtained serially from the dogs that were undergoing doxorubicin chemotherapy; samples were collected before doxorubicin (30 mg/m2) administration and then 1, 5, 7, and 14 days after administration throughout 6 cycles for a cumulative total dose of 180 mg/m2. All normal dogs, dogs with untreated neoplasia, and dogs with asymptomatic dilated cardiomyopathy had cTnT concentrations below the lower limits of detection for the assay used (<0.05 ng/mL). Detectable concentrations of cTnT were found in 3 dogs with congestive heart failure and in 2 dogs with skeletal muscle trauma. Detectable concentrations also were found in both dogs that had received 180 mg/m2 of doxorubicin. We conclude that dogs with congestive heart failure and those with skeletal muscle trauma and dogs with neoplasia receiving high-dose doxorubicin chemotherapy may have increased serum cTnT concentration, which may be suggestive of myocardial damage.     

Tachycardia-induced cardiomyopathy in a young Boxer dog with supraventricular tachycardia due to an accessory pathway

A 1-year-old male Boxer dog presented with sustained supraventricular tachycardia and tachycardia-induced cardiomyopathy. Conversion to sinus rhythm was achieved initially with intravenous lignocaine and subsequently with oral procainamide. Oral procainamide treatment was relatively successful in maintaining normal sinus rhythm with no side effects apart from a reversible change in coat colour. Electrophysiological studies demonstrated the presence of an accessory pathway connecting the right atrium to the right ventricle and confirmed the diagnosis of orthodromic atrioventricular reciprocating tachycardia. Radiofrequency catheter ablation of the accessory pathway led to permanent resolution of the supraventricular tachycardia and for 9.5 years the dog has had no further signs of cardiac disease. The successful treatment of this condition highlights the importance of differentiating tachycardia-induced cardiomyopathy from dilated cardiomyopathy.     

Plication of the free wall of the left ventricle in dogs with doxorubicin-induced cardiomyopathy

OBJECTIVE: To evaluate plication of the free wall of the left ventricle, which reduces the left ventricular area and volume, as a method to improve the left ventricular systolic function without cardiopulmonary bypass. ANIMALS: 8 mixed-breed adult dogs. PROCEDURE: Dilated cardiomyopathy (DCM) was induced in each dog by administration of doxorubicin (30 mg/m2, i.v., q 21 d for 168 days).Two dogs died during induction of cardiomyopathy. Plication surgery was performed in 4 dogs. Two dogs did not ondergo to surgery (control group). Values for cardiac output (CO), 2-dimensional and M-mode echocardiography, arterial blood pressure, electrocardiography, blood cell counts, and serum biochemical analyses were recorded after induction of DCM (baseline) and 1, 2, 7, 15, 21, 30, 60, 90, 120, 150, and 180 days after plication surgery. Ambulatory ECG (Holter) recordings were conducted for 24 hours on the day of surgery. RESULTS: 1 dog died after plication surgery. The remaining dogs undergoing ventricular plication had a significant improvement in CO, ejection fraction, and fractional shortening and reductions of left ventricular area and volume after surgery. Electrocardiographic and Holter recordings revealed premature ventricular complexes, which resolved without treatment during the first week after surgery. Clinical condition of the control dogs declined, and these 2 dogs died approximately 40 days after induction of cardiomyopathy. CONCLUSIONS AND CLINICAL RELEVANCE: Plication of the free wall of the left ventricle improved left ventricular systolic function in dogs with doxorubicin-induced cardiomyopathy. Additional studies are needed to evaluate its application in dogs with naturally developing DCM.     

Echocardiographic and clinical signs of canine dilated cardiomyopathy

The clinical signs, electrocardiograms and echocardiograms of 12 dogs with dilated cardiomyopathy of large breeds and congestive heart failure were reviewed. There was a high prevalence of males (11 dogs) and of the Doberman breed (7 dogs). Seven dogs had atrial fibrillation. The echocardiograms revealed significant increases in left ventricular and left atrial dimensions. The shortening fraction (%ΔD), aortic root excursion and left ventricular wall excursion were all significantly decreased, documenting a decrease in contractile function of the left ventricle that, together with the cardiac enlargement characterize this disease. The advantages of obtaining these functional parameters non-invasively are emphasized.     

Myocardial L-carnitine deficiency in a family of dogs with dilated cardiomyopathy

Dilated cardiomyopathy in a family of dogs was found to be associated with decreased myocardial L-carnitine concentrations, when compared with those in control dogs. In 2 affected dogs, treatment with high doses of L-carnitine was associated with increased myocardial L-carnitine concentration and greatly improved health and myocardial function. Withdrawal of L-carnitine supplementation from these dogs resulted in development of myocardial dysfunction and clinical signs of dilated cardiomyopathy.     

The potential role of myocardial serotonin receptor 2B expression in canine dilated cardiomyopathy

Serotonin signalling in the heart is mediated by receptor subtype 2B (5-HTR2B). A contribution of serotonin to valvular disease has been reported, but myocardial expression of 5-HTR2B and its role in canine dilated cardiomyopathy (DCM) is not known. The aim of the present study was to investigate myocardial 5-HTR2B mRNA expression in dogs with DCM and to correlate results with expression of markers for inflammation and remodelling. Myocardial samples from eight healthy dogs, four dogs with DCM, five with cardiac diseases other than DCM and six with systemic non-cardiac diseases were investigated for 5-HTR2B mRNA expression using quantitative PCR (qPCR). The results were compared to mRNA expression of selected cytokines, matrix metalloproteinases (MMP) and tissue inhibitors of matrix metalloproteinase (TIMP). Laser microdissection with subsequent qPCR and immunohistochemistry were employed to identify the cells expressing 5-HTR2B.The myocardium of control dogs showed constitutive 5-HTR2B mRNA expression. In dogs with DCM, 5-HTR2B mRNA values were significantly greater than in all other groups, with highest levels of expression in the left ventricle and right atrium. Myocytes were identified as the source of 5-HTR2B mRNA and protein. A significant positive correlation of 5-HTR2B mRNA with expression of several cytokines, MMPs and TIMPs was observed. The findings suggest that serotonin might play a role in normal cardiac structure and function and could contribute to myocardial remodelling and functional impairment in dogs with DCM.     

Echocardiographic evaluation of diastolic parameters in dogs with dilated cardiomyopathy

Echocardiography is a valuable tool for the evaluation of systolic and diastolic cardiac function. A high correlation between measurements of diastolic mitral inflow parameters analyzed with Doppler echocardiography and invasive methods makes the former valuable. The aim of this study was to ascertain if significant differences occur in diastolic myocardial parameters between dogs with no heart disease and dogs with subclinical or clinical dilated cardiomyopathy. Furthermore the aim of the study was to determine whether heart failure in dilated cardiomypathy is a result of systolic dysfunction alone or both systolic and diastolic dysfunction. Eleven parameters were analyzed: E wave, E-AT, E-DT, E time, A wave, A-AT, A-DT, A time, E+A time, E/A ratio, and IVRT. The study confirmed the value of noninvasive echocardiographic assessment of diastolic function in dogs with dilated cardiomyopathy. Significant differences were found in E wave, E-AT, E time, E/A ratio and IVRT between healthy dogs and dogs with dilated cardiomyopathy. All are characterized by a significant decrease compared to healthy dogs after taking into account age and body weight except for the E/A ratio, which significantly increased in value. There were no significant changes in any of the Doppler parameters for diastolic evaluation in subclinical cases of DCM. Advanced heart failure in dilated cardiomyopathy entails systolic and diastolic dysfunction.     

RIGHT HEART ENLARGEMENT IN HEARTWORM-INFECTED DOGS

Radiographically, the size of the right ventricle of 54 heartworm-infected dogs was graded subjectively as normal, 1 +, 2 +, and 3 + and served to classify the dogs into groups A, B, C, and D. With M-mode echocardiograms, right ventricular enlargement ratios (RVE ratios) were determined for each dog by dividing the measured right ventricular internal diastolic dimension (RVIDd) by the expected RVIDd of a normal dog of the same body weight. The normal RVIDd relation to body weight was derived from 25 healthy heartworm-free control dogs. These two variables were linearly related with a correlation coefficient r²= 0.59. Means and standard deviations of the RVE ratio were calculated for each group. Despite wide ranges and considerable overlap, the ratio was significantly different (t-test, p < 0.005) between groups with the exception of groups A and B, and C and D. The incidence of electrocardiographic signs of right ventricular hypertrophy was also determined for each group; it was 38% in group C and 62% in group D. From this data, it was concluded that M-mode echocardiography is a very sensitive technique for the documentation of right ventricular dilatation in heartworm-infected dogs, correlating with radiographic impressions of right ventricular enlargement.     

Correlation of mitochondrial protein expression in complexes I to V with natural and induced forms of canine idiopathic dilated cardiomyopathy

OBJECTIVE: To identify qualitative and quantitative differences in cardiac mitochondrial protein expression in complexes I to V between healthy dogs and dogs with natural or induced dilated cardiomyopathy (DCM). SAMPLE POPULATION: Left ventricle samples were obtained from 7 healthy dogs, 7 Doberman Pinschers with naturally occurring DCM, and 7 dogs with DCM induced by rapid right ventricular pacing. PROCEDURES: Fresh and frozen mitochondrial fractions were isolated from the left ventricular free wall and analyzed by 2-dimensional electrophoresis. Protein spots that increased or decreased in density by 2-fold or greater between groups were analyzed by matrix-assisted laser desorption/ionization time-of-flight mass spectrometry or quadrupole selecting, quadrupole collision cell, time-of-flight mass spectrometry. RESULTS: A total of 22 altered mitochondrial proteins were identified in complexes I to V. Ten and 12 were found in complex I and complexes II to V, respectively. Five were mitochondrial encoded, and 17 were nuclear encoded. Most altered mitochondrial proteins in tissue specimens from dogs with naturally occurring DCM were associated with complexes I and V, whereas in tissue specimens from dogs subjected to rapid ventricular pacing, complexes I and IV were more affected. In the experimentally induced form of DCM, only nuclear-encoded subunits were changed in complex I. In both disease groups, the 22-kd subunit was downregulated. CONCLUSIONS AND CLINICAL RELEVANCE: Natural and induced forms of DCM resulted in altered mitochondrial protein expression in complexes I to V. However, subcellular differences between the experimental and naturally occurring forms of DCM may exist.     

Canine dilated cardiomyopathy: a retrospective study of signalment, presentation and clinical findings in 369 cases

O bjective : To review the clinical and diagnostic findings and survival of dilated cardiomyopathy from a large population of dogs in England.
M ethods : A retrospective study of the case records of dogs with dilated cardiomyopathy collected between January 1993 and May 2006.
R esults : There were 369 dogs with dilated cardiomyopathy of which all were pure-bred dogs except for four. The most commonly affected breeds were dobermanns and boxers. Over 95 per cent of dogs weighed more than 15 kg and 73 per cent were male. The median duration of signs before referral was three weeks with 65 per cent presenting in stage 3 heart failure. The most common signs were breathlessness (67 per cent) and coughing (64 per cent). The majority of dogs (89 per cent) had an arrhythmia at presentation and 74 per cent of dogs had radiographic signs of pulmonary oedema or pleural effusion. The median survival time was 19 weeks.
C linical S ignificance : Dilated cardiomyopathy occurs primarily in medium to large breed pure-bred dogs, and males are more frequently affected than females. The duration of clinical signs before referral is often short and the survival times are poor. Greater awareness of affected breeds, clinical signs and diagnostic findings may help in early recognition of this disease which often has a short clinical phase.     

Dilated cardiomyopathy and sinoatrial dysfunction in an Estrela mountain dog

A 1 yr old male Estrela mountain dog was evaluated as a part of a screening program for dilated cardiomyopathy. The dog came from a family with a history of dilated cardiomyopathy but was asymptomatic. Occult dilated cardiomyopathy and sino-atrial dysfunction were diagnosed based on echocardiography and electrocardiography. These two disorders may be associated given that related dogs have been diagnosed with the same disorders. The dog has remained asymptomatic for 4 years following initial evaluation.