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Giornale Italiano di Cardiologia 1982

Echocardiographic assessment of left ventricular wall motion in hypertrophic cardiomyopathy.

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G Gullace
M Knippel
P Ravizza
M T Savoia

Keywords

Abstract

M-mode and two-dimensional parasternal long axis view echocardiography, and left anterior oblique cineangiography were employed to assess the left ventricular wall motion in 10 normal subjects (N) and in 25 patients with hypertrophic cardiomyopathy: 7 patients with symmetric hypertrophy (SH) and 6 patients with apical cardiomyopathy (AHCM) and no intraventricular gradient; 12 patients with hypertrophic obstructive cardiomyopathy and asymmetric septal hypertrophy with resting intraventricular gradient (6 pts) (HOCM-R) or gradient occurring only after isoproterenol infusion (6 pts) (HOCM-I). The left ventricle was divided into five portions: upper and lower septum, upper and lower posterior wall and apex. The excursion and thickness of the upper and lower portions of the septum and posterior wall were measured in all patients and compared to 10 normal subjects (N). From the superimposed end-diastolic and end-systolic echo frames and angio silhouettes a chordal and a radial-chordal method were used, respectively, to measure the motion of the left ventricular wall segments. In SH the left ventricular wall motion was qualitatively similar to N but a little reduced; the thickness was increased and no pressure gradient was present. In AHCM the lower septum, posterior wall, and apex showed significantly increased thickness and motion compared to N and compared to the upper portions of the septum and posterior wall. No gradient was present. In HOCM-R the upper septum moved towards the apex, the lower septum, upper posterior wall and lower posterior wall moved towards the left ventricular cavity. The upper posterior wall was hyperkinetic compared to N and compared to the lower posterior wall, resting gradient and SAM was present in all. In HOCM-I the upper septum moved towards the apex; the posterior wall was hyperkinetic (the excursion was a little wider in the lower posterior wall than in the upper posterior wall). No gradient was recorded at rest, but it could be provoked by isoproterenol. Echocardiography provides precise information on left ventricular wall motion in hypertrophic cardiomyopathy. Hyperkinesis of the lower left ventricular wall is related to AHCM; hyperkinesis of the upper posterior wall and the motion of the upper septum towards the apex are related to HOCM-R. Hyperkinesis of the lower posterior wall is related to HOCM-I. SAM and pressure gradients may be related to the hyperkinesis of the upper posterior wall. Finally, the septum is not an immobile structure in HOCM, since it moves mainly from the base to the apex and a less (or not at all) towards the posterior wall.

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