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.     

RADIOGRAPHIC AND ECHOCARDIOGRAPHIC ASSESSMENT OF LEFT ATRIAL SIZE IN 100 CATS WITH ACUTE LEFT‐SIDED CONGESTIVE HEART FAILURE

The aims of this study were to evaluate left atrial size in cats with acute left‐sided congestive heart failure. We hypothesized that left atrial size as determined by thoracic radiography can be normal in cats with acute left‐sided congestive heart failure. One hundred cats with acute left‐sided congestive heart failure in which thoracic radiography and echocardiography were performed within 12 h were identified. Left atrial size was evaluated using right lateral and ventrodorsal radiographs. Measurements were compared to two‐dimensional echocardiographic variables of left atrial size and left ventricular size. On echocardiography, left atrial enlargement was observed in 96% cats (subjective assessment) whereas maximum left atrial dimension was increased (>15.7 mm) in 93% cats. On radiographs left atrial enlargement (subjective assessment) was found in 48% (lateral view), 53% (ventrodorsal view), and 64% (any view) of cats whereas left atrial enlargement was absent in 36% of cats in both views. Agreement between both methods of left atrial size estimation was poor (Cohen's kappa 0.17). Receiver operating characteristic curve analysis identified a maximum echocardiographic left atrial dimension of approximately 20 mm as the best compromise (Youden index) between sensitivity and specificity in the prediction of radiographic left atrial enlargement. Left atrial enlargement as assessed by thoracic radiography may be absent in a clinically relevant number of cats with congestive heart failure. Therefore, normal left atrial size on thoracic radiographs does not rule out presence of left‐sided congestive heart failure in cats with clinical signs of respiratory distress.     

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.     

Hypercoagulability in cats with cardiomyopathy

BACKGROUND: Arterial thromboembolism (ATE) is a common complication of feline cardiomyopathy; however, the pathogenesis of ATE is unknown. HYPOTHESIS: Systemic activation of the coagulation cascade (hypercoagulability) and endothelial injury promote ATE in cardiomyopathic cats. ANIMALS: Healthy cats (n = 30) and 3 groups of cardiomyopathic cats: Group (1) left atrial enlargement only (LAE [n = 11]), ie, left atrial to aortic ratio >1.4; Group (2) LAE with spontaneous echocardiographic contrast, atrial thrombi or both (SEC-T [n = 16]); and Group (3) acute ATE with LAE (n = 16). METHODS: Hypercoagulability was defined by 2 or more laboratory abnormalities reflecting coagulation factor excess (high fibrinogen concentration or Factor VIII coagulant activity), inhibitor deficiency (low antithrombin activity), or thrombin generation (high thrombin-antithrombin complex [TAT] and d-dimer concentrations). High von Willebrand factor antigen concentration (vWF : Ag) was considered a marker of endothelial injury. Data were analyzed using nonparametric statistics. RESULTS: The 3 groups of cats with cardiac disease had higher median fibrinogen concentrations than did the healthy cats. Criteria of hypercoagulability were found exclusively in cats with SEC-T (50%) and ATE (56%). Hypercoagulability was not associated with left atrial size or congestive heart failure (CHF). ATE cats had significantly higher median vWF : Ag concentration than did the other groups. CONCLUSION AND CLINICAL IMPORTANCE: Systemic hypercoagulability is evident in many cardiomyopathic cats, often without concurrent CHF or overt ATE. Hypercoagulabilty may represent a risk factor for ATE. High vWF : Ag in ATE cats was attributed to downstream endothelial injury from the occlusive thrombus.     

Use of pimobendan in 170 cats (2006–2010)

Hypothesis/ObjectivesTo describe the therapeutic use of pimobendan in cats, describe the patient population to which it was administered, document potential side effects and report the clinical course following administration of pimobendan in conjunction with standard heart failure therapy. It is hypothesized that cats with advanced heart disease including congestive heart failure from a variety of causes will tolerate pimobendan with a minimum of side effects when used in treatment in conjunction with a variety of other medications.Animals, materials and methodsOne hundred and seventy client owned cats with naturally occurring heart disease, one hundred and sixty four of which had congestive heart failure. Medical records were reviewed and owners and referring veterinarians were contacted for follow-up data. Data collected included pimobendan dose, other medications administered concurrently, data collected at physical examination, presence or absence of heart failure, adverse effects, classification of heart disease, echocardiographic data and survival time. The data were analyzed for significance between the initial visit and any follow-up visits.ResultsAll cats were treated with pimobendan. The median pimobendan dose was 0.24 mg/kg q 12 h. Pimobendan was used in combination with multiple concurrent medications including angiotensin converting enzyme inhibitors, diuretics and anti-thrombotics. Five cats (3.0%) had potential side effects associated with pimobendan. One cat (0.6%) had presumed side effects severe enough to discontinue pimobendan use. Median survival time for 164 cats with congestive heart failure after initiation of pimobendan was 151 days (range 1–870).ConclusionPimobendan appears to be well tolerated in cats with advanced heart disease when used with a variety of concurrent medications. Randomized controlled studies need to be performed to accurately assess whether it is efficacious for treatment of congestive heart failure in cats.     

Congenital supravalvular mitral stenosis in 14 cats

ObjectivesTo describe the clinical features of congenital supravalvular mitral stenosis (SVMS) in cats.BackgroundSupravalvular mitral stenosis is an uncommon congenital cardiac defect that has not been previously reported in a series of cats.Animals14 cats with SVMS.MethodsMedical records, relevant diagnostic studies and preserved pathology specimens were reviewed.ResultsCats were presented over a wide age range (5 months–10 years; median 3 years); males (n = 9) and the Siamese breed were over-represented. Presenting complaints included respiratory distress (n = 6), hindlimb paralysis due to aortic thromboembolism (n = 5) and asymptomatic heart murmur (n = 3). Echocardiographic examination often identified pulmonary hypertension (PHT) (n = 7) and concurrent cardiac abnormalities (n = 7), especially partial atrioventricular septal defect (PAVSD) (n = 4). Status 12 months following diagnosis was known for 9 cats; 8 of these had died or were euthanized.ConclusionsCats with SVMS are usually presented as young adults for respiratory signs attributable to congestive heart failure, aortic thromboembolism or incidental murmur identification. Congestive heart failure, PHT and concurrent congenital cardiac abnormalities (specifically PAVSD) are common. Long-term prognosis for symptomatic cats is poor.     

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.     

Can ventricular function be assessed by echocardiography in chronic canine mitral valve disease?

Mitral regurgitation (MR) related to chronic degenerative valvular disease is the most important cause of heart failure in dogs. Ultrasound examination of the heart can identify valve lesions, confirm the presence of valvular regurgitation, document cardiac remodeling, estimate intracardiac pressures, and quantify systolic ventricular function. These findings can influence prognosis or selection of medical therapy. Reductions in ventricular systolic function may be detected on serial echocardiographic examinations in some dogs with MR. However the changes in ventricular loading that accompany MR often complicate these measurements. For example, shortening and ejection fractions are often increased in severe MR, even in the setting of congestive heart failure. Echocardiography with Doppler is also used to assess ventricular diastolic function and filling pressures. This information helps predict the risk of congestive heart failure. However these findings are often rendered ambiguous by age-related impairment of ventricular relaxation, elevations in left atrial pressure due to MR, and effects of volume overload on myocardial tissue velocities. These factors limit the usefulness of ventricular filling and tissue velocities, as well as derived ratios such as the E/E' ratio, for predicting congestive heart failure in MR. More advanced Doppler and tissue echocardiographic methods, as well as prospective clinical studies, are needed to reduce the ambiguity involved with assessment of ventricular function and filling pressures in the setting of MR.     

Congestive heart failure in horses: 14 cases (1984-2001)

OBJECTIVE: To identify clinical signs, underlying cardiac conditions, echocardiographic findings, and prognosis for horses with congestive heart failure. DESIGN: Retrospective study. ANIMALS: 14 horses. PROCEDURE: Signalment; history; clinical signs; clinicopathologic, echocardiographic, and radiographic findings; treatment; and outcome were determined by reviewing medical records. RESULTS: All 14 horses were examined because of a heart murmur; tachycardia was identified in all 14. Twelve horses had echocardiographic evidence of enlargement of 1 or more chambers of the heart. Other common clinical findings included jugular distention or pulsation, crackles, cough, tachypnea, and ventral edema. Nine horses had signs consistent with heart failure for > 6 days. Underlying causes for heart failure included congenital defects, traumatic vascular rupture, pericarditis, pulmonary hypertension secondary to heaves, and valvular dysplasia. Seven horses were euthanatized after diagnosis of heart failure; 5 were discharged but were euthanatized or died of complications of heart disease within 1 year after discharge. The remaining 2 horses were discharged but lost to follow-up. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that congestive heart failure is rare in horses. A loud heart murmur accompanied by either jugular distention or pulsation, tachycardia, respiratory abnormalities (crackles, cough, tachypnea), and ventral edema were the most common clinical signs. Echocardiography was useful in determining the underlying cause in affected horses. The long-term prognosis for horses with congestive heart failure was grave.     

Fatal acute lung injury after balloon valvuloplasty in a dog with pulmonary stenosis

A one-year-old French Bulldog was referred for the management of a severe form of pulmonary valve stenosis (PS) complicated by right-sided congestive heart failure.Echocardiography showed severe valvular PS with right ventricular concentric hypertrophy, dilatation and severe right atrial enlargement. A pulmonary balloon valvuloplasty (PBV) was performed with a balloon-to-pulmonary annulus ratio of 1.36. Echocardiography immediately after PBV showed a significant reduction in right atrial and ventricular size, improved opening and mobility of the pulmonary valve leaflets, and a 75% reduction in the pulmonary pressure gradient from 158 mmHg pre-operative to 40 mmHg post-operative. The dog recovered well from anesthesia, but 2 h later, it suddenly showed severe respiratory distress. Focus cardiac ultrasound showed increased left cardiac size with echocardiographic signs of high left ventricular filling pressure. Bedside lung ultrasound showed diffuse numerous-to-confluent B lines, compatible with a severe alveolar-interstitial syndrome. The dog was treated with furosemide, helmet continuous positive airway pressure, and then mechanical ventilation but without success.At post-mortem evaluation, histological examination of the lung showed diffuse, severe broncho-alveolar edema with mixed leukocyte, fibrin, and red blood cell infiltrate. Moreover, severe congestion and multifocal alveolar hemorrhages were evident. All findings were compatible with fatal acute lung injury after PBV secondary to pulmonary reperfusion-ischemia injury and increased pulmonary capillary hydrostatic pressure. Based on the present case, acute lung injury should be considered as a rare but serious complication of PBV.     

Multiple cardiac anomalies in a cat.

A 7-week-old domestic shorthair cat was examined because of congestive heart failure. Echocardiography and angiography were used to identify multiple cardiac anomalies. Because of the uncorrectable nature of the defects, the cat was euthanatized. Necropsy revealed persistent left vena cava, patent foramen ovale, and a right atrial/left ventricular canal. The right atrioventricular valve was replaced by a small ostium, and no chordae tendinae or papillary muscles were observed around the ostium. The pulmonary trunk originated from the right atrium. The right ventricular free wall was approximately 1 mm thick.     

Evaluation of circulating amino terminal-pro-B-type natriuretic peptide concentration in dogs with respiratory distress attributable to congestive heart failure or primary pulmonary disease

OBJECTIVE: To evaluate assessment of circulating amino terminal-pro-B-type natriuretic peptide (NT-proBNP) concentration as a means to discriminate between congestive heart failure and primary pulmonary disease in dogs. DESIGN: Prospective case series. ANIMALS: 46 dogs with signs of respiratory distress or coughing. PROCEDURES: All dogs underwent physical and thoracic radiographic examinations. Dogs with evidence of heart disease (eg, murmur, arrhythmia, or large cardiac silhouette detected by radiography) also underwent echocardiography. Dogs with no evidence of heart disease or failure were included if they underwent bronchoalveolar lavage (with cytologic examination and bacterial culture of the lavage fluid). Blood samples for NT-proBNP assay were obtained within 12 hours of the diagnosis of heart failure or prior to bronchoalveolar lavage in dogs with primary pulmonary disease. Circulating concentrations of NT-proBNP were compared between groups and correlated with radiographic and echocardiographic measures of cardiac size. RESULTS: Congestive heart failure and primary pulmonary disease were diagnosed in 25 and 21 dogs, respectively. Dogs with congestive heart failure had significantly higher median serum or plasma NT-proBNP concentration (2,554 pmol/L; interquartile [25% to 75%] range, 1,651.5 to 3,475.5 pmol/L) than dogs with primary pulmonary disease (357 pmol/L; interquartile range, 192.5 to 565.5 pmol/L). Radiographic vertebral heart score and echocardiographic left atrial-to-aortic diameter ratio were not correlated with NT-proBNP concentration. Left ventricular end-diastolic diameter (measured echocardiographically) and NT-proBNP concentration were weakly correlated. CONCLUSIONS AND CLINICAL RELEVANCE: Serum or plasma NT-proBNP concentration assessment may be useful for discrimination of congestive heart failure from primary pulmonary disease in dogs with respiratory distress or cough.     

Cardiac Troponin‐I Concentration,Myocardial Arteriosclerosis,and Fibrosis in Dogs with Congestive Heart Failure because of Myxomatous Mitral Valve Disease

Background

Few previous studies have investigated the association between biomarkers and cardiac disease findings in dogs with naturally occurring myxomatous mitral valve disease (MMVD).

Aim

To investigate if histopathological changes at necropsy could be reflected by in vivo circulating concentrations of cTnI and aldosterone, and renin activity, in dogs with naturally occurring congestive heart failure because of MMVD.

Animals

Fifty privately owned dogs with MMVD and heart failure.

Methods

Longitudinal Study. Dogs were prospectively recruited and examined by clinical and echocardiographical examination twice yearly until time of death. Blood was stored for batched analysis of concentrations of cTnI and aldosterone, and renin activity. All dogs underwent a standardized necropsy protocol.

Results

cTnI were associated with echocardiographic left ventricular end‐diastolic dimension (P < .0001) and proximal isovolumetric surface area radius (P < .004). Furthermore, in vivo cTnI concentrations reflected postmortem findings of global myocardial fibrosis (P < .001), fibrosis in the papillary muscles (P < .001), and degree of arterial luminal narrowing (P < .001) Aldosterone or renin activity did not reflect any of the cardiac disease variables investigated.

Conclusion and clinical importance

Cardiac fibrosis and arteriosclerosis in dogs with MMVD are reflected by circulating cTnI concentration, but not by aldosterone concentration or renin activity. Cardiac troponin I could be a valuable biomarker for myocardial fibrosis in dogs with chronic cardiac diseases.     

Third-degree atrioventricular block in 21 cats (1997-2004)

The effect of 3rd-degree atrioventricular block on long-term outcome in cats is unknown. Clinical findings and long-term outcome of 21 cats with 3rd-degree atrioventricular block were studied retrospectively. Median age of cats studied was 14 years (range 7-19 years). Presenting signs included respiratory distress or collapse, but 6 cats had no clinical signs of disease. Eight cats had congestive heart failure (CHF) at the time that 3rd-degree atrioventricular block was detected. Heart rates ranged from 80 to 140 beats per minute (bpm; median 120 bpm) with no difference in heart rate between cats with and those without CHF. Eleven of 18 cats that had echocardiograms had structural cardiac disease, and 6 cats had cardiac changes consistent with concurrent systemic disease. No atrioventricular nodal lesions were detected by echocardiography. One cat had atrioventricular nodal lesions detected on histologic examination. Median survival of 14 cats that died or were euthanized was 386 days (range 1-2,013 days). Survival did not differ between cats with or without CHF or between cats with or without structural cardiac disease. Thirteen cats with 3rd-degree atrioventricular block survived > 1 year after diagnosis, regardless of presenting signs or underlying cardiac disease. Third-degree heart block in cats is often not immediately life threatening. Survival was not affected by the presence of underlying heart disease or congestive heart failure at the time of presentation. Even cats with collapse might survive > 1 year without pacemaker implantation.     

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.     

Reversible pulmonary hypertension in a cat

A 13-year-old, neutered female domestic shorthair cat was presented for sudden respiratory distress following palliative radiotherapy and the combined administration of a single dose of carboplatin for the treatment of recurrent fibrosarcoma. Clinical and radiographic findings were suggestive of pleural effusion. Echocardiography revealed marked right-sided cardiac enlargement associated with tricuspid regurgitation and Doppler evidence of pulmonary hypertension. After 25 days of treatment for congestive heart failure and suspected pulmonary thromboembolism, clinical signs and echocardiographic and Doppler evidence of right-sided cardiac enlargement and pulmonary hypertension had completely resolved. To the best of the authors' knowledge, this is the first report of reversible pulmonary hypertension, likely secondary to pulmonary thromboembolism, in a cat.     

Echocardiographic changes in heart size in hypohydrated horses

Background: Hypohydration causes transient echocardiographic changes in pigs, dogs, humans, and cats. These changes mask the diagnosis of some cardiac diseases (valvular regurgitation, dilated cardiomyopathy) and promote the diagnosis of others (hypertropic cardiomyopathy and infiltrative disease), thus inhibiting accurate echocardiographic evaluation. Objectives: To describe the echocardiographic changes associated with hypohydration in normal horses. Animals: Ten adult horses without detectable cardiac disease. Methods: Experimental study. Echocardiographic examinations were performed on horses in the euhydrated and hypohydrated states. Horses were hypohydrated by combined water deprivation and furosemide administration until a 4–7% reduction in bodyweight was achieved. Statistical analyses were performed by paired t‐tests. Results: Hypohydration decreased left ventricular internal diameter in systole (0.8 ± 0.6 cm) and diastole (1.7 ± 0.9 cm), left atrial diameter (1.5 ± 0.4 cm) and left ventricular volume (490 ± 251 mL) (P‐values < .01), and increased septal wall thickness in diastole (0.6 ± 0.3 cm), free wall thickness in diastole (0.5 ± 0.3 cm), mean wall thickness (0.5 ± 0.2 cm) and relative wall thickness (0.2 ± 0.1 cm) (P‐values < .01). Conclusions and Clinical Importance: Hypohydration produces changes in left ventricular and atrial size that could mask or promote the severity of cardiac disease. The thickened, “pseudohypertrophied” appearance of the left ventricle in hypohydrated horses could affect interpretation of echocardiographic variables that are applied to the prediction of athletic performance. Echocardiography may prove a noninvasive method of monitoring volume status and response to fluid therapy in hypovolemic horses.     

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.     

M-MODE ECHOCARDIOGRAPHY AS A DIAGNOSTIC AID FOR FELINE CARDIOMYOPATHY

Normal cats and cats with congestive cardiomyopathy (CCM) and hypertrophic cardiomyopathy (HCM) were examined using M-mode echocardiography to determine its diagnostic capabilities. Sixteen normal cats were examined to verify previously reported data and to add further echocardiographic inforamtion (left atrial/aortic root ratio, left posterior wall thickness at end systole and end diastole, amplitude of mitral valve excursions, and velocity of valve opening and closure) to aid in differential diagnosis. Significant (p<0.05) changes were detected between the normal cats and those with cardiomyopathy. In each type of cardiomyopathy, alterations in left atrial dimension, left atrial/aortic root ratio, left ventricular dimension, left ventricular wall thickness and percentage of ventricular dimensional change were identified. Altered mitral valve motion was found with HCM. Echocardiography was found to be an accurate technique for definitive diagnosis of feline cardiomyopathy.     

Treatment of three cats with hyperviscosity syndrome and congestive heart failure using plasmapheresis

Three cats were evaluated at a veterinary teaching hospital for congestive heart failure (CHF) secondary to hyperviscosity syndrome from plasma cell neoplasia. All cats had severe hyperproteinemia due to hyperglobulinemia. Multiple myeloma or plasma cell neoplasia was diagnosed based on cytopathology and post mortem examination. The cats presented with signs of CHF including acute collapse, tachypnea, increased respiratory effort, and pulmonary crackles. All cats had heart murmurs and echocardiographic signs consistent with hypertrophic cardiomyopathy. An enlarged left atrium was found in all cats and two of three cats also had spontaneous echocardiographic contrast. Plasmapheresis (centrifugal plasma exchange) was performed on all three cats by the removal of whole blood and the infusion of a balanced electrolyte solution while the whole blood was centrifuged and separated. The RBCs were then washed before being readministered to the patient. Plasmapheresis alleviated the clinical signs of CHF (tachypnea) in all three cats. Plasmapheresis should be considered in cases of CHF secondary to hyperviscosity syndrome to rapidly alleviate clinical signs associated with heart failure while diagnosis of the underlying cause is made and appropriate therapy implemented.