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CHAPTER 7   Myocardial Diseases of the Dog   149





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                          FIG 7.4
                          Paroxysmal ventricular tachycardia at a rate of almost 300 beats/min in a Boxer with
                          arrhythmogenic right ventricular cardiomyopathy. Note the typical upright (left bundle
                          branch block–like) appearance of the ventricular ectopic complexes in the caudal leads.
                          Lead II, 25 mm/sec.




            clear. However, Animal Registry of Certified Health guide-  Treatment
            lines (ARCH,  http://www.archcertify.org/) suggest the fol-  Antiarrhythmic treatment is indicated for Boxers with clini-
            lowing classifications: fewer than 50 single monomorphic   cal signs from tachyarrhythmias (i.e., syncope). Asymp-
            VPCs/24-hour period is interpreted as normal; between 50   tomatic dogs with Holter findings of greater than 1000 single
            and 300 single monomorphic VPCs/24-hour period is    VPCs/24 hour, ventricular tachycardia, or close coupling of
            equivocal (ARVC cannot be definitively diagnosed or   VPCs to the preceding QRS on Holter monitoring are usually
            excluded); and greater than 300 VPCs/24-hour period, or   given antiarrhythmic therapy as well. However, the best
            periods of couplets, triplets, or runs of ventricular tachycar-  regimen(s) and when to institute therapy are still not clear.
            dia (VT), is abnormal and consistent with a diagnosis of   Sotalol and mexiletine have each shown efficacy in reducing
            ARVC. Frequent VPCs or episodes of ventricular tachycar-  VPC frequency and complexity. Either of these drugs is gen-
            dia signal an increased risk for syncope and sudden death.   erally considered acceptable first-line therapy for dogs with
            The occurrence of ventricular arrhythmias appears to be   ARVC, and combination therapy is common. Other drugs
            widely distributed throughout the day, and there can be   that can be used or added in refractory cases include amio-
            enormous variability (up to 85%) in the number of VPCs   darone, procainamide, or other β-blockers such as atenolol
            between repeated Holter recordings in the same dog. Longi-  (see Chapter 4). The addition of an omega-3 fatty acid sup-
            tudinal studies of Boxer dogs show that the onset of ven-  plement might also reduce VPC frequency. Magnesium
            tricular arrhythmias in ARVC is relatively abrupt, with a   supplementation (usually in the form of magnesium oxide)
            sudden increase in VPC number from <50 VPCs/24 hour    is used occasionally.
            in the year preceding ARVC diagnosis to an average of    The goals of antiarrhythmic drug therapy are to decrease
            ~1200 VPCs/24 hour at time of diagnosis. The biomarkers   number and complexity of VPCs, reduce frequency of
            cardiac troponin I and NT-proBNP do not reliably discrimi-  syncope, and, ideally, reduce risk of sudden death. Holter
            nate between normal and affected dogs, except possibly in   monitoring is used to monitor efficacy of antiarrhythmic
            dogs with DCM phenotype.                             therapy; given biologic variability in daily VPC number in
              Annual Holter recordings are recommended beginning at   dogs with ARVC, a reduction in VPCs of at least 85% gener-
            age 2 to 3 years to screen for development and monitor pro-  ally is needed to conclude adequate antiarrhythmic effect.
            gression of ARVC in Boxer dogs. Once Holter criteria for   Unfortunately, sudden death remains possible even with
            ARVC are met, annual echocardiography is also recom-  apparently good control of arrhythmias.
            mended to screen for development of DCM phenotype.     Therapy for dogs with DCM phenotype is similar to that
            Genetic testing for the striatin mutation is highly recom-  described for dogs with idiopathic DCM. Pimobendan and
            mended for animals considered for breeding and may also   ACEI are typically prescribed once LV systolic dysfunction
            provide  prognostic  information about  an individual dog   is documented, although benefit of these drugs has not been
            (particularly the likelihood of developing the DCM pheno-  evaluated in this specific setting. Once CHF occurs, furose-
            type). Homozygous-positive dogs should not be bred, and   mide and spironolactone are added. Antiarrhythmics are
            heterozygous-positive dogs should be bred only to dogs   prescribed or continued as previously discussed; caution
            negative for the striatin mutation. Dogs meeting Holter diag-  should be used with sotalol in the setting of DCM phenotype
            nostic criteria for ARVC (greater than 300 VPCs/24 hour or   and acute CHF, because the mild β-blocking effects of this
            dogs with complex ventricular ectopy) also should not be   drug may exacerbate LV systolic dysfunction. Myocardial
            bred, regardless of genotype.                        carnitine deficiency has been documented in some Boxers
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