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.     

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.     

Analysis of 8 Sarcomeric Candidate Genes for Feline Hypertrophic Cardiomyopathy Mutations in Cats with Hypertrophic Cardiomyopathy

Background: Hypertrophic cardiomyopathy (HCM) is the most common heart disease in cats. Causative mutations have been identified in the Maine Coon (MC) and Ragdoll breed in the cardiac myosin binding protein C gene (MYBPC3). HCM is thought to be inherited in other breeds.
Hypothesis: That a causative mutation for HCM in the British Shorthair (BSH), Norwegian Forest (NWF), Siberian, Sphynx, or MC cats would be identified in the exonic and splice site regions of 1 of 8 genes associated with human familial HCM.
Animals: Three affected BSH, NWF, Siberians, Sphynx, 2 MC (without the known MC mutation), and 2 Domestic Shorthair cats (controls) were studied.
Methods: Prospective, observational study. Exonic and splice site regions of the genes encoding the proteins cardiac troponin I, troponin T, MYBPC3, cardiac essential myosin light chain, cardiac regulatory myosin light chain, α tropomyosin, actin, and β–myosin heavy chain were sequenced. Sequences were compared for nucleotide changes between affected cats, the published DNA sequences, and control cats. Changes were considered to be causative for HCM if they involved a conserved amino acid and changed the amino acid to a different polarity, acid-base status, or structure.
Results: A causative mutation for HCM was not identified, although several single nucleotide polymorphisms were detected.
Conclusions and Clinical Importance: Mutations within these cardiac genes do not appear to be the only cause of HCM in these breeds. Evaluation of additional cardiac genes is warranted to identify additional molecular causes of this feline cardiac disease.     

Prevalence of the myosin-binding protein C mutation in Maine Coon cats

BACKGROUND: An autosomal dominant mutation has been identified in the myosin-binding protein C (MYBPC3) gene of Maine Coon cats. This mutation changes a conserved amino acid and computationally alters the protein conformation of this gene in Maine Coon cats with hypertrophic cardiomyopathy. The prevalence of this mutation is unknown. OBJECTIVE: To determine the genetic prevalence of the MYBPC3 mutation in a large cohort of predominantly Maine Coon cats. ANIMALS: Three thousand three hundred and ten DNA samples (blood or buccal swab) from cats. METHODS: This retrospective study reviewed the Veterinary Cardiac Genetics Laboratory database at Washington State University for samples submitted for evaluation of the Maine Coon MYBPC3 mutation. The data were analyzed with respect to the breed of cat, mutation status (negative, heterozygous, homozygous), and geographic origin of the submission. RESULTS: In the population of cats studied, Maine Coon cats accounted for 100% of all cats positive for the mutation, and the worldwide percentage of Maine Coon cats carrying the MYBPC3 mutation was 34%. CONCLUSIONS AND CLINICAL IMPORTANCE: The prevalence of the mutation (heterozygous or homozygous) was very similar among countries of submission, suggesting that the 34% mutation rate of the tested samples is a reasonable estimate of the true prevalence of the mutation within the breed. Because of the high prevalence of this mutation, a breeding recommendation to eliminate all cats with the mutation could have a substantial impact on the gene pool. Additional studies are indicated to explore the relationship between genotype and clinical outcome in affected cats.     

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.     

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.     

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).     

Measurement of M-mode echocardiographic parameters in healthy adult Maine Coon cats

OBJECTIVE: To determine reference values for M-mode echocardiographic parameters in nonsedated healthy adult Maine Coon cats and compare those values with data reported for nonsedated healthy adult domestic cats. DESIGN: Prospective study. ANIMALS: 105 healthy adult Maine Coon cats. PROCEDURE: Over a 3-year period, M-mode echocardiographic examinations (involving a standard right parasternal transthoracic technique) were performed on Maine Coon cats as part of prebreeding evaluations; values of M-mode parameters in healthy individuals were collected, and mean values were calculated for comparison with those reported for healthy adult domestic cats. RESULTS: The mean +/- SD weight of Maine Coon cats was significantly greater than that of domestic cats. Mean values of left ventricular internal dimension at end diastole and end systole (LVIDd and LVIDs, respectively), interventricular septal thickness at end systole (IVSs), left ventricular posterior wall thickness at end systole (LVPWs), left atrial dimension at end systole (LADs), and aortic root dimension (Ao) in Maine Coon cats differed significantly from values in healthy domestic cats. The greatest differences detected between the 2 groups involved values of LVIDd, LADs, and Ao. Linear regression analysis revealed a weak but significant correlation between weight and each of LVIDd, LVPWs, IVSs, Ao, LADs, and left ventricular posterior wall thickness at end diastole. CONCLUSIONS AND CLINICAL RELEVANCE: Values of several M-mode echocardiographic parameters in Maine Coon cats differ from those reported for domestic cats; these differences should be considered during interpretation of echocardiographic findings to distinguish between cardiac health and disease in this breed.     

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.     

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.     

Hypertrophic cardiomyopathy in the Sphynx cat: a retrospective evaluation of clinical presentation and heritable etiology

Hypertrophic cardiomyopathy is an inherited disease in some feline breeds including the Maine Coon and Ragdoll. In these breeds, distinct causative genetic mutations have been identified. The two breeds appear to have slightly different clinical presentations, including age of diagnosis. The observation that these two breeds may have different clinical presentations, as well as different genetic mutations, suggests that hypertrophic cardiomyopathy is a diverse disease in the cat. Hypertrophic cardiomyopathy is poorly described in the Sphynx. The objective of this study was to phenotypically characterize Sphynx hypertrophic cardiomyopathy and to evaluate for a familial etiology. Records of 18 affected cats (11 female, seven male) were evaluated. Age of affected cats ranged from 0.5 to 7 years (median, 2 years). Four affected cats were from a single family and included an affected cat in each of four generations (three females, one male). Further studies are warranted to evaluate for a causative mutation and better classify the phenotypic expression.     

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.     

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.     

Breed Dependency of Reference Intervals for Plasma Biochemical Values in Cats

Background: Reference intervals (RI) are pivotal in clinical pathology. The influence of breed on RI has been poorly documented in cats. Hypothesis/Objectives: RI for plasma biochemistry variables are breed‐dependent in cats. Animals: Five hundred and thirty‐six clinically healthy, fasted, client‐owned cats from 4 breeds: Holly Birman (n = 132), Chartreux (n = 129), Maine Coon (n = 139), and Persian (n = 136). Methods: Prospective observational study: Blood samples were collected from the cephalic vein into capillary tubes containing lithium heparin. Plasma glucose, urea, creatinine, total proteins, albumin, calcium, phosphate, sodium, potassium, chloride, and total CO₂ concentrations and the activities of alanine aminotransferase and alkaline phosphatase were assayed with a dry slide biochemical analyzer. RI were defined as central 95% intervals bounded by the 2.5th and 97.5th percentiles. Data were analyzed by a linear mixed effects model with type I error rate of 0.05. Results: A significant (P < .05) breed effect was observed for 9/13 variables. The magnitude of the differences between breeds could be clinically relevant for creatinine, glucose, and total protein. Age, body weight, sex, and housing conditions had significant (P < .05) breed‐related effects on different variables. Conclusions and Clinical Importance: Breed‐specific RI should be considered for cats.     

Characteristics of pedigree cat breeding in the Netherlands: breeds, population increase and litter size

A survey of the Dutch Cat Fancy was carried out to determine reproductive, patterns of pedigree cats. The data of the present study were obtained by questioning the pedigree registers of the cat clubs participating in the foundation 'Overleg Platform van de Nederlandse Cat Fancy'. The Dutch Cat Fancy registers 34 different cat breeds. From 1992 up to 1996 a total of 25.985 litters were registered. Over this period the number of litters increased from 4989 to 5313. Litters from Longhair and Exotic Shorthair cats comprised the biggest group and accounted for 55% of the total number of litters. However, over this period, the number of Longhair and Exotic Shorthair litters decreased by 9%. Litters from British Shorthair, Birman, Maine Coon and Norwegian Forrest Cat increased in number as did litters from small breeds such as Ragdoll, Bengal and Sphynx. Litters from Abyssinian, Siamese, Oriental Shorthair cats remained relatively the same. The average litter size of the total cat population, based on pedigree certificates, was calculated at 3.3 kittens per litter. For different breeds litter size varied from 2.7 (Longhair and Exotic Shorthair) to 4.3 (Burmese and Maine Coon). Taking into account an average age of 14 years, the total Dutch pedigree cat population was estimated at 240,000 viz. about 10% of the total cat population.     

Hypertrophic cardiomyopathy in young Maine Coon cats caused by the p.A31P cMyBP-C mutation - the clinical significance of having the mutation

Background

In Maine Coon (MC) cats the c.91G > C mutation in the gene MYBPC3, coding for cardiac myosin binding protein C (cMyBP-C), is associated with feline hypertrophic cardiomyopathy (fHCM). The mutation causes a substitution of an alanine for a proline at residue 31 (p.A31P) of cMyBP-C. The pattern of inheritance has been considered autosomal dominant based on a single pedigree. However, larger studies are needed to establish the significance of cats being heterozygous or homozygous for the mutation with respect to echocardiographic indices and the probability of developing fHCM. The objective of the present study was to establish the clinical significance of being homozygous or heterozygous for the p.A31P cMyBP-C mutation in young to middle-aged cats.

Methods

The cohort consisted of 332 MC cats, 282 cats < 4 years (85%). All cats were examined by 2-D and M-mode echocardiography. DNA was extracted from blood samples or buccal swabs and screened for the p.A31P cMyBP-C mutation in exon 3 of the gene, using polymerase chain reaction followed by DNA sequencing.

Results

The fHCM prevalence was 6.3% in the cohort. Eighteen cats were homozygous and 89 cats were heterozygous for the mutation. The odds ratio for having fHCM for homozygous cats was 21.6 (95% confidence interval 7.01-66.2) - when the group of equivocal cats was categorized as non-affected. Overall, 50% of the cats that were homozygous for the mutation had fHCM. p.A31P heterozygosity was not associated with a significant odds ratio for fHCM. In cats in the 4 to 6 years of age range a similar, non significant, odds ratio was seen in heterozygous cats. Only two cats over four years were homozygous and both were diagnosed with fHCM.

Conclusion

As there is no significant odds ratio associated with being heterozygous for the pA31P cMyBP-C mutation at this age, the mutation must have a very low penetrance in this group. From our data it would appear that most MC cats that develop fHCM due to the p.A31P mutation prior to the age of approximately 6 years do so because they are homozygous for this mutation.     

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.     

Platelet function in clinically healthy cats and cats with hypertrophic cardiomyopathy: analysis using the Platelet Function Analyzer‐100

Background: There is currently no simple analytical tool for the evaluation of hypercoagulability in cats. The Platelet Function Analyzer‐100^® (PFA‐100; Dade Behring Inc., Deerfield, IL, USA) is a bench‐top machine that evaluates platelet function by measuring closure time (CT) in citrated whole blood under high shear conditions. We hypothesized that cats with hypertrophic cardiomyopathy (HCM) have up‐regulated platelet function, which shortens their CT and increases their risk for thromboembolic events. Objectives: The goals of this study were to: (1) establish a feline reference interval for CT using the PFA‐100, (2) measure CT in blood from cats with HCM, and (3) determine if there is a measurable difference between the CT of healthy cats compared with cats with HCM. Methods: Citrated blood samples from 42 clinically healthy cats and 30 cats with HCM were analyzed according to manufacturer's specifications. CT was measured in triplicate and the mean value was used for analysis. Transformed data were compared between clinically healthy cats and cats with HCM using a Student's t‐test, and among cats with mild, moderate, or severe HCM using ANOVA. Results: The median CT of clinically healthy cats was 64 seconds (range 43–176 seconds). The median CT of cats with HCM was 74 seconds (range 48–197 seconds). There was no significant difference in CT between cats with HCM and clinically healthy cats. There also were no significant differences in cats with mild, moderate, or severe HCM. Conclusions: A feline reference interval for PFA‐100 CT will be useful in future studies of platelet function in cats. Cats with HCM do not have shorter CTs when compared with clinically healthy cats.     

Peritoneopericardial diaphragmatic hernia: a retrospective study of 31 cats and eight dogs

The records of 31 cats and eight dogs undergoing surgical correction of peritoneopericardial diaphragmatic hernia (PPDH) from 2000 through 2007 were reviewed. Weimaraners and long-haired cats of varying breeds, particularly Maine Coon cats, appear to be at higher risk of PPDH. Presenting complaints were most commonly related to the respiratory and gastrointestinal tracts in both dogs and cats, although respiratory signs were more prevalent in cats, and gastrointestinal signs were more common in dogs. The most common herniated organs were liver, gallbladder, and small intestine. Mortality associated with surgical repair of PPDH in cats and dogs was low in the first 2 weeks postoperatively, and prognosis for return to normal function was excellent. Peri-and postoperative complications were typically minor and self-limiting.     

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.