Supraventricular trigeminy in a dog with myxomatous mitral valve disease/Trigeminismo supraventricular em um cao com doenca mixomatosa da valva mitral.
A 15-year-old intact male mongrel dog weighing 13kg and with a history of heart murmur, cough, dyspnea, and ascites was referred for cardiac evaluation. Although, the dog was being treated with 5mg of enalapril twice daily for a year, he had never been subjected to ancillary tests for cardiac evaluation. On physical examination, cardiac auscultation revealed a grade V/VI systolic murmur at the mitral area and a grade IV/VI systolic murmur at the tricuspid area. His heart rate was 130 beats per minute and consisted of an irregular rhythm, hypokinetic and asynchronous femoral pulse. Mucous membrane color and capillary refill time (1 second) were normal, besides abdominal distention characteristic of ascites.
For Doppler echocardiographic examination (Sonosite Micromaxx, sector transducer frequencies of l-5MHz), M-mode, two-dimensional, and spectral Doppler were used. The patient was not sedated and gently restrained in left and right lateral recumbency to obtain images of the right parasternal, left caudal (apical) parasternal, and left cranial parasternal locations. The examination revealed: a thickened and prolapsed mitral valve with severe regurgitation; a thickened tricuspid valve with severe regurgitation and a pressure gradient of 41.9mmHg, which is characteristic of mild pulmonary hypertension; severe left atrial enlargement (LA/Ao ratio of 2.4); right atrial enlargement; eccentric hypertrophy of the left ventricle; and preserved systolic function. These findings were consistent with a diagnosis of myxomatous mitral and tricuspid valves disease with a severe hemodynamic compromise.
For electrocardiographic evaluation (ECG-PC TEB), the dog was not sedated and gently restrained in right lateral recumbency. The ECG tracing was obtained from leads I, II, III, aVR, aVL, and aVF. Examination revealed a sinus arrhythmia with isolated supraventricular premature complexes, supraventricular couplets, and periods of supraventricular trigeminy lasting up to fifteen seconds (Figure 1).
Treatment consisted of ascites drainage, digoxin (0.004mg [kg.sup.-1] twice daily), furosemide (1.5mg [kg.sup.-1] twice daily), spironolactone (1.9mg [kg.sup.-1] once daily), pimobendan (0.15mg [kg.sup.-1] twice daily), and sildenafil (1.0mg [kg.sup.-1] twice daily). Furthermore, it was recommended to repeat the electrocardiogram after 30 days of treatment and to collect blood samples for a complete blood count and biochemical profile. However, the patient did not return and died after 60 days owing to pulmonary edema.
Myxomatous mitral valve disease is the most common cardiac disease in dogs and prevalence is greatest in small geriatric populations. In most cases, the tricuspid valve is affected, such as in the present case. Cardiac arrhythmias may complicate prognosis of mitral endocardiosis. Most often arrhythmias have a supraventricular origin reflecting atrial stretch (TILLEY, 1992; CROSARAet al., 2010). Some echocardiographic parameters (e.g., LA/Ao ratio) provide valuable prognostic information for dogs with MMVD (BORGARELLI et al., 2008; SARGENT et al., 2015). Furthermore, echocardiographic abnormalities may be associated with a risk of developing arrhythmias. The LA/Ao ratio is a measure that evaluates atrial stretch. Dogs with MMVD that showed a LA/Ao>1.7 had more supraventricular rhythm disturbances, suggesting that this parameter is associated with a risk of developing arrhythmias of supraventricular origin (CROSARA et al., 2010). Electrophysiological mechanisms by which atrial stretch leads to supraventricular arrhythmias are not fully understood, but studies suggest that volume and pressure overload in the heart can activate stretch-activated ion channels inducing atrial premature beats (NAZIR & LAB, 1996; KAMKIN et al., 1999). Another risk factor for the arrhythmogenic substrate in the dog of the present report is the presence of pulmonary hypertension which can modulate autonomic activity and delay cardiac repolarization (HONG-LIANG et al., 2009; RAJDEV et al., 2012).
Besides atrial enlargement secondary to valvular insufficiency, supraventricular premature complexes can be associated with conditions such as atrial neoplasia, congenital cardiac defects, drug toxicities (e.g., general anesthesia, diuretics and digitalis), and electrolyte imbalances (TILLEY, 1992). In the present report, the patient's clinical history and echocardiogram refute all of these potential causes except electrolyte imbalance, since he did not undergo a blood draw to evaluate his biochemical profile.
Supraventricular trigeminy has not been reported by retrospective (APTEKMANN et al., 2010) and prospective (VARSHNEY et al., 2013; KUMAR et al., 2014) studies that evaluated cardiac arrhythmias in dogs. In studies evaluating cardiac arrhythmias in dogs with MMVD using conventional and Holter (24 hours) ECG, despite the higher incidence of arrhythmias of supraventricular origin supraventricular trigeminy is not reported. One of the studies revealed that a significant percentage (69%) of dogs demonstrated isolated supraventricular premature complexes; however, the Holter monitoring did not indicate trigeminy (CROSARA et al., 2010; RASMUSSEN et al., 2012; OLIVEIRA et al., 2014). Some studies reported the occurrence of trigeminy; however, it was of ventricular origin (CROSARA et al., 2010). In veterinary medicine, there is one report of supraventricular trigeminy in a foal (RISBERG et al., 2005).
Detecting and treating cardiac arrhythmias is an important therapeutic goal in cardiology. Digoxin is an inotropic positive and antiarrhythmic agent that acts by inhibiting sarcolemmal Na K+ATPase, resulting in increased intracellular sodium. Additionally, the drug slows conduction through the atrioventricular node. Digoxin is administered to patients with congestive heart failure and supraventricular arrhythmias (ATKINS & HAGGSTROM, 2012). The lack of a 24-hour Holter ECG and a second electrocardiogram to evaluate the effectiveness of digoxin antiarrhythmic therapy for supraventricular trigeminy are limitations of the present report.
The present report indicated that supraventricular trigeminy may occur in dogs with MMVD with severe hemodynamic compromise, and is probably related to atrial enlargement. Also, this case reinforces the importance of performing ECG in dogs with MMVD, since it complements the echocardiogram and enables a better therapeutic approach.
BIOETHICS AND BIOSSECURITY COMMITTEE APPROVAL
The authors of the article titled " Supraventricular trigeminy in a dog with myxomatous mitral valve disease" declare that for all due purposes, the project that gave rise to the present data lias not been submitted to the Ethics Committee of the University / Research Institute "Centra Universitario Ritter dos Reis" for evaluation but they are aware of the content of the Brazilian resolutions of the Conselho Nacional de Controle de Experimentacao Animal (CONCEA) <http://www.mct.gov.br/index. php/content/view/310553.html> if it involves animals.
Thus, the authors assume full responsibility for the presented data and are available for possible questions should they be required by competent authorities.
Returned by the author 07.22.17 CR-2016-0338.R3
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Frederico Aecio Carvalho Soares (1)
(1) Faculdade de Veterinaria, Centro Universitario Ritter dos Reis--UniRitter, Avenida Manoel Elias, 2001, 91240-261, Porto Alegre, RS, Brasil.
E-mail: fredaecioMgmail.com. * Corresponding author.
Caption: Figure 1--ECG tracing (leads I, II, III, aVR, aVL e aVF) of a 15-year -old male mongrel dog demonstrating a period of supraventricular trigeminy characterized by a condition in which every third beat is a supraventricular premature beat (arrows).
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|Title Annotation:||clinica y cirugia; texto en ingles|
|Author:||Soares, Frederico Aecio Carvalho|
|Date:||Sep 1, 2017|
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