Christopher Stauthammer

Influence of Beta Blockers on Survival in Dogs with Severe Subaortic Stenosis

Background Subaortic stenosis (SAS) is one of the most common congenital cardiac defects in dogs. Severe SAS frequently is treated with a beta adrenergic receptor blocker (beta blocker), but this approach largely is empirical. Objective To determine the influence of beta blocker treatment on survival time in dogs with severe SAS. Methods Retrospective review of medical records of dogs diagnosed with severe, uncomplicated SAS (pressure gradient [PG] ≥80 mmHg) between 1999 and 2011. Results Fifty dogs met the inclusion criteria. Twenty‐seven dogs were treated with a beta blocker and 23 received no treatment. Median age at diagnosis was significantly greater in the untreated group (1.2 versus 0.6 years, respectively; P = .03). Median PG at diagnosis did not differ between the treated and untreated groups (127 versus 121 mmHg, respectively; P = .2). Cox proportional hazards regression was used to identify the influence of PG at diagnosis, age at diagnosis, and beta blocker treatment on survival. In the all‐cause multivariate mortality analysis, only age at diagnosis (P = .02) and PG at diagnosis (P = .03) affected survival time. In the cardiac mortality analysis, only PG influenced survival time (P = .03). Treatment with a beta blocker did not influence survival time in either the all‐cause (P = .93) or cardiac‐cause (P = .97) mortality analyses. Conclusions Beta blocker treatment did not influence survival in dogs with severe SAS in our study, and a higher PG at diagnosis was associated with increased risk of death.

Structural and functional cardiovascular changes and their consequences following interventional patent ductus arteriosus occlusion in dogs: 24 cases (2000–2006)

OBJECTIVE To investigate cardiovascular changes and survival times following complete interventional device occlusion of uncomplicated left-to-right shunting patent ductus arteriosus in dogs. DESIGN Retrospective cohort study. ANIMALS 24 dogs with uncomplicated patent ductus arteriosus that was fully occluded and reevaluated within 24 hours, approximately 3 months, and 1 year after the procedure. PROCEDURES Information on medical history, diagnostic imaging findings, treatment received, and survival times were obtained from medical records. Patients were allocated into 2 groups on the basis of age (< 1 year [n = 14] and ≥ 1 year [10]) at the time of the procedure. Additional follow-up information was obtained through interviews of owners and referral veterinarians. RESULTS Following ductal occlusion, decreases were detected in vertebral heart scale size, left ventricular chamber diameter in diastole and in systole, left atrial dimension, fractional shortening, aortic velocity, and ventricular wall thickness. There were no differences between age groups for postocclusion changes except vertebral heart scale size. Systolic dysfunction was detected in 14 (58%) patients on the final visit. Median survival time for all dogs after ductal occlusion was > 11.5 years. CONCLUSIONS AND CLINICAL RELEVANCE Complete ductal occlusion resulted in immediate removal of the volume overload state and eventual return of cardiac chamber dimensions to reference range, suggesting regression of eccentric hypertrophy. Systolic dysfunction persisted in some dogs but appeared to be clinically unimportant. Most cardiovascular changes were independent of patient age at the time of the procedure.

Caudal vena cava obstruction caused by redundant pacemaker lead in a dog.

Inferior vena cava obstruction, a rare but serious complication of transvenous pacemaker lead placement in humans, has not been reported in dogs. We describe this complication in a dog that developed ascites 8 months after pacemaker implantation. Radiography disclosed a loop of redundant lead within the caudal vena cava (CVC), and angiography demonstrated obstruction to blood flow. Withdrawal of the loop from the CVC did not restore blood flow. Persistent obstruction was suspected secondary to fibrosis resulting from vascular damage caused by the loop of lead. Angioplasty of the CVC obstruction restored blood flow and resolved the dogs clinical signs.

Palliative balloon angioplasty in a cat with right pulmonary arterial branch stenoses and concurrent absence of the left pulmonary artery.

Unilateral absence of the left or right pulmonary artery with concurrent contralateral pulmonary arterial branch stenoses is an exceptionally rare disorder. We describe this anomaly in a cat with severe exercise intolerance and respiratory distress. Transthoracic echocardiography and angiography demonstrated the absence of the left pulmonary artery with concurrent right pulmonary branch stenosis. Palliative balloon angioplasty of the right pulmonary artery substantially reduced right ventricular systolic pressure load and alleviated the patients clinical signs.

Stent placement for palliation of cor triatriatum dexter in a dog with suspected patent foramen ovale

An 11 month old spayed, female dog presented with exercise intolerance and cyanosis upon exertion. Echocardiography revealed an imperforate cor triatriatum dexter with mild tricuspid valve dysplasia, an underfilled right ventricle and significant right to left shunting across a presumptive patent foramen ovale. Balloon dilation of the abnormal atrial membrane was initially successful in creating a communication between the right atrial chambers, but stenosis of the original perforation and persistent clinical signs prompted a second intervention. A balloon expandable biliary stent was placed across the abnormal partition, improving caudal venous return to the right ventricle and reducing the right to left shunt. Three months after stent placement, resting oxygen saturation had normalized. Six months after stent placement, exercise tolerance had improved and exertional cyanosis had resolved. Long term follow up will be necessary to assess for remodeling of the right ventricle with improved venous return. Stent placement can be considered as a palliative treatment option for cor triatriatum dexter, especially for stenosis post-balloon dilation.

A case of an unexplained eosinophilic myocarditis in a dog

An 8-year-old spayed female Munsterlander was evaluated for a chronic low grade fever and a two month history of exercise intolerance. On physical examination, tachycardia and a grade II/VI right systolic heart murmur were detected. Echocardiography revealed marked thickening of the atrial and ventricular walls with mixed echogenicity and concentric hypertrophy of the left and right ventricles and equivocal systolic dysfunction. Serum cardiac troponin I level was markedly elevated. Endomyocardial biopsy was attempted; however, the patient arrested during the procedure and resuscitation was unsuccessful. Post-mortem examination revealed severe, chronic atrial and ventricular eosinophilic myocarditis associated with marked interstitial fibrosis. Serological testing, histopathology and immunohistochemistry staining did not reveal an underlying infectious agent or neoplasm. To our knowledge, this is the first reported case of primary eosinophilic myocarditis in the absence of a peripheral eosinophilia and multi-organ eosinophilic inflammation in a dog.

International collaborative study to assess cardiovascular risk and evaluate long‐term health in cats with preclinical hypertrophic cardiomyopathy and apparently healthy cats: The REVEAL Study

Background Hypertrophic cardiomyopathy is the most prevalent heart disorder in cats and principal cause of cardiovascular morbidity and mortality. Yet, the impact of preclinical disease is unresolved. Hypothesis/Objectives Observational study to characterize cardiovascular morbidity and survival in cats with preclinical nonobstructive (HCM) and obstructive (HOCM) hypertrophic cardiomyopathy and in apparently healthy cats (AH). Animals One thousand seven hundred and thirty client‐owned cats (430 preclinical HCM; 578 preclinical HOCM; 722 AH). Methods Retrospective multicenter, longitudinal, cohort study. Cats from 21 countries were followed through medical record review and owner or referring veterinarian interviews. Data were analyzed to compare long‐term outcomes, incidence, and risk for congestive heart failure (CHF), arterial thromboembolism (ATE), and cardiovascular death. Results During the study period, CHF, ATE, or both occurred in 30.5% and cardiovascular death in 27.9% of 1008 HCM/HOCM cats. Risk assessed at 1, 5, and 10 years after study entry was 7.0%/3.5%, 19.9%/9.7%, and 23.9%/11.3% for CHF/ATE, and 6.7%, 22.8%, and 28.3% for cardiovascular death, respectively. There were no statistically significant differences between HOCM compared with HCM for cardiovascular morbidity or mortality, time from diagnosis to development of morbidity, or cardiovascular survival. Cats that developed cardiovascular morbidity had short survival (mean ± standard deviation, 1.3 ± 1.7 years). Overall, prolonged longevity was recorded in a minority of preclinical HCM/HOCM cats with 10% reaching 9‐15 years. Conclusions and Clinical Importance Preclinical HCM/HOCM is a global health problem of cats that carries substantial risk for CHF, ATE, and cardiovascular death. This finding underscores the need to identify therapies and monitoring strategies that decrease morbidity and mortality.

Survival time with pacemaker implantation for dogs diagnosed with persistent atrial standstill

OBJECTIVES To evaluate survival time in dogs with persistent atrial standstill after pacemaker implantation and to compare the survival times for cardiac-related vs. non-cardiac deaths. Secondary objectives were to evaluate the effects of breed and the presence of congestive heart failure (CHF) at the time of diagnosis on survival time. ANIMALS Twenty dogs with persistent atrial standstill and pacemaker implantation. METHODS Medical records were searched to identify dogs diagnosed with persistent atrial standstill based on electrocardiogram that underwent pacemaker implantation. Survival after pacemaker implantation was analyzed using the Kaplan-Meier method. RESULTS The median survival time after pacemaker implantation for all-cause mortality was 866 days. There was no significant difference (p=0.573) in median survival time for cardiac (506 days) vs. non-cardiac deaths (400 days). The presence of CHF at the time of diagnosis did not affect the survival time (P=0.854). No difference in median survival time was noted between breeds (P=0.126). CONCLUSIONS Dogs with persistent atrial standstill have a median survival time of 866 days with pacemaker implantation, though a wide range of survival times was observed. There was no difference in the median survival time for dogs with cardiac-related deaths and those without. Patient breed and the presence of CHF before pacemaker implantation did not affect median survival time.

Pulmonary atresia with intact ventricular septum and hypoplastic right ventricle in an Arabian foal.

Pulmonary atresia with intact ventricular septum, rudimentary tricuspid valve, hypoplastic right ventricle, and right-to-left atrial shunting were identified in a four-day-old, male Arabian foal with clinical signs of cyanotic heart disease. Pulmonary blood flow was apparently derived from a ductus arteriosus. Echocardiographic evaluation revealed the majority of cardiac abnormalities and also findings compatible with right-sided congestive heart failure. Congenital cardiac defects have a high incidence in this breed, and this is the first description of this combination of congenital cardiac defects.

Overexpression of copper/zinc superoxide dismutase in the median preoptic nucleus improves cardiac function after myocardial infarction in the rat

Previous reports indicate that overexpression of copper/zinc superoxide dismutase (CuZnSOD), an intracellular superoxide (O2•−) scavenging enzyme, in the brain subfornical organ improves cardiac function in a mouse model of heart failure (HF). A downstream hypothalamic site, the MnPO, may act as a relay centre for O2•− to serve as a mediator in the pathophysiology of HF. To test the hypothesis that elevated O2•− in the MnPO contributes to the pathophysiology of HF and decreased cardiac function, we injected adenovirus encoding CuZnSOD (AdCuZnSOD, n=7) or control empty adenovirus vector (AdEmpty, n=7) into the MnPO of normal rats. Subsequently, rats were subjected to coronary artery ligation to create a myocardial infarct (MI) of the left ventricle. Cardiac function was monitored via echocardiography. Upon completion, rat brains were examined for CuZnSOD expression in MnPO via immunofluorescence and histopathological analyses of cardiac infarct size were conducted. Baseline (EF) ejection fractions (%) of AdCuZnSOD and AdEmpty rats were 73 ± 1 and 71 ± 1, respectively. Two weeks after MI, EF was significantly decreased in both groups of rats (AdCuZnSOD: 51 ± 3, AdEmpty: 46 ± 1). In contrast, by 4 weeks post MI, EF had improved to 64 ± 2 in AdCuZnSOD rats, yet was only 52 ± 1 in AdEmpty rats, and this was accompanied by lower plasma noradrenaline levels in AdCuZnSOD rats (0.49 ± 0.19 ng/mL) compared to AdEmpty rats (1.20 ± 0.32 ng/mL). In conclusion, despite decreases in EF early after MI, overexpression of CuZnSOD in the MnPO was related to an improvement in left ventricular function and concomitant decreased plasma noradrenaline levels 4 weeks post MI.