Congenital cardiac disease in dogs

Pulmonic stenosis is caused by a malformed pulmonic valve, stricture of the right ventricular outflow tract or stricture of the pulmonary artery. English Bulldogs, Beagles, Samoyeds, Fox Terriers and Chihuahuas are predisposed. Clinical signs in severely affected dogs include exercise intolerance, stunting, dyspnea, syncope and ascites. Auscultation reveals a high-frequency, crescendo-decrescendo murmur during systole, loudest over the left side of the thorax, near the sternal cardiac border. An ECG may reveal a right-axis deviation of greater than 120 degrees, S waves in leads I, II and III, deep S waves in CV6LL, CV6LU and V10, Q waves deeper than 0.5 mv in leads II, III and AVF, and positive T waves in lead V10. Plain film LAT thoracic radiographs reveal an elevated carina, increased sternal contact of the heart, loss of the cranial cardiac waist and a widened cardiac silhouette, with normal pulmonary vasculature. A DV projection reveals an inverted "D" shape of the right ventricle and a pulmonary artery bulge. A nonselective angiocardiogram reveals poststenotic dilation of the main pulmonary artery. Treatment involves surgical correction of the stenosis.     

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

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.     

Auscultation and echocardiographic findings in Bull Terriers with and without polycystic kidney disease

OBJECTIVE: To investigate a possible association between Bull Terrier polycystic kidney disease (BTPKD) and cardiac disease, to determine the prevalence of mitral valve disease (MVD) and left ventricular outflow tract obstruction (LVOTO) in the Australian Bull Terrier population, and to compare auscultation and echocardiography in detection of cardiac disease in Bull Terriers. DESIGN: Ninety-nine Bull Terriers, ranging in age from 8 weeks to 13 years and 11 months were auscultated and examined using renal ultrasonography; 86 were also examined using echocardiography. The prevalence and severity of heart defects in dogs with BTPKD was compared with that in dogs without BTPKD. RESULTS: Nineteen of these 99 dogs were diagnosed with BTPKD. Forty-two percent of Bull Terriers with BTPKD and 28% of those without BTPKD had murmurs characteristic of mitral regurgitation or LVOTO. How recently an animal was descended from an ancestor with BTPKD was associated with presence (P = 0.008) and loudness of a murmur (P = 0.009). Overall, echocardiography detected MVD in 39% of Bull Terriers, with increased prevalence in older animals (P = 0.003). Mitral stenosis was found in eight cases. Fifty-three percent of dogs in this study had evidence of LVOTO, with obstruction consisting of a complex of lesions including dynamic or fixed subvalvular LVOTO, significantly narrowed left ventricular outflow tract or valvular aortic stenosis. Dogs with BTPKD, or those descended from dogs with BTPKD, were more likely to have MVD (P = 0.006), and while LVOTO was not more common in these dogs, if they did have LVOTO, they were more likely to have severe obstruction than dogs with no ancestors with BTPKD (analysed in three ways P = 0.028 to 0.001). In this study, 46% of Bull Terriers without a murmur or arrhythmia had cardiac disease detected on echocardiographic examination. CONCLUSION: Cardiac disease, especially MVD and LVOTO, was common in Bull Terriers in this study, and those with BTPKD had an increased risk of cardiac abnormalities. Auscultation did not detect a significant number of Bull Terriers with cardiac disease.     

Echocardiographic parameters in 14 healthy English Bull Terriers

OBJECTIVE: To determine the range of various cardiac parameters using echocardiography in apparently normal, healthy English Bull Terriers. DESIGN: Fourteen English Bull Terriers were selected for study. Cardiac auscultation of the parents of these dogs was normal. Echocardiographic examination of one parent of each animal showed: no mitral or aortic valve abnormalities; no myocardial lesions; no two dimensional evidence of fixed or dynamic left ventricular outflow tract obstruction; and no systolic aortic or left ventricular outflow tract turbulence on colour flow Doppler examination. The 14 selected dogs did not have arrhythmias or murmurs, and on echocardiographic examination had similar findings to their parents. Systolic blood pressure was measured in all dogs and they had no clinical evidence of Bull Terrier polycystic kidney disease or Bull Terrier hereditary nephritis. PROCEDURE: All dogs were auscultated and subjected to a sequential global echocardiographic assessment of the heart, including two dimensional long and short axis, and colour flow Doppler interrogation of the mitral and aortic valves. Dimensional measurements, including those from the left atrium, aortic annulus and left ventricle, were taken from a right parasternal window, and derived values such as fractional shortening, stroke volume and left atrial to aortic annulus ratio were calculated. Peak systolic aortic velocity was measured from the left parasternal window using two dimensional-guided pulsed wave Doppler with angle correction. Systolic blood pressure was measured using a Doppler monitor. The absence of Bull Terrier polycystic kidney disease was determined using renal ultrasonography, and of Bull Terrier hereditary nephritis using urinary protein to creatinine ratio. RESULTS: These 14 dogs had greater left ventricular wall thickness and smaller aortic root diameters than those reported as normal for other breeds of comparable body size. Left atrial dimensions were also larger, however this may have been due to the "maximising" method of measurement. These apparently normal English Bull Terriers also had higher aortic velocities than those reported for other breeds, possibly due to a smaller aortic root diameter or other anatomic substrate of the left ventricular outflow tract, lower systemic vascular resistance, or breed-specific "normal" left ventricular hypertrophy. While these dogs were selected to be as close to normal as possible, the breed may have a particular anatomy that produces abnormal left ventricular echocardiographic parameters. CONCLUSION: These echocardiographic parameters may be used to diagnose left ventricular outflow tract obstruction and left ventricular hypertrophy, and inaccurate diagnoses may result if breed-specific values are not used.     

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.     

Effect of various thoracic radiographic projections on the appearance of selected thoracic viscera

OBJECTIVES: To assess the effect of different radiographic projections on thoracic width, as well as position and visibility of the trachea, principal bronchi, cardiac silhouette, aorta, caudal vena cava (CVC) and oesophagus. METHODS: Right lateral recumbency (RLR), left lateral recumbency (LLR), dorsoventral (DV) and ventrodorsal (VD) thoracic radiographs of 42 dogs were reviewed retrospectively. RESULTS: In 78 per cent of cases the thoracic width was significantly larger on the VD projection than on the DV projection. The angle of divergence formed by the principal bronchi was significantly larger on the VD projection than on the DV projection in 80 per cent of dogs. A cardiac silhouette bulge at 1 to 2 o'clock was apparent on the VD projection in 22 per cent of dogs but was never seen on DV projections. The descending aorta was more visible at the 4 to 5 o'clock cardiac silhouette level on the DV projection and laterally at the T8 level on LLR projections. The CVC was better seen on VD and LLR projections. The oesophagus was visible as a soft tissue opacity in LLR in large dogs with normal thoracic conformation in 35 per cent of cases. CLINICAL SIGNIFICANCE: The DV projection appears to be more reliable for assessing the cardiac silhouette, the descending aorta and the angle of divergence of the principal bronchi. The VD projection should be considered for evaluating the CVC. LLR should be used for assessing the descending aorta and CVC.     

Echocardiography, electrocardiography, and radiography of cats with dilatation cardiomyopathy, hypertrophic cardiomyopathy, and hyperthyroidism

The echocardiographic, ECG, and radiographic findings of sequentially examined cats with dilatation cardiomyopathy (DCM, n = 7), hypertrophic cardiomyopathy (HCM, n = 8), and hyperthyroidism (HT, n = 20) were compared with those of healthy control cats (n = 11). Cats with DCM were easily differentiated from healthy cats by echocardiography and from cats with HCM and HT by a dilated left ventricle at end-diastole with a mean +/- SD of 2.20 +/- 0.36 cm, reduced fractional shortening (2.9% +/- 3.7%), reduced aortic amplitude (0.07 +/- 0.05 cm), reduced left ventricular wall amplitude (0.09 +/- 0.09 cm), and increased E-point septal separation (0.83 +/- 0.29 cm). The cats with HCM were most consistently recognized echocardiographically by increased left ventricular wall thickness at end-diastole (0.75 +/- 0.12 cm). Some cats with HT had abnormal echocardiograms with left ventricular wall hypertrophy. These cats could usually be differentiated from the cats with HCM because of normal or increased ventricular wall amplitude, aortic amplitude, or percentage of thickening of the left ventricular wall and interventricular septum. Left atrial enlargement (left atrial diameter greater than 1.57 cm or left atrium/aorta greater than 1.75) was commonly detected by the echocardiogram in cats with DCM, HCM, or HT. The echocardiogram was helpful in differentiating the type of cardiomyopathy (DCM, HCM, or HT) when plain thoracic radiographs indicated that cardiomegaly existed. The ECG may have indicated incorrectly that there was left ventricular enlargement in some cats with HT, and it did not indicate consistently that left ventricular enlargement existed when present in cats with DCM or HCM. The ECG was a poor indicator of left atrial enlargement in all cats.     

Ventricular septal defect with aortic valve insufficiency in a New Zealand White rabbit

A heart murmur was detected in a 10 mo old, female New Zealand White rabbit. Auscultation revealed cardiac murmurs both at the left and right hemithorax. Phonocardiography confirmed the systolic-diastolic nature of the left-sided and the systolic character of the right-sided murmur. Electrocardiography showed normal sinus rhythm; tall R waves and large T waves in lead II; and deep S waves in leads II, III, and aVF. Thoracic radiography demonstrated generalized cardiomegaly with prominent pulmonary vasculature. Echocardiography revealed a perimembraneous ventricular septal defect with aortic insufficiency. Signs of biventricular volume overload, relative pulmonic stenosis, and pulmonary valve insufficiency were also seen as consequences of the defect. Necropsy demonstrated a ventricular septal defect just below the aortic valve, a dilated pulmonary trunk, dilated and hypertrophied ventricles, dilated atria, and rightward displacement of the aortic root. Cardiac histopathology showed ventricular cardiomyocyte degeneration (swelling and hypereosinophilia of the cytoplasm with a loss of cross striation, and nuclear hyperchromasia), cartilaginous metaplasia of the aorta, and subendocardial fibrosis of the right ventricular flow tract.     

CLINICAL AND ELECTROCARDIOGRAPHIC FINDINGS IN SUSPECTED VIRAL MYOCARDITIS OF PUPS

Surviving puppies from three separate litters in which deaths had occurred from suspected viral myocarditis were examined clinically and electrocardiographically. Of 11 puppies examined, 5 subsequently died or were euthanised within 11 days of initial examination. ECG changes present in these puppies for 1 to 11 days prior to death were small R waves (less than 0.4 mV in lead II), S-T segment elevation, QRS notching and paroxysmal ventricular tachycardia (PVT). No clinical signs referable to the ECG changes were present before the terminal episodes of apparent sudden death or death following a brief period of dyspnoea. Multifocial subacute myocarditis was present on post-mortem examination. A sixth puppy with small R waves remained clinically normal for a further 4 weeks. It then developed severe dyspnoea which persisted for 24 hours before euthanasia. Extensive fibrosis of the left ventricle was present on post-mortem examination.     

Hypertropic cardiomyopathy and hyperthyroidism in the cat

In a 21/2-year period, hypertrophic cardiomyopathy was found at necropsy of 23 cats that died (13 cats) or were euthanatized (10) because of problems associated with hyperthyroidism. Of these, 4 (17%) also had evidence of cardiac failure (pulmonary edema or pleural effusion). The mean body weight of the cats with hyperthyroidism and hypertrophic cardiomyopathy was significantly less (P less than 0.001) than that of clinically normal cats and cats with primary cardiomyopathy (congestive or restrictive) or excessive moderator band cardiomyopathy. In addition, the ratio of heart weight to body weight was significantly greater (P less than 0.001) in the 23 hyperthyroid cats than in the normal cats and cats with primary cardiomyopathy. Twenty (87%) of the cats had symmetric hypertrophy of the ventricular septum and left ventricular free wall, whereas the remaining 3 cats had disproportionate thickening of the ventricular septum, compared with the free wall, similar to what is found in cats with asymmetric hypertrophic cardiomyopathy. Histologic cardiac abnormalities included large, hyperchromatic nuclei, interstitial fibrosis, endocardial fibroplasia, fibrosis of the atrioventricular node, and marked disorganization of cardiac muscle cells. The study showed that hypertrophic cardiomyopathy develops in most hyperthyroid cats, some of which also develop congestive heart failure. Although the signs of heart disease in primary myocardial disease and thyrotoxic disease are similar, the characteristic signalment and clinical signs of hyperthyroidism should lead one to suspect the association of hypertrophic cardiomyopathy with the hyperthyroidism.     

Review of left-to-right shunting patent ductus arteriosus and short term outcome in 98 dogs

The case records of 98 dogs with a left-to-right shunting patent ductus arteriosus (PDA) were reviewed. There were 35 breeds represented, with a female to male ratio of 3:1. Forty per cent of the dogs were older than one year at initial presentation and 31 per cent had clinical signs attributable to PDA. A left heart base continuous murmur of grade IV/VI or higher was noted in 90 per cent of the dogs. On electrocardiography, the most common abnormalities were tall R waves (63 per cent) and deep QII waves (62 per cent). The radiographic triad of dilation of the descending aorta with enlargement of the main pulmonary artery segment and left atrium, typical of PDA, was noted in only 26 per cent of cases. Two-dimensional (2D) and M-mode echocardiography detected left atrial enlargement (35 per cent) and an increased left ventricular diameter in diastole (82 per cent) and systole (84 per cent) as the most common abnormalities. Doppler echocardiography demonstrated increased aortic outflow velocities in 66 per cent of cases. The overall short-term successful outcome in this study was 95 per cent. There was no significant difference between surgical ductal ligation using a standard technique or the Jackson-Henderson technique in terms of survival, occurrence of haemorrhage or residual shunting. The number of interventional procedures used in this study was too low for statistical comparison, but there appeared to be a trend towards a higher rate of residual shunting and a lower fatality rate using a coil occlusion technique.     

Method of selective and non-selective angiocardiography for the horse

A practical and safe method of angiocardiography for the horse is described. The technique involved the rapid injection of 50 to 150 ml contrast agent via catheters in the right and left heart, pulmonary artery and aorta. The examination was carried out with the horse in the standing position or under general anaesthesia. Angiocardiograms were performed on 10 normal horses and satisfactory pictures of the right and left ventricles, pulmonary arteries, aorta and coronary circulation were obtained. The technique was also used in a foal with severe congenital heart disease. The most practical methods of recording the images in the standing position were cinefilm or video taperecording. In the recumbent position both cinefilm and radiographs were taken. No damage to the heart was inflicted by the catheters and only a few ventricular premature contractions (less than five) were produced by the pressure of injection. No signs of toxicity were recorded using repeated injections of contrast material (ie, less than 600 ml).     

CORRELATION OF RADIOGRAPHIC, ECHOCARDIOGRAPHIC, AND ELECTROCARDIOGRAPHIC SIGNS OF LEFT HEART ENLARGEMENT IN DOGS WITH MITRAL REGURGITATION

Thoracic radiographs of 40 dogs with mitral regurgitation were evaluated for signs of left heart enlargement and classified into three groups based on the degree of left atrial enlargement (mild = group A, moderate = group B, and severe = group C). Echocardiographic enlargement ratios were calculated for the left atrium (LAE_echo), the left ventricle (LVE_echo), and the aorta (AOE_echo) by dividing the measured dimension with the expected dimension normalized for body weight. The incidence of LVH patterns and p-mitrale was recorded on electrocardiograms. With advanced stages of the disease, there was good agreement of the radiographs and echocardiograms with significant differences of the left atrial enlargement ratio between groups. Nine of the 16 dogs from groups A and B, however, had LAE_echo ratios within the normal range. Sixteen dogs with radiographic signs of left ventricular enlargement had normal LVEecho ratios. These disagreements were interpreted as either cardiac enlargement not manifest in the dimensional change measured by the echocardiogram or as overreading of radiographs. The left ventricular wall thickness did not vary significantly between groups. The incidence of p-mitrale was 30%, but this ECG abnormality, when present, reliably identified enlarged left atrial dimensions. Left ventricular hypertrophy patterns of the ECG did not correlate with either the radiographic diagnosis of left ventricular enlargement or the echocardiographic enlargement ratios.     

Aortic foreign body (airgun pellet) embolism in a cat

A five-year-old female domestic shorthair cat presented with clinical signs typical of an aortic saddle thromboembolism. An echocardiogram and thoracic radiographs excluded cardiac disease as a source of the thrombus. Two heavy metal opacity, pellet-like objects were seen in the thoracic and abdominal radiographs. Abdominal ultrasound demonstrated occlusion of aortic blood flow by the abdominal pellet but could not indicate whether this was due to a penetrating aortic wound or pellet embolisation. A necropsy confirmed a penetrating left ventricular cardiac wound with subsequent embolisation of the pellet to the abdominal aorta.     

Influence of detomidine on echocardiographic function parameters and cardiac hemodynamics in horses with and without heart murmur

30 warmblood horses were examined before and after sedation with 20 micrograms/kg BW detomidine, to determine changes of cardiac function parameters, using B-mode, M-mode and Doppler echocardiography. 15 horses showed a heart murmur, but no clinical signs of cardiac heart failure, 15 horses had neither a heart murmur nor other signs of cardiac disease. After sedation with detomidine we could recognise a significant increase of end-diastolic left atrium diameter, an increase of end-systolic left ventricular diameter and aortic root diameter. The end-systolic thickness of papillary muscle and interventricular septum showed a decrease. Fractional shortening and amplitude of left ventricular wall motion was decreased after sedation. The mitral valve echogram revealed a presystolic valve closure and an inflection in the Ac slope (B-notch) in xy horses before sedation. Both increased after sedation with detomidine. Doppler echocardiography showed a decrease of blood flow velocity and velocity time integral (VTI) in the left and right ventricular outflow tract after sedation. Regurgitant flow signals were intensified following sedation in xy horses, especially at the mitral valve.     

Linear,logarithmic, and polynomial models of M-mode echocardiographic measurements in dogs

OBJECTIVE: To determine whether logarithmic and polynomial models are superior to simple linear models for predicting reference values for M-mode echocardiographic variables in dogs with a wide range of body weights. ANIMALS: 69 apparently healthy adult male and female dogs of various breeds, ages (range, 1 to 12 years; median, 3.5 years), and body weights (range, 3.9 to 977 kg; median, 25.4 kg). PROCEDURE: Echocardiographic M-mode measurements of the interventricular septum, left ventricular dimension (LVD), left ventricular wall, aorta, and left atrium were obtained. Simple linear, second-order polynomial, third-order polynomial, and logarithmic regression models were determined by use of the least-squares method to describe the relationship between M-mode measurements and body weight. Differences in adjusted R2 values of logarithmic and polynomial models were tested for significance of contribution, compared with the simple linear model. RESULTS: Significant differences in adjusted R2 were found when comparing simple linear with logarithmic or polynomial models for LVD-diastole, LVD-systole, aorta, and left atrium. Differences in adjusted R2 between second-order polynomial, third-order polynomial, and logarithmic models were not significant for any M-mode measurement. CONCLUSIONS AND CLINICAL RELEVANCE: In this study, logarithmic or second-order polynomial models predicted reference values of M-mode measurements for size of the cardiac chambers better than simple linear models for dogs with a wide range of body weights. Logarithmic and polynomial models were not superior to simple linear models for M-mode measurements of cardiac wall thickness.     

Survival time in dogs with spontaneous atrial fibrillation related to scintigraphically measured cardiac performance

In 40 canine patients with spontaneous atrial fibrillation (AF) cardiac performance was measured scintigraphically and correlated with the survival time (ST) following the diagnosis of AF. The parameters used for cardiac performance were heart rate (HR), end-diastolic left ventricular volume (EDV), ejection fraction of the left ventricle (EF), left ventricular regurgitation fraction (RF) and cardiac output (CO). ST varied from 3 days to 780 days. Two groups of animals were distinguished as previously described: group A (EF less than 0.3, n = 26) and group B (EF greater than or equal to 0.3, n = 14). The median ST (90 days) in group A was only weakly significant (p = 0.1) shorter than in group B (150 days). RF was significantly lower in group A than in group B (p less than 0.001). A weak correlation was found between ST and EF (r = 0.28; p = 0.04). It was concluded that the prognosis in the described AF patients is slightly favourable if EF is normal or only moderately reduced.     

Electrocardiographic and echocardiographic features of trypanosomiasis in dogs inoculated with North American Trypanosoma cruzi isolates.

Purebred Beagles were inoculated with Trypanosoma cruzi isolates from a North American opossum or armadillo (Tc-W), and dog (Tc-D). Although Tc-D established infection in dogs, the dogs did not develop cardiac abnormalities. Dogs inoculated with Tc-W developed acute myocarditis associated with increases in P-R interval, atrioventricular block, depression of R wave amplitude and shifts in mean electrical axis. Echocardiograms were normal during this stage. Three Tc-W-inoculated dogs died during the acute stage. Following the acute stage, 5 of 8 Tc-W-inoculated dogs entered an indeterminate stage in which ECG changes were minor and echocardiograms were normal. Progression to the chronic stage in 5 of the 8 Tc-W-inoculated dogs was indicated by development of ventricular-based arrhythmias, mainly ventricular premature contractions, between postinoculation days 60 and 170. In some dogs, ventricular premature contractions were multifocal. Electrocardiographic abnormalities progressively degenerated to various forms of ventricular tachycardia. Worsening ECG coincided with loss of left ventricular function as measured by echocardiography. Mean percent ejection fraction and percentage of fractional shortening decreased to 63% and 52% of control values, respectively. The left ventricular free wall (LVFW) thickness decreased and % septal: % LVFW thickening ratio increased, indicating a relative preservation of septal wall motion and LVFW hypokinesis.     

Canine hypertrophic cardiomyopathy.

Necropsy findings in 10 dogs with naturally occurring cardiac disease closely resembled hypertrophic cardiomyopathy in human beings and cats. Each dog had marked cardiac hypertrophy, and 8 dogs had disproportionate thickening of the ventricular septum with respect to the left ventricular free wall (compared with dogs with normal hearts or with cardiac hypertrophy due to acquired or congenital heart disease). Ratios of septum to free wall thickness in the 10 dogs ranged from 1.1 to 1.5, and 6 had ratios greater than or equal to 1.3. Marked cardiac muscle cell disorganization in the ventricular septum, characteristic of human patients with hypertrophic cardiomyopathy, was found in only 2 of the 10 dogs. Death occurred while the dogs were under anesthesia during the course of operative procedures (5 dogs) or unexpectedly in animals without previous manifestations of cardiac disease (3 dogs). Four dogs had clinical signs of congestive heart failure, including 2 with marked cardiac decompensation. Two of these 4 dogs with heart failure and 1 dog that died during unrelated surgery, but without prior signs of heart disease, had electrocardiographic evidence of complete heart block.