Long-term incidence and risk of noncardiovascular and all-cause mortality in apparently healthy cats and cats with preclinical hypertrophic cardiomyopathy.

BACKGROUND: Epidemiologic knowledge regarding noncardiovascular and all-cause mortality in apparently healthy cats (AH) and cats with preclinical hypertrophic cardiomyopathy (pHCM) is limited, hindering development of evidence-based healthcare guidelines. OBJECTIVES: To characterize/compare incidence rates, risk, and survival associated with noncardiovascular and all-cause mortality in AH and pHCM cats. ANIMALS: A total of 1730 client-owned cats (722 AH, 1008 pHCM) from 21 countries. METHODS: Retrospective, multicenter, longitudinal, cohort study. Long-term health data were extracted by medical record review and owner/referring veterinarian interviews. RESULTS: Noncardiovascular death occurred in 534 (30.9%) of 1730 cats observed up to 15.2 years. Proportion of noncardiovascular death did not differ significantly between cats that at study enrollment were AH or had pHCM (P = .48). Cancer, chronic kidney disease, and conditions characterized by chronic weight-loss-vomiting-diarrhea-anorexia were the most frequently recorded noncardiovascular causes of death. Incidence rates/risk of noncardiac death increased with age in AH and pHCM. All-cause death proportions were greater in pHCM than AH (65% versus 40%, respectively; P < .001) because of higher cardiovascular mortality in pHCM cats. Comparing AH with pHCM, median survival (study entry to noncardiovascular death) did not differ (AH, 9.8 years; pHCM, 8.6 years; P = .10), but all-cause survival was significantly shorter in pHCM (P = .0001). CONCLUSIONS AND CLINICAL IMPORTANCE: All-cause mortality was significantly greater in pHCM cats due to disease burden contributed by increased cardiovascular death superimposed upon noncardiovascular death.

Taurine deficiency and dilated cardiomyopathy in golden retrievers fed commercial diets.

INTRODUCTION: Golden retrievers are over-represented in cases of taurine-deficient dilated cardiomyopathy and recently a surge in cases has prompted further investigation. OBJECTIVE: To describe the clinical, dietary, and echocardiographic features in golden retrievers diagnosed with taurine deficiency and dilated cardiomyopathy, and to determine specific dietary associations. A second aim was to determine the whole blood taurine concentrations in a representative sample of healthy golden retrievers. ANIMALS: Twenty-four client-owned golden retrievers with documented taurine deficiency and dilated cardiomyopathy and 52 healthy client-owned golden retrievers. METHODS: In this multicenter prospective observational study, baseline and follow-up echocardiographic data, complete diet and medical histories, and whole blood, plasma, or serum taurine concentrations were obtained. Baseline and follow-up echocardiographic data were compared. Associations were evaluated between specific diets and taurine deficiency or congestive heart failure. The prevalence of low whole blood taurine concentrations in the healthy golden retrievers was calculated. RESULTS: Twenty-three of 24 dogs diagnosed with taurine deficiency and dilated cardiomyopathy were fed diets that were either grain-free, legume-rich, or a combination of these factors. None of these diets were feeding trial tested using Association of American Feed Control Officials (AAFCO) procedures. Twenty-three of 24 dogs had significant improvement in their echocardiographic parameters and normalization of taurine concentrations following diet change and taurine supplementation. Nine of 11 dogs diagnosed with congestive heart failure (CHF) had resolution of their congestion at follow-up with five no longer requiring diuretic therapy and four tolerating diuretic dose reduction by >50%. CONCLUSIONS: Certain diets and diet characteristics were associated with the development of taurine deficiency. Taurine deficiency and dilated cardiomyopathy in golden retrievers is likely multifactorial, including a combination of dietary, metabolic, and genetic factors.

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.

Correction: Taurine deficiency and dilated cardiomyopathy in golden retrievers fed commercial diets.

[This corrects the article DOI: 10.1371/journal.pone.0209112.].

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.

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.

Patent ductus arteriosus occlusion in small dogs utilizing a low profile Amplatz® canine duct occluder prototype.

OBJECTIVES: To develop procedural methodology and assess the safety, utility and effectiveness of a low profile Amplatz(®) canine duct occluder (ACDO) prototype in dogs deemed too small to undergo ductal occlusion with the commercially-available ACDO device. ANIMALS: Twenty-one dogs with left-to-right shunting patent ductus arteriosus (PDA). Dogs were ≥1.5 kg but considered too small to accommodate a 6 Fr catheter or 4 Fr sheath within the femoral artery. METHODS: Prospective canine study using a low profile ACDO prototype delivered through a 4 Fr catheter via a femoral arterial approach. Procedural methods, fluoroscopy time, perioperative complications, and residual ductal flow were evaluated, and angiographic ductal morphology and dimensions were tabulated. RESULTS: All 21 dogs underwent successful ductal occlusion using the prototype device, 4 Fr catheter, and right femoral artery approach. No perioperative complications or device embolization occurred. The median minimal ductal diameter was 1.9 mm (range, 0.4-3.4), and the median device size deployed was 4 mm (range, 3-6). Complete ductal occlusion was noted in 17 dogs (81%) on post-deployment angiography. Twenty dogs (95%) had no residual flow on echocardiography performed the following day. In the 17 dogs (81%) that returned for a long-term (≥3months) follow-up evaluation, all had complete ductal occlusion based on echocardiography. CONCLUSIONS: The low profile ACDO prototype is a safe and effective method of PDA occlusion in the small dog. The deployment procedure appears of similar technical difficulty to the commercially available ACDO.

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 patient's clinical signs.

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.

Minimally invasive per-catheter occlusion and dilation procedures for congenital cardiovascular abnormalities in dogs.

With ever-increasing sophistication of veterinary cardiology, minimally invasive per-catheter occlusion and dilation procedures for the treatment of various congenital cardiovascular abnormalities in dogs have become not only available, but mainstream. Much new information about minimally invasive per-catheter patent ductus arteriosus occlusion has been published and presented during the past few years. Consequently, patent ductus arteriosus occlusion is the primary focus of this article. Occlusion of other less common congenital cardiac defects is also briefly reviewed. Balloon dilation of pulmonic stenosis, as well as other congenital obstructive cardiovascular abnormalities is discussed in the latter part of the article.

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 dog's clinical signs.