A 13-year-old 5.5-kg (12.1-lb) spayed female Ocicat was evaluated by the cardiology service at the Lois Bates Acheson Veterinary Teaching Hospital at Oregon State University because of progressive lethargy and anorexia. Six days prior to the referral evaluation, thoracic radiography was performed by the referring veterinarian, which revealed that the cat had mild pleural effusion. At the veterinary teaching hospital, the cat was quiet, alert, and eupneic. Cardiac auscultation revealed a grade 3/6 left parasternal systolic murmur with a regular rhythm and a heart rate of 200 beats/min. Femoral arterial pulses were synchronous bilaterally and considered fair in quality. Echocardiography revealed evidence of hypertrophic obstructive cardiomyopathy without atrial enlargement and confirmed the presence of mild pleural effusion. Electrocardiographic limb lead monitoring during echocardiography confirmed a normal sinus rhythm. Thoracocentesis was performed, and a sample of the pleural fluid was submitted for cytologic examination and bacterial culture. Cytologic findings were consistent with a septic, suppurative exudate with a mixed bacterial population. Bacterial culture yielded heavy growth of anaerobes (Clostridium spp and Bacteroides spp [excluding Bacteroides fragilis]) and no aerobic bacterial growth. A diagnosis of pyothorax was made, and the cat was transferred to the surgery service for thoracic CT examination followed by exploratory thoracotomy.
The CT examination revealed bilateral moderate to severe pleural fluid and thick pleurae, mild pneumothorax attributable to thoracocentesis, and a multifocal interstitial to alveolar pulmonary pattern suspected to be due to atelectasis. Within the fluid, soft tissue strands were present, which were considered to be fibrin or focal abscesses. Exploratory thoracotomy did not reveal a nidus for infection, although there was gross evidence of pleuritis and pericarditis, and most of the lungs were atelectatic despite positive-pressure ventilation. Pericardiectomy was performed, and the thoracic cavity was lavaged and closed. Histologic examination of sections of the pericardium and diaphragm confirmed pleuritis, pericarditis, and pyothorax. The cat recovered initially without complications and was treated supportively with analgesic drugs, antimicrobials (including potentiated penicillin), and fluid therapy at a rate of 10 mL/h. However, 3 days after surgery, an increase in respiratory rate and effort was noted. Thoracic radiography revealed moderate pleural effusion and an unstructured interstitial pulmonary pattern. Thoracocentesis yielded pleural fluid of low cellularity and low total protein concentration (1.4 g/dL), consistent with a transudate. Recheck echocardiography was performed, and severe biatrial dilation and mild biventricular dilation were identified. Doppler echocardiographic evaluation revealed absence of A waves on the mitral valve inflow as well as absent A’ waves on tissue Doppler evaluation of the mitral valve annulus. Concurrent bradycardia was detected, and a 6-lead ECG examination was performed (Figure 1).
Initial 6-lead ECG tracings obtained from a 13-year-old cat with progressive lethargy and anorexia. These tracings were obtained at the time of diagnosis of congestive heart failure, bradycardia, and myocarditis. Notice the atrial standstill characterized by the absence of P waves and a supraventricular origin rhythm with a heart rate of 120 beats/min, consistent with a junctional escape rhythm. A ventricular escape beat (arrow) is preceded by a longer R-R interval (instantaneous heart rate, 107 beats/min). Mild ST-segment elevation is also present. Paper speed = 50 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 250, 11; 10.2460/javma.250.11.1242
ECG Interpretation
The initial ECG examination revealed a junctional escape rhythm with a heart rate of 120 beats/min and an absence of P waves (Figure 1). Infrequent ventricular escape beats preceded by a slightly longer R-R interval were also present. Mild ST-segment elevation was noted. The absence of P waves with a bradycardic junctional escape rhythm was consistent with atrial standstill. Other differential diagnoses included atrial fibrillation with atrioventricular node block, an escape rhythm with retrograde P waves hidden within the QRS complex, a sinoventricular rhythm, and concurrent disease of the sinus and atrioventricular nodes.1,2 Serum electrolyte concentrations at the time of the ECG examination were within reference intervals, with the exception of mild hyperchloridemia (120 mEq/L; reference interval, 104 to 116 mEq/L). Serum cardiac troponin I (cTnI) concentration was severely high (8.2 ng/mL; reference interval, < 0.2 ng/mL). The cat was treated for congestive heart failure with furosemide and oxygen therapy, and administration of antimicrobials was continued.
Two days later, the cat's clinical condition had improved and its heart rate had normalized. Another 6-lead ECG examination was performed (Figure 2). Evaluation of the ECG tracings revealed a normal sinus rhythm with persistent ST-segment elevation that was most notable in lead III (0.15 mV above baseline).
Six-lead ECG tracing obtained from the cat in Figure 1 after resumption of a normal heart rate 2 days after the initial evaluation. There is a normal sinus rhythm with P waves (arrowheads) preceding every QRS complex, and a heart rate of 176 beats/min. Persistent mild ST-segment elevation (0.15 mV above baseline) is most apparent in lead III (asterisks). Paper speed = 50 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 250, 11; 10.2460/javma.250.11.1242
The cat was discharged from the hospital shortly after restoration of normal sinus rhythm, and the owner was instructed to administer furosemide (0.9 mg/kg [0.41 mg/lb]), PO, every 12 hours; amoxicillin-clavulanic acid (13.6 mg/kg [6.18 mg/lb]), PO, every 8 hours; and maropitant citrate (1.1 mg/kg [0.5 mg/lb]), PO, every 24 hours.
A week after discharge from the hospital, the cat was progressively inappetent, and a diagnosis of chronic kidney disease exacerbated by dehydration was made. Recheck echocardiography revealed normalization of atrial size. The cat received fluid therapy and appetite stimulants, and administration of furosemide was discontinued. The cTnI concentration decreased to 0.8 ng/mL at 12 days after surgery and to 0.6 ng/mL at the 6-week postoperative recheck examination. Electrocardiography was performed 6 weeks after the initial evaluation as part of ongoing management of hypertrophic obstructive cardiomyopathy (Figure 3). Evaluation of the ECG tracing revealed a normal sinus rhythm with a heart rate of approximately 200 beats/min and a normal ST segment.
Lead II ECG tracing obtained from the cat in Figure 1 six weeks after initial diagnosis of myocarditis and transient atrial standstill. Normal sinus rhythm is present with a heart rate of 207 beats/min and a normal ST segment. Paper speed = 50 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 250, 11; 10.2460/javma.250.11.1242
Discussion
For the cat of the present report, atrial standstill was suspected on the basis of the lack of P waves on the surface ECG tracings with a bradycardic junctional escape rhythm. Doppler echocardiographic evaluation revealed no evidence of mechanical atrial activity. However, atrial standstill was not confirmed through an electrophysiologic study or atrial pressure tracing. Therefore, alternative diagnoses were considered for a junctional or high-ventricular escape rhythm with hidden P waves. A sinoventricular rhythm with conduction along internodal tracts but without generalized atrial depolarization was also considered.
Atrial standstill is caused by a lack of electrical and mechanical activity of the atrial myocardium, including the sinus node and internodal tracts. There is loss of sinus node pacemaker activity or disrupted conduction, with a resultant junctional or ventricular escape rhythm. No P waves or very low–amplitude P waves are evident on surface ECG tracings.3,4 Atrial standstill can either be persistent or transient. Transient atrial standstill can occur in animals with hyperkalemia, digitalis toxicosis, or hypothermia.4 Persistent atrial standstill in humans and other animals can be a consequence of atrial fibrosis, inflammation, amyloidosis, chronic cardiac disease, or genetic mutations including those associated with muscular dystrophy.1,4 Persistent atrial standstill has been identified in cats with dilated cardiomyopathy3,5 as well as in a cat with biatrial dilation and histopathologic evidence of connective tissue and fatty infiltration of the atrial mycoardium.1 The latter case did not have evidence of inflammation; on the basis of medical history, that cat was thought to have had a protracted course of atrial disease, which was unlike the cat of the present report.
In the cat of the present report, atrial standstill was postulated to be a consequence of myocarditis secondary to pyothorax, either via direct bacterial inoculation of the myocardium after pericardiectomy or from extension of local or systemic inflammation. Bacterial myocarditis in cats is extremely rare, although infection with Bartonellae henselae may result in myocarditis6,7 and there is a report of a cat with Streptococcus canis myocarditis.8 Myocardial inflammation may be present with vegetative endocarditis, which is also rare in cats.9 Feline toxoplasmosis may also result in myocarditis.10
In addition to the echocardiographic findings, results of ECG examinations and assessment of serum cTnI concentration supported the clinical diagnosis of myocarditis for the cat of the present report. Broadly, ST-segment elevation is a sign of myocardial ischemia and can be associated with acute myocarditis.11,12 The ST-segment elevation in this cat during the immediate postoperative period was coincident with generalized chamber dilation as well as a markedly high serum cTnI concentration, which are characteristic of myocarditis.13,14 Troponin is a myocardial protein, and the presence of circulating cTnI is a sensitive marker for cardiomyocyte injury or necrosis but is not specific for an underlying cause.14 At the time of the initial ECG examination, the serum cTnI concentration was 8.2 ng/mL, which decreased to 0.8 ng/mL within 2 weeks and to 0.6 ng/mL at 6 weeks after surgery. Six weeks after surgery, the previously noted ECG abnormalities had completely resolved, the cat was doing clinically well at home, and the echocardiographic findings were consistent with hypertrophic obstructive cardiomyopathy without atrial enlargement. The severe, transient elevation in serum cTnI concentration was consistent with an acute myocardial insult that resolved over time; mild increases in serum cTnI concentration can develop in cats with hypertrophic cardiomyopathy, and persistent mildly high cTnI concentration is supportive of resolution of myocardial inflammation.15,16 Myocarditis is a histopathologic diagnosis and therefore was not conclusively diagnosed in the cat of the present report. However, the parallel patterns of posttreatment improvement in the ECG and echocardiographic findings and serum cTnI concentration, as well as the presence of bacterial infection within the thoracic cavity, led to the presumptive diagnosis of myocarditis with transient atrial standstill in this cat.
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