Deterioration of Myocardial Function in Paradoxical Low-Flow Severe Aortic Stenosis: Two-Dimensional Strain Analysis

Background: The diagnosis and management of paradoxical low-flow (PLF) aortic stenosis (AS) is challenging in clinical practice. In addition, its pathophysiology has not been fully understood. The aim of this study was to test the hypothesis that left ventricular (LV) myocardial function is deteriorated in PLF AS and that it is closely related to global LV afterload. Methods: Echocardiographic data from 103 patients with severe AS (aortic valve area <1.0 cm(2)) with normal LV ejection fractions were prospectively collected. Global longitudinal and circumferential myocardial strain was analyzed using two-dimensional speckle-tracking imaging. PLF AS was defined as a stroke volume index <35 mL/m(2). Results: Sixteen patients were classified as having PLF AS. Compared with those with normal-flow AS, patients with PLF AS were more likely to have worse functional status (mean New York Heart Association functional class, 2.38 +/- 0.70 vs 1.96 +/- 0.62; P = .02), worse global longitudinal strain (GLS) ( 12.6 +/- 4.4% vs -16.4 +/- 4.0%, P < .01), lower aortic valve area (0.53 +/- 0.15 vs 0.78 +/- 0.19 cm(2), P < .01), and higher valvuloarterial impedance (5.62 +/- 1.33 vs 3.65 +/- 0.83 mm Hg . m(2)/mL, P < .01). GLS showed a significant negative linear relationship with stroke volume index (r = -0.324, P = .001) and a positive relationship with E/E' ratio (r = 0.367, P < .001). Multivariate analysis showed that age (beta = 0.08, P = .07) and valvuloarterial impedance (beta = 1.54, P < .01) were significant predictors of GLS. Conclusions: GLS is depressed in patients with PLF AS. This implies that subclinical myocardial dysfunction may be more prominent in PLF AS compared with normal-flow AS and suggests the possible diagnostic and prognostic value of two-dimensional global strain in identifying PLF AS. In addition, global LV afterload is an important determinant of myocardial dysfunction in patients with severe AS. (J Am Soc Echocardiogr 2011; 24: 976-83.)