Introduction

A 4-year-old neutered male domestic shorthair cat was presented to the University of Minnesota. Veterinary Medical Center emergency room because of an acute onset of inappropriate behavior, tachypnea, and ataxia. On physical examination, the patient was lethargic, hypothermic (36.6 °C), tachypneic (60 breaths/min), and tachycardic (300 beats/min); no murmur was auscultated. Initial bloodwork showed respiratory acidosis (pH, 7.207; base excess, –9 mEq/L; Pco₂, 48.3 mm Hg) and slightly high BUN (35 mg/dL; reference interval, 8 to 35 mg/dL) and creatinine (1.7 mg/dL; reference interval, 0.8 to 1.5 mg/dL) concentrations. Results of a focused assessment with sonography for trauma were negative for free fluid in the pericardial, pleural, and peritoneal cavities. Thoracic radiography demonstrated substantial left atrial enlargement and a soft tissue opacity in the right caudal lung field considered to most likely be atelectasis or early cardiogenic pulmonary edema. Echocardiography revealed diffuse myocardial thickening (diastolic left ventricular free wall thickness, 7.4 mm; reference interval,¹ 3.48 to 5.33 mm) and spontaneous echogenic contrast within the enlarged left atrium (left atrial-to-aortic diameter ratio, 2.1; reference interval for a 4-kg cat,² < 1.43). Serum troponin I concentration was also high (2.69 ng/mL; reference interval, < 0.03 ng/mL). Differential diagnoses that were considered included primary hypertrophic cardiomyopathy and transient myocardial thickening. Left ventricular hypertrophy secondary to hyperthyroidism, hypertension, or acromegaly was considered unlikely given the patient’s age. A 6-lead ECG was obtained with the cat in right lateral recumbency (Figure 1).

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Six-lead ECG obtained from a 4-year-old neutered male domestic shorthair cat examined because of an acute onset of inappropriate behavior, tachypnea, and ataxia. The ECG shows tachycardia (360 beats/min) with regular R-R intervals and QRS complexes that are normal in duration (40 milliseconds; reference interval,³ < 40 milliseconds). The tachycardia was determined to be supraventricular in origin. No P waves were identified in this ECG recording. Paper speed = 50 mm/s; 10 mm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 260, 13; 10.2460/javma.20.07.0399

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ECG Interpretation

The ECG revealed a narrow QRS complex tachycardia that was considered to be supraventricular in origin, with a rate of 360 beats/min and regular R-R intervals. The QRS complexes were normal in duration (40 milliseconds; reference interval,³ < 40 milliseconds) and amplitude (0.3 mV; reference interval, < 1.0 mV). The mean electrical axis in the frontal plane was +20° (reference interval,³ 0 to +90°). P waves were difficult to appreciate owing to the severe tachycardia; however, given the normal QRS morphology, paroxysmal supraventricular tachycardia (SVT) was suspected. Vagal maneuvers, including digital compression of the carotid sinuses and ocular pressure, were attempted but failed to terminate or alter the rhythm. The patient was subsequently given a bolus of esmolol (0.25 mg/kg, IV) followed by a second bolus (0.12 mg/kg, IV), which successfully converted the SVT to sinus rhythm with a heart rate of 140 beats/min (Figure 2). During sinus rhythm, delta waves were observed in addition to short PQ intervals (40 milliseconds; reference interval,³ 50 to 90 milliseconds) despite treatment with a β-adrenoceptor blocker, which would have been expected to prolong the PQ interval by slowing conduction through the atrioventricular node.⁴ The final diagnosis was ventricular preexcitation associated with an accessory pathway between the atria and ventricles and orthodromic atrioventricular reentrant tachycardia (OAVRT), also known as Wolff-Parkinson-White syndrome. The patient was maintained on a constant rate infusion of esmolol (50 μg/kg/min, IV) for 3 hours, affording time for oral atenolol (6.25 mg) absorption. The patient’s clinical status markedly improved following conversion to a sinus rhythm. The patient stayed in sinus rhythm for the remainder of the hospitalization period and was discharged later that day with a prescription for atenolol (6.25 mg, PO, q 12 h).

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Six-lead ECG recording obtained after 2 boluses of esmolol were administered. The transition from supraventricular tachycardia (approx 300 beats/min) to sinus rhythm (approx 136 beats/min; arrow) is accompanied by the introduction of delta waves in the upstroke of the QRS complex (arrowheads) and a short PQ interval. This is indicative of ventricular preexcitation and anterograde conduction through an accessory pathway. Paper speed = 50 mm/s; 10 mm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 260, 13; 10.2460/javma.20.07.0399

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Discussion

SVT represents a large category of tachyarrhythmias that originate above the bundle of His and may involve the sinus node, atrial myocardium, or atrioventricular nodal tissue.⁵ Current guidelines in human medicine divide SVTs into 6 classes: sinus tachycardia, atrial tachycardia (focal or multifocal), atrioventricular nodal reentrant tachycardia, atrioventricular reentrant tachycardia (AVRT), junctional tachycardia, and atrial flutter.⁵ AVRT is a reentrant-type arrhythmia that is characterized by an accessory pathway that allows conduction between the atria and ventricles outside of the atrioventricular node.⁵ The reentrant circuit created by this accessory pathway allows for retrograde conduction from the ventricular myocardium into the atrial myocardium and subsequent anterograde conduction through the atrioventricular node, restimulating the ventricles (OAVRT). Alternatively, anterograde flow through the accessory pathway from the atria into the ventricles results in ventricular preexcitation, as the wave of depolarization is able to bypass the atrioventricular node and enter the ventricles earlier than expected and usually outside the normal conduction system. This is manifested by an abnormally short PQ interval and distortion of the initial portion of the QRS complex, referred to as a delta wave (Figure 2).⁶ The morphology of the delta wave is dependent on the insertion site of the accessory pathway in the ventricles and the conduction velocity through the accessory pathway relative to that through the atrioventricular node. Delta waves may be positive or negative, of variable duration, or nonexistent.^7,8 The hallmark of Wolff-Parkinson-White syndrome is an SVT with evidence of preexcitation during sinus rhythm,^5,6 as seen in the cat described in the present report. In humans, accessory pathway formation is known to occur during early development, when bridging myocardial tissue fails to regress past 20 weeks of gestation, leaving a conductive pathway between the atrium and ventricle outside of the atrioventricular node and His bundle.⁹ To the authors’ knowledge, there is no veterinary literature regarding the developmental nature of accessory pathways in dogs or cats.

OAVRT was diagnosed in this case on the basis of the upright and narrow QRS morphology during paroxysmal tachycardia, prior to conversion to a sinus rhythm. The most common findings in dogs with OAVRT are retrograde P′ waves in the ST segment and a shortened R-P′ interval (80 to 85 milliseconds) with longer P′R intervals.^8,10 P′ waves represent the wave of depolarization reentering and propagating across the atria as a result of retrograde conduction from the ventricles through the accessory pathway. Although there were no visible P or P′ waves in conjunction with the tachycardia in our patient, they were suspected to be buried in the ST segment. The shortened PQ interval and slurred positive upstroke of the QRS complex were consistent with ventricular preexcitation secondary to an accessory pathway.¹¹

Treatment for SVT relies on interrupting the reentrant circuit through the accessory pathway and atrioventricular node by inducing a functional block in 1 or both limbs of the reentrant circuit.¹¹ This can be achieved with class Ia drugs (eg, quinidine or procainamide), which increase the retrograde refractory period of the accessory pathway, and class IV drugs (eg, diltiazem), which increase the refractory period of the atrioventricular node.^4,11 Class III drugs (eg, sotalol) are also known to be effective in treating SVTs by prolonging the refractory period in nodal tissue and subsequent conduction through the atrioventricular node.¹² Lidocaine has recently been found to be successful in converting 84% of dogs with OAVRT despite its typical poor response in atrial tachyarrhythmias.¹³

There are only a handful of reports of cats with SVTs.^14–19 Correspondingly, OAVRT is apparently a rare phenomenon in cats, with only 1 other case reported to the authors’ knowledge.¹⁶ In that case, the abnormal rhythm spontaneously converted to sinus rhythm. Not surprisingly, therefore, optimal antiarrhythmic treatment for cats with OARVT is not reported. Treatment with a β-adrenoceptor blocker was used in this case on the basis of the authors’ experience with favorable responses in other cats with SVTs. Class II β-adrenoceptor blockers (eg, esmolol and atenolol) can be beneficial by reducing atrioventricular nodal conduction and were successful in this case for both conversion to sinus rhythm and maintenance of sinus rhythm long-term. For dogs with accessory pathway–mediated SVTs, electrophysiologic mapping with radiofrequency catheter ablation of the accessory pathway is well documented to provide improved outcomes with the possibility of no long-term antiarrhythmic therapy.^8,20 This interventional treatment is often limited to very few locations and, to the authors’ knowledge, has not been performed in a cat to date. This may in part be due to the small size of the heart and difficulty of vascular access in cats.

At a 3-week recheck examination, the diffuse myocardial thickening seen on initial presentation of the cat was markedly reduced (diastolic left ventricular free wall thickness, 4.0 mm) and atrial size was improved (left atrial-to-aortic diameter ratio, 1.2). The improvement in myocardial thickening, patient’s young age, and initially high cardiac troponin I concentration were consistent with either transient myocardial thickening or tachycardia-induced pseudohypertrophy. Transient myocardial thickening is thought to be caused by an antecedent stressful event,²¹ which in this case could have been the OAVRT. Pseudohypertrophy of the ventricular walls, along with high troponin I concentrations, has also been documented with severe tachycardia.²² A recheck ECG showed that patient remained in sinus rhythm with ventricular preexcitation. Accordingly, oral treatment with atenolol was continued.