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.     

Echocardiographic findings in 103 cats with hyperthyroidism

Using M-mode echocardiography, cardiac abnormalities were studied in 103 cats with untreated hyperthyroidism. In addition, follow-up echocardiography was performed on 24 of these cats to assess the long-term (4 to 21 months) effect of treatment (thyroidectomy or radioiodine) on thyrotoxic cardiac disease. The most common echocardiographic abnormality in the 103 untreated hyperthyroid cats was hypertrophy of the left ventricular caudal wall (71.9%). Hypertrophy of the interventricular septum also was documented in 39.8% of the 103 cats. Other abnormalities included high values for left atrial diameter (70.0%), aortic root diameter (18.5%), and left ventricular diameter at end diastole (45.6%). In some of these cats, indices of contractility were enhanced; in 21.4% and 14.6% of the cats, values for shortening fraction and velocity of circumferential fiber shortening, respectively, were greater than those values measured in clinically normal cats. After treatment of the hyperthyroidism, left ventricular hypertrophy resolved or improved in many of the cats, as indicated by decreases in left ventricular caudal wall and interventricular septum thicknesses. Hyperdynamic wall motion resolved in all cats after treatment, as evidenced by consistent decreases in shortening fraction and velocity of circumferential fiber shortening. Despite these improvements, some cats had one or more persistently abnormal echocardiographic values after treatment. These results suggested that in cats, hyperthyroidism commonly is associated with largely reversible cardiomyopathy. In those cats in which cardiomyopathy persists or worsens after treatment, underlying primary cardiomyopathy or thyroid hormone-induced cardiac structural damage may exist.     

猫肥厚型心肌病与心肌纤维化

肥厚型心肌病是猫最常见的原发性心脏疾病,典型特征为心脏左心室肥厚。心肌纤维化是猫肥厚型心肌病的标志性病理变化,其可导致心脏功能障碍和节律异常,是心肌病患猫预后不良的重要因素。对于猫肥厚型心肌病与心肌纤维化,目前缺乏针对性治疗,新型治疗方法亟需开发。本综述总结了猫肥厚型心肌病的病理特征以及目前关于猫心肌纤维化发病机制的研究进展,拟通过探索心肌纤维化的发病机制,从而为猫肥厚型心肌病新型治疗药物的开发寻找突破点。     

Excessive moderator bands in the left ventricle of 21 cats

Excessive numbers of moderator bands bridging the left ventricular septum and free wall and entangling papillary muscles were associated with heart failure and death in 21 cats. Clinical findings included dyspnea, anorexia, hypothermia, cardiomegaly, pleural effusion, plumonary edema, heart murmurs, gallop rhythm, electrocardiographic abnormalities (especially conduction disturbances), increased left ventricular end-diastolic pressure, angiocardiographic evidence of left ventricular restriction, and aortic thromboembolism. Pathologic changes included a morphologically distinct network of abnormal numbers of moderator bands in the left ventricle, left ventricular hypertrophy (younger cats--mean age, 4 years) or dilatation (older cats--mean age, 8.7 years), left atrial enlargement and hypertrophy, and pulmonary edema with heart failure cells in the alveoli. Heart weights of affected cats were significantly less than those of cats with congestive, hypertrophic, and restrictive cardiomyopathy (endocardial fibrosis), but were not significantly less than heart weights of clinically normal cats. Pathologic changes were characteristic of the syndrome grossly and histologically, but clinical findings were not clearly definable.     

Congestive heart failure associated with hyperthyroidism in cats

Hyperthyroidism was diagnosed in 4 cats with congestive heart failure. Dyspnea and anorexia were observed in 3 of the 4 cats. In each cat, a holosystolic left and/or right apical heart murmur was auscultated. In 3 cats, a prominent extra heart sound (gallop rhythm) was auscultated. All cats had a palpably large thyroid lobe(s) and weight loss. The laboratory and ECG changes were similar to those reported for feline hyperthyroidism. Moderate-to-severe pleural effusion and cardiomegaly were detected via radiography in all cats. Some cats had radiographic signs of pulmonary venous engorgement and pulmonary edema. Echocardiography revealed cardiac dilatation and low left ventricular shortening fraction (wall motion) in all cats. Three cats responded initially to cardiac drugs and propylthiouracil or thyroidectomy. One of these died later, presumably from an adverse reaction to propylthiouracil, and the others died from recurrent congestive heart failure (1) or postoperative cardiac arrest (1). One cat did not respond to treatment, and died 2 days after diagnosis.     

Risk factors, clinical signs, and survival in cats with a clinical diagnosis of idiopathic hypertrophic cardiomyopathy: 74 cases (1985-1989).

Population characteristics, risk factors, and survival characteristics were evaluated in 74 cats with hypertrophic cardiomyopathy (HC) seen at North Carolina State University veterinary teaching hospital from 1985 to 1989, and compared with 82 clinically normal cats. The mean (+/- SD) age of cats with HC was 6.5 (4.0) years. Neutered males were at significantly greater risk (odds ratio 3.1) than neutered females. Breed, body weight, or coat color were not determined to be risk factors for HC. Tricolor cats were significantly underrepresented, probably reflecting the male predisposition for HC and not a true risk reduction associated with coat color. Forty-one cats were without clinical signs of heart disease (murmur and/or gallop sound only), 24 were in congestive heart failure, and 9 had systemic arterial embolism, 3 of which had concomitant congestive heart failure. The median survival time for 61 cats with HC, for which survival information could be obtained and that were not euthanatized on day 1, was 732 days. Survival was not affected by age at diagnosis, breed, body weight, or sex. However, clinical signs were important in determining prognosis; cats with heart rates greater than 200 beats/min survived significantly longer (median survival greater than 1,830 days) than those with heart rates greater than or equal to 200 beats/min (median survival = 152 days). Cats without clinical signs (median survival greater than 1,830 days) survived longer than those with clinical signs, and cats in heart failure survived a median of 92 days, compared with 61 days for those with systemic arterial embolism. Analysis of survival revealed no significant difference between the 2 groups of cats with clinical signs; however, all cats with embolism and only 60% of cats with heart failure were dead 6 months after diagnosis.     

Increased Serum Growth Hormone Concentration in Feline Hypertrophic Cardiomyopathy

Serum growth hormone concentration was measured by radioimmunoassay in 31 cats with hypertrophic cardiomyopathy, 38 normal cats, and 35 cats with other cardiac disease. Cats with hypertrophic cardiomyopathy had a significantly increased serum growth hormone concentration when compared with normal cats and cats with other cardiac disease. The serum growth hormone concentration in cats with hypertrophic cardiomyopathy was less than that previously reported in cats with growth hormone secreting pituitary tumors. Pituitary tumors were not identified in eight of the cats with hypertrophic cardiomyopathy examined at necropsy. An increased serum growth hormone concentration may be measured in cats with hypertrophic cardiomyopathy but it is unclear if the increased serum growth hormone concentration is a cause or effect of hypertrophic cardiomyopathy.     

Pathology of end-stage remodeling in a family of cats with hypertrophic cardiomyopathy

End-stage hypertrophic cardiomyopathy (ES-HCM), affecting 5-10% of human hypertrophic cardiomyopathy (HCM) patients, is characterized by relative thinning of the ventricular walls and septum with dilation of the ventricular lumen, decreased fractional shortening, and progression to heart failure. C. J. Baty and others recently documented similar progressive changes to ES-HCM in a family of four cats through serial echocardiograms. At the time of heart failure, these cats exhibited changes similar to those exhibited by human ES-HCM patients. Our objectives were to describe the pathologic alterations associated with ES-HCM and investigate the pathogenesis in three of the four cats. Grossly, there was left atrial dilation with relative thinning of the interventricular septum (IVS) and left ventricular free wall (LVFW). The left atrium contained large thrombi in two of the three cats, and all three cats died following thromboembolization of the aortic bifurcation. Histologically, all three cats had subendocardial and myocardial fibrosis, predominantly of the IVS and LVFW, and one cat had acute, multifocal, myocardial infarcts with mononuclear inflammatory cell infiltrates. The pathogenesis of ES-HCM is uncertain, but theories implicate occlusion of the coronary blood flow by thickening of the coronary vessels, coronary vascular thromboembolism or coronary vessel spasm, apoptosis of myocytes, and myocardial hypertrophy beyond the ability of the vasculature to supply blood. Apoptosis assays did not reveal any apoptotic myocytes. Considering the hypercoagulative state of these cats, coronary vascular thromboembolism could be a major contributing factor. We cannot exclude apoptosis or coronary vessel spasm on the basis of the data presented.     

Assessment of left atrial appendage flow velocity and its relation to spontaneous echocardiographic contrast in 89 cats with myocardial disease

The hypotheses of this prospective study were that (1) left atrial appendage (LAA) blood flow velocities can be recorded in cats with myocardial disease by transthoracic Doppler echocardiography, (2) LA enlargement, LA mechanical dysfunction, and left ventricular (LV) diastolic abnormalities are associated with decreased LAA flow velocities, and (3) low LAA flow velocities predict the appearance of spontaneous echocardiographic contrast in cats with cardiomyopathy. Transthoracic 2-dimensional, M-mode, and Doppler echocardiographic studies were performed in 89 cats with hypertrophic, restrictive, dilated, or unclassified cardiomyopathy or with hyperthyroid heart disease. Maximal LAA flow velocity (LAAmax) was decreased (P < .001) in cats with cardiomyopathy (median, 0.28 m/s; range, 0.08-1.35) compared to normal cats. Associated with decreased LAA flow velocities were increased LA size, decreased LA function, increased severity of LV diastolic dysfunction, and the presence of congestive heart failure. Multivariate logistic regression analysis detected an LAAmax <0.20 m/s as the only independent variable to predict LA spontaneous echocardiographic contrast (odds ratio, 30.1; 95% confidence interval [CI], 4.1 222.3; P < .001). Receiver operating characteristic analysis performed to predict spontaneous echocardiographic contrast indicated an area under the curve of 0.88 (95% CI, 0.80-0.95; P < .001) with sensitivities of 100 and 74% and specificities of 69 and 83% for LAAmax <0.25 and <0.20 m/s, respectively. Thus, low LAA flow velocities identified a subgroup of patients at increased risk of spontaneous echocardiographic contrast and possible thromboembolism. These findings may have important clinical implications for anticoagulation therapy and prognostication in cats with cardiomyopathy.     

Preferences of veterinarians for drugs to treat heart disease in dogs and cats

SUMMARY Responses (473) were collated from a questionnaire sent to 5054 veterinarians in Australia enquiring about drug preferences for treating cardiac disease in dogs and cats. When treating a small breed dog with endocardiosis and mild left congestive heart failure, 74% of 472 respondents used a diuretic, 67% a theophylline derivative, 27% a vasodilator and 20% a positive inotrope. Frusemide was the preferred diuretic and digoxin the preferred inotrope, but vasodilator use varied. Low sodium diets were “often recommended” by 71% of respondents. Propranolol was preferred to diltiazem for treating feline hypertrophic cardiomyopathy. Digoxin was clearly preferred for treating supraventricular dysrhythmias, while lignocaine and digoxin were preferred equally for ventricular dysrhythmias. Respondents appeared more willing than US veterinarians to use theophylline derivatives and prasozin, and less inclined to employ nitrates, hydralazine, inotropes other than digoxin, and low sodium diets.     

Dietary patterns of cats with cardiac disease

OBJECTIVE: To determine nutrient intake and dietary patterns in cats with cardiac disease. DESIGN: Prospective study. ANIMALS: 95 cats with congenital cardiac disease or primary cardiomyopathy. PROCEDURES: Owners completed a standardized telephone questionnaire regarding their cat's diet and a 24-hour food recall to determine daily intake of calories, fat, protein, sodium, magnesium, and potassium. RESULTS: Of the 95 cats, 18 (19%) had a history of congestive heart failure and 73 (77%) had no clinical signs of cardiac disease. Fifty-five percent (52/95) of cats had concurrent disease. Inappetance was reported in 38% (36/95) of all cats and in 72% (68/95) of cats with a history of congestive heart failure. Most (57% [54/95]) cats received treats or table scraps on a regular basis. Approximately half the cats were receiving orally administered medications, supplements, or both. Only 34% (32/68) of owners used food to administer medications to cats. Cats consumed more than the Association of American Feed Control Officials (AAFCO) minimums for protein, sodium, potassium, and magnesium, and nearly all cats consumed more than the AAFCO minimum for fat. Daily nutrient intake was variable for all of the nutrients assessed. CONCLUSIONS AND CLINICAL RELEVANCE: Dietary intake in cats with cardiac disease was variable, but results for dietary supplement use, food use for medication administration, and treat feeding were different from those found in a similar study of dogs with cardiac disease. This information may be useful for treating and designing nutritional studies for cats with cardiac disease.     

Cardiac troponin I in feline hypertrophic cardiomyopathy

Measurement of plasma cardiac troponin I concentration ([cTnI]) is a sensitive and specific means for detecting myocardial damage in many mammalian species. Studies have shown that [cTnI] increases rapidly after cardiomyocyte injury. The molecular structure of cTnl is highly conserved across species, and current assays developed for its detection in humans have been validated in many species. In this study, [cTnI] was quantified using a 2-site sandwich assay in plasma of healthy control cats (n = 33) and cats with moderate to severe hypertrophic cardiomyopathy (HCM) (n = 20). [cTnI] was significantly higher in cats with HCM (median, 0.66 ng/mL; range, 0.05-10.93 ng/mL) as compared with normal cats (median, <0.03 ng/mL; range, <0.03-0.16 ng/mL) (P < .0001). An increase in [cTnI] was also highly sensitive (sensitivity = 85%) and specific (specificity = 97%) for differentiating cats with moderate to severe HCM from normal cats. [cTnI] was weakly correlated with diastolic thickness of the left ventricular free wall (r2 = .354; P = .009) but not with the diastolic thickness of the interventricular septum (P = .8467) or the left atrium: aorta ratio (P = .0652). Furthermore, cats with congestive heart failure at the time of cTnI analysis had a significantly higher [cTnI] than did cats that had never had heart failure and those whose heart failure was controlled at the time of analysis (P = .0095 and P = .0201, respectively). These data indicate that cats with HCM have ongoing myocardial damage. Although the origin of this damage is unknown, it most likely explains the replacement fibrosis that is consistently identified in cats with moderate to severe HCM.     

Feline heart disease: An update

Heart disease is relatively common in cats and our understanding of feline cardiomyopathy has improved considerably over the last two decades, in part as a result of the improved sophistication of non-invasive diagnostic techniques. The incidence of feline dilated cardiomyopathy has declined markedly since the discovery of taurine deficiency as an aetiological factor and subsequent modification of commercial diets. Hypertrophic cardiomyopathy now seems to be the commonest primary form and is characterised by unexplained left ventricular hypertrophy and diastolic dysfunction. Intermediate forms of cardiomyopathy are also recognised. Secondary cardiomyopathies are common; examples of causes include hyperthyroidism, systemic hypertension and acromegaly. Congenital cardiac disease is also well recognised and may lead to clinical signs even late in life.     

Hypertrophic cardiomyopathy in an aged dog

A 14-year-old female Yorkshire terrier was presented with the complaint of cardiac murmur and convulsive seizure. Thickened mitral valve, left atrial enlargement, excess motions of the left ventricular (LV) free wall and the ventricular septum, and tricuspid, mitral and aortic valve regurgitations were recognized on echocardiography. Follow-up echocardiography revealed the progression of concentric LV hypertrophy and LV outflow obstruction. Clinical symptoms associated with cardiac failure did not develop during the observation period. The pathological examination of the heart revealed that the dog had the morphological hallmarks of hypertrophic cardiomyopathy: massive ventricular hypertrophy, disorganization of cardiac muscle cells, interstitial myocardial fibrosis, and abnormal intramural coronary arteries.     

Indirect determination of nitric oxide in cats with cardiomyopathy and arterial thromboembolism

Objective: To determine nitric oxide concentration in cats with hypertrophic or intermediate forms of cardiomyopathy and arterial thromboembolism (ATE) compared to healthy controls and to determine the association between nitric oxide concentration and the presence of ATE, congestive heart failure (CHF), and echocardiographic measurements. Design: Case–control study. Setting: Veterinary teaching hospital. Animals: Client‐owned cats with cardiomyopathy, cardiomyopathy and ATE, and normal cats. Interventions: None. Measurements: All cats underwent 2‐dimensional and M‐mode echocardiography. Nitric oxide was assessed indirectly by measuring the concentration of plasma nitrite+nitrate (NN), end products of nitric oxide metabolism. Plasma arginine concentration and dietary arginine content were also assessed since arginine is a precursor for nitric oxide production. Main results: Twenty‐six cats with cardiomyopathy, 26 cats with cardiomyopathy and ATE, and 29 nor‐mal cats were enrolled. Compared with healthy controls, median NN concentration was significantly higher in cats with cardiomyopathy and cats with both cardiomyopathy and ATE. There was no difference between cats with cardiomyopathy alone and cats with cardiomyopathy and ATE. Nitrate+ nitrite concen‐tration in cats with cardiac disease was unrelated to the presence of CHF, plasma arginine concentration, or dietary arginine content. In cats with cardiac disease, the left atrial diameter, left ven‐tricular diameter in diastole, and age were negatively correlated with NN concentrations. Conclusions: Nitric oxide concentration is elevated in cats with cardiac disease, but the elevation appears to be independent of ATE and CHF.     

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.     

Anesthetic concerns for patients with cardiomyopathy.

Hypertrophic cardiomyopathy usually affects cats. The overall cardiac dysfunction associated with hypertrophic cardiomyopathy relates to a decrease in diastolic function. Anesthetic regimens that minimize increases in heart rate and stress-related catecholamine release are desirable. Patients with dilative cardiomyopathy can present asymptomatic or in congestive heart failure. The overall myocardial defect is a depression of systolic function. An anesthetic regimen that minimizes myocardial depression is essential.     

Assessment of hypertension in 40 cats with left ventricular hypertrophy by Doppler-shift sphygmomanometry

Forty cats with left ventricular hypertrophic disease had blood pressure evaluated indirectly by Doppler-shift sphygmomanometry. Disease categories included hyperthyroidism, chronic renal insufficiency and hypertrophic cardiomyopathy unrelated to either of the first two disorders. Nineteen (47-5 per cent) of the 40 cats had systemic hypertension, nine had high systolic blood pressure only, 10 had high systolic and diastolic blood pressure, and none had only isolated diastolic hypertension. Blood pressure did not correlate with the degree of left ventricular thickness. The results of this study suggest a high prevalence of both left ventricular hypertrophy and systemic hypertension. Cause and effect relationships require further evaluation.     

A retrospective study of heart disease in doberman pinscher dogs

The prevalence of gross and/or histological cardiac lesions was found to be much greater in Doberman pinscher dogs (16/26 or 62%) than in non-Doberman dogs (124/417 or 30%). At least some of the affected Dobermans were unrelated. Middle aged (mean age 4.7 yr) Dobermans of both sexes (11 M:5F) were affected. Four of the Dobermans with heart lesions had congestive cardiomyopathy; three of these four had congestive heart failure and the other one died suddenly. Prominent gross lesions were ventricular dilation and atrioventricular valvular endocardiosis. Histological lesions noted were prominent myocardial fibrosis, myofiber degeneration with fatty replacement, myofiber vacuolation and arterial intimal cushion formation. A spectrum of myocardial disease exists in Dobermans and clinically overt congestive cardiomyopathy represents one end of this spectrum.     

Primary pulmonic infundibular stenosis in 12 cats: Natural history and the effects of balloon valvuloplasty

ObjectivesTo evaluate the natural history of primary pulmonic infundibular stenosis in cats and the effects of balloon valvuloplasty.BackgroundPrimary pulmonic infundibular stenosis is an uncommon congenital defect in cats. The natural history of the disease has not been described. Information regarding balloon valvuloplasty in the cat is limited.AnimalsRecords between January 1, 1999 and December 31, 2005 were reviewed and cats with a confirmed echocardiographic diagnosis of primary pulmonic infundibular stenosis, a complete medical history, and no evidence of significant systemic disease were identified.MethodsEchocardiographic, electrocardiographic, and radiographic findings are described. The natural history of those with severe disease was compared to those with mild to moderate disease. Balloon valvuloplasty was performed in six of the cats. The technique used is described.ResultsA stenotic gradient ≥70 mmHg and a right ventricular outflow tract (measured at the level of the stenosis) to pulmonary valve annulus ratio of ≤0.25 were consistent with clinical and echocardiographic severe disease. Cats with severe disease had a very guarded prognosis with a high incidence of congestive heart failure (CHF). Balloon valvuloplasty was successfully performed in 4 of the cats and appeared to improve prognosis, especially if performed prior to the development of CHF. Concurrent hypertrophic cardiomyopathy complicated the outcome in some cats.ConclusionsSevere primary pulmonic infundibular stenosis carries a very guarded prognosis in the cat. Balloon valvuloplasty should be considered in the presence of severe disease and should be performed prior to the development of CHF if possible. The presence of concurrent hypertrophic cardiomyopathy may complicate the prognosis.