Affected boxer dogs may die suddenly and unexpectedly during vigorous exercise, leisurely walking, or while sleeping. Persistently high sympathetic tone was not found to be a consistent feature of boxer dogs with ARVC/D . Syncope is common and has been recorded in approximately half of severely affected dogs, including up to two-thirds of those that subsequently died suddenly, but there was no significant difference in the mode of death, sudden vs. nonsud-den, in dogs with this symptom. Although less common, congestive heart failure may occur when systolic dysfunction is present.
Commonly, the physical examination is unremarkable. Tachycardia may be detected and abnormal jugular venous pulse may accompany arrhythmias. In some dogs, auscultation may reveal an S3 gallop or soft, systolic, regurgitant heart murmur heard loudest over the tricuspid valve. Signs that may be asso ciated with heart failure include tachypnea, ascites, hepatosplenomegaly, jugular venous distension, and respiratory crackles.
Ventricular premature complexes (PVCs) with left bundle branch block morphology are commonly detected during 24-h Holter ECG recording  and may occur in up to three-quarters of affected boxer dogs. This arrhythmia is consistent with RV origin . Ventricular tachycardia with left bundle branch block occurs in almost half of ARVC/D dogs (Fig. 8.4). One of the authors (PF) considers such arrhythmias in the boxer breed as surrogate markers of ARVC/D, particularly in combination with familial history of this disease, or with other clinical signs such as syncope or heart failure. Other arrhythmias including PVCs of right bundle branch block morphology as well as supraventricular arrhythmias may also be observed, particularly if myocardial failure and severe atrial dilation are present. The role of the ECG in screening and assessing animal models of ARVC/D, however, has not been clarified. QT interval duration and dispersion have not been found to correlate with disease severity , although the use of signal-averaged ECG may identify some individual dogs at risk for sudden death .
Thoracic radiographs are often unremarkable. Some affected dogs may have right-sided heart enlargement. Animals with myocardial failure have generalized cardiac enlargement and pulmonary edema may be detected. With right-sided congestive heart failure, pericardial, pleural, or abdominal effusion is present.
Transthoracic echocardiographic examination is frequently unremarkable. RV dilation or thinning of apical RV myocardium is evident in some dogs, and animals with myocardial failure display reduced systolic function and cardiac chamber dilation.
ARVC/D hearts display high transmural signal intensity in the anterolateral and/or infundibular regions of RV. This is particularly evident in hearts with fatty replacement, and corresponds anatomically to those areas of RV fat identified with histopathology (Fig. 8.5) .
Heart failure can occur in dogs with ARVC/D, particularly when left ventricular dysfunction is present. Standard therapy includes diuretics, angiotensin-converting enzyme inhibitors, and digitalis. The calcium channel agent diltiazem is added to control ventricular heart rate when atrial fibrillation occurs.
There is substantial spontaneous variability in the frequency of ventricular arrhythmias in boxer dogs with ARVC/D, and changes of up to 80% in PVC frequency have been recorded by Holter monitor . Several antiarrhythmic drugs have been studied in boxer dogs with ARVC/D with regard to their effects on heart rate, the frequency of PVCs, the severity of arrhythmia, and the influence on syncope. Treatment with mexiletine combined with atenolol, or with so-talol alone, significantly reduced the frequency of PVCs, arrhythmia severity, and heart rate. In contrast, treatment with either atenolol or procainamide did not significantly affect these parameters. Neither of these treatment groups significantly affected the occurrence of syncope .
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