Echocardiographic assessment of apical morphology and dynamics in hypertension and apical hypertrophic cardiomyopathy

Figures

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  Fig. 1. The schematic diagrams and echocardiographic images depicted the 4 and 5-chamber view used to measure the blood flow velocity. Pulse Doppler velocities were measured at the LV apex (at 1/6 of the LV long axis, image (a) and the LVOT (just underneath the aortic annulus, image (b). The velocity of the apical cavity (Vap) (under the baseline) in normal, hypertension and AHCM group respectively (c, d, e). AHCM = apical hypertrophic cardiomyopathy; LV = left ventricle; LVOT = left ventricular outflow tract; LA = left atrium; LV = left ventricle; RA = right atrium; RV = right ventricle.

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  Fig. 2. The echocardiographic measurements of apical angle were based on Wu’s research6 (left, MRI image). Noncontrast (middle) and contrast-enhanced (right) echocardiographic images of two AHCM patients. In the zoom-apical four chamber view, two lines were drawn from the endocardial apex to the two points of the endocardium at 1/6 of the long axis length of the LV. The angle between the two additional lines was defined as the apical angle (apA). The apical angle was easily measured when the apical endocardial border was completely visualized by routine surface echocardiography or contrast echocardiography.

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  Fig. 3. Comparison of the apical morphological and dynamic parameters among three study groups. AHCM = apical hypertrophic cardiomyopathy; ABR = apical basal wall thickness ratio; apA-d = apical angle at end-diastole; apA-s = apical angle at end-systole; ΔapA = apA-d - apA-s; apA%=ΔapA/apA-d; Vap= pulsed Doppler velocity at apex; Vlvot=pulsed Doppler velocity at left ventricular outflow tract; LS = longitudinal strain; RALS = relative apical longitudinal strain [apical longitudinal strain (LSapical)/sum of basal and mid LS (LSbasal +LSmiddle)].

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  Fig. 4. Representative examples of two-dimensional echocardiographic images (a1, b1, c1) and segmental longitudinal strain images in normal, hypertension and AHCM group respectively (a2, b2, c2). The reduction of LSbasal was more pronounced in hypertensive patients(b2). AHCM patients had a more remarkable decrease in LSapical (c2). In healthy and hypertension group, LS increased from the base to apex. However, AHCM patients lost this trend. LS = longitudinal strain.