A 10-month-old 4.62-kg (10.16-lb) neutered male domestic longhair cat was evaluated because of acute lethargy and labored breathing. The cat had been previously healthy with no notable medical history.
Physical examination findings revealed the cat had a dull mentation, but it was responsive. Rectal temperature was 37.7°C (99.8°F). Cardiac auscultation revealed a heart rate > 300 beats/min with a regular rhythm and no murmur or gallop sound. The femoral pulse quality was weak. The cat was tachypneic with a respiratory rate of 60 breaths/min and mild respiratory effort. Lung auscultation revealed harsh lung sounds. Thoracic radiography was performed, and the images were reviewed by a board-certified veterinary radiologist; findings included mild cardiomegaly and mild diffuse bronchial pattern, but there was no evidence of congestive heart failure.
The cat underwent echocardiography, which revealed severe left ventricular concentric hypertrophy (in a 2-D long-axis view, the left ventricular posterior wall thickness in diastole was 0.8 cm [reference interval,1 0.31 to 0.41 cm] and interventricular septal wall thickness in diastole was 0.6 cm [reference interval,1 0.29 to 0.39 cm]) and marked left atrial and moderate left auricular dilation (left atrial-to-aortic root diameter ratio, 3.00; reference interval,1 1.13 to 1.68). The left ventricle appeared volume underloaded, and systolic function appeared adequate despite the severe tachyarrhythmia. The suspected diagnosis was juvenile-onset hypertrophic cardiomyopathy (HCM). Transient myocardial thickening was considered; however, there was no antecedent event identified, and severe cardiac remodeling and concomitant arrhythmias in association with that disease entity in cats have not previously been reported.2 Given the cat's young age, left ventricular hypertrophy secondary to hyperthyroidism, acromegaly, or systemic hypertension was considered unlikely. Electrocardiography was performed.
ECG Interpretation
The cat was placed in right lateral recumbency, and 6-lead ECG was performed (Figure 1) Mean heart rate was between 360 and 390 beats/min. P waves were not readily identifiable in any lead tracing. The QRS complexes were negative in leads II, III, and aVF. The QRS-complex duration was high-normal at 40 milliseconds (reference interval,3 < 40 milliseconds), and QRS-complex morphology alternated in a bigeminal pattern, with variable notching of the complexes (most notable in the lead II tracing) in an SrS' pattern consistent with aberrant conduction. The mean electrical axis varied in a bigeminal pattern, alternating between right and left axis shifts.
On the basis of the findings for the cat, a diagnosis of suspected supraventricular tachycardia (SVT) with variable partial bundle branch block was made. Electrical alternans was likely related to the SVT with phasic aberrant conduction (because no pericardial or pleural effusion was present). The possibility of ventricular tachycardia was considered less likely given the narrow QRS complexes and presence of electrical alternans (although a high ventricular focus could have potentially been responsible). A vagal maneuver failed to terminate the arrhythmia. Treatment with diltiazem hydrochloride was initiated with 2 IV bolus doses of 0.46 mg each (0.1 mg/kg [0.05 mg/lb]) administered 20 minutes apart, followed by a third bolus of 0.92 mg of diltiazem (0.2 mg/kg [0.09 mg/lb], IV) and then a brief continuous rate infusion of diltiazem at a rate of 13.8 μg/min (3 μg/kg/min [1.36 μg/lb/min], IV), but failed to reduce the heart rate. Given the cat's lack of response, 0.46 mg of esmolol (0.1 mg/kg, IV) was administered as a bolus 10 minutes later, and the rhythm immediately converted to sinus rhythm with a heart rate of 140 beats/min. The cat's demeanor improved, and it became bright and interactive. Diltiazem administration was discontinued, and the cat received atenolol (1.35 mg/kg [0.61 mg/lb], PO, q 12 h) and clopidogrel (4 mg/kg [1.8 mg/lb], PO, q 24 h). Electrocardiographic monitoring of the cat was continued throughout the period of hospitalization, and no further arrhythmias were detected.
Recheck 6-lead ECG was performed the following morning and revealed that the cat had a sinus rhythm with a heart rate of 140 beats/min (Figure 2) The duration of QRS complexes (20 milliseconds) was normal, and the mean electrical axis was normal. Electrical alternans had also resolved, as expected with resolution of the SVT.
Discussion
Supraventricular tachycardia describes any arrhythmia that originates anywhere other than in the ventricles, namely the sinus node, atrial myocardium, atrioventricular (AV) node, and junctional tissue, and includes arrhythmias that rely on accessory pathways for reenetry. Regular SVTs can be a result of abnormal automaticity or reentry and include atrial tachycardias, such as focal atrial tachycardia (FAT), atrial flutter, sinoatrial reentrant tachycardia, and intra-atrial reentry, as well as junctional tachycardias, such as AV nodal reentrant tachycardias and AV reentrant tachycardias (orthodromic AV reciprocating tachycardia and antidromic AV reciprocating tachycardia). In cats with HCM, arrhythmias are uncommon, occurring in approximately 6.5% of cases, and SVT is exceedingly uncommon, occurring in only approximately 3.3% of cases.4 The specific mechanism of SVT can be difficult to determine by use of surface 6-lead ECG, and a definitive diagnosis would be made on the basis of electrophysiologic study findings; however, certain features of a case, such as electrical alternans and response to treatment, can help elucidate possible mechanisms.
Atrial tachyarrhythmias are associated with atrial enlargement in dogs and cats.5 The development of atrial tachyarrhythmias in cats with HCM seems to be mechanistically related to ultrastructural changes of the atria and their transmembrane action potentials. Cats with severe left atrial enlargement (LAE) have a higher proportion of degenerating cells, compared with hypertrophied cells, as well as thickening of the basement membranes of all cells, which may affect ion flux. In addition, abnormal arrangement of myofibers and increased connective tissue between fibers may slow impulse conduction and promote reentry. Cats with HCM and moderate to severe LAE have atrial cells with reduced resting membrane potential and action potential amplitudes, compared with findings for cats with mild left atrial dilation. It has been shown that HCM-affected hearts contain cells that are not excited by an external electrical stimulus, and this is correlated with severity of LAE.5 Both of these changes may also cause slow conduction or a block in variable cardiac tissue regions, resulting in intra-atrial reentry.5
Electrical alternans has been detected in dogs and cats with SVTs and occurs in association with both FAT and orthodromic AV reciprocating tachycardia, but less commonly with FAT.6,7 The mechanism of electrical alternans in the context of SVT is unknown but likely involves an alternating aberrancy in conduction and resultant intermittent axis shift.8 Variable bundle branch block can occur with various tachyarrhythmias, including SVT with functional aberrancy, preexcited reentrant tachycardia involving an atriofascicular accessory pathway as the antegrade limb, SVT with a bystander atriofascicular pathway, and bundle branch reentrant ventricular tachycardia. For the cat of the present report, a functional bundle branch block secondary to the severely rapid heart rate was considered the most likely of these possibilities. In people, this most commonly occurs with orthodromic AV reciprocating tachycardia, but may occur with any SVT as a consequence of the Ashman phenomenon.9 The Ashman phenomenon is the occurrence of a supraventricular premature beat with bundle branch block morphology as a result of early impulse conduction through the His-Purkinje system while it is still in its refractory period from the preceding impulse. Right bundle branch block is typical with single supraventricular complexes because the right bundle branch has a longer refractory period, compared with the left bundle branch; however, at faster heart rates, the left bundle branch has a longer refractory period, thereby causing a rate-dependent left bundle branch block.10
In the case described in the present report, the cat's lack of response to diltiazem with subsequent conversion to sinus rhythm following administration of a β-adrenergic receptor blocker was of interest. With regard to atrial reentrant tachyarrhythmias, both nondihydropyridine calcium channel blockers and β-adrenergic receptor blockers may enhance the AV block and slow the ventricular response rate but typically do not convert the arrhythmia to sinus rhythm. Conversion of atrial reentry typically requires prolongation of the refractory period with class IA drugs such as procainamide or class III drugs such as sotalol or amiodarone. Lidocaine has been reported to successfully convert SVTs in dogs.11 Other options for chemical cardioversion of atrial tachyarrhythmias include class IC drugs, such as flecainide and propafenone. When antiarrhythmic medications have been ineffective, the treatment of choice for SVTs, including AV nodal reentrant tachycardia, atrial tachycardia, and tachycardias caused by an accessory pathway (eg, Wolff-Parkinson-White syndrome), in people is radiofrequency ablation.12 Pacemakers and implantable cardiac defibrillators may also be used to convert certain SVTs in humans. Atrial reentrant tachycardias (eg, atrial flutter) and FAT attributable to enhanced automaticity may be susceptible to conversion by atrial anti-tachycardia pacing with short bursts of rapid pacing or programmed stimulation to overdrive suppress the arrhythmogenic focus.13
For the cat of the present report, long-term treatment with atenolol, a β-1 adrenergic receptor-selective antagonist, was chosen on the basis of the cat's response to esmolol. Evidence for administration of esmolol in the treatment of arrhythmias in cats is lacking, and its use is largely extrapolated from human medicine because of its theoretical effectiveness based on its mechanism of action. Additional potential beneficial effects of treatment with atenolol for the cat of the present report, given the patient's severe HCM, included indirect positive lusitropic effects and a potential neuroendocrine modulating effect.14 Survival time for cats with clinical signs of HCM is approximately 15 months from the time of diagnosis.4 For cats with HCM and an arrhythmia at the time of diagnosis, the risk of death is approximately 3 times that for cats with HCM and no arrhythmia.15 Given the cat's severe LAE, risks of congestive heart failure and arterial thromboembolism were emphasized to the owner. A follow-up telephone call with the client 3 months after the initial evaluation of the cat revealed that it was doing well with no clinical signs at home.
References
1. Boon JA. Appendix 4. In: Boon JA, ed. Veterinary echocardiography. 2nd ed. Chichester, England: Wiley-Blackwell, 2011;1682.
2. Novo Matos J, Pereira N, Glaus T, et al. Transient myocardial thickening in cats associated with heart failure. J Vet Intern Med 2018;32:48–56.
3. Tilley LP, Smith FWK Jr. Electrocardiography. In: Tilley LP, Smith FWK Jr, Oyama MA, et al. Manual of canine and feline cardiology. 4th ed. St Louis: WB Saunders, 2008;270–274.
4. Ferasin L, Sturgess CP, Cannon MJ, et al. Feline idiopathic cardiomyopathy: a retrospective study of 106 cats (1994–2001). J Feline Med Surg 2003;5:151–159.
5. Boyden PA, Tilley LP, Albala A, et al. Mechanisms for atrial arrhythmias associated with cardiomyopathy: a study of feline hearts with primary myocardial disease. Circulation 1984;69:1036–1047.
6. Santilli RA, Perego M, Crosara S, et al. Utility of 12-lead electrocardiogram for differentiating paroxysmal supraventricular tachycardia in dogs. J Vet Intern Med 2008;22:915–923.
7. Ferasin L. Recurrent syncope associated with paroxysmal supraventricular tachycardia in a Devon Rex cat diagnosed by implantable loop recorder. J Feline Med Surg 2009;11:149–152.
8. Brembilla-Perrot B, Lucron H, Schwalm F, et al. Mechanism of QRS electrical alternans. Heart 1997;77:180–182.
9. Neiger JS, Trohman RG. Differential diagnosis of tachycardia with a typical left bundle branch block. World J Cardiol 2011;3:127–134.
10. Alraies MC, Eisa N, Alraiyes AH, et al. The long and short of it: Ashman's phenomenon. Am J Med 2013;126:962–963.
11. Johnson MS, Martin M, Smith P. Cardioversion of supraventricular tachycardia using lidocaine in five dogs. J Vet Intern Med 2006;20:272–276.
12. Hebbar AK, Hueston WJ. Management of common arrhythmias: part I. Supraventricular arrhythmias. Am Fam Physician 2002;65:2479–2486.
13. Epstein AE, DiMarco JP, Ellenbogen KA, et al. 2012 ACCF/AHA/HRF focused update incorporated into the ACCF/AHA/HRS 2008 guidelines for device-based therapy of cardiac rhythm abnormalities. J Am Coll Cardiol 2013;61:e6–e75.
14. Gordon SG, Cote E. Pharmacotherapy of feline cardiomyopathy: chronic management of heart failure. J Vet Cardiol 2015;17:S159–S172.
15. Payne JR, Borgeat K, Conolly DJ, et al. Prognostic indicators in cats with hypertrophic cardiomyopathy. J Vet Intern Med 2013;27:1427–1436.