Clinical findings using echocardiography and plasma cardiac troponin I and pathological findings in dogs with hypertrophic cardiomyopathy: A retrospective study

Abstract

Background: Hypertrophic cardiomyopathy (HCM) is considered rare in dogs, and there is a lack of clinical data. Cardiac  troponin I (cTnI) is a biomarker of cardiomyocyte damage and necrosis and can be used to diagnose cat and  human HCM.

Aim: We investigated whether the presence of cTnI in clinical data can be used in conjunction with   echocardiography to diagnose canine HCM.

Methods: This study comprised client-owned dogs with clinical evidence of concentric hypertrophy on echocardiographic images, serum total thyroxine levels of ≤5 µg/dl, systolic blood pressure of ≤180 mmHg, and absence  of aortic stenosis. All cases were necropsied.

Results: Cardiomyocyte hypertrophy (mean diameter, 18.3 ± 1.8 µm),  myocardial fiber disarray (70%), interstitial fibrosis (80%), and small vessel disease (100%) were assessed. In dogs with  HCM, the left ventricles were concentric, almost symmetrical, and hypertrophied above the aortic diameter. The end- diastolic interventricular septum normalized to body weight [intraventricular septal thickness in diastole (IVSDN)] was  0.788 [interquartile range (IQR), 0.7–0.92], which exceeded the normal range (5%–95%, IQR: 0.33–0.52). In total, 70% of  the dogs with HCM had syncope and dyspnea, and all dogs had high cTnI levels (median, 3.94 ng/ml), exceeding the  upper limit of normal (0.11 ng/ml) and indicating cardiomyocyte damage. IVSDN and serum cTnI levels were correlated  (ρ = 0.839, p = 0.01).

Conclusion: Ventricular wall thickening and high serum cTnI levels can provide a presumptive  diagnosis of HCM and prompt the initiation of treatment or additional diagnostic investigations