RV function, dilatation and wall motion abnormalities were estimated visually by one investigator, blinded to the number of VPCs, and categorised as mild, moderate and severe. RVOT size was measured at end-diastole in the parasternal short axis, from the anterior RV wall to the aortic valve when echocardiographic loops of appropriate quality and the correct plane were available ( 15). Diastolic function was assessed by mitral inflow pattern using PW-Doppler ( 18). AS was defined by a AV max velocity ≥2.25 m/s ( 17). The presence of aortic stenosis (AS) was determined using standard Doppler assessment of AV flow. Ejection fraction was calculated using the Simpson’s method of disks ( 15).ĭCM was defined by LVIDd > 5.18 cm, LVIDs > 3.63 cm and FS < 23% which are the 95 th and 5 th percentiles in normal boxers, respectively ( 16). Left ventricular end-diastolic (LVIDd) and end systolic (LVIDs) diameter were measured in echocardiograms in the parasternal long-axis view using 2D images. 24h-ECGs were excluded if the printout quality was sub-optimal for analysis. R-on-T phenomenon was defined as a VPC superimposed on the T wave from other sinus beats as postulated ( 14). Couplets, triplets and VTs were defined as polymorphic if they displayed different morphologies within their single beats. The duration and rate of supraventricular and ventricular arrhythmias was recorded. The most commonly appearing morphology was used to describe the overall vector. Monomorphic VPCs had the same visual vector, polymorphic VPCs had > 1 vector. The morphology of VPCs, couplets, triplets and VTs were evaluated and defined as monomorphic or polymorphic.
24h-ECGs and echocardiograms were analysed retrospectively.Ģ4h-ECGs were analysed for the number of VPCs, couplets, triplets, and episodes of VT. The reason for referral, clinical signs, and medications were obtained from clinical records. Previously used diagnostic criteria are shown in the Supplemental Material, Table 1.Īll Boxer dogs admitted to the cardiology service of The Royal Veterinary College between 20 were included. However, there is no consensus on diagnostic criteria for ARVC in Boxer dogs resulting in a discrepancy of diagnostic criteria between different studies, which prevents direct comparison between them. Subsequent research focused on arrhythmogenic risk and the genetic causes of the disease (Supplemental Material, Table 1) and it was suggested that Boxer dogs might serve as a naturally occurring model for the human disease, based on the close clinical and pathological resemblances of the two conditions ( 12). ACM in humans can imitate dilated cardiomyopathy (DCM), however it usually presents with a severity of ventricular arrhythmia disproportionate to the extent of LV dilatation ( 10).Īrrhythmogenic right ventricular cardiomyopathy (ARVC), a disease similar to ACM in humans, was first described in Boxer dogs in 1983, which unlike cardiomyopathies in other dogs, lacked ventricular dilation and atrial fibrillation but was distinguished by extensive histological alterations including fibrofatty replacement of cardiomyocytes, ventricular premature complexes (VPCs) and frequent ventricular tachycardia (VT) ( 11) and can concern both RV and LV ( 12, 13).
However, a significant percentage of patients experiences little or no symptoms ( 9).
The criteria include structural changes identified by cardiac MRI, echocardiography or RV angiography, histopathology, as well as characteristic ECG-changes, documentation of arrhythmias, and family history ( 8).ĪCM can lead to recurrent sustained or non-sustained ventricular tachyarrhythmia and/or myocardial failure and possible death. The clinical diagnosis is based on criteria defined by the European Society of Cardiology Task Force in 1994( 7), revised in 2010( 8). Dilatation and regional wall motion abnormalities of the RV are frequently seen( 5) and may occur at any time during the disease ( 6). The fibrofatty replacement affects intercellular electrical conduction increasing the risk of life-threatening ventricular arrhythmias ( 4). Although these abnormalities predominantly occur in the RV they may also involve the left ventricle (LV) producing a dilated phenotype ( 3). Arrhythmogenic cardiomyopathy (ACM) is a genetically determined myocardial disorder defined histologically by progressive replacement of the right ventricular (RV) myocardium with adipose and fibrous tissue ( 1, 2).
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