A 12-year-old 22.3-kg (49.1-lb) spayed female Australian Shepherd was presented for a cardiac recheck evaluation. Approximately 1 month earlier, a diagnosis of left-sided congestive heart failure (CHF) secondary to presumptive myxomatous mitral valve disease had been made for the dog on the basis of radiographic evidence of left-sided cardiomegaly and left-sided congestive heart failure and auscultation of a loud, grade 4/6 left apical systolic heart murmur. The dog was treated with furosemide (2 mg/kg [0.9 mg/lb], PO, q 12 h), pimobendan (0.25 mg/kg [0.11 mg/lb], PO, q 12 h), and benazepril (0.5 mg/kg [0.23 mg/lb], PO, q 24 h). The dog initially had responded well to treatment; however, during the 2-day period prior to the recheck evaluation, the dog had showed signs of relapse of CHF.
At the recheck evaluation, a brief thoracic ultrasonographic examination was performed, which revealed no evidence of pleural or pericardial effusion. On physical examination, the dog's heart rate was approximately 180 beats/min with a rapid irregular rhythm. Femoral pulses were present with variable pulse quality and no pulsus paradoxus or jugular venous distention noted. Single-lead ECG was performed.
ECG Interpretation
The lead II ECG (Figure 1) tracing revealed a rapid irregular arrhythmia characterized by the absence of P waves and a rapid ventricular response rate suggestive of atrial fibrillation (AF). A regularly alternating amplitude of the QRS complexes was suggestive of electrical alternans (EA).
Lead II ECG recording obtained during a recheck evaluation of a 12-year-old Australian Shepherd with left-sided congestive heart failure secondary to presumptive myxomatous mitral valve disease. Notice the lack of defined P waves and irregular rhythm indicative of atrial fibrillation. The ventricular rate is 250 complexes/min. The alternating amplitude of the QRS complexes is characteristic of electrical alternans. Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 257, 7; 10.2460/javma.257.7.707
Discussion
Atrial fibrillation is the most common supraventricular tachyarrhythmia in dogs and is often described as an irregularly irregular rhythm.1 There are 3 primary theories postulated for the underlying causative mechanism of AF. These theories include rapid firing of an ectopic focus that propagates irregularly owing to varying capacity of the atria to respond, a single reentry circuit that propagates to the atrial tissue irregularly owing to varying responsiveness of the atria, and multiple coexisting atrial reentry circuits.2 In dogs with experimentally induced CHF, the CHF leads to the development of myocardial fibrosis that separates atrial muscle bundles and results in localized slowing of conduction, which stabilizes reentry and can promote development of AF.1,3 This process is known as structural remodeling.3 Atrial dilation is another common finding in animals with concurrent CHF and AF, and in affected dogs that are in a tachycardic state, atrial size can increase dramatically.4 Increased atrial size predisposes to the development of AF because atrial stretch is associated with increased dispersion of refractoriness and altered electrical propagation.5,6 Experimentally induced mitral valve disease also supports the initiation of AF as the disease worsens atrial dilation, interstitial fibrosis, and inflammation.7 Once AF begins, it leads to changes in the electrophysiologic function of the atria, including a decrease in the L-type Ca2+ current and an increase in the rectifier background K+ current, that favors maintenance of AF.8,9 The former current is responsible for the slowed depolarization found within the pacemaker cells, which helps propagate an action potential, whereas the latter current helps maintain a negative potential prior to the onset of depolarization.10 When the ionic homeostasis is altered, the normal atrial refractory period is shortened, thereby promoting the development of AF.1,8,9
The dog of the present report also had ECG evidence of EA. Electrical alternans is characterized by beat-to-beat changes of at least 0.1 mV in the amplitude of the P waves, QRS complexes, or T waves.11,12 Electrical alternans is classified as repolarization alternans (changes in the ST segments or T waves), conduction alternans (changes in the P waves, PQ intervals, and QRS complexes), and alternans attributable to cardiac movements.12 Electrical alternans as a result of cardiac movements appears to be the most common clinical cause of EA in dogs with pericardial effusion.13,14 For the dog of the present report, the brief thoracic ultrasonographic examination failed to identify any evidence of pericardial effusion. As such, it seems likely that the dog had conduction alternans, which has been reported in patients with supraventricular tachycardia.15,16 Electrical alternans was initially postulated to be indicative of orthodromic reciprocating tachycardia involving an accessory atrioventricular connection as the retrograde limb of the tachycardia circuit.15 However, a later study16 revealed that EA is also frequently present in humans with atrial tachycardia and atrioventricular node reentrant tachycardia. It appears that the mechanism of EA during SVT is rate dependent and attributable to oscillation of action potential duration and refractoriness within the His-Purkinje system.16,17 In addition, changes in heart volume (Brody effect),18,19 ischemia,20,21 or a change in contractility22 or electrical axis23 may also contribute to the development of EA. The authors suspect it was likely a combination of the electrophysiologic alterations and changes in heart volume and contractility as a result of AF that contributed to the development of EA in the dog of the present report.
Results of previous studies23,24 have indicated a high prevalence of AF in medium- to large-breed dogs with myxomatous mitral valve degeneration and concurrent CHF, and the case described in the present report involved an Australian Shepherd that had CHF secondary to presumptive myxomatous mitral valve disease and AF. In dogs with myxomatous mitral valve degeneration, concurrent CHF, and AF, the mean survival time is significantly shorter than that for dogs with myxomatous mitral valve degeneration and CHF without AF.23,24
There are 2 strategies used to treat AF, namely rate control, in which ventricular response rate is slowed, and rhythm control, in which AF is terminated.25 Because recurrence of AF after cardioversion is relatively common, rate control of AF is typically pursued in veterinary species.26,27 In addition, rates of complication and death in humans with AF receiving rate control versus rhythm control are similar.25 The current treatment recommendation for dogs with AF is to maintain heart rate < 125 beats/min, if possible.24 This is most likely to be achieved by treatment with a combination of diltiazem and digoxin.28 The dog of the present report was prescribed single-agent treatment with diltiazem (1 mg/kg [0.45 mg/lb], PO, q 8 h), which has been shown to decrease heart rate and improve cardiac function in dogs with experimentally induced AF.29 Monotherapy was instituted initially to evaluate whether the dog would develop adverse effects from the single-agent anti-arrhythmic treatment; a combination treatment of diltiazem and digoxin was initiated 1 week later because the heart rate remained high. Eventually, rate control was achieved with a combination of diltiazem (3 mg/kg [1.36 mg/lb], PO, q 8 h) and digoxin (0.003 mg/kg [0.001 mg/lb], PO, q 12 h). The dog was doing well 5 months after the time of initial diagnosis of CHF.
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