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Natalia M. Llado-Calderon Department of Cardiology, Garden State Veterinary Specialists, Tinton Falls, NJ

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Andrew J. M. White Department of Cardiology, Garden State Veterinary Specialists, Tinton Falls, NJ

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Introduction

A 16-year-old 4.94-kg castrated male domestic shorthair cat was referred to Garden State Veterinary Specialists for further treatment of congestive heart failure, azotemia, collapse, and an arrhythmia. The referring emergency veterinarian had performed a single-lead ECG that raised concerns for atrioventricular (AV) block and concurrent ventricular tachycardia. The cat had a history of chronic kidney disease (creatinine, 3.0 mg/dL 2 weeks prior to presentation) that had been static over the preceding 3 months, well-managed hyperthyroidism, and heart disease characterized by normal left ventricular wall thickness (values not reported), moderate left atrial enlargement (left atrial diameter, 18.9 mm; reference range,1 < 15.7 mm), and mitral regurgitation with suspected congestive heart failure (scant pericardial and pleural effusion) diagnosed ultrasonographically 6 months prior to presentation. The cat was managed on pimobendan (1.25 mg, PO, q 12 h), enalapril (0.625 mg, PO, q 24 h), and furosemide (6.25 mg, PO, q 12 h initially, tapered to 3.125 mg, PO, q 48 h).

Immediately prior to referral, thoracic radiography had been performed, which revealed moderate generalized cardiomegaly (vertebral heart score, 9.5; reference range,2 < 8.0) with pulmonary venous distension and a mild diffuse interstitial pulmonary pattern predominantly in the cranial and caudoventral lung fields, consistent with congestive heart failure. A CBC and serum biochemical profile revealed moderate nonregenerative anemia (Hct, 24.4%; reference range, 30.3% to 52.3%), a mild stress leukogram, progressive azotemia (BUN, 66 mg/dL [reference range, 16 to 36 mg/dL]; creatinine, 4.4 mg/dL [reference range, 0.8 to 2.4 mg/dL]), and hyperphosphatemia (9.0 mg/dL; reference range, 3.1 to 7.5 mg/dL). The cat was receiving methimazole (5 mg, PO, q 12 h) for the hyperthyroidism, and serum total thyroxine concentration was within reference limits (1.4 μg/dL; reference range, 0.8 to 4.0 µg/dL).

On presentation, the cat was bradycardic (heart rate, 60 beats/min) with an irregular rhythm and paroxysms of tachycardia. A grade IV/VI parasternal systolic murmur was present, and femoral pulses were strong and symmetric with frequent pulse deficits. There was increased respiratory effort with mildly increased bronchovesicular lung sounds in all fields. Cardiac troponin I (cTnI) concentration was markedly high (12.75 ng/mL; reference range, 0.03 to 0.11 ng/mL), suggestive of recent or ongoing myocardial damage.

Echocardiography revealed moderate interventricular septal thickening (7.2 mm; reference range,3 < 6 mm), moderate to severe mitral and tricuspid regurgitation with moderate biatrial enlargement (left atrium, 18.6 mm; right atrium, 16.4 mm; reference range,1,4 < 13.7 mm), scant pericardial effusion, and a restrictive transmitral filling profile on pulsed-wave and tissue Doppler imaging. These findings were consistent with a diagnosis of hypertrophic cardiomyopathy with restrictive filling and congestive heart failure.

Six-lead ECG recordings were obtained at the time of presentation (Figures 1 and 2). The patient was treated conservatively with furosemide (1 mg/kg, IV, q 8 h). The following day (after administration of 2 doses of furosemide), the cat was eupneic with resolved pulmonary edema on thoracic radiographs but progressive azotemia (creatinine, 7.3 mg/dL).

Figure 1
Figure 1

Six-lead ECG recording obtained from a 16-year-old cat referred for further treatment of congestive heart failure, azotemia, collapse, and an arrhythmia. Notice the atrioventricular dissociation with an atrial rate of 211 beats/min (arrows) and ventricular escape complexes with a rate of 83 beats/min (asterisks), consistent with atrioventricular block. Toward the end of the recording, there is initiation of wide complex tachycardia (heart rate, 211 beats/min) with left bundle branch block morphology (cross). Paper speed, 50 mm/s; 10 mm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 260, 15; 10.2460/javma.21.01.0012

Figure 2
Figure 2

Continuation of the ECG recording showing cessation of the paroxysmal wide complex tachycardia and a return to the persistent atrioventricular block with ventricular escape. The P waves (arrowheads) occur at the end of the preceding T waves with a constant P-R interval during the period of tachycardia. This is consistent with periodic sinus capture with a 1:1 atrioventricular conduction and left bundle branch block pattern, rather than ventricular ectopy. Paper speed, 50 mm/s; 10 mm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 260, 15; 10.2460/javma.21.01.0012

ECG Interpretation

The initial ECG recordings demonstrated complete AV dissociation with an atrial rate of 211 beats/min with normal P-wave morphology (duration, 40 milliseconds [reference range, < 40 milliseconds]; amplitude, 0.15 mV [reference range, < 0.2 mV]) and electrical axis (49°; reference range, 0° to +90°), wide complex escape beats (QRS duration, 70 milliseconds [reference range, < 40 milliseconds]; QRS amplitude, 0.52 mV [reference range, < 0.9 mV]) with a ventricular rate of 83 beats/min, and periods of wide complex tachycardia (ventricular rate, 211 beats/min) with complete (truncal) left bundle branch block (LBBB) morphology (QRS duration, 70 milliseconds; QRS amplitude, 1.26 mV) and mean electrical axis of 100° (reference range,5 0° to 160°).

These findings were consistent with the initial presumptive diagnosis of complete (third-degree) AV block and ventricular tachycardia. However, examination revealed the faster rhythm conducted with LBBB morphology was associated with a consistent P-R interval (75 milliseconds; reference range, 40 to 90 milliseconds) with the P waves at the end of the preceding T waves, a regular R-R interval matching that of the underlying atrial rate (approx 211 beats/min), and unchanged P-wave morphology and electrical axis. These findings were more consistent with trifascicular block characterized by high-grade, second-degree AV block and ventricular escape beats alternating with periods of sinus capture conducted with a 1:1 AV ratio with complete LBBB at a rate of approximately 211 beats/min. No treatment was initiated for the arrhythmia, and periods of sinus capture increased, leading to predominant sinus tachycardia with occasional periods of second-degree AV block throughout hospitalization (Figure 3). However, the LBBB pattern persisted.

Figure 3
Figure 3

Six-lead ECG recording obtained during hospitalization and treatment. Notice the predominant 1:1-conducted sinus rhythm (heart rate, 190 beats/min) with infrequent periods of second-degree atrioventricular block. However, there remains evidence of bifascicular block, as there is persistence of the left bundle branch block pattern. Paper speed, 25 mm/s; 10 mm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 260, 15; 10.2460/javma.21.01.0012

Progressive azotemia developed during days 3 and 4 of hospitalization despite supportive care (creatinine, 8.2 mg/dL). The owners were advised of the poor prognosis and elected to take the cat home. Further testing was declined, and the patient was euthanized in the following weeks because of worsening clinical signs.

Discussion

Trifascicular block is diagnosed when there is evidence of conduction block of each of the 3 (right, left anterior, and left posterior) intraventricular fascicles. This can be observed as alternating complete LBBB and right bundle branch block or bifascicular block (LBBB or right bundle branch block with partial LBBB [left anterior or left posterior fascicular block]) with concurrent periods of second-degree AV block.5,6 This case demonstrated the latter, with evidence of complete LBBB during 1:1 conduction of sinus beats and periods of advanced second-degree AV block. This combination of abnormalities results from periodic disruption of impulse conduction in all 3 fascicles.

Trifascicular block appears to be an uncommon conduction abnormality in animals but has recently been reported in cats in association with suspected myocarditis, as determined by high cTnI concentration with or without transient myocardial thickening or other evidence of cardiac disease.6,7 In people, conduction disturbances associated with myocarditis have been attributed to myocardial interstitial edema that disrupts normal electrical conduction, resulting in various degrees of AV and intraventricular block in the acute stage. Improvement in interstitial edema is accompanied by resolution of the conduction blocks in most cases,8,9 but temporary transvenous pacing is often needed for hemodynamic support in the acute phase with permanent pacemaker implantation considered only if clinically important conduction block does not improve within 1 week.9 Pacemaker placement should be considered in cats if the bradyarrhythmia is causing substantial hemodynamic derangements but was not considered in this case. Additionally, conduction disturbances in cats with suspected myocarditis in previous reports6,7 were not causing clinical signs related to bradycardia and improved with supportive care.

The cat described in the present report had a markedly high cTnI concentration consistent with substantial recent or ongoing myocardial damage and myocarditis. Myocarditis in cats has been associated with FIV, feline coronavirus, Streptococcus canis, Toxoplasma gondii, and Bartonella henselae infection,1014 but no underlying cause other than previous nonspecific heart disease was identified in this case.

A high serum cTnI concentration is not specific for myocarditis, and other factors could have contributed to the high cTnI concentration in this cat. Both congestive heart failure and azotemia have been shown to increase cTnI concentrations,1416 and a previous report17 described cTnI as an accurate marker for hypertrophic cardiomyopathy and cardiac causes of respiratory distress in cats. However, there is considerable overlap in concentrations among asymptomatic cats with and without left atrial enlargement.15 Azotemia has been shown to increase cTnI concentration independent of cardiac disease, although there is no apparent correlation between severity of azotemia and cTnI concentration.16 The cTnI concentration in our case was high, compared with median values reported for cats with congestive heart failure (1.703 ng/mL; interquartile [25th to 75th percentile] range, 0.378 to 4.383 ng/mL) and azotemia (0.345 ng/mL; range, 0.06 to 3.39 ng/mL),15,16 suggesting there may have been some degree of myocarditis. A recent report18 describing transient myocardial thickening with congestive heart failure mimicking hypertrophic cardiomyopathy also reported high cTnI concentrations, compared with concentrations in cats with decompensated idiopathic hypertrophic cardiomyopathy (although a significant difference was not identified), suggesting that myocardial thickening was due to inflammatory infiltrates.

Given the previously reported normal ventricular wall thickness, markedly high cTnI concentration, and improved conduction through the His-Purkinje system during hospitalization in our case, some degree of myocarditis was considered the likely cause of the conduction disturbance. Persistence of the LBBB is worth noting in that it may have continued to improve if solely due to myocardial edema or inflammatory infiltrates or would have persisted if it was a consequence of permanent injury to the conduction system. Unfortunately, follow-up was not obtained to demonstrate further improvement in the heart rhythm. This case demonstrates an uncommon arrhythmia and the importance of scrutinizing wide complex tachycardia so as to not lead to misdiagnosis and mistreatment of ventricular tachycardia.

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