A 2-year-old castrated male Blue Heeler was referred to the Texas A&M University Veterinary Medical Teaching Hospital for evaluation of suspected second-degree atrioventricular (AV) block after a cardiac arrhythmia was auscultated during an annual examination by the referring veterinarian. The dog was reported to have no clinical signs of cardiac disease.
On physical examination, the dog was bright, alert, and responsive. Thoracic auscultation revealed frequent premature beats, which occurred in a bigeminal pattern. No cardiac murmurs were auscultated. Femoral pulses were strong, but deficits associated with the premature beats were evident. No additional physical examination abnormalities were detected.
A 6-year-old spayed female Basset Hound was re-ferred to the Texas A&M University Veterinary Medical Teaching Hospital for evaluation of sudden onset of lethargy, polyuria-polydipsia, peripheral edema, abdominal distention, diarrhea, and hypoalbuminemia. The dog had a history of hypothyroidism, hyperadrenocorticism, and recurrent urinary tract infections. At the time of this initial evaluation, it was being treated with thyroid hormone supplementation, trilostane, nitrofurantoin, vitamin C (to control urine pH), and diphenhydramine (for seasonal allergies).
At the initial examination, the dog was bright, alert, and mildly tachypneic (respiratory rate, 42 breaths/ min). Thoracic auscultation revealed normal bronchovesicular sounds, muffled heart sounds,
10-year-old 20-kg (44-lb) spayed female Brittany was examined by a veterinarian because of acute onset of lethargy and inappetence. Tachycardia was detected on physical examination and confirmed via ECG; in all leads, the QRS complexes were wide. Lidocaine hydrochloride (2 mg/kg [0.9 mg/lb]) was administered IV, which slowed the heart rate slightly. The dog was subsequently transferred to a local emergency clinic for supervision overnight. Because of the incomplete response to lidocaine, the dog was referred to the Veterinary Medical Teaching Hospital at Texas A&M University for further evaluation the following morning.
A 13-year-old Thoroughbred gelding was referred to the Texas Veterinary Medical Center, Texas A&M College of Veterinary Medicine and Biomedical Sciences, for echocardiographic evaluation. The horse had been hospitalized at the referring veterinarian's clinic for approximately 1 week for fever, tachycardia, limb edema, and lethargy Results of a CBC revealed marked leukocytosis (20,390 WBCs/μL; reference range, 5,400 to 14,300 WBCs/μL). Treatment included antimicrobials, glucocorticoids, and NSAIDs. The sudden onset of a loud right-sided heart murmur prompted referral for further evaluation. At the time of admission, the horse was quiet and alert and afebrile, with mild sinus tachycardia (heart rate,
Case Description—A 12-year-old Miniature Dachshund with a history of permanent endocardial pacemaker implantation performed 7 weeks previously was admitted for routine dental prophylaxis.
Clinical Findings—Preanesthetic ECG revealed normal ventricular capture. Thoracic radiographic findings included caudomedial displacement of the endocardial pacemaker lead. Echocardiography revealed moderate chronic degenerative valve disease with moderate left atrial and ventricular dilation. After induction of anesthesia, loss of ventricular capture was detected. The dog recovered from anesthesia and had improved ventricular capture. The following day, surgical exposure of the cardiac apex revealed perforation of the right ventricular apex by the passive-fixation pacemaker lead.
Treatment and Outcome—A permanent epicardial pacemaker was implanted through a transxiphoid approach. Appropriate ventricular capture and sensing were achieved. The dog recovered without complications. Approximately 2 months later, the dog developed sudden respiratory distress at home and was euthanized.
Clinical Relevance—In dogs with permanent pacemakers and loss of ventricular capture, differential diagnoses should include cardiac perforation. If evidence of perforation of the pacemaker lead is found, replacement of the endocardial pacemaker lead with an epicardial pacemaker lead is warranted.
Case Description—A 3-year-old sexually intact male Standard Poodle was admitted to the veterinary teaching hospital for transcatheter closure of a large atrial septal defect (ASD).
Clinical Findings—The dog had exercise intolerance and was thin. Findings on physical examination were within normal limits with the exception of a left base systolic heart murmur (grade 5/6). The dog was not receiving any medications. Echocardiography and thoracic radiography confirmed the diagnosis of ASD and revealed compensatory changes consistent with a large left to right shunting ASD. Results of serum biochemical analysis and CBC were within reference range limits.
Treatment and Outcome—Transcatheter ASD closure with an atrial septal occluder (ASO) was performed and failed. An open heart surgical approach under cardiopulmonary bypass was declined by the dog's owners. The dog underwent a novel hybrid approach involving active device fixation under temporary inflow occlusion after transatrial device deployment. The dog recovered with some manageable postoperative complications. As of the last follow-up examination, the dog had 10 months of event-free survival.
Clinical Relevance—Transcatheter closure by use of an ASO and open heart patch repair with cardiopulmonary bypass to surgically treat dogs with ASD has been reported. Transcatheter closure is not possible in dogs with large ASD. The novel hybrid procedure reported herein represented a viable alternative to euthanasia.
Objective—To report the outcome of minimally invasive surgical treatment of heartworm caval syndrome in a series of dogs and to provide information on long-term survival of patients with this condition.
Design—Retrospective case series.
Animals—42 client-owned dogs with a diagnosis of heartworm caval syndrome.
Procedures—Information on history, clinical, laboratory, and diagnostic imaging findings and treatment was obtained from medical records. When possible, additional follow-up information was obtained through telephone interviews with referring veterinarians and owners.
Results—Of the 42 dogs with caval syndrome, 21 underwent minimally invasive surgical treatment consisting of transvenous heartworm extraction. Two of the 21 dogs died during the procedure, and after surgery, 4 died. Following induction of anesthesia, heartworms migrated into the distal portion of the pulmonary artery in 1 dog; therefore, extraction was not attempted. Transvenous heartworm extraction was completed successfully in 14 dogs, and all 14 of these dogs were discharged from the hospital. Mean follow-up time in these 14 dogs was 24.4 ± 17.7 months with a range of 2 to 56 months. At the time of final follow-up, 10 of these 14 dogs had survived at least 18 months and 7 had survived > 24 months. By the end of the study, 1 dog was lost to follow-up and 3 had been euthanatized for unrelated reasons.
Conclusions and Clinical Relevance—Results of the study reported here suggest that dogs with caval syndrome that undergo successful transvenous heartworm extraction and survive to discharge have a good long-term prognosis.
Objective—To determine the effect of PO administration of pimobendan on clinical and echocardiographic variables and survival time in cats with heart failure characterized by ventricular systolic dysfunction.
Design—Retrospective cohort study.
Animals—27 client-owned cats (16 male and 11 female) with heart failure, treated with pimobendan (mean ± SD dosage, 0.26 ± 0.08 mg/kg [0.118 ± 0.036 mg/lb], PO, q 12 h).
Procedures—Information on medical history, laboratory results, diagnostic imaging findings, treatments received, and survival time were obtained from medical records of cats that received pimobendan because of cardiac disease. When possible, additional follow-up information was obtained through telephone interviews with referring veterinarians and owners.
Results—The mean ± SD age of all 27 cats was 8.9 ± 5.2 years. All cats had received several cardiac medications. Types of heart disease represented included unclassified cardiomyopathy (CM; n = 11 [41%]), dilated CM (8 [30%]), arrhythmogenic right ventricular CM (4 [15%]), congenital heart disease (3 [11 %]), and hypertrophic CM with regional hypokinesis (1 [4%]). All cats had ventricular systolic dysfunction. One cat with systolic anterior motion of the mitral valve became severely hypotensive after initial administration of pimobendan and was excluded from the survival analysis. Median survival time was 167 days (95% confidence interval, 32 to 339 days).
Conclusions and Clinical Relevance—Pimobendan appeared to be well tolerated in cats with heart failure characterized by ventricular systolic dysfunction of various etiologies. Cats with systolic anterior motion of the mitral valve may develop systemic hypotension when treated with pimobendan. Additional studies are needed to establish dosages for pimobendan and its effects before it can be recommended for treatment of cats with CHF.