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.     

Determination of β-adrenoceptors and cAMP in muscle from normal and splayleg Belgian Landrace pigs

-Adrenoceptors were identified and characterized by [³H]dihydroalprenolol ([³H]DHA) binding experiments in muscle membrane preparations from piglets. The [³H]DHA binding was rapid, reversible and stereoselective. Catecholamines competed for specific binding with a rank order of potency (-)-isopropylnoradrenaline > (-)-epinephrine » (-)-norepinephrine, indicating a -subtype of adrenoceptor. Saturation binding experiments with [³H]DHA showed no significant difference for either the number of binding sites or the equilibrium dissociation constants in normal and splayleg pigs.Adenylate cyclase assays indicated that the basal adenylate cyclase activity and the prostaglandin E₁ (PGE₁)-, (-)-isopropylnoradrenaline (ISO)-, 5-guanylyl-imidodiphosphate (GppNHp)- and sodium fluoride (NaF)-stimulated values were not significantly different in normal and splayleg pigs. In both groups, PGE₁ did not affect basal activity, whereas ISO and GppNHp stimulated adenylate cyclase activity significantly (p<0.001) to about 40% above basal level. NaF induced a significant (p<0.001) increase of cAMP in normal and splayleg pigs amounting to 48% and 61% respectively. Significant correlations between absolute adenylate cyclase responses to ISO (r=0.83^***), NaF (r=0.72^**) and GppNHp (r=0.61^*) and basal activity in the splayleg pigs were the most striking findings. In contrast, these correlations could not be detected in the normal pigs. Whether or not this observation reflects an alteration in the signal transduction system needs to be further investigated.To the best of our knowledge this is the first biochemical study which relates an altered -adrenoceptor function and porcine splayleg.     

Assessment of Left Ventricular Systolic Function by Strain Imaging Echocardiography in Various Stages of Feline Hypertrophic Cardiomyopathy

Background: Diastolic dysfunction occurs in many cats with hypertrophic cardiomyopathy (HCM). Less is known about systolic function in various stages of HCM. Myocardial strain analysis by tissue Doppler imaging (TDI) is a noninvasive echocardiographic method to assess systolic function that has not been reported previously in cats. Objectives: To evaluate systolic function in various stages of feline HCM by measurement of myocardial strain. Animals: Two hundred and sixty‐three cats. Methods: Cats were classified by echocardiography into one of the following groups: clinically healthy (control) group (n = 160), mild HCM (n = 22), moderate HCM (n = 39), and severe HCM (n = 42). Peak myocardial strain, measured by TDI in the basal and midventricular segment of the interventricular septal wall (IVS) and the left ventricular posterior wall (LVPW), was compared among different HCM and control groups. Results: Whereas conventional echocardiography demonstrated an apparently normal or supernormal contractile state based on percentage of fractional shortening, myocardial strain in all HCM groups was significantly decreased compared with the control group (P < .001). There was a significant correlation between strain values and wall thickness (P < .001). Reproducibility of strain analysis was 6.3% in the IVS and 9.7% in the LVPW. Conclusions and Clinical Importance: Myocardial strain analysis is a new, valuable, and reproducible method in cats. This method allows noninvasive detection of abnormal systolic deformation in cats with HCM despite apparently normal left ventricular systolic function as assessed by conventional echocardiography. The abnormal systolic deformation already was present in mild HCM and increased with progressive left ventricular concentric hypertrophy.     

Effects of clopidogrel therapy on whole blood platelet aggregation,the Plateletworks® assay and coagulation parameters in cats with asymptomatic hypertrophic cardiomyopathy: a pilot study

Background: Although scientific evidence is limited, clopidogrel is frequently used as prophylaxis for arterial thromboembolism in cats with hypertrophic cardiomyopathy (HCM).

Objectives: Evaluating effects of clopidogrel therapy in asymptomatic cats with HCM on (1) conventional whole blood aggregation (WBA), (2) alternative platelet aggregation assessed with tubes of the Plateletworks® assay and (3) standard coagulation parameters.

Animals and methods: Prospective, randomized, double-blind, placebo-controlled pilot study. Fourteen asymptomatic HCM cats were randomly allocated to receive placebo (n = 5) or clopidogrel (18.75 mg/cat q24h, n = 9) as part of a larger study. Aggregation responses (to 20 µM adenosine diphosphate (ADP) and 10 µg/ml collagen) in WBA and the Plateletworks® assay and standard coagulation parameters were evaluated at baseline and after seven days of therapy.

Results: Clopidogrel therapy significantly reduced aggregation responses to ADP and collagen in the Plateletworks® agonists tubes (ADP and collagen: P < 0.001), but did not significantly reduce aggregation responses to ADP and collagen in the WBA technique (ADP: P = 0.07, collagen: P = 0.30). Clopidogrel therapy did not show a significant effect on prothrombin time, activated partial thromboplastin time, antithrombin, D-dimers and fibrinogen concentrations.

Conclusion and clinical importance: Clopidogrel therapy at a dose of 18.75 mg/cat q24h for seven days causes a significant decrease in in vitro platelet aggregation evaluated with the Plateletworks® assay, without affecting standard coagulation parameters in cats with asymptomatic HCM.     

Measurements of plasma endothelin immunoreactivity in healthy cats and cats with cardiomyopathy

Plasma concentrations of endothelin-1 (ET-1), the most potent endogenous pressor substance discovered to date, are abnormally high in humans with congestive heart failure (CHF), and they correlate with the degree of functional impairment. We sought first to validate a human sandwich ELISA kit that targets that portion of the amino acid sequence that is identical in cats. The assay demonstrated linearity (R2 = .9968) and parallelism (P = .5339), recovery of spiked human ET-1 in cat plasma averaged 98.7%, and intraassay precision had a coefficient of variation <10%. We subsequently determined ET-1 immunoreactivity in healthy cats and in cats with myocardial disease with and without CHF, systemic thromboembolism (STE), or both. Plasma ET-1 immunoreactivity was measured in 12 healthy cats and in 28 cats with primary myocardial disease, including hypertrophic cardiomyopathy (HCM), dilated cardiomyopathy (DCM), or restrictive or unclassified cardiomyopathy (RCM and UCM), respectively. Plasma ET mean (95% CI) concentrations were 0.777 (0.6536-0.924) fmol/mL in the control cats, 1.427 (0.922-2.209) fmol/mL in 12 cats with cardiomyopathy (HCM = 11, RCM/UCM = 1) but without CHF or evidence of STE, and 2.360 (1.666-3.343) fmol/mL in 16 cats with cardiomyopathy (HCM = 8, RCM/UCM = 7, DCM = 1) and CHF (n = 15) or STE (n = 4). Plasma immunoreactivity of ET-1 was significantly higher in cats with myocardial disease without CHF/STE versus normal cats (P < .05) and in cats with myocardial disease with CHF/STE versus normal cats (P < .001).     

Prevalence of hypertrophic cardiomyopathy in a cohort of British Shorthair cats in Denmark

Background: Familial hypertrophic cardiomyopathy (HCM) has been described previously in British Shorthair cats (BSH), but until now, no reports have been published describing the prevalence of the disease within this breed. Objectives: The aim of this study was to assess the prevalence of HCM in a large cohort of BSH and to evaluate the effect of sex, weight, and increasing age as potential risk factors for this disease. Animals: Three hundred and twenty‐nine BSH presented for routine HCM screening during a 4‐year period. Methods: Prospective cross‐sectional study in which all cats were screened for HCM by conventional echocardiography. Results: A total of 329 cats were examined, 214 females and 115 males, with a median age of 2.3 years (range, 0.8–14.1). Twenty‐eight cats (8.5%) were classified as HCM‐positive, 14 (4.3%) as equivocal, 282 (85.7%) as HCM‐negative, and 5 (2.1%) were diagnosed with other cardiac diseases. The median age for diagnosis of HCM was 2.7 years (range, 0.9–14.1). Male cats had a significantly higher occurrence of HCM (20.4%) compared with the females (2.1%) corresponding to an odds ratio of 7.89 (95 % CI, 2.54–28.08) for males versus females adjusted for age and weight (P < .001). Conclusion: The BSH in our cohort had a high prevalence of HCM, often of early onset and with a significant male sex predisposition. We strongly recommend echocardiographic screening in this breed, especially cats used for breeding.     

Endotoxin-induced microvascular injury in isolated and perfused pig lungs

The lungs of 13 healthy Landrace piglets were isolated, perfused and maintained in an isogravimetric state under zone III conditions. By applying vascular occlusion methods, the total blood flow resistance (Rt) was partitioned into four components: arterial (Ra), pre- (Ra) and post-capillary (Rv), and venous (Rv). The capillary filtration coefficient (K _f,c) was evaluated using a gravimetric technique. A bolus of 55 µg ofEscherichia coli endotoxins (LPS) per 100 g of lung was injected into the arterial reservoir of eight lungs, followed by an infusion of LPS at a rate of 55 µg per 100 g of lung per hour for 180 min. A bolus of theophylline (85 mg per 100 g of lung weight) was injected into the arterial reservoir after the last determination of theK _f,c value. All the parameters were evaluated again when the lungs reached a new steady state. Endotoxin induced a significant increase inRt from 54.7 ± 7.0 at zero time to 184.7±44.2 cm H₂O min L^–1 (100 g)^–1 180 minutes later, which can be ascribed to the increase inRa andRv. These haemodynamic modifications were related to the increases in the arterial pressure and in the pressure at the distal end of the arterial segment and to the decreases in the pressure at the proximal end of the venous segment and in the blood flow. The capillary pressure and the lung weight remained unchanged. Endotoxin infusion infusion induced an increase in theK _f,c value from 0.208±0.011 (att=0) to 0.391±0.034 ml min^–1 (cmH₂O)^–1 (100 g)^–1 (att=180). Administration of theophylline significantly reducedRt,Ra,Ra andRv towards or under the baseline values and also induced a significant increase in the lung weight and in theK _f,c value. It was concluded that the endotoxin-induced increase in the total blood flow resistance can be ascribed to a vasospasm occurring at the level of the pre- and post-capillary small vessels and that changes in the permeability of the endothelium greatly contribute to the development of the pulmonary oedema observed in endotoxaemic pigs.     

Transient Myocardial Thickening in Cats Associated with Heart Failure

Background

Cats with hypertrophic cardiomyopathy (HCM) and congestive heart failure (CHF) can have resolution of both left ventricular hypertrophy and CHF.

Objectives

To describe the clinical characteristics of cats with transient myocardial thickening (TMT) and CHF compared with a control population of cats without resolution of HCM.

Animals

A total of 21 cats with TMT, 21 cats with HCM.

Methods

Retrospective study. Clinical records at 4 veterinary centers were searched for TMT cases and a control group of cats with HCM and CHF. TMT was defined as initial maximal left ventricular wall thickness (LVWT) ≥6 mm with left‐sided CHF, with subsequent resolution of CHF, reduction in left atrium/aorta (LA/Ao), and LVWT<5.5 mm. HCM was defined as persistent LVWT ≥6 mm.

Results

Cats with TMT were younger (2 [0.4–11.4] years) than cats with HCM (8 [1.6–14] years) (P < 0.0001), and antecedent events were more common (15/21 versus 6/21, respectively) (P = 0.01). In cats with TMT, LVWT normalized from 6.8 [6.0–9.7] mm to 4.8 [2.8–5.3] mm and LA/Ao decreased from 1.8 [1.6–2.3] to 1.45 [1.2–1.7] after a mean interval of 3.3 (95% CI: 1.8–4.7) months. CHF recurred in 1 of 21 TMT and 15 of 21 cats with HCM. Cardiac treatment was discontinued in 20 of 21 cats with TMT and 0 of 21 HCM cats. All cats with TMT survived, whereas 8 of 19 cats with HCM died during the study period.

Conclusions and Clinical Importance

TMT occurs in younger cats, and antecedent events are common. The prognosis is better in cats with CHF associated with TMT than HCM.     

Myocardial collagen deposition and inflammatory cell infiltration in cats with pre-clinical hypertrophic cardiomyopathy

The histological features of feline hypertrophic cardiomyopathy (HCM) have been well documented, but there are no reports describing the histological features in mild pre-clinical disease, since cats are rarely screened for the disease in the early stages before clinical signs are apparent. Histological changes at the early stage of the disease in pre-clinical cats could contribute to an improved understanding of disease aetiology or progression. The aim of this study was to evaluate the histological features of HCM in the left ventricular (LV) myocardium of cats diagnosed with pre-clinical HCM. Clinically healthy cats with normal (n = 11) and pre-clinical HCM (n = 6) were identified on the basis of echocardiography; LV free wall dimensions (LVFWd) and/or interventricular septal wall (IVSd) dimensions during diastole of 6–7 mm were defined as HCM, while equivalent dimensions <5.5 mm were defined as normal. LV myocardial sections were assessed and collagen content and inflammatory cell infiltrates were quantified objectively. Multifocal areas of inflammatory cell infiltration, predominantly lymphocytes, were observed frequently in the left myocardium of cats with pre-clinical HCM. Tissue from cats with pre-clinical HCM also had a higher number of neutrophils and a greater collagen content than the myocardium of normal cats. The myocardium variably demonstrated other features characteristic of HCM, including arteriolar mural hypertrophy and interstitial fibrosis and, to a lesser extent, myocardial fibre disarray and cardiomyocyte hypertrophy. These results suggest that an inflammatory process could contribute to increased collagen content and the myocardial fibrosis known to be associated with HCM.     

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.     

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.     

Reduced protein kinase C activity and endogenous protein phosphorylation in ethionine-induced fatty liver in cows

Protein kinase C (PKC) activity was evaluated and the phosphorylation of its endogenous substrates was explored in fatty liver induced by administration of ethionine (an analogue of methionine) to cows in order to assess the relevance of PKC-dependent phosphorylation in the development of fatty liver. PKC activity was decreased in both the cytosolic and the total particulate fractions from fatty livers, compared to the corresponding fractions from control liver. The mode of activation by the PKC cofactors (1-oleoyl-2-acetyl-sn-glycerol, 12-O-tetradecanoylphorbol-13-acetate, phosphatidylserine and Ca²⁺) was similar in both control and fatty livers, suggesting a quantitative but not a qualitative change in PKC in fatty liver. At least three substrate proteins (34 kDa, 26 kDa and 19 kDa) were found in the cytosolic fraction and their phosphorylation was reduced in fatty liver. These results suggest that impairment of the signal transduction pathway mediated by PKC is involved in the pathogenesis of fatty liver in cows.Abbreviations ATP adenosine triphosphate - EGTA ethylene glycol bis(-aminoethylether)-N,N,N,N-tetraacetic acid - NEFA non-esterified fatty acid - OAG 1-oleoyl-2-acetyl-sn-glycerol - PKC protein kinase C - PS phosphatidylserine - SDS-PAGE sodium dodecyl sulphate-polyacrylamide gel electrophoresis - TG triglyceride - TPA 12-O-tetradecanoylphorbol-13-acetate     

Heart rate and arrhythmia frequency of normal cats compared to cats with asymptomatic hypertrophic cardiomyopathy

ObjectivesTo compare heart rate and arrhythmia frequency and complexity in a normal population of cats to a population of cats with hypertrophic cardiomyopathy (HCM).Animals17 cats with HCM and 15 cats with normal echocardiograms.MethodsResults for echocardiography, electrocardiography, Doppler blood pressure, and 24-h Holter monitoring were compared between groups.ResultsThere was no difference in heart rate between HCM cats and normal cats regardless of modality used. All (17/17) HCM cats had ventricular arrhythmias (geometric mean 124 complexes/24 h) with 82% (14/17) exhibiting complex arrhythmias (couplets, triplets, or ventricular tachycardia). Most (14/15) normal cats had ventricular arrhythmias (geometric mean 4 complexes/24 h), but only 20% (3/15) exhibited complexity. HCM cats had significantly more total ventricular complexes, ventricular premature complexes and accelerated idioventricular rhythm than normal cats (P < 0.0001, P < 0.0001, and P = 0.01, respectively). Eighty eight percent (15/17) of HCM cats had supraventricular arrhythmias (geometric mean 9 complexes/24 h) with 23% (4/17) exhibiting complexity. Sixty percent (9/15) of normal cats had supraventricular arrhythmias (geometric mean 1 complex/24 h) with 13% (2/15) exhibiting complexity. Cats with hypertrophic cardiomyopathy had significantly more supraventricular complexes than normal cats (P = 0.0148).ConclusionCats with asymptomatic HCM have more frequent and complex ventricular and supraventricular arrhythmias than normal cats but do not have different overall heart rates compared to normal cats. Further studies are needed to determine if these arrhythmias are associated with an increased risk of sudden cardiac death or influence long-term survival.     

Effect of Cadmium in Feed on Organs and Meat Colour of Growing Pigs

One hundred and ninety-two barrows (Duroc × Landrace × Yorkshire, initial weight 27.7 kg) were used to investigate the effects of cadmium in feed on the function of selected organs and meat colour of growing pigs. The pigs were randomly allocatted into four different treatments. Each treatment included three replications with 16 pigs per replicate. The animals were fed corn–soybean basal diet and supplemented with 0, 0.5, 5.0, 10.0 mg/kg cadmium (as CdCl₂), respectively. The feeding trial ended when the average body weight of the pigs reach 90 kg. The results showed that, compared with controls, addition of 10 mg/kg cadmium to the diet resulted in significant elevations of relative weight of liver and spleen by 18.3% (p < 0.05) and 19.7% (p < 0.05) respectively, and of serum glutamic-pyruvic transaminase (GPT) and glutamic-oxaloacetic transaminase (GOT) activities by 17.8% (p < 0.05) and 27.4% (p < 0.05) respectively; and significant decreases of Na⁺/K⁺-ATPase activity in the liver by 24.6% (p < 0.05), the redness of longissimus dorsi by 26.6% (p < 0.05) and 24.9% (p < 0.05) at 0.75 h and 16 h post mortem, respectively, and of the myoglobin content of longissimus dorsi by 19.4% (p < 0.05). No changes were found in these indices above when the pigs were fed the diet supplied with 0.5 or 5 mg/kg cadmium (p > 0.05), nor in renal functions among cadmium-treatment treatments (p > 0.05) as indicated is the activities of urinary N-acetyl-β-d-glucosaminidase (NAG) and alkaline phosphatase (ALP) and the content of urinary protein. The study indicated the adverse effects of 10 mg/kg cadmium in feed on liver functions and meat colour of growing pigs.     

Desmin as a possible immunohistochemical marker for feline hypertrophic cardiomyopathy

Desmin has been suggested as a possible histopathological marker for hypertrophic cardiomyopathy (HCM) in humans. To test whether a similar pattern of desmin staining applies to HCM in cats, we conducted an immunohistochemical study on myocardial samples from 13 cats (HCM 4, other cardiomyopathies (OCM) 4, and control 5). The pattern of staining for desmin in HCM cats was not the same as that reported in humans, but was weaker than in OCM cats and controls. This suggested that desmin may be a possible histochemical marker for feline HCM, but our data was insufficient to clearly confirm this.     

Utility of measuring plasma N-terminal pro-brain natriuretic peptide in detecting hypertrophic cardiomyopathy and differentiating grades of severity in cats

Background: Cats with hypertrophic cardiomyopathy (HCM) often have no clinical signs or subtle signs. Measurement of N‐terminal pro‐brain natriuretic peptide (NT‐proBNP) has been demonstrated in people to be highly specific for heart disease and also correlates with severity of HCM. NT‐proBNP may also be valuable in detecting and grading HCM in cats, but results to date have been equivocal. Objectives: The aims of this study were to evaluate NT‐proBNP as a screening test for diagnosis of HCM in cats and determine an appropriate cut‐off value and to determine if NT‐proBNP concentrations correlated with severity of HCM in cats. Methods: Plasma NT‐proBNP concentrations were measured in 201 cats using an ELISA designed for use in cats. Cats were classified using echocardiography as clinically healthy controls (n=99) or cats with equivocal (n=9), mild (n=15), moderate (n=17), or severe (n=61) HCM. Results: NT‐proBNP concentrations (median; 25th–75th interquartile percentiles) in mildly (216.1; 87.6–392.5 pmol/L), moderately (282.7; 131.9–466.6 pmol/L), and severely (839.5; 655.3–1046.4 pmol/L) affected cats were significantly higher than those in healthy controls (18.9; 3.4–62.4 pmol/L). Concentrations in severely affected cats were significantly higher than in cats from other HCM groups. There was no significant difference between mild and moderate HCM. Cut‐off values >49 pmol/L had a sensitivity of 97.8% and specificity of 66.7%; >100 pmol/L had a sensitivity of 92.4% and specificity of 93.9%; and >150 pmol/L had a sensitivity of 88% and a specificity of 100%. Conclusions: NT‐proBNP with a cut‐off value of >100 pmol/L was useful in detecting even mild HCM. Cats with increased NT‐proBNP concentrations should be examined by echocardiography.     

Structural and biochemical evidence of mitochondrial depletion in pigs with hypertrophic cardiomyopathy

Pig hearts with naturally occurring hypertrophic cardiomyopathy (HCM) were isolated to investigate the effects of mitochondrial deficiency at biochemical and molecular levels. Enzyme activities of mitochondrial-encoded cytochrome c oxidase and NADH dehydrogenase in the HCM hearts (n=12) were lower than that in the controls (n=12) by 41+/-29% (P<0.01) and 43+/-21% (P<0.001), respectively. Additionally, Southern blot analysis was conducted to quantify the relative amount of mitochondrial DNA (mtDNA) from the HCM and controls. The relative amount of mtDNA in the HCM hearts was significantly 57+/-19% (P<0.001) lower than that in the controls. Both mitochondrial enzyme deficiency and mtDNA depletion were significantly correlated with the degree of cardiac hypertrophy judged based on the ratio of heart/body weight. In conclusion, our results reveal that a secondary effect of tissue-specific mtDNA depletion and mitochondrial dysfunction is in response to the 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.     

Effect of treatment with atenolol on 5-year survival in cats with preclinical (asymptomatic) hypertrophic cardiomyopathy

ObjectivesTo investigate the effect of treatment with atenolol on 5-year survival in cats with preclinical hypertrophic cardiomyopathy (HCM).Animals63 Client-owned cats with preclinical HCM and 31 healthy control cats.MethodsProspective, observational, open-label, clinical cohort study. Cats with HCM were diagnosed by echocardiography, treated with atenolol (6.25–12.5 mg q12h, PO; n = 42) or untreated (n = 21), and were observed for 5 years after enrollment. The study end point was death from any cause. Cats of similar body weight, age, gender, and breed without evidence of heart disease were studied concurrently and served as controls.ResultsDuring the observational period, 27 cats with HCM died; 14 (22%) due to cardiac disease and 13 (21%) due to non-cardiac disease. Ten control cats (32%) died of non-cardiac disease. There was no significant difference (P = 0.307) in all-cause mortality between control and HCM. Cardiac mortality was higher in cats with HCM compared to control cats (P = 0.005). There was no significant difference in all-cause mortality (P = 0.729) and cardiac mortality (P = 0.897) between cats with HCM treated or untreated with atenolol. Age and left atrial size at diagnosis were the only predictors of 5-year outcome.ConclusionsOur study failed to demonstrate an effect of atenolol on 5-year survival in cats with preclinical HCM.     

Prospective echocardiographic and tissue Doppler screening of a large Sphynx cat population: Reference ranges,heart disease prevalence and genetic aspects

Objectives(1) To investigate heart morphology and function using echocardiography and tissue Doppler imaging (TDI), (2) to determine heart disease prevalence and characteristics, and (3) to assess potential genetic features in a population of Sphynx cats presented for cardiovascular screening.AnimalsA total of 147 echocardiographic examinations, including 33 follow-ups, were performed by trained observers on 114 Sphynx cats of different ages (2.62 ± 1.93 years [0.5–10.0]) from 2004 to 2011.MethodsSphynx cats underwent a physical examination, conventional echocardiography, and, if possible, two-dimensional color TDI.ResultsConventional echocardiographic findings included 75/114 normal (65.8%) and 39/114 (34.2%) abnormal examinations with a diagnosis of either congenital heart diseases (n = 16) or hypertrophic cardiomyopathy (HCM, n = 23). In adult healthy cats, a significant body weight effect was observed for several echocardiographic variables, including end-diastolic left ventricular (LV) free wall (P < 0.01), interventricular septum (P < 0.001), and LV diameter (P < 0.001). Mitral valve dysplasia (MVD) was observed as a single or associated defect in 15/16 cats with congenital heart diseases. A significant increase in HCM prevalence (P < 0.001) was observed according to age. The pedigree analysis of a large family (n = 81) suggested an autosomal dominant mode of inheritance with incomplete penetrance for HCM.ConclusionsBody weight should be taken into account when interpreting values of diastolic myocardial wall thicknesses in Sphynx cats. Additionally, HCM and MVD are two relatively common heart diseases in this feline breed. More pedigree data are required to confirm the inheritance pattern of HCM at the breed level.