A 12-year-old, spayed female, mixed breed dog was referred due to arrhythmia, which was observed on preoperative examination for dental treatment. Auscultation revealed a left apical Grade II/VI systolic murmur, bradycardia, and rhythm irregularity. The patient was diagnosed with complete atrioventricular block (CAVB) by electrocardiography. Administration of cilostazol was initiated per ownerʼs request, but CAVB was not controlled. CABV is caused by blockage of excitatory conduction within the atrioventricular conduction system and may result in bradyarrhythmia and sudden death, therefore pacemaker implantation (PMI) was performed. One day after PMI, the heart rate was stable at 88 bpm, however, two days after PMI, the patientʼs condition deteriorated rapidly and cardiopulmonary arrest occurred. Post-mortem histopathologic examination revealed moderate to severe, acute myocarditis in the ventricular septum, including the area where the pacemaker was implanted in the right ventricular apex, and inflammation was widespread in the septal myocardium. Previous reports of histopathologic evaluation for etiology and outcome of CAVB and PMI are limited. Here we describe clinicopathologic findings of CAVB associated with severe ventricular septal fibrosis and developed acute myocarditis at the site of PMI in a dog.
A 12-year-old spayed Chihuahua with a medical history of myxomatous mitral valve disease (MMVD) was brought to our hospital for sudden collapse. Clinical examinations revealed pulmonary edema, pericardial effusion, right atrial collapse and decreased atrioventricular lumen volume. In addition, mitral regurgitation flow was decreased compared to the patientʼs previous echocardiographic records. Based on these findings, the patient was tentatively diagnosed with cardiac tamponade due to left atrial rupture, and medical treatment was initiated. To avoid the risk of provoking hemorrhage from the rupture site, pericardiocentesis was not conducted. Clinical symptoms resolved within a few hours after the initial treatment, and improvement of cardiac tamponade was achieved. However, the patient collapsed again on the next day, and investigations showed recurrence of cardiac tamponade and probable hypoxic hepatitis. To prevent persistent recurrence of cardiac tamponade caused by left atrial rupture associated with MMVD, the patient underwent surgical repair of the mitral valve. Intraoperative findings revealed blood coagulation at the left atrial rupture site. The surrounding tissue was vulnerable and further repair procedure against the rupture site was not required. The patient showed good prognosis and no recurrent atrial rupture or progress of cardiac failure from MMVD have been reported eighteen months after the surgery. Early choice of mitral valve repair may be a curative and permanent treatment for recurrent cardiac tamponade from left atrial rupture due to MMVD.