Assessment of left atrial function by volumetric indices and tissue Doppler imaging in ischaemic and idiopathic dilated cardiomyopathy

Abstract

Left atrial (LA) contractility plays an important role in maintenance of cardiac output in patients with left ventricular systolic dysfunction. Although left atrial contractile dysfunction has been reported in dilated cardiomyopathy of ischemic and non-ischemic etiology, the mechanism of LA dysfunction and the pathophysiologic determinants of left atrial size and function have not been adequately investigated in these patients. The aim of this study was to evaluate LA size and contractile function in patients with dilated cardiomyopathy of ischemic and idiopathic etiology and to explore the mechanism and determinants of LA dilation and contractile dysfunction in these patients. 35 patients with ischemic dilated cardiomyopathy, 15 patients with idiopathic dilated cardiomyopathy and 30 control subjects were studied with transthoracic conventional echocardiography, tissue Doppler imaging (TDI) and coronary angiography (CA). Left ventricular (LV) size, systolic and diastolic functions as well as mitral regurgitation (MR) were evaluated. Left atrial volume at mitral valve opening (Vmax), onset of atrial systole, determined by onset of the P wave of the electrocardiogram (Vp) and mitral valve closure (Vmin) was determined with two-dimensional echocardiography. The left atrial contractile function was assessed by means of active emptying fraction (ACTEF = {Vp − Vmin}/Vp%) and TDI for assessment of late diastolic velocity of the mitral annulus and left atrial free wall. Left atrial Vmax was greater while ACTEF and left atrial wall velocity were lower in cardiomyopathy patients compared with the control subjects (79 ± 32 vs. 59 ± 18; P < 0.05, 27.6 ± 13 vs. 42 ± 15; P < 0.05 and 10.2 ± 4.7 vs. 16.2 ± 5.4; P < 0.05, respectively). Vmax , ACTEF and left atrial wall velocity were similarly affected in both types of cardiomyopathy, ischaemic and idiopathic, under the same loading conditions (74 ± 24 vs. 91 ± 46; P > 0.05, 29 ± 12 vs. 27 ± 13; P > 0.05 and 10 ± 5 vs. 11 ± 4; P > 0.05, respectively). The determinants of ACTEF were left atrial volume, left ventricular ejection fraction (EF), E/e’ and MR severity. Left atrial enlargement and contractile dysfunction are common in patients of dilated cardiomyopathy regardless of its aetiology, with the same degree of contractile dysfunction in both ischemic and idiopathic cardiomyopathies under similar loading conditions. This dysfunction is related to worse LV systolic and diastolic function, more severe mitral regurgitation and larger LA volume rather than to the aetiology of cardiomyopathy.