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.     

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.     

Comparison of myocardial contrast enhancement via cardiac magnetic resonance imaging in healthy cats and cats with hypertrophic cardiomyopathy

OBJECTIVE: To quantify myocardial contrast enhancement (MCE) of the left ventricle (LV) by use of cardiac magnetic resonance imaging (CMRI) in healthy cats and cats with hypertrophic cardiomyopathy (HCM) and to compare MCE between the 2 groups. ANIMALS: 10 healthy cats and 26 Maine Coon cats with moderate to severe HCM but without clinical evidence of congestive heart failure. PROCEDURE: Anesthetized cats underwent gradient echo CMRI examination. Short-axis images of the LV were acquired before and 7 minutes after IV administration of gadolinium dimeglumine. Regions of interest were manually traced in the quadrants of 5 mid-LV slices acquired at end systole, and the MCE percentage was calculated from summed weight-averaged data from all slices. Doppler tissue imaging echocardiography was performed to measure the early diastolic myocardial velocity (Em) as an index of diastolic function. Three-way repeated-measures ANOVA was used to determine differences in MCE between cats with HCM and healthy cats. Simple linear regression was used to assess whether MCE was correlated with LV mass, LV mass index (LVMI), or Em. A Student t test was used to compare the SDs of the postcontrast myocardial signal intensity between the 2 groups. RESULTS: There was no difference in MCE between cats with HCM and healthy cats. There was no correlation of MCE with LV mass, LVMI, or Em. There was no difference in heterogeneity of signal intensities of LV myocardium between the 2 groups. CONCLUSIONS AND CLINICAL RELEVANCE: Contrast-enhancement CMRI was not useful in detecting diffuse myocardial fibrosis 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.     

Reference range values of regional left ventricular myocardial velocities and time intervals assessed by tissue Doppler imaging in young nonsedated Maine Coon cats

OBJECTIVE: To describe and analyze the left ventricular free wall (LVFW) radial and longitudinal motions in a population of healthy Maine Coon cats by use of quantitative 2-dimensional color tissue Doppler imaging (TDI). ANIMALS: 23 healthy young Maine Coon cats (mean +/- SD: age, 2.1 +/- 0.9 years; weight, 5.0 +/- 1.0 kg). PROCEDURE: TDI was performed by the same trained observer (VC) on all cats. Radial LVFW velocities were recorded in endocardial and epicardial LVFW segments, and longitudinal velocities were recorded in the mitral annulus and in basal and apical LVFW segments. Isovolumic contraction and relaxation times were calculated in each myocardial segment, and the coefficients of variation (CVs; %) were determined for each TDI parameter. RESULTS: LVFW velocities were significantly higher in the endocardial layers than in the epicardial layers and also significantly higher in the basal than in the apical segments. Annular velocities were significantly higher than basal myocardial velocities in systole and early diastole. Coefficient of variation values were lower for radial velocities, particularly in systole, and were also lower for time intervals (16% to 22%) than for myocardial velocities (19% to 62%). CONCLUSIONS AND CLINICAL RELEVANCE: Because Maine Coon cats are predisposed to an inherited hypertrophic cardiomyopathy, which is a common cause of death in this breed, TDI could provide a useful tool for early detection of the disease. Tissue Doppler imaging indices may complete the conventional analysis of the left ventricular function in Maine Coon cats. However, the usefulness of TDI indices in the early detection of myocardial dysfunction needs to be clarified.     

Assessment of left ventricular longitudinal function in cats with subclinical hypertrophic cardiomyopathy using tissue Doppler imaging and speckle tracking echocardiography

Hypertrophic cardiomyopathy (HCM) in cats is characterized by concentric left ventricular (LV) hypertrophy and both diastolic and systolic dysfunction. Although impaired cardiac function detected by tissue Doppler imaging (TDI) in cats with HCM was previously reported, reference ranges of TDI in normal cats and cats with HCM have been reported as widely variable. Two-dimensional speckle tracking echocardiography (STE) was useful for assessment of cardiac function in human patients with HCM, but clinical utility was not known in cats. The aim of this study was to assess global and segmental LV myocardial function using STE in cats with HCM whose TDI variables were within the reference range. A total of 35 cats of different breeds were enrolled in this study. The HCM group (n=22) was cats diagnosed as HCM without left atrial enlargement and with normal TDI measurements. HCM cats were further divided into a segmental hypertrophy (S-HCM) group and a diffuse hypertrophy (D-HCM) group. The control group consisted of 13 clinically healthy cats. No cats in any group showed any clinical symptoms. Conventional echocardiography, TDI, and global and segmental STE indices were evaluated and compared between groups. Only the longitudinal strain rate during early diastole was significantly decreased in both HCM groups, even in all segments including those without hypertrophy in S-HCM group. This study suggests that STE parameters are the more sensitive variables compared with conventional TDI parameters to detect early myocardial diastolic dysfunction in cats with HCM.     

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.     

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.     

NT-proBNP measurement fails to reliably identify subclinical hypertrophic cardiomyopathy in Maine Coon cats

The purpose of this study was to evaluate the value of measuring plasma NT-proBNP concentration as a screening tool in cats with varying severity of subclinical hypertrophic cardiomyopathy (HCM). Plasma NT-proBNP concentration was measured in 35 cats that had previously been classified as normal, equivocal, moderate HCM or severe HCM via echocardiography. No cat had ever been in congestive heart failure. Cats with severe HCM had a significantly higher NT-proBNP concentration compared to the other groups (P<0.0003), however, the sensitivity of NT-proBNP for diagnosing cats with severe disease was only 44% (cutoff≤100pmol/l) to 55% (cutoff≤40pmol/l). There was no significant difference in NT-proBNP concentration between normal, equivocal and moderate categories (sensitivity for detecting moderate HCM was 0%). Based on the results of this study, NT-proBNP concentration is not considered adequate as a screening test for detecting mild to moderate HCM in Maine Coon cats and it appears that it may miss many cats with severe HCM.     

QUANTIFICATION OF LEFT VENTRICULAR MASS USING CARDIAC MAGNETIC RESONANCE IMAGING COMPARED WITH ECHOCARDIOGRAPHY IN DOMESTIC CATS

The hypotheses were that cardiac magnetic resonance imaging (cMRI) would accurately determine LV mass in domestic cats and would do so more accurately than echocardiography (ECHO). ECHO was performed on seven sedated cats. LV mass was calculated using the truncated ellipse formula from a right parasternal long-axis view. T1 weighted gradient echo cMRI was acquired from anesthetized cats during multiple phases of the cardiac cycle. Short-axis images were obtained by acquiring 3 mm thick contiguous slices perpendicular to the cardiac long axis. LV mass was determined using Simpson's rule. Endocardial and epicardial borders were traced on each slice at end-systole, end-diastole, and mid-cycle and the difference in areas was myocardial area. Myocardial area was multiplied by slice thickness to calculate myocardial volume. Total (summated) myocardial volume was multiplied by myocardial density (1.05) to obtain LV mass at three measured phases of the cardiac cycle. Cats were euthanized and the LV was dissected and weighed to determine true mass. CMRI at end-systole most accurately quantified LV mass and was more accurate than echocardiography (P = 0.0078). Actual LV mass ranged from 6.5 to 10.5 g (mean = 8.5 g, SD = 1.6 g) compared with MRI LV mass at end-systole, which ranged from 6.7 to 11.1 g (mean = 8.7 g, SD = 1.7 g) and echocardiographic LV mass at enddiastole, which ranged from 5.2 to 9.1 g (mean= 7.1 g, SD = 1.8 g). Inter- and intraobserver variability for cMRI was 2%. CMRI obtained at end-systole accurately and reliably quantifies LV mass in domestic cats. It is more accurate than the echocardiographic method used in this study.     

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.     

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.     

Investigation into the use of plasma NT-proBNP concentration to screen for feline hypertrophic cardiomyopathy

ObjectiveTo evaluate the utility of feline NT-proBNP plasma concentration [NT-proBNP] as a screening tool for cats with subclinical hypertrophic cardiomyopathy (HCM).Animals, materials and methodsForty adult Maine Coon or Maine Coon crossbred cats from the feline HCM research colony at the University of California, Davis were studied. All cats had previously been genotyped as heterozygous or negative for the A31P myosin binding protein C (MYBPC) mutation. Echocardiograms were performed to assess the severity of HCM in each cat. Blood samples were collected for evaluation of [NT-proBNP].ResultsIn these cats with severe HCM, [NT-proBNP] was significantly elevated (P < 0.0001) when compared to all other groups of cats and an [NT-proBNP] > 44pmol/L accurately predicted the presence of severe HCM. However, [NT-proBNP] was not increased in cats with moderate or equivocal HCM when compared to normal cats. Cats heterozygous for the MYBPC mutation had a significantly elevated [NT-proBNP] when compared to cats without the A31P mutation (P = 0.028).ConclusionsMeasurement of [NT-proBNP] has a high sensitivity and specificity as a means of detecting severe HCM in cats, but it is not sensitive for the identification of moderate HCM as judged by the evaluation of Maine Coon and Maine Coon cross cats in our colony. Consequently, we conclude that this test cannot be used to screen cats for the presence of mild to moderate HCM.     

Prevalence of myocardial hypertrophy in a population of asymptomatic Swedish Maine coon cats

Background

Maine coon cats have a familial disposition for developing hypertrophic cardiomyopathy (HCM) with evidence of an autosomal dominant mode of inheritance [1]. The current mode to diagnose HCM is by use of echocardiography. However, definite reference criteria have not been established. The objective of the study was to determine the prevalence of echocardigraphic changes consistent with hypertrophic cardiomyopathy in Swedish Maine coon cats, and to compare echocardiographic measurements with previously published reference values.

Methods

All cats over the age of 8 months owned by breeders living in Stockholm, listed on the website of the Maine Coon breeders in Sweden by February 2001, were invited to participate in the study. Physical examination and M-mode and 2D echocardiographic examinations were performed in all cats.

Results

Examinations of 42 asymptomatic Maine coon cats (10 males and 32 females) were performed. The age of the cats ranged from 0,7 to 9,3 years with a mean of 4,8 ± 2,3 years. Four cats (9,5%) had a diastolic interventricular septal (IVSd) or left ventricular free wall (LVPWd) thickness exceeding 6,0 mm. In 3 of these cats the hypertrophy was segmental. Two cats (4,8%) had systolic anterior motion (SAM) of the mitral valve without concomitant hypertrophy. Five cats (11,9%) had IVSd or LVPWd exceeding 5,0 mm but less than 6,0 mm.

Conclusion

Depending on the reference values used, the prevalence of HCM in this study varied from 9,5% to 26,2%. Our study suggests that the left ventricular wall thickness of a normal cat is 5,0 mm or less, rather than 6,0 mm, previously used by most cardiologists. Appropriate echocardiographic reference values for Maine coon cats, and diagnostic criteria for HCM need to be further investigated.     

Association of A31P and A74T Polymorphisms in the Myosin Binding Protein C3 Gene and Hypertrophic Cardiomyopathy in Maine Coon and Other Breed Cats

Background: Hypertrophic cardiomyopathy (HCM) is an inherited autosomal dominant trait in cats. The A31P single nucleotide polymorphism (SNP) in the myosin binding protein C 3 gene is thought to be the causative mutation in Maine Coon cats. Additionally, the A74T SNP is offered as a genetic test for HCM. Objectives: To evaluate the genetic association between the above‐mentioned SNPs and phenotypes. Animals: Eighty‐three Maine Coon cats and 68 cats of other breeds. Methods: The study was performed prospectively. Cats were phenotyped as healthy or HCM with echocardiography. Taqman genotyping assays were used for genotyping; results were confirmed by sequencing analysis. Results: A31P was found in 18/83 (22%) Maine Coon cats. Fifteen of 18 Maine Coons (83%) with the A31P mutation were healthy on echocardiographic examination (mean age 65 months). A74T was present in 28/79 (35%) of Maine Coons and in 42/68 (62%) of other cat breeds. Twenty‐two of 28 (79%) of Maine Coons and 21/42 (62%) of other breed cats with the A74T mutation were healthy at a mean age of 72 months and 91 months, respectively. Of 12 Maine Coons with HCM, 9 (75%) were genotype‐negative for A31P and 6 (50%) for A74T. Allele frequencies did not differ significantly (P= .47) between phenotype groups. None of the evaluated genetic tests was able to provide useful predictive information of disease outcome. Conclusions and Clinical Importance: The value of currently available genetic tests is low in the cats of this study. The mutations analyzed appear to have a low penetrance, and even homozygote cats can remain healthy.     

Naturally Occurring Biventricular Noncompaction in an Adult Domestic Cat

A definitively diagnosed case of left ventricular noncompaction (LVNC) has not been previously reported in a non‐human species. We describe a Maine Coon cross cat with echocardiographically and pathologically documented LVNC. The cat was from a research colony and was heterozygous for the cardiac myosin binding protein C mutation associated with hypertrophic cardiomyopathy (HCM) in Maine Coon cats (A31P). The cat had had echocardiographic examinations performed every 6 months until 6 years of age at which time the cat died of an unrelated cause. Echocardiographic findings consistent with LVNC (moth‐eaten appearance to the inner wall of the mid‐ to apical region of the left ventricle (LV) in cross section and trabeculations of the inner LV wall that communicated with the LV chamber) first were identified at 2 years of age. At necropsy, pathologic findings of LVNC were verified and included the presence of noncompacted myocardium that consisted of endothelial‐lined trabeculations and sinusoids that constituted more than half of the inner part of the LV wall. The right ventricular (RV) wall also was affected. Histopathology identified myofiber disarray, which is characteristic of HCM, although heart weight was normal and LV wall thickness was not increased.     

Pulsed tissue Doppler imaging of the left ventricular septal mitral annulus in healthy dogs

This study evaluated pulsed TDI variables including the isovolumic time interval and duration of the major wave in a population of large healthy dogs. Longitudinal myocardial motion at the septal mitral annulus was evaluated with pulsed TDI in 45 healthy adult dogs. Maximal myocardial velocities, isovolumic time intervals, and duration of the myocardial waves were measured. The correlation between time intervals and velocity variables was also investigated. The mean maximal systolic velocity was 6.92 ± 1.78 cm/sec, the mean early diastolic velocity (Em) was 6.58 ± 1.81 cm/sec, the mean late diastolic velocity (Am) was 5.10 ± 2.00 cm/sec, the mean isovolumic contraction time (IVCT) was 53.61 ± 95.13 msec, and the mean isovolumic relaxation time (IVRT) was 26.74 ± 57.24 msec. The early diastolic mitral inflow velocity (E)/Em ratio was 10.94 ± 3.27 while the Em/Am ratio was 1.40 ± 0.40. There was a negative correlation between Am duration and Am amplitude, and a positive correlation between the IVRT and Em/Am ratio (p < 0.05). The normal LV parameter using pulsed TDI method could be used as the reference range for identifying myocardial dysfunction in dogs.     

TWO-DIMENSIONAL COLOR TISSUE DOPPLER IMAGING DETECTS MYOCARDIAL DYSFUNCTION BEFORE OCCURRENCE OF HYPERTROPHY IN A YOUNG MAINE COON CAT

A 20-month-old healthy male Maine Coon cat was referred for a cardiovascular evaluation. Physical examination and electrocardiogram were normal. The end-diastolic subaortic interventricular septal thickness (6 mm; reference range: < or = 6mm) and the mitral flow late diastolic velocity (0.89 m/s; reference range: 0.2-0.8m/s) were within the upper ranges. However, M-mode echocardiography did not reveal any sign of hypertrophic cardiomyopathy (HCM). Tissue Doppler imaging (TDI) identified a marked left ventricular free wall dysfunction characterized by decreased myocardial velocities in early diastole, increased myocardial velocities in late diastole and the presence of postsystolic contractions both at the base and the apex for the longitudinal motion. One year later, the diagnosis of HCM was confirmed by conventional echocardiography and the cat died suddenly 2 months later. This report demonstrates for the first time in spontaneous HCM the sensitivity of TDI for early diagnosis of myocardial dysfunction and suggests that TDI should form part of the screening techniques for early diagnosis of feline HCM.     

Assessment of left ventricular function using pulsed tissue Doppler imaging in healthy dogs and dogs with spontaneous mitral regurgitation

Pulsed tissue Doppler imaging (pulsed TDI) has been demonstrated to be useful for the estimation of left ventricular (LV) systolic and diastolic functions in various human cardiac diseases. The objectives of this study were to investigate the relationship between pulsed TDI and LV function by using cardiac catheterization in healthy dogs and to evaluate the clinical usefulness of pulsed TDI in dogs with spontaneous mitral regurgitation (MR). The peak early diastolic velocity (E'), peak atrial systolic velocity (A'), and peak systolic velocity (S') were detectable in the velocity profiles of the mitral annulus in all the dogs. In the healthy dogs, S' and E' were correlated with LV peak +dP/dt and -dP/dt, respectively. E' was lower in dogs with MR than in dogs without cardiac diseases. E/E' in the MR dogs with decompensated heart failure was significantly increased in comparison with those with compensated heart failure. The sensitivity and specificity of the E/E' cutoff value of 13.0 for identifying decompensated heart failure were 80% and 83%, respectively. In addition, E/E' was significantly correlated with the ratio of left atrial to aortic diameter. These findings suggest that canine pulsed TDI can be applied clinically for estimation of cardiac function and detection of cardiac decompensation and left atrial volume overload in dogs with MR.     

Systolic and diastolic myocardial dysfunction in cats with hypertrophic cardiomyopathy or systemic hypertension

BACKGROUND: Hypertrophic cardiomyopathy (HCM) and chronic systemic hypertension (SHT) can both lead to left-ventricular hypertrophy (LVH) in cats. Assessment of LVH-associated myocardial dysfunction could provide new insights in the understanding of the pathophysiology of these diseases. HYPOTHESIS: Quantification of left-ventricular free-wall (LVFW) motion using tissue Doppler imaging (TDI) could permit differentiation of feline HCM from SHT-related LVH (LVH-SHT). ANIMALS: A total of 108 cats of different breeds were enrolled in this study: 35 cats with HCM, 17 with concentric LVH and SHT, and 56 healthy cats as a control group. METHODS: All cats were examined by conventional echocardiography and 2-dimensional color TDI. RESULTS: Radial and longitudinal diastolic LVFW velocities were similarly altered in cats with HCM and LVH-SHT, compared to controls. Systolic velocities were also lower in the groups with hypertrophy than in the controls, for longitudinal but not radial motion. To determine whether these diastolic and systolic alterations could also be observed in cats without LVFW hypertrophy, we performed a subgroup analysis in cats with a normal M-mode examination, that is, with only a localized subaortic interventricular septum hypertrophy. A significant radial and longitudinal diastolic dysfunction was still observed in both the HCM and LVH-SHT groups compared to controls, and systolic dysfunction was detected in the longitudinal motion. CONCLUSIONS: LVFW motion is similarly altered in cats with HCM and LVH-SHT. This dysfunction occurs independently of the presence of myocardial hypertrophy, demonstrating that TDI is capable of detecting systolic and diastolic segmental functional changes in nonhypertrophied wall segments in cats with HCM and SHT.