Abstract
Myocardial deformation analysis by speckle-tracking echocardiography (STE) has been used for analysis of myocardial viability and myocardial fibrosis. Patients with severe aortic stenosis are known to develop myocardial fibrosis. This study evaluated the association between myocardial fibrosis determined by late gadolinium enhancement (LGE) cardiac magnetic resonance (CMR) and 2-dimensional STE in patients with severe aortic stenosis. In 30 patients (78±7 years) with severe aortic stenosis (mean gradient 53±21 mm Hg), peak systolic circumferential strain based on 2-dimensional echocardiographic parasternal short-axis views and peak systolic longitudinal strain based on apical views were determined for analysis of regional function. LGE CMR was performed to define the amount of fibrosis in each segment within 24 hours of echocardiography. Relative amount of fibrosis was determined based on LGE CMR as gray-scale threshold 6 SDs above the mean signal intensity of the normal remote myocardium. There was a decrease in LGE from base to apex (14.4±8.7% for basal segments, 3.4±3.0% for midventricular segments, and 2.1±3.0% for apical segments; p<0.001). Simultaneously, there was an increase in myocardial deformation expressed as peak systolic longitudinal strain from base to apex (-11.6±7.0% for basal segments, -16.9±6.5% for midventricular segments, and -17.4±7.7% for apical segments; p=0.001). There was a negative correlation between the amount of myocardial fibrosis determined by LGE CMR and peak systolic longitudinal strain for the total left ventricle (r=-0.538, p=0.007). Myocardial fibrosis defined as LGE>10% could be identified by peak systolic longitudinal strain less than -11.6%, with a sensitivity of 65% and a specificity of 75% (area under the receiver operating characteristic curve 0.69). In conclusion, myocardial fibrosis increases from apical to basal left ventricular segments in patients with severe aortic stenosis. There is an association between severity of myocardial fibrosis defined by LGE CMR and myocardial deformation by STE.
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