Effect of spironolactone on diastolic function and left ventricular mass in Maine Coon cats with familial hypertrophic cardiomyopathy

BACKGROUND: Myocardial fibrosis occurs in cats with hypertrophic cardiomyopathy (HCM), and is one factor that leads to diastolic dysfunction. Spironolactone (SPIR) reduces myocardial fibrosis in several models of HCM and in humans with cardiac disease. HYPOTHESIS: SPIR will improve diastolic function and reduce left ventricular (LV) mass in Maine Coon cats with HCM. METHODS: Maine Coon cats with familial HCM were included if there was concentric hypertrophy (> or =6 mm end diastolic wall thickness) and decreased early lateral mitral annular velocity (Em) or summated early and late mitral annular velocity (EAsum) measured by pulsed wave tissue Doppler imaging echocardiography. Cats were paired by Em-EAsum and randomized to receive 2 mg/kg SPIR (n = 13) or placebo (n = 13) PO q12 h for 4 months. Em-EAsum, systolic velocity, LV mass, and the ratio of left atrial to aortic diameter were measured at baseline, 2 months, and 4 months. Statistical analysis included 2-way repeated measures analysis of variance and the Student's t-test. RESULTS: Plasma aldosterone concentration increased in cats treated with SPIR (235 ng/mL, baseline; 935 ng/mL, 2 months; 1,077 ng/mL, 4 months; P < .001 at 2 and 4 months). No significant treatment effect was identified for early or early-late summated diastolic mitral annular velocity or any other variable except plasma aldosterone concentration. Severe facial ulcerative dermatitis developed in 4 of 13 cats treated with SPIR, requiring discontinuation of the drug. CONCLUSION: SPIR did not improve Em or EAsum of the lateral mitral annulus or alter LV mass over 4 months. One third of cats treated with SPIR developed severe ulcerative facial dermatitis.     

Evaluation of the Calcium Channel-Blocking Agents Diltiazem and Verapamil for Treatment of Feline Hypertrophic Cardiomyopathy

To determine the efficacy of and clinical response to several pharmacologic agents for treatment of idiopathic hypertrophic cardiomyopathy in cats, 17 symptomatic cats were randomized to treatment with either propranolol, diltiazem, or verapamil. Clinical, laboratory, radiographic, electrocardiographic, and echocardiographic data were obtained before treatment and after 3 and 6 months of chronic oral therapy. Too few of the cats receiving propranolol or verapamil survived long enough to obtain long-term data needed to make statistical comparisons between groups. However, all 12 cats ultimately treated with diltiazem became asymptomatic, and no adverse effects from this drug were noted in any of these cats. Treatment with diltiazem was associated with a significant reduction of pulmonary congestion assessed radiographically (P less than 0.01), and improved ventricular filling based on echocardiographic measurements of left atrial size (P less than 0.05), left ventricular internal diastolic dimension (P less than 0.05), and relaxation time index (P less than 0.001). There was also a drug-related improvement in jugular venous oxygen tension (P less than 0.001) and blood lactate concentration (P less than 0.01) suggesting improved peripheral perfusion in the cats receiving diltiazem. The results indicate that diltiazem provides an effective and apparently safe treatment for the management of feline hypertrophic cardiomyopathy.     

Colour M-mode tissue Doppler imaging in healthy cats and cats with hypertrophic cardiomyopathy

OBJECTIVES: To determine whether decreased diastolic and systolic myocardial velocity gradient between the endocardium and the epicardium exist in the left ventricle of cats with hypertrophic cardiomyopathy. METHODS: Myocardial velocity gradient and mean myocardial velocities were measured by colour M-mode tissue Doppler imaging in the left ventricular free wall of 20 normal cats and 17 cats with hypertrophic cardiomyopathy. RESULTS: The peak myocardial velocity gradient (sec(-1)) during the first (E1) (5.71+/-1.75 versus 11.38+/-3.1, P<0.001) and second phase (E2) (3.09+/-1.53 versus 7.02+/-3.1, P=0.005) of early diastole and also the maximum early diastolic myocardial velocity gradient (Emax) (6.12+/-2.1 versus 10.76+/-3.2, P<0.001) were reduced in cats with hypertrophic cardiomyopathy compared with normal cats. Peak myocardial velocity gradient during early systole (Se) was lower in affected cats than in normal cats (6.26+/-2.08 versus 8.67+/-2.83, P=0.006). Affected cats had a lower peak mean myocardial velocities (mm/s) during the two isovolumic periods (IVRb and IVCb) compared with normal cats (2.97+/-6.76 versus 12.74+/-5.5 and 22.28+/-9.96 versus 38.65+/-10.1, P<0.001, respectively). CLINICAL SIGNIFICANCE: This study shows that hypertrophic cardiomyopathy cats have decreased myocardial velocity gradient during both diastole and systole and also altered myocardial motion during the two isovolumic periods. Myocardial velocity gradients recorded by colour M-mode tissue Doppler imaging can discriminate between the healthy and diseased myocardium.     

The effect of atenolol on NT-proBNP and troponin in asymptomatic cats with severe left ventricular hypertrophy because of hypertrophic cardiomyopathy: a pilot study

Background: Atenolol often is used empirically in cats with hypertrophic cardiomyopathy (HCM) before the onset of heart failure, although evidence of efficacy is lacking. Cardiac biomarkers play a critical role in the early detection of subclinical cardiac disease, in the prediction of long‐term prognosis, and in monitoring the response to therapy in humans. Hypothesis: Circulating concentrations of the biomarkers N‐terminal pro‐B type natriuretic peptide (NT‐proBNP) and cardiac troponin I (cTnI) will decrease after chronic administration of atenolol PO to cats with severe HCM but no signs of heart failure. Animals: Six Maine Coon or Maine Coon cross cats with severe HCM. Methods: Cats were treated with atenolol (12.5 mg PO q12 h) for 30 days. No cat had left ventricular dynamic outflow tract obstruction caused by systolic anterior motion of the mitral valve. The concentrations of NT‐proBNP and cTnI were assayed before and on the last day of drug administration. Results: There was no statistically significant change in NT‐proBNP (median before, 394 pmol/L; range, 71–1,500 pmol/L; median after, 439 pmol/L; range, 24–1,500 pmol/L; P = .63) or in cTnI (median before, 0.24 ng/mL; range, 0.10–0.97 ng/mL; median after, 0.28 ng/mL; range, 0.09–1.0 ng/mL; P = .69) after administration of atenolol. Conclusions: Atenolol administration did not decrease NT‐proBNP or cTnI concentrations in cats with severe left ventricular hypertrophy caused by hypertrophic cardiomyopathy. These results suggest that atenolol did not decrease myocardial ischemia and myocyte death in these cats. A larger clinical trial is warranted to verify these findings.     

Use of relaxation half-time as an index of ventricular relaxation in clinically normal cats and cats with hypertrophic cardiomyopathy

Relaxation half-time (t1/2) was evaluated as a measure of isovolumic ventricular relaxation in clinically normal cats and cats with hypertrophic cardiomyopathy. Relaxation half-time was determined directly from the left ventricular pressure tracing as the time required for the left ventricular pressure at the beginning of isovolumic relaxation to decrease by half. The value of t1/2 was unaffected by moderate changes in heart rate, inotropic state, and afterload in clinically normal cats. However, t1/2 increased significantly (P = 0.003) with increased preload. The value of t1/2 was significantly higher (P = 0.0003) in a group of cats with hypertrophic cardiomyopathy, compared with that of a group of clinically normal cats. Although t1/2 must be interpreted in the context of changes in loading conditions, the index is useful as a measure of relaxation in clinically normal cats and cats with hypertrophic cardiomyopathy.     

The effect of ramipril on left ventricular mass, myocardial fibrosis, diastolic function, and plasma neurohormones in Maine Coon cats with familial hypertrophic cardiomyopathy without heart failure

BACKGROUND: Hypertrophic cardiomyopathy (HCM) is the most common heart disease of cats, resulting in left ventricular (LV) hypertrophy, myocardial fibrosis, and diastolic dysfunction. HYPOTHESIS: Ramipril will reduce LV mass, improve diastolic function, and reduce myocardial fibrosis in cats with HCM without congestive heart failure (CHF). ANIMALS: This prospective, blinded, placebo-controlled study included 26 Maine Coon and Maine Coon cross-bred cats with familial HCM but without CHF. METHODS: Cats were matched for LV mass index (LVMI) and were randomized to receive ramipril (0.5 mg/kg) or placebo q24h for 1 year, with investigators blinded. Plasma brain natriuretic peptide (BNP) concentration, plasma aldosterone concentration, Doppler tissue imaging (DTI), and systolic blood pressure were measured at baseline and every 3 months for 1 year. Cardiac magnetic resonance imaging (cMRI) was performed to quantify LV mass and myocardial fibrosis by delayed enhancement (DE) cMRI at baseline and 6 and 12 months. Plasma angiotensin-converting enzyme (ACE) activity was measured on 16 cats 1 hour after PO administration. RESULTS: Plasma ACE activity was adequately suppressed (97%) in cats treated with ramipril. LV mass, LVMI, DTI, DE, blood pressure, plasma BNP, and plasma aldosterone were not different in cats treated with ramipril compared with placebo (P = .85, P = .94, P = .91, P = .89, P = .28, P = .18, and P = .25, respectively). CONCLUSION: Treatment of Maine Coon cats with HCM without CHF with ramipril did not change LV mass, improve diastolic function, alter DE, or alter plasma BNP or aldosterone concentrations in a relevant manner.     

Pharmacokinetic and Pharmacodynamic Properties of Conventional and CD-Formulated Diltiazem in Cats

The IV and apparent steady-state kinetics of diltiazem HCI (DLT) and slow-absorption long-acting diltiazem (CD) given PO were investigated in cats. The effects of PO diltiazem on heart rate and PR interval were also studied. Plasma diltiazem concentrations were determined by ultraviolet high-performance liquid chromatography (UV-HPLC), using vera-pamil as the internal standard. Heart rate and PR interval determinations were evaluated over a 24–hour period for the PO formulations and compared with values under diltiazem-free conditions. The mean systemic clearance and apparent volume of distribution of IV diltiazem were 15.0 mL/min/ kg and 2.70 L/kg, respectively. The elimination half-life of diltiazem after IV and PO DLT administration were approximately 120 minutes. In contrast, the terminal half-life of CD was 460 minutes. The mean apparent bioavailability of DLT PO was 71%, which was significantly higher than that observed with CD (36%). Heart rate and PR intervals in cats receiving the 2 formulations at steady-state were not different from those measured in the drug-free state. We conclude that DLT at 1 mg/kg PO tid and CD at 10 mg/kg PO sid provide plasma concentrations that are known to have pharmacodynamic effects in other species.     

Tolerability and efficacy of benazepril in cats with chronic kidney disease

The objective of the study was to test the effect of the angiotensin-converting enzyme inhibitor (ACEI) benazepril in cats with chronic kidney disease (CKD). A total of 192 cats with CKD with an initial plasma creatinine concentration > or = 2 mg/dL (> or = 177 micromol/L) and urine specific gravity < or = 1.025 were recruited into a double-blind, parallel-group, prospective, randomized clinical trial. Cats received daily (q24h) PO placebo (n = 96) or benazepril x HCl at a dosage of 0.5-1.0 mg/kg (n = 96) for up to 1,119 days. Most cats were fed exclusively a diet containing low amounts of phosphate, protein, and sodium. Benazepril produced a significant reduction in proteinuria, assessed by the urine protein-to-creatinine ratio (UPC, P = .005). This effect of benazepril was present in all subgroups tested, including cats with UPC <0.2, although the effect was largest in cats with higher UPCs. Plasma protein was maintained at higher concentrations with benazepril as compared with placebo during treatment in cats with initial UPC <1 (P = .038 versus P = .079 for all cats). There was no difference in renal survival time between the 2 groups when all 192 cats were compared. Mean +/- SD renal survival times were 637 +/- 480 days with benazepril and 520 +/- 323 days with placebo (P = .47). Mean +/- SD renal survival times in the 13 cats with initial UPC > or = 1 were 402 +/- 202 days with benazepril and 149 +/- 90 days with placebo (P = .27). Cats with initial UPC > or = 1 treated with benazepril had better appetite (P = .017) as compared with those treated with placebo. Benazepril was well tolerated. In conclusion, benazepril decreased proteinuria in cats with CKD.     

Tissue Doppler imaging and gradient echo cardiac magnetic resonance imaging in normal cats and cats with hypertrophic cardiomyopathy

Cats with hypertrophic cardiomyopathy (HCM) often develop diastolic dysfunction, which can lead to development of left congestive heart failure. Tissue Doppler imaging (TDI) echocardiography has emerged as a useful, noninvasive method for assessing diastolic function in cats. Cardiac magnetic resonance imaging (cMRI) has been performed in cats and accurately quantifies left ventricular (LV) mass in normal cats. However, assessment of cardiac function in cats by cMRI has not been performed. Six normal Domestic Shorthair cats and 7 Maine Coon cats with moderate to severe HCM were sedated, and TDI of the lateral mitral annulus was performed. Peak early diastolic velocity (Em) was measured from 5 nonconsecutive beats. Cats were anesthetized with propofol and electrocardiogram-gated gradient echo cMRI was performed during apnea after hyperventilation. Short-axis images of the LV extending from the mitral annulus to the apex were obtained throughout the cardiac cycle. LV mass at end systole and LV volumes throughout the cardiac cycle were quantified according to Simpson's rule. To assess the possible influence of propofol on diastolic function, TDI was performed on the 7 cats with HCM while sedated and then while anesthetized with propofol. Em was significantly lower in cats with HCM than normal cats (6.7 +/- 1.3 cm/s versus 11.6 +/- 1.9 cm/s, P < .001, respectively). There was no difference in the cMRI indices of diastolic function in normal and HCM cats. Propofol did not reduce diastolic function (Em) in cats with HCM but mildly reduced systolic myocardial velocity (S) in Maine Coon cats with HCM that were anesthetized with propofol (P = .87 and P = .03, respectively).     

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.     

Quantification of left ventricular diastolic wall motion by Doppler tissue imaging in healthy cats and cats with cardiomyopathy

OBJECTIVE: To assess Doppler tissue imaging (DTI) for evaluating left ventricular diastolic wall motion in healthy cats and cats with cardiomyopathy. ANIMALS: 20 healthy cats, 9 cats with hypertrophic cardiomyopathy (HCM), and 9 cats with unclassified cardiomyopathy (UCM). PROCEDURE: A pulsed wave DTI sample gate was positioned at a subendocardial region of the left ventricular free wall in the short axis view and at the lateral mitral annulus in the apical 4-chamber view. Indices of diastolic wall motion were measured, including peak diastolic velocity (PDV), mean rate of acceleration and deceleration of the maximal diastolic waveform (MDWaccel and MDWdecel, respectively), and isovolumetric relaxation time (IVRT). RESULTS: The PDV of cats with HCM and 6 of 9 cats with UCM was significantly decreased, compared with that of healthy cats. In the 3 cats with UCM that had a PDV that was not different from healthy cats, MDWaccel and MDWdecel were greater, and IVRT was shorter than those of healthy cats. The IVRT in cats with HCM was longer than that of other cats. CONCLUSIONS AND CLINICAL RELEVANCE: Indices of diastolic function in cats with HCM, and in many cats with UCM, differed from those of healthy cats and were similar to those reported in humans with HCM and restrictive cardiomyopathy, respectively. However, the hemodynamic abnormality was not the same for all cats with UCM; some cats with an enlarged left atrium and a normal left ventricle (ie, UCM) had abnormal left ventricular wall motion consistent with restrictive cardiomyopathy while others did not.     

Population characteristics and survival in 127 referred cats with hypertrophic cardiomyopathy (1997 to 2005)

Objectives : To evaluate the characteristics and survival of a recent population of cats with hypertrophic cardiomyopathy. Methods : Records at the Royal Veterinary College Queen Mother Hospital for Animals were searched for cats diagnosed with hypertrophic cardiomyopathy between 1997 and 2005. Referring veterinarians and owners were contacted to determine survival times. Results : Cats with hypertrophic cardiomyopathy were evaluated for population characteristics (n=127) and survival times (n=109). Overall median survival from date of hypertrophic cardiomyopathy diagnosis at the Queen Mother Hospital for Animals was 1276 days. Cats with hypertrophic cardiomyopathy were younger (P=0·009), and more likely to be male (P<0·001) compared to a hospital control group (n=1473), and Ragdolls were over-represented (P<0·05). Characteristics associated with increased survival in univariate analysis included younger age (P=0·007), asymptomatic status (P<0·001), normal left atrial size (P<0·001) and presence of systolic anterior motion of the mitral valve (P=0·003). Systolic anterior motion was associated with asymptomatic status, and did not influence survival in asymptomatic cats or those in congestive heart failure. Age, left atrial size and breed were significantly associated with survival time in a multivariate analysis. Clinical Significance : Cats with hypertrophic cardiomyopathy and left atrial enlargement have a poorer prognosis. The positive influence of systolic anterior motion on survival is likely to be linked to its association with asymptomatic status.     

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.     

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.     

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.     

Prospective Echocardiographic and Tissue Doppler Imaging Screening of a Population of Maine Coon Cats Tested for the A31P Mutation in the Myosin-Binding Protein C Gene: A Specific Analysis of the Heterozygous Status

Background: A mutation in the sarcomeric gene coding for the myosin-binding protein C gene has been identified in a colony of Maine Coon cats with hypertrophic cardiomyopathy (MyBPC3-A31P mutation). However, the close correlation between genotype and phenotype (left ventricular hypertrophy [LVH] and dysfunction) has never been assessed in a large population, particularly in heterozygous (Hetero) cats.
Objectives: To investigate LV morphology and function with echocardiography and tissue Doppler imaging (TDI) in a population of Maine Coon cats tested for the MyBPC3-A31P mutation with focus on Hetero animals.
Animals: Ninety-six Maine Coon cats.
Methods: Prospective observational study. Cats were screened for the MyBPC3-A31P mutation and examined with both echocardiography and 2-dimensional color TDI.
Results: Fifty-two out of 96 cats did not have the mutation (wild-type genotype, Homo WT), 38/96 and 6/96 were Hetero- and homozygous-mutated (Homo M) cats, respectively. Only 11% of Hetero cats (4/38) had LVH and 29% (10/34) of Hetero cats without LVH were >4 years old (4.1–11.5 years). LVH was also detected in 2 Homo WT cats (4%). A significantly decreased ( P < .05) longitudinal E/A (ratio between early and late diastolic myocardial velocities) in the basal segment of the interventricular septum was observed in Hetero cats without LVH (n = 34) compared with Homo WT cats without LVH (n = 50), thus confirming that the Hetero status is associated with regional diastolic dysfunction ( P < .05).
Conclusions: The heterozygous status is not consistently associated with LVH and major myocardial dysfunction. Moreover, Homo WT cats can also develop LVH, suggesting that other genetic causes might be implicated.     

Pulsed tissue Doppler imaging in normal cats and cats with hypertrophic cardiomyopathy

Myocardial motion was quantified in normal cats (n = 25) and cats with hypertrophic cardiomyopathy (HCM) (n = 23) using the pulsed tissue Doppler imaging (TDI) technique. A physiologic nonuniformity was documented in the myocardial motion of normal cats, which was detected as higher early diastolic velocities, acceleration, and deceleration in the interventricular septum compared with the left ventricular free wall (LVFW). HCM cats exhibited lower early diastolic velocities, acceleration, and deceleration and also prolonged isovolumic relaxation time compared with normal cats. These differences were detected mainly along the longitudinal axis of the heart. A cutoff value of E' in the LVFW along the longitudinal axis >7.2 cm/s discriminated normal from HCM cats with a sensitivity of 92% and a specificity of 87%. The physiologic nonuniformity of myocardial motion during diastole was lost in affected cats. Systolic impairment (decreased late-systolic velocities in most segments along the longitudinal axis and decreased early systolic acceleration in both mitral annular sites) was evident in HCM cats irrespective of the presence of left ventricular outflow tract obstruction and congestive heart failure. Postsystolic thickening was recorded in the LVFW along the longitudinal axis only in affected cats (n = 6) and was another finding indicative of systolic impairment in the HCM of this species. This study identified both diastolic and systolic impairment in cats with HCM compared with normal cats. The study also documents the normal physiologic nonhomogeneity in myocardial motion in cats and the subsequent loss of this feature in the HCM diseased state.     

Effect of pimobendan on case fatality rate in Doberman Pinschers with congestive heart failure caused by dilated cardiomyopathy

BACKGROUND: Despite traditional therapy of a diuretic, angiotensin converting enzyme inhibitor, digoxin, or a combination of these drugs, survival of dogs with dilated cardiomyopathy (DCM) is low. Pimobendan, an inodilator, has both inotropic and balanced peripheral vasodilatory properties. HYPOTHESIS: Pimobendan when added to conventional therapy will improve morbidity and reduce case fatality rate in Doberman Pinschers with congestive heart failure (CHF) caused by DCM. ANIMALS: Sixteen Doberman Pinschers in CHF caused by DCM. METHODS: A prospective randomized, double-blind, placebo-controlled study with treatment failure as the primary and quality of life (QoL) indices as secondary outcome variables. Therapy consisted of furosemide (per os [PO] as required) and benazepril hydrochloride (0.5 mg/kg PO q12h) and dogs were randomized in pairs and by sex to receive pimobendan (0.25 mg/kg PO q12h) or placebo (1 tablet PO q12h). RESULTS: Pimobendan-treated dogs had a significant improvement in time to treatment failure (pimobendan median, 130.5 days; placebo median, 14 days; P= .002; risk ratio = 0.35, P= .003, lower 5% confidence limit = 0.13, upper 95% confidence limit = 0.71). Number and rate of dogs reaching treatment failure in the placebo group precluded the analysis of QoL. CONCLUSIONS AND CLINICAL IMPORTANCE: Pimobendan should be used as a first-line therapeutic in Doberman Pinschers for the treatment of CHF caused by DCM.     

Pulsed Doppler assessment of left ventricular diastolic function in normal and cardiomyopathic cats.

Left ventricular (LV) diastolic function was evaluated in 16 cats with primary hypertrophic cardiomyopathy (HCM) using pulsed Doppler (PD) assessment of transmitral flow and isovolumic relaxation time. Data obtained was compared to data from 12 healthy, adult, research cats. Compared to normal cats, the HCM group showed significantly (p value less than 0.05) reduced early LV inflow velocities (mean +/- standard error [SE], peak velocity of 0.70+/-0.04 m/s versus 0.54+/-0.04 m/s and integrated velocity of 0.48+/-0.08 m/s versus 0.37+/-0.03 m/s); a reduced rate of deceleration of early inflow (mean+/-SE, -12.0+/-1.0 m/s2 versus -5.1+/-1.1 m/s2); prolonged isovolumic relaxation time (mean +/- SE, 45.7+/-3.3 ms versus 76.0+/-3.1 ms); and increased atrial systolic flow velocities (mean +/- SE, peak velocity of 0.29+/-0.04 m/s versus 0.48+/-0.04 m/s and integrated velocity of 0.21+/-0.03 m/s versus 0.34+/-0.03 m/s). The results suggest that PD provides a noninvasive method of identifying and quantifying functional diastolic impairment in cats with HCM.     

Tissue Doppler imaging in Maine Coon cats with a mutation of myosin binding protein C with or without hypertrophy

BACKGROUND: The cardiac myosin binding protein C gene is mutated in Maine Coon (MC) cats with familial hypertrophic cardiomyopathy. HYPOTHESES: Early diastolic mitral annular velocity is incrementally reduced from normal cats to MC cats with only an abnormal genotype to MC cats with abnormal genotype and hypertrophy. ANIMALS: Group 1 consisted of 6 normal domestic shorthair cats, group 2 of 6 MC cats with abnormal genotype but no hypertrophy, and group 3 of 15 MC cats with hypertrophy and abnormal genotype. METHODS: The genotype and echocardiographic phenotype of cats were determined, and the cats were divided into the 3 groups. Tissue Doppler imaging (TDI) of the lateral mitral annulus from the left apical 4-chamber view was performed. Five nonconsecutive measurements of early diastolic mitral annular velocity (EM) or summated early and late diastolic velocity (EAsum) and heart rate were averaged. RESULTS: There was an ordered reduction in Em-EAsum as group number increased (group 1, range 9.7-14.7 cm/s; group 2, range 7.5-13.2 cm/s; group 3, range 4.5-14.1 cm/s; P = .001). Using the lower prediction limit for normal Em-EAsum, the proportion of cats with normal Em-EAsum decreased as the group number increased (P = .001). However, Em-EAsum was reduced in only 3 of 6 cats in group 2. CONCLUSION: The incremental reduction of Em-EAsum as group severity increased indicates that diastolic dysfunction is an early abnormality that occurs before hypertrophy development. TDI measurement of Em or EAsum of the lateral mitral annulus is an insensitive screening test for identification of phenotypically normal, genotypically affected cats.