A 10-year-old 37-kg (81.4-lb) spayed female pit bull-type mixed-breed dog was presented to the emergency service for evaluation of multiple syncopal events. The dog had a previous medical history of recurrent urinary tract infections. Salient physical findings were obesity (body condition score, 9/9), heart rate of 120 beats/min with a regular rhythm, and a grade 2 right apical systolic murmur. The dog's systolic arterial blood pressure was measured 3 times by use of a Doppler technique, and the mean value was 140 mm Hg.
Thoracic radiography revealed mild generalized cardiomegaly with no evidence of pulmonary vascular congestion or cardiogenic pulmonary edema. Results of a CBC were unremarkable apart from mild neutrophilia. Whole blood biochemical analysis revealed mildly high alanine aminotransferase and aspartate aminotransferase activities and moderately high alkaline phosphatase and γ-glutamyltransferase activities. Results of urinalysis were unremarkable. Resting plasma cortisol concentration was mildly high (5.9 μg/dL; reference interval, 1.0 to 5.0 μg/dL).
ECG Interpretation
After initial diagnostic testing had been completed, the dog underwent a 6-lead ECG examination (Figure 1). This recording revealed an underlying sinus arrhythmia with a heart rate of approximately 120 beats/min. The QRS complexes were narrow, and the QRS complex duration (0.06 seconds) was within reference limits. There were deep S waves present in the lead I, II (−1.2 mV), III, and aVF traces. There was a right-axis deviation1 in the frontal plane with a mean electrical axis of −120 degrees. There was fragmentation (or splintering) of the QRS complexes evident in the lead I, II, III, aVR, and aVF traces. The QRS complexes in the lead II trace had the morphology of qrSR'S complexes; the QRS complexes in the lead III and aVF traces had a similar appearance. In the lead I, II, III, and aVF traces, there was concave ST-segment elevation. The ECG diagnosis was sinus arrhythmia with fragmented, narrow QRS complexes and a right-axis deviation.
Electrocardiographic tracings (6 leads) obtained during evaluation of a dog with a history of syncope and a right-sided heart murmur. Notice the narrow QRS complexes with a splintered appearance in leads I, II, III, aVR, and aVF. Echocardiography was subsequently performed, and a 5.8-cm-diameter mass located in the right ventricular outflow tract with corresponding echocardiographic evidence of severe right ventricular hypertrophy was detected. Paper speed = 50 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 256, 11; 10.2460/javma.256.11.1215
On the basis of the ECG findings, echocardiography was performed. There was severe right ventricular dilation with concurrent concentric hypertrophy, severe right atrial enlargement, and mild tricuspid valve regurgitation. The left atrium and left ventricle appeared structurally and functionally normal. There was a large (approx 5.8-cm-diameter) mass located in the right ventricular outflow tract (RVOT) that was homogeneous in echogenicity with a stalk observed in the infundibular RVOT. There was severe turbulence in the RVOT because of near total luminal obstruction, with an RVOT velocity (3.75 m/s) that was considered moderately high.
Differential diagnoses for a mass in this anatomic location included ectopic thyroid tissue (struma cordis), myxoma or myxosarcoma, and hemangiosarcoma. Recommendations for further workup of the dog included CT, transesophageal echocardiography, and nuclear scintigraphy to identify ectopic thyroid tissue. Treatment options included surgical resection (with inflow occlusion or cardiac bypass), radiation therapy, chemotherapy (ie, oral administration of toceranib phosphate), and radioactive iodine treatment. The dog was discharged from the hospital, and the owner was instructed to administer trazodone and to avoid exposure of the dog to situations in which it might become excited, thereby causing exacerbation of clinical signs. The dog was lost to follow-up.
Discussion
Fragmented QRS complexes, commonly referred to as splintered QRS complexes in veterinary medicine, are used in human medicine as indicators of myocardial scarring and prognostic indicators for other cardiac diseases.2–6 The most commonly used definition of a fragmented QRS complex is a QRS complex with an additional R wave (R’ wave) that notches at the nadir of the S or R wave or the presence of > 1 R’ wave in 2 contiguous leads on a 12-lead ECG recording.7 Originally, this definition only included narrow QRS complexes but has been expanded to include complexes of bundle branch block morphology and paced QRS complexes.7 Recently, a new classification of fragmented QRS complexes has been proposed that is designed to be more specific in the determination of pathological versus nonpathological fragmented QRS complexes.8
In human medicine, the disease processes for which fragmented QRS complexes are used as markers or prognostic indicators include coronary artery disease, sarcoidosis, dilated cardiomyopathy, arrhythmogenic right ventricular hypertrophy, Brugada syndrome, and congenital diseases.2–6,9,10 Myocardial single-photon emission tomography has been used to detect regional perfusion abnormalities, most often secondary to myocardial scarring from previous myocardial infarction. For humans with known or suspected coronary artery disease, increased perfusion and functional abnormalities are detected with single-photon emission tomography when fragmented QRS complexes are present on ECG tracings.11 The presence of fragmented QRS complexes has high sensitivity for the diagnosis of coronary artery disease in humans, although the presence of fragmented QRS complexes has been associated with other conditions and may be evident on ECG recordings obtained from healthy humans.2,4,7
The presence of fragmented QRS complexes has also been associated with the development of arrhythmias in humans with dilated cardiomyopathy.3,12 Fragmented QRS complexes represent disruptions in conduction from inhomogeneous activation in the ventricular myocardium.13,14 These areas of altered conduction may serve as an arrhythmogenic substrate, leading to malignant ventricular arrhythmia. In humans with nonischemic dilated cardiomyopathy, the presence of fragmented QRS complexes is associated with dyssynchronous conduction, and it is thought that such patients may benefit from resynchronization therapy.13,14 However, in approximately 5% of healthy adult humans, fragmented QRS complexes may be detected on ECG examination, indicating that this finding is not highly specific for cardiac disease in general.15
In veterinary species, the most common disease associated with splintered QRS complexes is tricuspid valve dysplasia. In 1 study,16 21 of 39 dogs and 4 of 6 cats with right atrioventricular valve malformation had evidence of splintered QRS complexes. In humans, fragmented QRS complexes are associated with Ebstein anomaly. Ebstein anomaly is a condition in which the septal and posterior leaflets of the tricuspid valve adhere abnormally to the underlying right ventricular myocardium and the inlet portion of the right ventricle becomes integrated with the right atrium, thereby creating a so-called atrialized right ventricle.10 Histologic evaluation of an atrialized right ventricle has revealed a decrease in the number of cardiomyocytes and the presence of myocardial fibrosis.9 It is speculated that progressive right ventricular enlargement and myocardial fibrosis lead to intraventricular conduction disturbances and QRS complex fragmentation in these patients.9 In an electrophysiologic study17 of humans with Ebstein anomaly, late depolarization during the fragmented R’ wave is evident, which suggests that there may be a second QRS complex that is produced by the atrialized right ventricular tissue. Humans with Ebstein anomaly who have detectable fragmented QRS complexes have greater severity of disease and a higher risk of development of tachyarrhythmias, compared with findings for persons affected with Ebstein anomaly who do not have ECG evidence of fragmented QRS complexes.9,10,16
For the dog of the present report, the splintered QRS complexes identified during 6-lead ECG prompted echocardiographic investigation of underlying causes of conduction disturbance. It is possible that there was major myocardial ischemia and scarring secondary to the severe right ventricular hypertrophy, which led to development of splintered QRS complexes. Alternatively, the mass identified may have invaded the myocardium, thereby causing disruption of normal ventricular conduction that led to the development of splintered QRS complexes. The dog's syncopal events may have been associated with dynamic obstruction of the RVOT that resulted in sudden decreases in cardiac output. However, consideration must be given to transient ventricular tachyarrhythmias as the cause, given their association with fragmented QRS complexes.
References
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