Congenital cardiac disease in dogs

Thoracic conformation, age, amount of body fat, and stage of respiration and cardiac contraction affect the cardiac silhouette. Deep-chested dogs have an upright, narrow cardiac silhouette about 2 1/2 intercostal spaces wide, while barrel-chested dogs have a round, wide silhouette about 3 1/2 intercostal spaces wide. On LAT films the vessels to a lung lobe should be of equal size and 0.25-1.2 times the diameter of the upper third of the 4th rib at the 4th intercostal space. On DV projections, vessels to the caudal lung lobe should be no larger than the diameter of the 9th rib. Signs of right ventricular enlargement include loss of the cranial waist, increased width of the cardiac silhouette, increased sternal contact of the heart, and an elevated cardiac apex. Signs of left ventricular enlargement include an elevated carina, loss of the caudal waist, and a more perpendicular caudal cardiac border. Signs of left atrial enlargement include separation of mainstem bronchi, compression of the bronchus to the left caudal lung lobe, and an increased distance from the carina to the dorsal border of the caudal vena cava. Enlargement of the aorta and main pulmonary artery segment on a LAT view appears as a soft tissue density obscuring the cranial waist. Pulmonary vascular fields are usually hypervascular in patent ductus arteriosus and interventricular septal defects, normal in uncomplicated aortic or pulmonic stenosis, and hypovascular in tetralogy of Fallot.     

Congenital cardiac disease in dogs

Patent ductus arteriosus (PDA) is thought to be inherited and occurs twice as often in females as in males, most commonly in Poodles, Collies, Cocker Spaniels and Shetland Sheepdogs. About half of untreated dogs develop left-sided heart failure by 8 months of age. Clinical signs include coughing, decreased exercise tolerance, pulmonary edema, a "machinery" murmur in the pulmonic-aortic region, and a bounding pulse. An ECG may reveal an increased amplitude of the R wave and a lengthened P wave. Plain LAT films reveal loss of the cranial and caudal cardiac waists, increased sternal contact of the heart, increased width and straightened caudal border of the cardiac silhouette, elevated carina, and an enlarged left atrium. Changes on plain DV films include an elongated cardiac silhouette, enlarged right ventricle, and 3 bulges on the left side of the cardiac silhouette. Nonselective angiocardiography can be used for a definitive diagnosis and to demonstrate a reverse right-to-left PDA, in which the ascending aorta, brachiocephalic trunk and left subclavian artery are not opacified by contrast medium. Animals with a right-to-left shunt PDA are cyanotic in caudal body parts. Treatment of left-to-right shunt PDA involves ligation with 2 nonabsorbable sutures. A right-to-left shunt PDA should not be ligated but is treated by restricted exercise and periodic phlebotomy.     

Congenital cardiac disease in dogs

Patent ductus arteriosus, aortic stenosis, ventricular septal defect, pulmonic stenosis and tetralogy of Fallot are the most frequently reported cardiac anomalies of dogs. Systolic murmurs occur after the first heart sound but before the second, while diastolic murmurs occur after the second heart sound. Murmurs associated with the pulmonic, aortic and mitral valves are best heard at the left intercostal spaces 3, 4 and 5, respectively, and those of the tricuspid valve at the right intercostal space 3 or 4. Mucosae at both ends of the animal should be examined for cyanosis. Right ventricular enlargement is characterized by a mean electrical axis greater than 100 degrees, a Q wave amplitude greater than 0.5 mv in leads II, III and AVF, and a positive T wave in lead V10. Left ventricular enlargement causes an axis of less than 40 degrees, a QRS complex duration greater than 0.06 seconds, an R wave amplitude greater than 3 mv, and a slurred or depressed ST segment. Atrial enlargement is characterized by a P wave duration greater than 0.04 seconds and a P wave amplitude greater than 0.4 mv. The cardiac silhouette is more upright and round on DV radiographs than on VD projections.     

Congenital cardiac disease in dogs

Ventricular septal defect (VSD) generally occurs high in the membranous septum rather than lower in the muscular portion. The English Bulldog and Siberian Husky may be predisposed. Clinical signs include a holosystolic or crescendo-decrescendo murmur best heard low on the right side at the 3rd-4th intercostal space and, with large defects, pulmonary congestion, exercise intolerance, cyanosis and ascites. The ECG is normal unless the right ventricle is hypertrophied, which causes right axis deviation and other electrocardiographic signs of right-sided heart enlargement. Plain film thoracic radiographs reveal signs of right-sided heart enlargement but often are not diagnostic. Nonselective angiocardiography is often not useful in diagnosing VSD with a left-to-right shunt of blood. Selective angiocardiography, in which contrast medium is injected directly into the left ventricle via a catheter, is the method of choice for diagnosis of VSD. Dogs with a small VSD remain asymptomatic, but those with large defects require surgical correction with a prosthetic septal pathic or pulmonary artery band.     

Congenital cardiac disease in dogs

Aortic stenosis is a heritable cardiac anomaly most common in German Shepherds, Boxers and Newfoundlands, and less common in Pugs, English Bulldogs, Boston Terriers, Fox Terriers, Schnauzers and Bassets. Clinical signs are associated with secondary left-sided heart failure and include coughing, moist rales, exercise intolerance, arrhythmias and a weak femoral pulse. It causes an ejection-type crescendo-decrescendo, systolic murmur best heard on the left side near the elbow. The ECG may be normal or may show signs of left ventricular hypertrophy, including an axis of less than 40 degrees, a QRS complex of greater than 60 seconds in duration, R waves greater than 3 mv in amplitude, ST segment slurring or depression, or T waves of an amplitude greater than 25% of that of R waves. A LAT radiograph usually reveals an enlarged cardiac silhouette, loss of the cranial cardiac waist, and normal pulmonary vasculature, while DV projections show an elongated cardiac silhouette, rounding of the left ventricular border, and a normal descending aorta. Nonselective angiocardiography reveals poststenotic dilatation of the aorta. Treatment of severely affected dogs involves surgical correction.     

Congenital heart disease in dogs and cats

The presence of congenital heart disease in dogs and cats is usually indicated by a cardiac murmur. There may or may not be further signs of cardiac failure. The type and site of a murmur often suggests the nature of the underlying lesion, but electrocardiography and radiography can give further indications of the nature of the defect. Advanced diagnostic procedures include cardiac catheterisation for angiography, blood pressure recording and blood gas analysis, but this technique is now being superseded in many cases by cardiac ultrasound. Some lesions can be demonstrated directly by echocardiography, but the source of the murmur and the severity of the deformity can be defined precisely by Doppler. Congenital cardiovascular disorders can increasingly be relieved by sophisticated surgery.     

Congenital cardiac diseases in dogs: a retrospective analysis

In a time period of 6 years, 158 congenital cardiac defects were diagnosed in 146 dogs at the Clinic for Small Animal Medicine University of Zurich. In respect to all dogs with cardiac disease, these were 23.5% of the cases. Most common defects were subaortic stenosis (SAS, 31.5%), pulmonic stenosis (PS, 23.3%), ventricular septal defect (VSD, 14.4%), patent ductus arteriosus (PDA, 13.7%) and tricuspid dysplasia (TD, 7.5%). Complex defects were found in 8.2% of the dogs. Although single dogs per breed were affected by various defects, some breed-related tendencies could be observed. We found PS more numerously in boxers and Jack Russell Terriers whereas SAS, VSD and TD were also found in breeds reported to be predisposed. Congenital cardiac defects are an important clinical entity, and knowledge of prevalence is helpful when considering the differential diagnosis and for making a tentative diagnosis in an individual case.     

Cardiac troponin-I concentration in dogs with cardiac disease

Cardiac troponin-I (cTnI) is a highly sensitive and specific marker of myocardial injury and can be detected in plasma by immunoassay techniques. The purpose of this study was to establish a reference range for plasma cTnI in a population of healthy dogs using a human immunoassay system and to determine whether plasma cTnI concentrations were high in dogs with acquired or congenital heart disease, specifically cardiomyopathy (CM), degenerative mitral valve disease (MVD), and subvalvular aortic stenosis (SAS). In total, 269 dogs were examined by physical examination, electrocardiography, echocardiography, and plasma cTnI assay. In 176 healthy dogs, median cTnI was 0.03 ng/mL (upper 95th percentile = 0.11 ng/mL). Compared with the healthy population, median plasma cTnI was increased in dogs with CM (0.14 ng/mL; range, 0.03-1.88 ng/mL; P < .001; n = 26), in dogs with MVD (0.11 ng/mL; range, 0.01-9.53 ng/mL; P < .001; n = 37), and in dogs with SAS (0.08 ng/mL; range, 0.01-0.94 ng/mL; P < .001; n = 30). In dogs with CM and MVD, plasma cTnI was correlated with left ventricular and left atrial size. In dogs with SAS, cTnI demonstrated a modest correlation with ventricular wall thickness. In dogs with CM, the median survival time of those with cTnI >0.20 ng/mL was significantly shorter than median survival time of those with cTnI <0.20 ng/mL (112 days versus 357 days; P = .006). Plasma cTnI is high in dogs with cardiac disease, correlates with heart size and survival, and can be used as a blood-based biomarker of cardiac disease.     

Non-invasive real-time measurements of cardiac vagal tone in dogs with cardiac disease

In dogs with spontaneous heart disease, an electronically generated measurement of cardiac vagal tone, the cardiac index of parasympathetic activity, was a sensitive, simple and inexpensive measure of the severity of heart failure. Dogs with cardiac disease and an index score less than 3 were at 15.8 (95 per cent confidence interval 2.9 to 87.2) times the risk of dying within a year than those with a score of 3 and over. The measurement of the index provided an objective and reliable beat-by-beat measurement of cardiac vagal tone, which was prognostically useful in dogs with heart disease.     

Evaluation of dietary patterns in dogs with cardiac disease

OBJECTIVE: To determine the dietary patterns and intake of nutrients of concern in dogs with cardiac disease. DESIGN: Prospective study. ANIMALS: 82 dogs with dilated cardiomyopathy (DCM) or chronic valvular disease. PROCEDURE: Owners of dogs were contacted and given a standardized telephone questionnaire regarding diet and a 24-hour food recall to determine daily intake of calories, protein, fat, sodium, potassium, and magnesium. RESULTS: Among the 82 dogs, 71% had no congestive heart failure (CHF), and 29% had CHF or a history of CHF. Sixty-one percent of dogs had concurrent diseases. Anorexia was or had been evident in 34% of dogs and was significantly more common in the CHF group and in dogs with DCM. Most dogs (92%) received some treats and table food, with a median percentage of daily calories from treats of 19% (range, 0% to 100%). Most owners (57%) that administered pills used human or pet foods for pill administration. Most dogs ate more than the Association of American Feed Control Officials (AAFCO) minimum values for fat and protein. Daily sodium intake varied from 14 to 384 mg/100 kcal, compared with the AAFCO minimum of 17 mg/100 kcal. A median of 25% of total daily sodium came from treats and table food (range, 0% to 100%). Dogs with CHF ate significantly more sodium, compared with dogs with no CHF. CONCLUSIONS AND CLINICAL RELEVANCE: Dietary intake for dogs with cardiac disease is highly variable and often not optimal.     

Congenital and acquired neuromuscular disease of young dogs and cats

Neuromuscular disorders in small animals include a diverse group of congenital and acquired diseases. The prognosis will vary according to the disorder and the portion of the motor unit affected. A number of diseases might be satisfactorily treated (for example, myasthenia gravis, congenital myotonia), whereas others may be self-limiting (for example, hereditary myopathy of Labrador Retrievers). Accurate diagnosis is necessary for establishing a prognosis and treatment plan suitable to the patient and client. Specific diagnosis in the absence of specialized tests is difficult, although not always impossible (for example, congenital myotonia in the Chow Chow). A knowledge of the neuromuscular diseases that might affect small animals, a detailed history, and a thorough physical examination will help in the presumptive diagnosis. Specialized laboratory examinations may need to be applied (for example, antiacetylcholine receptor antibody titer for acquired myasthenia gravis). Referral may be necessary for more detailed diagnostic workup (for example, electromyographic examination, nerve or muscle biopsy examination). In the case of inherited neuromuscular disorders, a knowledge of inheritance patterns will allow genetic counseling to avoid future problem breedings.     

Serum nitrate and nitrite in dogs with spontaneous cardiac disease

The purpose of this study was to determine whether nitric oxide (NO) concentrations are high in dogs with chronic valvular disease (CVD) and dilated cardiomyopathy (DCM) compared to healthy controls and to determine whether NO concentrations are correlated with type of cardiac disease, disease severity, medical therapy, or serum tumor necrosis factor (TNF) and interleukin-1 (IL-1). Blood was collected from 32 dogs with DCM, from 10 dogs with CVD, and from 10 healthy controls. Indirect determination of NO concentrations was performed by a commercial photoabsorbance assay that uses a Greiss reagent to measure the concentration of nitrite and nitrate (NN), end products of NO metabolism. TNF and IL-1 activities were measured by bioassay. Mean NN concentrations were significantly higher in dogs with heart disease (median, 4.57 microM; range, 0.00-31.05 microM) than in controls (median, 0.00 microM; range, 0.00-6.16 microM; P = .04). NN concentrations in dogs with cardiac disease were not correlated with type or severity of cardiac disease, medication type, or TNF and IL-1 concentrations. NN concentrations were inversely correlated with fractional shortening. The results of this study suggest that metabolites of NO are increased in some dogs with cardiac disease, but these increases appear to be independent of disease severity, TNF and IL-1 concentrations, and type of pharmacologic intervention.     

Congenital dilatation of the bile ducts (Caroli's disease) in young dogs

We describe 8 young dogs with congenital dilatation of the intra- and extrahepatic bile ducts and diffuse cystic kidney disease, compatible with Caroli's disease in humans. The dogs were referred between 1980 and 2000 because of chronic disease at an age of 6 months to 3 years. These dogs included 3 Collies, 2 Frisian Stabyhouns, 2 Jack Russell Terriers, and 1 mixed-breed dog. The most common signs were vomiting (6/6), polyuria and polydipsia (4/6), and anorexia (4/6). Ascites was a common finding (4/6). Clinicopathologic abnormalities were available for 6 dogs. All had increased plasma alkaline phosphatase activity and fasting bile acids: increased alanine aminotransferase activity and urea and creatinine concentrations were present in 50% of dogs. Ultrasound examination of the liver showed severely dilated bile ducts without evidence of obstruction, and calcification in all cases but 1. Postmortem examination revealed severe dilatation of the larger intra- and extrahepatic bile ducts. The common bile duct and gall bladder were normal, and the bile system was patent. The ducts contained a clear viscid fluid often with calcified material. Microscopically, marked portal fibrosis was present, often with abnormally structured dilated bile ducts lined with columnar or cuboid epithelium and regularly small calcifications. The lesion was complicated by ascending cholangitis in 1 dog. The kidneys showed marked cortical and medullary fibrosis with a diffuse radial cystic pattern; only slight renal fibrosis was found in the oldest dog. Seven dogs were euthanized without treatment; the oldest dog was alive and well 5 months after diagnosis and was maintained on a protein-restricted diet.     

Congenital lobar emphysema in two dogs

Congenital lobar emphysema is described in two dogs. The condition was characterized by progressive dyspnoea and cyanosis from a very young age. There was marked expiratory effort, and wheezing and crackling were evident on auscultation. Radiographic examination revealed overdistension and emphysema of the right middle lobe with displacement of the heart and mediastinum to the opposite side. The pathology and possible treatments are discussed.     

Congenital anorectal abnormalities in six dogs

Congenital anorectal abnormalities were diagnosed in three male and three female dogs. One dog had anal stenosis, three had a persistent anal membrane, and the other two had an imperforate anus associated with a rectovaginal fistula. Five of the dogs were treated surgically, and four of them which were followed up for periods ranging from one to five years continued to pass faeces normally.