Long-term Outcome of Irish Wolfhound Dogs with Preclinical Cardiomyopathy, Atrial Fibrillation, or Both Treated with Pimobendan, Benazepril Hydrochloride, or Methyldigoxin Monotherapy.

BACKGROUND: Dilated cardiomyopathy (DCM) is a common cause of morbidity and mortality in the Irish Wolfhound (IW). However, the benefit of medical treatment in IW dogs with preclinical DCM, atrial fibrillation (AF), or both has not been demonstrated. OBJECTIVES: Compare the time to develop congestive heart failure (CHF) or sudden death in IW dogs with preclinical DCM, AF, or both receiving monotherapy with pimobendan, methyldigoxin, or benazepril hydrochloride. ANIMALS: Seventy-five client-owned IW dogs. METHODS: Irish Wolfhound dogs were prospectively randomized to receive pimobendan (Vetmedin®), benazepril HCl (Fortekor®), or methyldigoxin (Lanitop®) monotherapy in a 1:1:1 ratio in a blinded clinical trial. The prospectively defined composite primary endpoint was onset of CHF or sudden death. To assure stringent evaluation of treatment effect, data from dogs complying with the study protocol were analyzed. RESULTS: Sixty-six IW fulfilling the study protocol included 39 males, 27 females; median (interquartile range) age, 4.0 years (3.0-5.0 years) and weight, 70.0 kg (63.0-75.0 kg). Primary endpoint was reached in 5 of 23 (21.7%) IW receiving pimobendan, 11 of 22 (50.0%) receiving benazepril HCl, and 9 of 21 (42.9%) receiving methyldigoxin. Median time to primary endpoint was significantly longer for pimobendan (1,991 days; 65.4 months) compared to methyldigoxin (1,263 days; 41.5 months; P = .031) or benazepril HCl-(997 days; 32.8 months; P = .008) treated dogs. CONCLUSIONS AND CLINICAL IMPORTANCE: In IW dogs with preclinical DCM, AF or both, pimobendan monotherapy significantly prolonged time to onset of CHF or sudden death than did monotherapy with benazepril HCl or methyldigoxin.

Cardiac pathology in Irish wolfhounds with heart disease.

OBJECTIVES: To evaluate gross and histopathologic lesions in Irish wolfhounds (IWs) with atrial fibrillation (AF) and/or primary dilated cardiomyopathy (DCM) in different stages of disease. METHODS: Twenty-six formalin-fixed IW hearts were studied. Clinical diagnosis was based upon results of their most recent cardiovascular examinations including electrocardiography and echocardiography and categorized as normal (n = 4); preclinical (asymptomatic) DCM with AF (n = 6); DCM with congestive heart failure and AF (n = 4); AF with left ventricular reverse remodeling after DCM diagnosis (n = 3); AF without DCM (n = 7); and DCM with sinus rhythm (n = 2). All hearts were evaluated by one pathologist (HA) blinded to the clinical diagnosis. RESULTS: Ten of 15 DCM hearts showed mild to moderate multifocal myocardial fibrosis with variable diffuse adipocyte infiltration within the left and right ventricular myocardium. In five DCM hearts, there were no histopathological findings identified. Right atrial appendages from AF dogs with and without DCM had significantly more myocardial fibrosis and adipocyte infiltration compared with normal hearts and compared to left atrial appendages. CONCLUSIONS: Gross and histological findings in the ventricular myocardium of IWs with clinical diagnosis of DCM were variable; in some dogs, histopathology was normal. In IWs, the etiology of DCM might be different from that in other breeds with conditions causing functional impairment rather than evident histological changes. Right and left atrial appendages from IWs with AF displayed substantial pathology (interstitial fibrosis and adipocytes) most prevalent in the right atrial appendages which may be correlated to the pathogenesis of AF. These preliminary findings merit further study.

Complex segregation analysis of dilated cardiomyopathy (DCM) in Irish wolfhounds.

The objective of the present study was to analyse the mode of inheritance for dilated cardiomyopathy (DCM) in Irish wolfhounds using regressive logistic models by testing for mechanisms of genetic transmission. Insights from this spontaneous animal model should aid importantly in understanding basic pathogenic mechanisms with regard to genetics and molecular biology of DCM in humans. Moreover, a procedure for the simultaneous prediction of breeding values and the estimation of genotype probabilities for DCM is expected to markedly improve breeding programmes. Results of cardiovascular examinations of 1018 dogs carried out between 1987 and 2003 by one veterinarian were analysed. Data of 878 dogs from 531 litters in 147 different kennels were used for complex segregation analyses. Pedigree information was available for more than 15 generations. Male dogs were affected significantly more often by DCM than female dogs. The segregation analysis showed that among all other tested models a mixed monogenic-polygenic model including a sex-dependent allele effect best explained the segregation of affected animals in the pedigrees. A pure monogenic inheritance of DCM could be significantly rejected in favour of the major gene and most general model. The gene action of the major gene was significantly different between female and male dogs.

The prevalence of cardiomyopathy in the Irish wolfhound: a clinical study of 500 dogs.

The prevalence of cardiomyopathy in Irish wolfhounds was evaluated by retrospective review of the results of cardiovascular examinations carried out in 500 dogs presented for veterinary services at the author's practice. Abnormalities were found in 209 (41.8%) of the dogs examined. Dilated cardiomyopathy (DCM) was diagnosed in 121 (24.2%) of the dogs and was accompanied by atrial fibrillation in 106 dogs. Seventeen dogs were suffering from advanced congestive heart failure (CHF), and 55 dogs were suffering from mild to moderate CHF as a result of DCM. Congestive heart failure was most commonly characterized by mild to severe pleural effusion due to right-sided heart failure in addition to pulmonary edema. Rhythm disturbances without evidence of DCM were detected in 48 dogs. Forty dogs had echocardiographic abnormalities without signs of DCM. Soft to moderate mitral regurgitations were diagnosed in 13 (2.6%) of these 40 dogs examined. In 39 dogs that died as a result of DCM, the median survival time from the time of diagnosis was 5.1 months, and in 59 dogs with DCM that are still alive, the median survival time is 15.7 months.

Echocardiographic measurements in the Irish wolfhound: reference values for the breed.

Out of 400 Irish wolfhounds cardiologically examined, echocardiographic measurements of 262 normal dogs were analyzed to obtain reference values for the breed. Based on regression analysis, several echocardiographic parameters showed significant linear correlation with body weight and with age, but coefficients of determination were low. Therefore, due to a high individual variability of echocardiographic measurements in adult Irish wolfhounds, the predictive value of body weight for echocardiographic measurements was clinically not relevant. Sex had no influence on echocardiographic values. For the estimation of myocardial function, end-systolic volume index (ESVI) (mean, 29.0 ml/m2 +/- standard deviation [SD], 5.9 ml/m2) was determined for the group of 262 normal dogs.

Use of echocardiography in the diagnosis of dilated cardiomyopathy in Irish wolfhounds.

The purpose of this study was to compare the echocardiographic features of Irish wolfhounds with clinically inapparent dilated cardiomyopathy (DCM) (n = 33) to dogs with advanced DCM (n = 33) and to normal dogs (n = 262). Significant differences were detected between the three groups. In dogs with DCM, the most sensitive diagnostic measurements were: end-systolic volume index (ESVI), E-point to septal separation (EPSS), fractional shortening (FS), and left ventricular internal dimensions (LVIDd and LVIDs). Left atrial diameter was increased markedly in dogs with DCM and 83.3% of affected Irish wolfhounds had concurrent atrial fibrillation. Compared with early DCM, in advanced DCM there was a significant increase in end-diastolic right ventricular diameter, often combined with extensive pleural effusion, the leading sign of congestive heart failure in Irish wolfhounds.