A 10-year-old 26-kg (57-lb) spayed female Boxer was referred to the Veterinary Teaching Hospital of the University of Pisa because of 2 episodes of syncope and progressive lethargy. When the dog was 1 year old, a systolic murmur was detected but was not further investigated by echocardiography. At the initial physical examination, the dog was cachectic (body condition score, 2/9) and had a dull mental status. It was unable to maintain a standing position. Rectal temperature was 39.6°C (103.28°F), mucous membranes were pale pink, and capillary refill time was 2 seconds. Respiratory rate was 36 breaths/min with normal auscultatory findings. The dog's heart rhythm was regular with a heart rate of 40 beats/min. The jugular pulse was absent. The femoral pulse was synchronous with the heartbeats and strong bilaterally. Cardiac auscultation revealed a pansystolic heart murmur (grade 5/6) with maximal intensity over the left heart base.
Thoracic radiography revealed moderate cardiomegaly and a mild diffuse pulmonary pattern compatible with interstitial pulmonary edema. Echocardiography revealed a large aortic valve vegetative lesion compatible with aortic endocarditis, high-velocity turbulent systolic aortic flow, severe aortic valve insufficiency, and moderate to severe left atrial and left ventricular enlargement, with normal left ventricular systolic function. In addition, a circular hypoechoic area was evident in the basal portion of the interventricular septum, compatible with a myocardial area of inflammation or abscess.
Results of a CBC indicated that the dog had leukocytosis (24,000 WBCs/μL; reference range, 5,000 to 17,000 WBCs/μL), neutrophilia (20,000 neutrophils/μL; reference range, 3,700 to 12,000 neutrophils/μL), monocytosis (2,200 monocytes/μL; reference range, 200 to 1.700 monocytes/μL), and mild thrombocytopenia (119,000 platelets/μL; reference range, 148,000 to 484,000 platelets/μL). Serum cardiac troponin I concentration was very high (5.50 ng/mL; reference range, 0.0 to 0.11 ng/mL). Results of a serum biochemical profile were within reference intervals. Urinalysis revealed no abnormalities, and results of microbiologic culture of a urine sample were negative. Abdominal ultrasonographic findings were considered normal. The result of a PCR-based blood test for Bartonella spp was negative. Electrocardiography was performed (Figure 1).
Six-lead ECG recording obtained from a dog that was evaluated for episodes of syncope and progressive lethargy. The dog had echocardiographic evidence of aortic endocarditis. Notice that the P waves are regular, with an atrial rate of 150 beats/min, but they are not associated with QRS complexes. The ventricular rate is 50 beats/min and regular. The QRS complexes are wide (duration, 100 milliseconds; reference range, < 70 milliseconds) and have a negative polarity in the caudal lead tracings (II, III, and aVF). These findings are indicative of a complete (third-degree) atrioventricular block (AVB) with a monomorphic ventricular escape rhythm. Paper speed = 50mm/s; 5 mm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 248, 9; 10.2460/javma.248.9.1004
ECG Interpretation
The 6-lead ECG recording (Figure 1) revealed an underlying third-degree atrioventricular block (AVB) with a mean heart rate of 50 beats/min. Given the critical medical condition of the dog and the risk of lead infection, pacemaker implantation was initially declined by the owner. The dog was hospitalized for medical treatment, and administration of cefazolin (25 mg/kg [11.36 mg/lb], IV q 12 h), ceftriaxone (30 mg/kg [13.64 mg/lb], IV q 12 h), enrofloxacin (5 mg/kg [2.27 mg/lb], IV q 24 h), furosemide (1 mg/kg [0.45 mg/lb], IV q 12 h), and benazepril (0.25 mg/kg [0.11 mg/lb], PO q 12 h) was initiated.
The dog underwent continuous ECG monitoring with a defibrillator device. After 3 days of hospitalization, the dog was more alert and able to maintain a standing position; its mucous membranes were pink with a capillary refill time of < 2 seconds. Femoral pulses were synchronous with heart beats and were rhythmic and strong bilaterally. The heart rate was 80 beats/min. A 6-lead ECG tracing (Figure 2) obtained at this time revealed regression of the third-degree AVB. A sinus rhythm associated with a first-degree AVB and a postdivisional left bundle branch block was evident.
Six-lead ECG recording of the dog with third-degree AVB in Figure 1 obtained after 3 days of hospitalization and medical treatment. The atrial and ventricular rates are 85 beats/min. The P-Q interval is severely prolonged (duration, 280 milliseconds; reference range, 60 to 130 milliseconds) but regular. There is a prolongation of QRS-complex duration (110 milliseconds) with positive complex polarity in the caudal lead tracings (II, III, and aVF). The presence of Q waves in lead I and in the caudal lead tracings indicates normal early depolarization of the interventricular septum. All of these findings are consistent with a sinus rhythm conducted with a first-degree AVB and a postdivisional left bundle branch block. Paper speed = 50 mm/s; 5 mm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 248, 9; 10.2460/javma.248.9.1004
Echocardiography revealed a fistula that crossed the interventricular septum starting from the hypoechoic area previously observed. A 24-hour Holter monitoring confirmed the presence of sinus rhythm with first-degree AVB and left bundle branch block for the entire recording time.
Ten days after hospital admittance, the dog was in a good clinical condition with no leukocytosis, and the sinus rhythm with first-degree AVB and left bundle branch block was still present. Echocardiographically, the endocarditic lesion was still present but appeared stable. After 17 days, the dog died suddenly. The owner declined permission for necropsy.
Discussion
In dogs, AVB is a relatively common cardiac arrhythmia that results from conduction abnormalities along the atrioventricular node or the His-Purkinje system. Dogs with third-degree AVB may have no clinical signs or have exercise intolerance, weakness, syncope, and sudden death related to bradycardia, ventricular arrhythmias, or both.1,2
In dogs, third-degree AVB has been associated with a variety of pathological conditions (degenerative, inflammatory, infectious, neoplastic, parasitic, or traumatic) affecting the AV bundle and branching, with different pathogenesis. Infective endocarditis is a known cause of AVB in dogs.3–7
In accordance with modified Duke criteria,7 the dog of the present report had aortic valve endocarditis; the diagnosis was made on the basis of echocardiographic findings and fever, a major and a minor criterion for this condition, respectively. Another minor criterion for infective endocarditis is a predisposing heart condition because certain preexisting lesions increase the risk of development of bacterial endocarditis. Among dogs, subvalvular aortic stenosis is a well-documented predisposing factor for aortic endocarditis, especially in Boxers.5–9 The dog of the present report had a history of a systolic murmur, which had never been investigated echocardiographically. Subaortic lesions were not identified via echocardiography, but aortic valvular stenosis, although less frequent, could not be ruled out in this case.
The detection of vascular or embolic phenomena is also a minor criterion for the diagnosis of infective endocarditis. In dogs with aortic bacterial endocarditis, infection can extend into the myocardium causing myocarditis or can induce myocardial infarction and abscess formation as a result of coronary embolization.10,11 Consequently, decreased cardiac function, tachyarrhythmias, or AVBs can be complications of infective endocarditis. In the case described in the present report, the very high serum concentration of cardiac troponin I was strongly suggestive of myocardial involvement associated with the infectious process in the aortic valve. High serum troponin I concentration can be an indicator of active myocarditis in dogs with AVB.2,12
The hypoechoic area observed in the basal part of the interventricular septum in the dog of the present report was compatible with an aortic perivalvular abscess with subsequent fistulization. This condition is well-known in human medicine, with an incidence of 30% in cases of infective endocarditis, and its presence worsens the course of the disease. In addition, 10% of humans with infective endocarditis and perivalvular abscesses have a high-grade AVB, and 40% have fistulization associated with abscesses.13
In humans, acute myocarditis causing transitory myocardial interstitial edema is the most common cause of transient AVB.14 In veterinary medicine, results of a study15 indicated that 13% of dogs with high-grade AVB have complete or partial regression of the conduction disturbance within 1 month following pacemaker implantation. In another study,12 2 dogs with third-degree AVB and a high serum cardiac troponin I concentration reverted to sinus rhythm within 6 months following pacemaker implantation. In both studies, the authors suggested acute myocarditis was the cause of transient AVB.
In the case described in the present report, the regression of the third-degree AVB supported a diagnosis of acute myocarditis secondary to endocarditis. In human medicine, the resolution of conduction disturbances associated with infectious endocarditis and myocardial involvement is described as occurring both spontaneously16,17 and after surgery.13 To the authors' knowledge, this is the first report of spontaneous regression of third-degree AVB in a dog with aortic endocarditis.
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