Prevalence of heart disease in symptomatic cats: an overview from 1998 to 2005

Riesen, Sabine C.; Kovačević, Alan; Lombard, Christophe W.; Amberger, C.

doi:10.1024/0036-7281.149.2.65

Cited by 55 publications

(52 citation statements)

References 11 publications

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“…HCM is the most common cardiac disease in domestic cats (11,42). Among them, gene mutations encoding cardiac myosin-binding protein C (MYBP-C3), which is known as a major mutation site in human HCM, have been found to be associated with HCM in two cat breeds (Maine Coon and Ragdoll cats) (36,37).…”

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confidence: 99%

Impaired cardiac mitochondrial oxidative phosphorylation and enhanced mitochondrial oxidative stress in feline hypertrophic cardiomyopathy

Christiansen

Dela

Koch

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Yokota T. Impaired cardiac mitochondrial oxidative phosphorylation and enhanced mitochondrial oxidative stress in feline hypertrophic cardiomyopathy. Am J Physiol Heart Circ Physiol 308: H1237-H1247, 2015. First published March 13, 2015; doi:10.1152/ajpheart.00727.2014.-Mitochondrial dysfunction and oxidative stress are important players in the development of various cardiovascular diseases, but their roles in hypertrophic cardiomyopathy (HCM) remain unknown. We examined whether mitochondrial oxidative phosphorylation (OXPHOS) capacity was impaired with enhanced mitochondrial oxidative stress in HCM. Cardiac and skeletal muscles were obtained from 9 domestic cats with spontaneously occurring HCM with preserved left ventricular systolic function and from 15 age-matched control cats. Mitochondrial OXPHOS capacities with nonfatty acid and fatty acid substrates in permeabilized fibers and isolated mitochondria were assessed using high-resolution respirometry. ROS release originating from isolated mitochondria was assessed by spectrofluorometry. Thiobarbituric acid-reactive substances were also measured as a marker of oxidative damage. Mitochondrial ADP-stimulated state 3 respiration with complex I-linked nonfatty acid substrates and with fatty acid substrates, respectively, was significantly lower in the hearts of HCM cats compared with control cats. Mitochondrial ROS release during state 3 with complex I-linked substrates and thiobarbituric acid-reactive substances in the heart were significantly increased in cats with HCM. In contrast, there were no significant differences in mitochondrial OXPHOS capacity, mitochondrial ROS release, and oxidative damage in skeletal muscle between groups. Mitochondrial OXPHOS capacity with both nonfatty acid substrates and fatty acid substrates was impaired with increased mitochondrial ROS release in the feline HCM heart. These findings provide new insights into the pathophysiology of HCM and support the hypothesis that restoration of the redox state in the mitochondria is beneficial in the treatment of HCM. hypertrophic cardiomyopathy; mitochondria; oxidative stress

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confidence: 99%

Impaired cardiac mitochondrial oxidative phosphorylation and enhanced mitochondrial oxidative stress in feline hypertrophic cardiomyopathy

Christiansen

Dela

Koch

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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“…Ventricular septal defect was the most frequent anomaly (56.3%), followed by mitral valve dysplasia (14.6%) and TVD (10.4%). Although congenital heart disease in cats seems to be more frequent in males, and the incidence of mitral valve dysplasia is reported most frequently (RIESEN et al, 2007), here we report a case of TVD in a female domestic cat. Cardiovascular malformations are important causes of morbidity and mortality in dogs and cats less than one year old (OLIVEIRA et al, 2011).…”

Section: Discussionmentioning

confidence: 99%

“…A retrospective study in cats with heart disease over a period of eight years (RIESEN et al, 2007) determined a prevalence of 11.8% (48/408) of congenital heart defects. Ventricular septal defect was the most frequent anomaly (56.3%), followed by mitral valve dysplasia (14.6%) and TVD (10.4%).…”

Section: Discussionmentioning

confidence: 99%

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Tricuspid valve dysplasia in a domestic feline: case report

Mantovani¹,

Gimenes²,

Castro³

et al. 2017

SCA

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Tricuspid valve dysplasia (TVD) is a congenital heart defect described in dogs and cats; however, in Brazil there are no reports of this condition in cats. Therefore, our goal was to report a case of TVD in a domestic cat. A four-year-old, female, domestic short hair cat that was seen at the Cardiology Service of the Veterinary Teaching Hospital, University of São Paulo, for apathy, appetite loss and dyspnea for five days. During physical examination, dyspnea with a restrictive respiratory pattern due to pleural effusion was observed. Thoracocentesis was performed and 450 mL of serosanguineous fluid was drained. Two-dimensional echocardiography in the right parasternal short-axis plane at the level of the papillary muscles showed right ventricular dilatation and paradoxical septal motion. On the left parasternal apical four-chamber view, significant dilatation of the right chambers, loss of mobility of the septal leaflet of the tricuspid valve and a thickened mural leaflet chordae with anomalous insertion were observed. Based on clinical and echocardiographic aspects, a diagnosis of TVD was given. Treatment was initiated with enalapril 0.5 mg/kg, furosemide 0.5 mg/kg and pimobendan 0.3 mg/kg every 12 hours, all per os. The patient experienced remission of clinical manifestations and survived for 50 days after diagnosis. Key words: Congenital heart disease. Echocardiography. Cat. Valvopathies. ResumoDisplasia valvar tricúspide (DVT) é um defeito cardíaco congênito descrito em cães e gatos. Entretanto no Brasil ainda não há relato desta cardiopatia em felinos. Desta forma, objetivou-se relatar um caso de DVT em um felino doméstico. Uma gata de pelo curto, com quatro anos de idade foi atendida no Serviço de Cardiologia do Hospital Veterinário da Universidade de São Paulo, apresentando apatia, perda de apetite e dispneia há cinco dias. Durante o exame físico observou-se dispneia com padrão respiratório restritivo devido a presença de efusão pleural. Foram drenados 450 mL de líquido serosanguinolento por meio de toracocentese. O ecocardiograma no modo bidimensional, pela janela paraesternal direita, ao eixo curto transversal ao nível dos músculos papilares, revelou hipertrofia excêntrica do ventrículo direito e movimento septal paradoxal. Pela vista apical quatro câmaras, na janela paraesternal esquerda, observou-se importante remodelamento de câmaras cardíacas direitas. A valva tricúspide apresentou-se com perda de mobilidade de sua cúspide septal e espessamento de cordoalha tendínea da cúspide mural, com inserção anômala. Com base nos aspectos clínicos e ecocardiográficos, instituiu-se o dianóstico de DVT. Iniciou-se o tratamento com enalapril (0,5 mg/kg), furosemida (0,5 mg/kg) e pimobendan (0,3 mg/kg), pela via oral a cada 12 horas. O paciente apresentou remissão das manifestações clínicas, sobrevivendo por 50 dias após o diagnóstico.

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“…In questo caso, solo l'esame clinico ed ecocardiografico ripetuti possono aiutare a determinare in modo affidabile la diagnosi eziologica ed a differenziare la HCM da tutte le forme secondarie di ipertrofia ventricolare sinistra. Rarität und eine dilatative ist bei Katzen nur noch selten zu beobachten (Riesen et al 2007). …”

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