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.     

A case of sustained atrial fibrillation in a cat with a normal sized left atrium at the time of diagnosis

This case illustrates an unusual presentation of atrial fibrillation in a 10-year-old male neutered Maine coon. At the time of diagnosis of the arrhythmia the size of the left atrium determined by echocardiography was within normal limits and no structural or functional heart or other systemic disease was identified. Traditionally it has been suggested that the atria must be of a sufficient size in order to sustain atrial fibrillation (multiple wavelet theory) and therefore only cats with significant cardiac disease can attain sufficiently large atria to sustain this arrhythmia. To the author's knowledge this is the first detailed case report of sustained atrial fibrillation in a cat with a normal sized left atrium and no obvious structural heart disease seen on cardiac ultrasound.     

Arterial thromboembolism in cats: acute crisis in 127 cases (1992-2001) and long-term management with low-dose aspirin in 24 cases

Records of 127 cats with arterial thromboembolism (ATE) were reviewed. Abyssinian, Birman, Ragdoll, and male cats were overrepresented. Tachypnea (91%), hypothermia (66%), and absent limb motor function (66%) were common. Of 90 cats with diagnostics performed, underlying diseases were hyperthyroidism (12), cardiomyopathy (dilated [8], unclassified [33], hypertrophic obstructive [5], hypertrophic [19]), neoplasia (6), other (4), and none (3). Common abnormalities were left atrial enlargement (93%), congestive heart failure (CHF, 44%), and arrhythmias (44%). Of cats without CHF, 89% were tachypneic. Common biochemical abnormalities were hyperglycemia, azotemia, and abnormally high serum concentrations of muscle enzymes. Of 87 cats treated for acute limb ATE, 39 (45%) survived to be discharged. Significant differences were found between survivors and nonsurvivors for temperature (P < .00001), heart rate (P = .038), serum phosphorus concentration (P = .024), motor function (P = .008), and number of limbs affected (P = .001). No significant difference was found between survivors and nonsurvivors when compared by age, respiratory rate, other biochemical analytes, or concurrent CHE A logistic regression model based on rectal temperature predicted a 50% probability of survival at 98.9 degrees F (37.2 degrees C). Median survival time (MST) for discharged cats was 117 days. Eleven cats had ATE recurrences, and 5 cats developed limb problems. Cats with CHF (MST: 77 days) had significantly shorter survival than cats without CHF (MST: 223 days; P = .016). No significant difference was found in survival or recurrence rate between cats receiving high-dose aspirin (> or = 40 mg/cat q72h) and cats receiving low-dose aspirin (5 mg/cat q72h). Adverse effects were less frequent and milder for the lower dosage.     

Familial Ventricular Arrhythmias in Boxers

The purposes of this study were to evaluate families of Boxers with ventricular arrhythmias to determine whether this disorder is a familial trait and, if so, to determine the mode of inheritance. Eighty-two Boxers were evaluated by physical examination, electrocardiogram, echocardiogram, and 24-hour ambulatory electrocardiogram. Dogs were considered affected if at least 50 premature ventricular complexes (PVCs) were observed during a 24-hour period. All dogs were at least 6 years of age at evaluation. Complete cardiovascular examinations were performed on dogs from 6 extended families. The 2 most complete pedigrees were used to determine the pattern of inheritance. The number of PVCs observed during a 24-hour period in affected dogs ranged from 112 to 4,894 (mean +/- SD, median; 1,309 +/- 2,609, 1,017). The number of PVCs observed during a 24-hour period in the unaffected dogs ranged from 0 to 16 (7 +/- 10, 12). Pedigree evaluation was performed to determine pattern of inheritance. An autosomal dominant pattern was determined to be most likely because a sex predisposition was not observed, affected individuals were observed in every generation, and 2 affected individuals produced unaffected offspring. We conclude that familial ventricular arrhythmias is inherited as an autosomal dominant trait in some Boxers.     

Role of cellular paracrine in the mechanism of cardiomyocyte hypertrophy induced by stretch

AIM: To investigate the role of cellular paracrine in the mechanism of cardiomyocyte hypertrophy induced by stretch. METHODS: [³H]-leu incorporation into cultured cardiomyocytes was measured when stimulated by conditioned-media of myocardial fibroblast and microvascular endothelial cell after stretch. RESULTS: [³H]-leu incorporation rate were both elevated significantly stimulated by conditioned-media of myocardial fibroblast and microvascular endothelial cell. And angiotensin II and endothelin of conditioned-media of myocardial fibroblast and microvascular endothelial cell were also elevated significantly. And [³H]-leu incorporation rate were inhibited significantly when the specific angiotensin II and endothelin receptor antagonist losartan(1μmol/L) and BQ123(1μmol/L) were added. [³H]-leu incorporation rate were inhibited over 80% when losartan(1μmol/L) and BQ123(1μmol/L) were added together.CONCLUSION: The activation of myocardial fibroblast and microvascular endothelial cell endocrine stimulated by stretch play a role through paracrine in the pathogenesis of pressure-overload heart hypertrophy.     

Two-dimensional echocardiographic assessment of the feline left atrium

Atrial size determined by echocardiography provides a surrogate measure of the hemodynamic burden of cardiac disease. Linear atrial dimensions often are indexed to aortic diameter. Whereas quantitative variables obtained from healthy cats, using 2-dimensional echocardiography (2DE), have been reported, indices from 2DE, have not. Using 2DE and M-mode echocardiography, we calculated indices of left atrial size and a single index of atrial function, left atrial fractional shortening, in 17 healthy cats. Specifically, left atrial dimensions from short- and long-axis 2DE planes were indexed to aortic diameter and also to end-diastolic left ventricular dimension. Additionally, left atrial circumference and area were indexed to aortic circumference and area, respectively. The same variables were obtained from 20 cats with hypertrophic cardiomyopathy (HCM), so that agreement between 2DE indices and indices from M-mode echocardiography could be evaluated over a clinically relevant range of atrial sizes. Atrial dimensions and indices of atrial size from cats with HCM exceeded those of healthy cats. Left atrial dimension from 2D short-axis images indexed to aortic diameter generally was less than the analogous index obtained from M-mode (mean bias, [95% limits of agreement] -0.13, [-0.42, 0.17]). Left atrial dimension from 2D long-axis images indexed to aortic diameter generally was greater than the index obtained from M-mode (0.15, [-0.28, 0.58]). We conclude that ratios of left atrial size and aortic diameter, from 2DE and M-mode echocardiography, are not interchangeable. Normative data that may serve as reference intervals for 2DE assessment of atrial size are presented.     

Tissue Doppler imaging for detection of radial and longitudinal myocardial dysfunction in a family of cats affected by dystrophin-deficient hypertrophic muscular dystrophy

Diagnosis of feline hypertrophic cardiomyopathy currently is based on the presence of myocardial hypertrophy detected using conventional echocardiography. The accuracy of tissue Doppler imaging (TDI) for earlier detection of the disease has never been described. The objective of this sudy was to quantify left ventricular free wall (LVFW) velocities in cats with hypertrophic muscular dystrophy (HFMD) during preclinical cardiomyopathy using TDI. The study animals included 22 healthy controls and 7 cats belonging to a family of cats with HFMD (2 affected adult males, 2 heterozygous adult females, one 2.5-month-old affected male kitten, and 2 phenotypically normal female kittens from the same litter). All cats were examined via conventional echocardiography and 2-dimensional color TDI. No LVFW hypertrophy was detected in the 2 carriers or in the affected kitten when using conventional echocardiography and histologic examination, respectively. The LVFW also was normal for 1 affected male and at the upper limit of normal for the 2nd male. Conversely, LVFW dysfunction was detected in all affected and carrier cats with HFMD when using TDI. TDI consistently detects LVFW dysfunction in cats with HFMD despite the absence of myocardial hypertrophy. Therefore, TDI appears more sensitive than conventional echocardiography in detecting regional myocardial abnormalities.