ECG Interpretation

The first 12-lead surface ECG tracing (Figure 1) revealed a regular rhythm with a mean heart rate of 120 beats/min. The P waves had a normal axis (63°; reference range,³ −18° to 90°) and amplitude (0.25 mV; upper reference limit,⁴ < 0.4 mV), but their duration was slightly prolonged (0.05 seconds; upper reference limit,⁴ < 0.04 seconds). Short and mildly variable PR intervals (0.04 to 0.06 seconds; reference range,⁴ 0.06 to 0.13 seconds) were followed by wide QRS complexes (0.1 seconds; upper reference limit,⁴ < 0.06 seconds) with a notch at the onset of each R wave (R-wave amplitude, 2 mV; upper reference limit,⁴ < 2.5 mV) that in positive leads had a slurred upslope. Moreover, QRS complexes were predominantly positive in caudoventral and precordial leads, but negative in leads I, aVL, and aVR (mean electrical axis, 100°; reference range,⁴ 40° to 110°). Precordial concordance was present, such that the polarity of the QRS complexes was the same (positive) for all the precordial leads. At this point, the 2 differential diagnoses were accelerated idioventricular rhythm (AIVR) with left bundle branch block (LBBB) morphology coupled to isorhythmic atrioventricular dissociation (IAVD), with synchronization type 2⁵ or sinus rhythm associated with ventricular preexcitation (VP).⁶

In the second ECG tracing (a direct continuation of the first ECG strip; Figure 2), a premature ventricular complex (VPC) with right bundle branch block morphology (negative in the caudoventral leads and positive in leads I, V4, V5, and V6) abruptly interrupted the aforementioned rhythm. Subsequently, a postextrasystolic pause occurred, followed by restoration of normal sinus rhythm. However, no notable change in heart rate was detected between the first and second tracings. Accurate examination of the last 6 beats revealed normalization of PQ intervals (duration, 0.1 seconds); moreover, remarkable changes in the QRS-complex shape (lack of notched morphology), duration (0.06 seconds), amplitude (1 mV), and mean electrical axis (90°) were evident.

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A second 12-lead ECG tracing representing the direct continuation of the ECG strip in Figure 1. Notice the abrupt end of the ectopic rhythm owing to the occurrence of a ventricular premature complex (VPC) with right bundle branch block morphology (asterisk). This VPC is followed by a postextrasystolic pause. Restoration of sinus rhythm subsequently occurs (arrow) with normalization of the PQ intervals as well as remarkable changes in QRS-complex duration, shape, amplitude, and mean electrical axis. Paper speed = 50 mm/s; 1 cm = 2 mV.

Citation: Journal of the American Veterinary Medical Association 247, 5; 10.2460/javma.247.5.484

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Discussion

Arrhythmogenic right ventricular cardiomyopathy is an inherited cardiac disease characterized by abnormalities of right ventricular structure and function that result from myocyte loss with fatty or fibrofatty replacement.⁷ In people, pathogenic mutation of desmosomal proteins has been detected in up to 50% of affected individuals.⁷ In dogs with ARVC, similar gene mutations have not been identified but lower expressions of cardiac ryanodine receptors, myocardial calstabin-2, and connexion 43 junction protein as well as mutation of striatin have been demonstrated.⁸ As a consequence, myocyte depolarization and repolarization abnormalities may occur, thereby promoting either ventricular or, less commonly, supraventricular arrhythmias.^7–9 In humans, ARVC most frequently affects the right ventricle, but it can also involve the left side of the heart. When the right ventricle is affected, the cardiomyopathy can either be diffuse or segmental, involving the subtricuspid valve region, right ventricular apex, or outflow tract.⁷ Interestingly, the segmental form of ARVC affecting the right ventricular outflow tract in an English Bulldog has been described.¹⁰ Moreover, characteristic clinical features of ARVC have been reported for several dogs of the same breed, suggesting a possible breed predisposition for the disease, as observed in Boxers.⁸

In the dog of the present report, several ECG features were identified as follows: a regular rhythm with mean ventricular rate of 120 beats/min, mildly variable and short PR intervals, and wide QRS complexes with notched R waves and normal mean electrical axis. Explanations for these findings include AIVR with LBBB morphology coupled to IAVD with synchronization type 2⁵ and sinus rhythm associated with VP.⁶ Control of the atria and ventricles by independent pacemakers defines atrioventricular (AV) dissociation.^11–13 The term isorhythmic is additionally used when rates of the independent pacemakers approximate each other over relatively long periods, despite different influences acting on each.^11–13 Because the sinus node has the fastest inherent automaticity (compared with other cardiac tissues that have inherent automaticity) under normal conditions, a subsidiary pacemaker (either junctional or ventricular) becomes apparent only when the sinus rate slows, the junctional or ventricular rate accelerates, or the AV conduction is disturbed or when these events occur simultaneously in some combination. This phenomenon is called synchronization, and it develops when separate and distinct cellular elements that have no anatomic continuity and possess inherently different rhythms are placed in contact with each other; subsequently, they can begin to discharge impulses simultaneously at a common rate.¹⁴ The term synchronization is used when the hook-up between cardiac elements is relatively long; when the phenomenon lasts for only a few beats, the term accrochage has been proposed.¹⁴

In humans and dogs, IAVD has been previously reported in cases of third-degree AV block, junctional tachycardia, and AIVR.^5,11–13 During IAVD, P waves may oscillate gradually back and forth across the QRS complexes, thereby resulting in rhythmic PQ-interval fluctuations (ie, synchronization type 1), or, conversely, may be coupled to correspondent QRS complexes at constant or almost constant PQ intervals with P waves always preceding R waves (ie, synchronization type 2).⁵ Different theories have been proposed to explain synchronization type 1, including cyclic fluctuations of arterial blood pressure and mechanical stretching of the sinus node.^5,13 The mechanism of synchronization type 2 has not been conclusively established.^5,13

The presence of highly similar atrial and ventricular rates with P waves preceding QRS complexes at fixed or mildly variable and short PQ intervals can lead to erroneous diagnosis of VP, suggestive of the presence of an accessory pathway (AP) with an antegrade conduction property.^6,15 Ventricular pre-excitation is an ECG phenomenon in which a supraventricular impulse travels over an AP and activates a portion or the entire ventricular muscle earlier than would be expected if the impulse travelled via the normal AV conduction system.⁶ Because the physiological AV conduction delay is bypassed, the ventricle is prematurely activated, resulting in a shortened PR interval.⁶ Moreover, the QRS complexes are often widened and characterized by a slurring at the onset of R waves (known as a delta wave), which is a result of summation of 2 fronts of ventricular excitation (the earliest activation front, which initiates the delta waves, travels over the AP; the other travels throughout the AV node in a normal manner).⁶ Correct identification of VP may be often difficult because of the wide range of VP patterns, including intermittent VP and preexcitation alternans that may be easily mistaken for frequent VPCs and ventricular bigeminy, respectively.⁶ Similarly, if VP persists for several beats, the rhythm can be misdiagnosed as an AIVR.⁶ On the other hand, late-coupled VPCs can sometimes mimic VP, especially when intraventricular conduction disturbances occur and result in notched R waves (thereby creating pseudo-delta waves).⁶

Definitive distinction of ectopic rhythms with IAVD from VP may be extremely challenging without electrophysiologic examination^6,15; nevertheless, a scrupulous analysis of surface ECG tracings (taking into account all findings recorded either during arrhythmia and sinus rhythm) has a key role in diagnosis. In the case described in the present report, AIVR with LBBB morphology was strongly hypothesized to be the underlying rhythm disorder for several reasons. First, ventricular arrhythmias with LBBB morphology (suggesting a right ventricular origin) represent the ECG hallmark of ARVC, being identified in > 80% of dogs with definitive histologic diagnosis.⁸ Second, the presence of precordial concordance strongly suggested the ventricular origin of the QRS complexes. However, a few exceptions may exist, for example when tachycardia involves a left posterior AP for the AV conduction.¹⁶ Third, simultaneous existence of ARVC and AP-mediated rhythm disturbances represents an exceptionally rare condition in people¹⁷ and, to the authors’ knowledge, has not been described for veterinary patients. Fourth, variations in PQ-interval durations are usual in cases of IAVD,^5,6 whereas the classic ECG pattern of VP has fixed PQ intervals.⁶ Lastly, remarkable modifications in QRS complexes were identified after restoration of sinus rhythm in the dog of this report. Such changes represent a typical finding of ventricular arrhythmias alternating with sinus beats. This ECG pattern would be unlikely in cases of intermittent VP during which QRS complex morphology and duration are expected to change (because of the delta wave's intermittent occurrence and disappearance), but QRS complex amplitude and mean electrical axis are less commonly affected.⁶

In the present report, an intriguing case of ARVC with somewhat confusing ECG characteristics in an English Bulldog has been described. This case highlights the fact that an ECG pattern of short PQ intervals followed by widened QRS complexes with notched R waves may not always indicate VP.^5,6 In such circumstances, less common differential diagnoses, including AIVR with IAVD, should be also considered.