Echocardiographic characterisation of cardiac dilatation induced by volume overload in a canine experimental model

Abstract

The aim of this study was to characterise the development of cardiac dilatation induced by chronic volume overload in 12 dogs. Bilateral arteriovenous fistulas were created between the common femoral arteries and the femoral veins, and the animals were serially studied with transthoracic echocardiography for a period of 12 weeks after the operation. Compared to the measurements obtained before the operation (week 0), the data obtained at the end of the experimental period showed significantly increased left ventricular volume measured by 2D-echocardiography (from 25.1 cm 3 to 43.8 cm 3 , p < 0.0001 in diastole and from 8.6 cm 3 to 16.8 cm 3 , p < 0.001 in systole), and left ventricular diameter measured by M-mode echocardiography (from 26.2 mm to 32.6 mm, p < 0.0001 in diastole and from 17.1 mm to 20.6 mm, p < 0.001 in systole). The size of the left atrium also increased in transversal (from 29.2 mm to 33.6 mm, p < 0.01) but not in longitudinal diameter. In spite of a significant cardiac chamber dilatation over the 12-week period, left ventricular systolic functional variables (fractional shortening, FS % and ejection fraction, EF %), and also the left ventricular systolic and diastolic free wall thickness remained unchanged. In this study we demonstrated that chronic progressive volume overload resulted in gradual dilatation of the canine heart, and that the pathological process can be monitored successfully by serial echocardiography. We found that left atrial dilatation occurred without the development of mitral regurgitation and/or detectable left ventricular dysfunction.