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Hypertrophic cardiomyopathy in a dog: a systematic diagnostic approach
Journal of Veterinary Cardiology ( IF 1.2 ) Pub Date : 2023-10-16 , DOI: 10.1016/j.jvc.2023.10.002
J Novo Matos 1 , J Silva 1 , S Regada 1 , S Rizzo 2 , M Serena Beato 3 , C Basso 2
Affiliation  

A seven-year-old female neutered Parson Russel terrier was referred for syncopal episodes. An electrocardiogram revealed paroxysmal atrial flutter followed by periods of sinus arrest, suggesting sick sinus syndrome. Echocardiography showed severe biventricular wall thickening (hypertrophic cardiomyopathy (HCM) phenotype) with no signs of fixed or dynamic left ventricular outflow tract obstruction. Blood pressure, abdominal ultrasound, serum total thyroxin and thyroid-stimulating hormone, and insulin-like growth factor-1 were all within normal limits. Cardiac troponin I was elevated (1.7 ng/mL, ref<0.07). Serological tests for common infectious diseases were negative. A 24-h Holter confirmed that the syncopal episodes were associated with asystolic pauses (sinus arrest after runs of atrial flutter) ranging between 8.5 and 9.6 s. Right ventricular endomyocardial biopsies (EMB) were performed at the time of pacemaker implantation to assess for storage or infiltrative diseases that mimic HCM in people. Histological analysis of the EMB revealed plurifocal inflammatory infiltrates with macrophages and lymphocytes (CD3+ > 7/mm) associated with myocyte necrosis, but no evidence of myocyte vacuolisation or infiltrative myocardial disorders. These findings were compatible with myocardial ischaemic injury or acute lymphocytic myocarditis. Molecular analysis of canine cardiotropic viruses were negative. The dog developed refractory congestive heart failure and was euthanised 16 months later. Cardiac post-mortem examination revealed cardiomyocyte hypertrophy and disarray with diffuse interstitial and patchy replacement fibrosis, and small vessel disease, confirming HCM. We described a systemic diagnostic approach to an HCM phenotype in a dog, where a diagnosis of HCM was reached by excluding HCM phenocopies.

中文翻译:

狗的肥厚性心肌病:系统的诊断方法

一只七岁的雌性绝育帕森拉塞尔梗犬因晕厥发作而被转诊。心电图显示阵发性心房扑动,随后出现一段时间的窦性停搏,提示病态窦房结综合征。超声心动图显示严重的双心室壁增厚(肥厚性心肌病(HCM)表型),没有固定或动态左心室流出道梗阻的迹象。血压、腹部超声、血清总甲状腺素、促甲状腺激素以及胰岛素样生长因子-1均在正常范围内。心肌肌钙蛋白 I 升高(1.7 ng/mL,参考值<0.07)。常见传染病血清学检测呈阴性。 24 小时动态心电图证实晕厥发作与 8.5 至 9.6 秒之间的心搏暂停(心房扑动后窦性停搏)有关。在起搏器植入时进行右心室心内膜心肌活检 (EMB),以评估是否存在类似于人类 HCM 的储存性疾病或浸润性疾病。 EMB 的组织学分析显示,巨噬细胞和淋巴细胞 (CD3+ > 7/mm) 的多灶性炎症浸润与肌细胞坏死相关,但没有证据表明肌细胞空泡化或浸润性心肌病。这些发现与心肌缺血性损伤或急性淋巴细胞性心肌炎相一致。犬类心肌病毒的分子分析结果为阴性。这只狗出现了顽固性充血性心力衰竭,16 个月后被安乐死。心脏尸检显示心肌细胞肥大和紊乱,伴有弥漫性间质和斑片状替代纤维化,以及小血管疾病,证实了 HCM。我们描述了一种针对狗 HCM 表型的系统诊断方法,通过排除 HCM 表型来诊断 HCM。
更新日期:2023-10-16
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