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1.
J Vet Intern Med ; 32(3): 930-943, 2018 May.
Article En | MEDLINE | ID: mdl-29660848

BACKGROUND: Hypertrophic cardiomyopathy is the most prevalent heart disorder in cats and principal cause of cardiovascular morbidity and mortality. Yet, the impact of preclinical disease is unresolved. HYPOTHESIS/OBJECTIVES: Observational study to characterize cardiovascular morbidity and survival in cats with preclinical nonobstructive (HCM) and obstructive (HOCM) hypertrophic cardiomyopathy and in apparently healthy cats (AH). ANIMALS: One thousand seven hundred and thirty client-owned cats (430 preclinical HCM; 578 preclinical HOCM; 722 AH). METHODS: Retrospective multicenter, longitudinal, cohort study. Cats from 21 countries were followed through medical record review and owner or referring veterinarian interviews. Data were analyzed to compare long-term outcomes, incidence, and risk for congestive heart failure (CHF), arterial thromboembolism (ATE), and cardiovascular death. RESULTS: During the study period, CHF, ATE, or both occurred in 30.5% and cardiovascular death in 27.9% of 1008 HCM/HOCM cats. Risk assessed at 1, 5, and 10 years after study entry was 7.0%/3.5%, 19.9%/9.7%, and 23.9%/11.3% for CHF/ATE, and 6.7%, 22.8%, and 28.3% for cardiovascular death, respectively. There were no statistically significant differences between HOCM compared with HCM for cardiovascular morbidity or mortality, time from diagnosis to development of morbidity, or cardiovascular survival. Cats that developed cardiovascular morbidity had short survival (mean ± standard deviation, 1.3 ± 1.7 years). Overall, prolonged longevity was recorded in a minority of preclinical HCM/HOCM cats with 10% reaching 9-15 years. CONCLUSIONS AND CLINICAL IMPORTANCE: Preclinical HCM/HOCM is a global health problem of cats that carries substantial risk for CHF, ATE, and cardiovascular death. This finding underscores the need to identify therapies and monitoring strategies that decrease morbidity and mortality.


Cardiomyopathy, Hypertrophic/veterinary , Cat Diseases/mortality , Age Factors , Animals , Cardiomyopathy, Hypertrophic/complications , Cardiomyopathy, Hypertrophic/mortality , Cardiovascular Diseases/etiology , Cardiovascular Diseases/mortality , Cardiovascular Diseases/veterinary , Case-Control Studies , Cats , Echocardiography/veterinary , Female , Incidence , Male , Retrospective Studies , Risk Factors , Survival Analysis
2.
J Vet Cardiol ; 15(3): 189-96, 2013 Sep.
Article En | MEDLINE | ID: mdl-23972628

OBJECTIVES: Taurine plays an important role in maintaining myocardial function. Irish wolfhound dogs (IW) are at risk for dilated cardiomyopathy (DCM), but a relationship between whole blood taurine (WBT) deficiency and DCM has not been established. Our aim was to determine prevalence of WBT deficiency in IW with and without DCM and assess its association with diet. ANIMALS: 115 privately owned IW. METHODS: Whole blood taurine was measured in IW that received cardiovascular examination. Dietary history was recorded; crude protein and energy intake were estimated. RESULTS: Forty-nine (42.6%) had DCM; 66 (57.4%) had no DCM. Dogs with DCM were older ([median; inter-quartile range or IQR] 5.3; 4.3, 6.2 years) than dogs without heart disease (3; 2, 4 years; P < 0.001). There was no significant relationship between WBT concentration and age (P = 0.64). Whole blood taurine was severely reduced (<130 nmol/mL) in 8 dogs (4 with and 4 without DCM) and moderately reduced (130-179.9 nmol/mL) in 32 dogs (12 with DCM and 20 without DCM). Follow up of dogs without DCM revealed that a higher proportion of dogs with any degree of WBT deficiency developed DCM later compared to dogs with normal WBT (P < 0.001). CONCLUSIONS: Whole blood taurine deficiency occurred in IW with and without DCM. Based on taurine measurement on a single occasion, there was no clear relationship between low WBT and presence of DCM in this population. Regardless of WBT, DCM affected predominantly older dogs, suggesting a relatively late onset disease in the IW.


Cardiomyopathy, Dilated/veterinary , Dog Diseases/blood , Echocardiography/veterinary , Taurine/blood , Animal Feed/analysis , Animal Feed/standards , Animals , Cardiomyopathy, Dilated/blood , Cardiomyopathy, Dilated/diagnostic imaging , Case-Control Studies , Diet/veterinary , Dog Diseases/diagnostic imaging , Dogs , Female , Male , Reproducibility of Results , Taurine/deficiency , Taurine/metabolism
3.
J Vet Cardiol ; 5(2): 7-19, 2003 Nov.
Article En | MEDLINE | ID: mdl-19081360

Dilated cardiomyopathy (DCM) is a major cause of morbidity and mortality in various dog breeds. The diagnosis of overt DCM is not normally problematic, although the importance of active exclusion of other causes of the dilated, hypokinetic heart is emphasised. Recent interest in human familial DCM has prompted a number of researchers to investigate the genetic basis of canine DCM. Prospective screening of dogs from lines with familial prevalence of DCM may identify dogs with pre-clinical ("occult") DCM. Dogs with other echocardiographic abnormalities or arrhythmias may also be identified. It is clear that dogs, like humans, have a prolonged pre-symptomatic phase of the disease extending over years. The ESVC DCM taskforce was established to provide the veterinary cardiology community with guidelines for the diagnosis of DCM, predominantly based on 2D and M-mode echocardiography. Diagnosis of DCM requires all of the following: (i) Left ventricular dilatation (ii) Reduced systolic function (iii) Increased sphericity of the left ventricle. We propose a scoring system for the identification of dogs in the pre-clinical stages. These include a number of major criteria and minor criteria. Future prospective longitudinal studies are required to test these in different breed populations to assess their predictive power and further refinements may be required. The importance of post mortem confirmation of disease is emphasised, and the two major histopathological features associated with DCM, the attenuated wavy fibre and the fibro-fatty infiltration-degenerative forms, require further investigation to identify the different aetiopathogenetic factors which may be involved.

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