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.

N-terminal atrial natriuretic peptide immunoreactivity in plasma of cats with hypertrophic cardiomyopathy.

Atrial natriuretic peptide (ANP) is an important regulator of fluid homeostasis and vascular tone. We sought to compare N-terminal ANP immunoreactivity (ANP-IR) in plasma from cats with and without hypertrophic cardiomyopathy (HCM). Secondarily, we evaluated relationships between ANP-IR and echocardiographical variables in cats with HCM and healthy cats. Venous blood samples were obtained from 17 cats with HCM and from 19 healthy cats. Plasma ANP-IR concentration was determined by an enzyme-linked immunoassay. Two cats with HCM had clinical evidence of congestive heart failure; the remainder had subclinical disease. Plasma ANP-IR concentration was higher in cats with HCM (3,808 +/- 1,406 fmol/L, mean +/- SD) than in control cats (3,079 +/- 1,233 fmol/L), but this difference was not statistically significant (P = .11; 95% confidence interval [CI] = -166 to 1,622). There was a significant, but modest correlation between plasma ANP-IR concentration and left ventricular posterior wall thickness (r = 0.42; P = .01). Additionally, plasma ANP-IR concentration was weakly correlated with left atrial size (r = 0.35; P = .03). A linear regression model was developed to further explore these relationships. Atrial size and wall thickness were included in the model; the 2 explanatory variables had an interactive effect on plasma ANP-IR concentration (R2 = 0.27; P = .02). There was no appreciable correlation between plasma ANP-IR concentration and any other echocardiographical variable. In a population that included cats with subclinical disease, those with HCM did not have significantly higher plasma ANP-IR concentration than did healthy cats. An exploratory multivariable regression analysis suggested a linear relationship between ANP-IR concentration and atrial size, wall thickness, and their interaction.

Comparison of Doppler-derived peak aortic velocities obtained from subcostal and apical transducer sites in healthy dogs.

The accuracy of Doppler-derived blood flow velocity depends on the angle of incidence between the ultrasound beam and the direction of flow. In dogs with subaortic stenosis, it is known that the subcostal transducer site provides higher left ventricular ejection velocities than does the apical site. Left ventricular ejection velocities obtained from the subcostal site in healthy dogs have not been reported; accordingly, we examined healthy, random-source dogs to test the hypothesis that aortic velocities obtained from the subcostal and apical transducer sites differ. In 38 unsedated dogs, high-pulsed repetition frequency (HPRF) and continuous-wave (CW) Doppler studies of the proximal aorta and left ventricular outflow tract were performed using two-dimensional echocardiographic guidance. The effects of Doppler modality, transducer site, and their interaction on peak aortic velocity were tested through the use of analysis of variance. P values less than 0.05 were considered to indicate significance. The mean (+/-SE) peak aortic velocities were as follows: subcostal site (HPRF) = 1.44 +/- 0.03; apical site (HPRF) = 1.39 +/- 0.03; subcostal site (CW) = 1.48 +/- 0.03; apical site (CW) = 1.39 +/- 0.03. Aortic velocities obtained from the subcostal site were significantly greater than those obtained from the cardiac apex (P = 0.0001). Lower and upper limits of 95% reference intervals for aortic velocities by method of measurement and transducer location are proposed. In a population of healthy dogs, peak aortic velocities obtained from the subcostal site exceeded those obtained from the cardiac apex but did so only to a marginal degree.