Canine infantile left ventricular noncompaction.

BACKGROUND: Left ventricular noncompaction (LVNC) is a rare form of cardiomyopathy currently described in humans and cats. It consists of a spongy myocardium characterized by prominent trabeculation and deep recesses involving more than 50% of the ventricular thickness. We describe the clinical and pathological features of LVNC combined with tricuspid valve dysplasia, double-orifice tricuspid valve and severe pulmonary stenosis in a puppy. In addition, we briefly review the LVNC causes, pathogenesis, forms and current diagnostic criteria. CASE PRESENTATION: A seven-week-old intact German Shorthaired Pointer-cross male was presented with a poor body condition, exercise intolerance and dyspnea. Clinical exam identified a bilateral systolic murmur (grade IV/VI over the right heart base and grade III/VI over the left heart base). Echocardiography identified tricuspid valve dysplasia, mild mitral regurgitation, and severe pulmonic stenosis with a trans-valvar systolic pressure gradient of 106 mmHg. Left ventricular noncompaction was diagnosed by necropsy and further confirmed histopathologically by the presence of two distinct myocardial layers: an inner noncompacted zone covering more than 50% of ventricular thickness containing prominent trabeculation and deep recesses, and an outer zone of compact myocardium. CONCLUSIONS: This is the first case describing LVNC in a canine patient, supporting the introduction of this form of heart disease as a differential diagnosis for cardiomyopathies in juvenile and adult dogs.

Successful management of ventricular fibrillation and ventricular tachycardia using defibrillation and intravenous amiodarone therapy in a cat.

OBJECTIVE: To describe the successful management of ventricular fibrillation (VF) and ventricular tachycardia (VT) using cardiopulmonary resuscitation, including defibrillation, followed by continuous rate infusion of IV amiodarone, in a cat with cardiac arrest secondary to tachyarrhythmia. CASE SUMMARY: A 12-year-old previously healthy neutered male Scottish Fold cat presented following an acute episode of collapse. Initial physical examination revealed severe tachycardia and cardiovascular collapse. Within a few minutes after arrival, the cat experienced cardiopulmonary arrest. Electrocardiographic assessment was suggestive of VF, and CPR was initiated, including 2 rounds of defibrillation (2 joule/kg each), resulting in return of spontaneous circulation with sustained VT. After procainamide and lidocaine failed to result in conversion to normal sinus rhythm (NSR), continuous IV amiodarone therapy was initiated, and NSR was achieved. Echocardiography demonstrated severe systolic dysfunction, and tachycardia-induced cardiomyopathy (TICM) secondary to chronic VT was suspected; however, dilated cardiomyopathy (DCM) or end-stage hypertrophic cardiomyopathy could not be ruled out. The patient was discharged the following day with oral amiodarone and pimobendan. During a recheck examination performed 7 months later the cat was in NSR, with no direct evidence of long-term amiodarone adverse effects. The cat died acutely at home 8 months after discharge. NEW OR UNIQUE INFORMATION PROVIDED: This report is the first to describe the successful use of IV amiodarone in a cat to manage sustained VT following CPR.

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.

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.

Combined double chambered right ventricle, tricuspid valve dysplasia, ventricular septal defect, and subaortic stenosis in a dog.

BACKGROUND: Double chambered right ventricle (DCRV) is a congenital heart anomaly where the right ventricle is divided into two chambers. We describe, for the first time, an unusual combination of DCRV combined with some other congenital heart defects. CASE PRESENTATION: A 1.2-year-old Golden Retriever was presented with lethargy, exercise intolerance and ascites. Physical examination revealed an irregularly irregular pulse and a grade V/VI, systolic, right cranial murmur. Electrocardiography revealed widened and splintered QRS complexes with a right bundle-branch block pattern. Radiography demonstrated right-sided cardiomegaly. Two-dimensional echocardiography identified a DCRV with tricuspid valve dysplasia. The patient died despite abdominocentesis and 4 days of oral pharmacotherapy, and necropsy revealed an anomalous fibromuscular structure that divided the right ventricle into two compartments. Another finding was tricuspid valve dysplasia with hypoplasia of the posterior and septal leaflets. The anterior leaflet was prominent, being part of the anomalous structure that divided the right ventricle. Necropsy also identified a perimembranous ventricular septal defect and mild subaortic stenosis. Histopathological examination of the fibromuscular band that separated the right ventricle identified longitudinally oriented layers of dense fibrous connective tissue and myocardial cells arranged in a plexiform pattern. The muscular component was well represented at the ventral area of the fibromuscular band, and was absent in the central zone. Superficially, the endocardium presented areas of nodular hyperplasia covering mainly the fibrous part of the abnormal structure. The nodules were sharply demarcated and were composed by loosely arranged connective tissue with myxoid appearance, covered by discrete hyperplastic endocardium. CONCLUSIONS: Concomitant cardiac malformations involving DCRV, tricuspid valve dysplasia, perimembranous ventricular septal defect and mild subaortic stenosis have not been previously described in veterinary medicine, and are reported here for the first time. Moreover, this is the first report of a canine patient with tricuspid valve dysplasia (TVD) and DCRV where the anterior leaflet is part of an anomalous structure dividing the right ventricle (RV) into two separate compartments.

Sleeping and resting respiratory rates in dogs with subclinical heart disease.

OBJECTIVE: To characterize sleeping respiratory rates (SRRs) and resting respiratory rates (RRRs), collected in the home environment, of dogs with subclinical heart disease that could result in left-sided congestive heart failure. DESIGN: Prospective cross-sectional study. ANIMALS: 190 adult dogs with subclinical left-sided heart disease. PROCEDURES: Most dogs had mitral valve disease or dilated cardiomyopathy of various severities. Clients collected ten 1-minute SRRs or RRRs during a period ranging from 1 week to 6 months. Clinicians provided echocardiographic and medical data on each patient. RESULTS: The within-dog mean SRR (SRRmean; 16 breaths/min) was significantly lower than the within-dog mean RRR (RRRmean; 21 breaths/min). Seven dogs had SRRmean and 33 dogs had RRRmean > 25 breaths/min; 1 dog had SRRmean and 12 dogs had RRRmean > 30 breaths/min; these dogs mostly had a left atrial (LA)-to-aortic ratio > 1.8. Dogs with moderate LA enlargement had a significantly higher SRRmean than did other dogs. However, median SRRmean for each of 4 levels of LA enlargement was < 20 breaths/min; median RRRmean for each of 4 levels of LA enlargement was < 25 breaths/min. Both within-dog SRR and RRR remained stable for 10 consecutive measurements. Treatment with cardiac medications or presence of pulmonary hypertension was not associated with SRRmean or RRRmean. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggested that dogs with confirmed subclinical left-sided heart disease of various severities generally had SRRmean < 25 breaths/min, which was infrequently exceeded at any time, and that SRR and RRR remained stable, regardless of individual within-dog SRRmean or RRRmean.

Expression of urocortin peptides in canine myocardium and plasma.

Urocortin (Ucn) peptides are the endogenous ligands for the corticotropin-releasing factor type 2 receptor (CRFR2). They have potentially important roles in cardiovascular physiology in health and disease, and show promise as therapeutics for congestive heart failure. Analysis of canine heart tissue showed mRNA expression of Ucn 1, Ucn 3 and CRFR2 in all heart chambers. Immunohistochemistry also demonstrated Ucns 1 and 3 expression in cardiomyocytes. To assess the potential usefulness of circulating Ucns as markers of heart disease, plasma samples from 45 dogs with cardiac disease and 15 controls were analysed by radioimmunoassay. Both Ucns 1 and 3 were measurable but the presence of cardiac disease did not alter their concentrations. Therefore, whilst Ucns are expressed in canine myocardium (where they may play a role in the endogenous neurohumoral response to cardiac disease or failure) they do not appear to be sensitive biomarkers of cardiac disease in our canine patient population.

Molecular detection of Bartonella henselae and Bartonella koehlerae from aortic valves of Boxer dogs with infective endocarditis.

Cardiac aortic valves from five dogs that died from acquired infective endocarditis were retrospectively molecularly screened for Bartonella infection. Identification was carried out using PCR targeting four gene fragments (rpoB, ribC, 16S rRNA and gltA), and the 16S-23S intergenic spacer (ITS). Bartonella henselae DNA was detected in aortic valve tissue from one Boxer dog with moderate subaortic stenosis (SAS). Bartonella koehlerae DNA was detected from the aortic valve of another Boxer dog with severe SAS. The latter dog was both a littermate and a housemate of the dog with the B. henselae infection. Other animals residing at the same household were also screened for Bartonella infection. B. henselae was molecularly detected in a spleen aspirate from the dogs' mother, and isolated and molecularly characterized from another housemate cat. This is the first molecular identification of B. henselae and B. koehlerae, two zoonotic Bartonella species, from valves of dogs with canine infective endocarditis, suggesting their role in the pathogenesis of this disease. Moreover, this is the first report describing the detection of B. koehlerae from dogs.

Ventricular rate control using a novel vagus nerve stimulating system in a dog with chronic atrial fibrillation.

A 4-year-old, intact male Dogue de Bordeaux dog with congenital valvular pulmonic stenosis, tricuspid valve dysplasia, and chronic atrial fibrillation underwent ultrasound-guided balloon valvuloplasty in addition to pharmacological treatment. Owner compliance to prescribed pharmacotherapy proved very poor, and concerns developed regarding the ability to successfully control heart rate and symptoms using drug therapy alone. These concerns were addressed by the implantation of a novel vagal stimulation system that was programmed to prevent a ventricular rate of >145 bpm. Consequently, post-operative ventricular response rate decreased from up to 250 to 140 bpm. Successful ventricular rate control was maintained for 291 days post-operatively, following which euthanasia was elected by the owner due to persistent right-sided congestive heart failure. To the authors' knowledge, this is the first report of successful continuous rate control using a vagal stimulating system in a closed-chest, client-owned dog with chronic atrial fibrillation secondary to spontaneously occurring organic heart disease.

Incomplete atrioventricular canal complicated by cardiac tamponade and bidirectional shunting in an adult dog.

An incomplete atrioventricular (AV) canal with bidirectional shunting and cardiac tamponade in a 6-year-old dog was initially diagnosed echocardiographically as a common atrium. The dog failed to respond to medical therapy and was euthanized. Upon necropsy, the defect was confirmed as an incomplete AV canal. A mechanism for the potential sequence of clinical events demonstrated in this dog is proposed.

Exhaustion of the Frank-Starling mechanism in conscious dogs with heart failure induced by chronic coronary microembolization.

The role of the Frank-Starling mechanism in the regulation of cardiac systolic function in the ischemic failing heart was examined in conscious dogs. Left ventricular (LV) dimension, pressure and systolic function were assessed using surgically implanted instrumentations and non-invasive echocardiogram. Heart failure was induced by daily intra-coronary injections of microspheres for 3-4 weeks via implanted coronary catheters. Chronic coronary embolization resulted in a progressive dilation of the left ventricle (12+/-3%), increase in LV end-diastolic pressure (118+/-19%), depression of LV dP/dt(max) (-19+/-4%), fractional shortening (-36+/-7%), and cardiac work (-60+/-9%), and development of heart failure, while the LV contractile response to dobutamine was depressed. A brief inferior vena caval occlusion in dogs with heart failure decreased LV preload to match the levels attained in their control state and caused a further reduction of LV dP/dt(max), fractional shortening, stroke work and cardiac work. Moreover, in response to acute volume loading, the change in the LV end-diastolic dimension-pressure (DeltaLVEDD-DeltaLVEDP) curve in the failing heart became steeper and shifted significantly to the left, while the increases in LV stroke work and cardiac work were blunted. Thus, our results suggest that the Frank-Starling mechanism is exhausted in heart failure and unable to further respond to increasing volume while it plays an important compensatory role in adaptation to LV dysfunction in heart failure.