Systolic anterior motion in the absence of asymmetric septal hypertrophy. A buckling phenomenon of the chordae tendineae.

Abstract

SUMMARY Systolic anterior motion (SAM) of the mitral valve in the absence of asymmetric septal hypertrophy or concentric left ventricular hypertrophy has been reported in several conditions. In this report we describe the clinical and echocardiographic findings in 15 patients who demonstrated SAM without associated organic heart disease (group 1, 10 patients) or in association with mitral valve prolapse (group 2, five patients). Cross-sectional echocardiography revealed the etiology of SAM in both groups to be early systolic anterior angular motion ("buckling") of mitral chordal structures, rather than movement of the body of the anterior mitral leaflet into the left ventricular outflow tract. In contrast to normal subjects and group 1, group 2 patients had auscultatory evidence of mitral prolapse, a slightly greater mean left ventricular ejection fraction (p < 0.05) (normals, 69 ± 5.2%, group 1, 72 ± 3.8%, group 2, 75 ± 5.6%), and a greater mean diastolic mitral valve (D-E) excursion (p < 0.05) (normals, 1.8 ± 0.2 cm, group 1, 2.2 ± 0.3 cm, and group 2, 2.6 ± 0.4 cm). This spectrum of mitral excursion and left ventricular ejection fraction supports the concept that the mitral valve prolapse syndrome may have as its basis a mitral valve abnormality and/or a hyperdynamic state that predispose to both chordal buckling and mitral leaflet prolapse.SYSTOLIC ANTERIOR MOTION (SAM) of the mitral valve was initially described in conjunction with asymmetric septal hypertrophy as one of the two echocardiographic hallmarks of idiopathic hypertrophic subaortic stenosis or hypertrophic obstructive cardiomyopathy.'~' The presence of SAM was considered to be the M-mode echocardiographic manifestation of the left ventricular outflow obstruction in hypertrophic cardiomyopathy.' ' Furthermore, the amount of SAM (i.e., the degree and duration of the approximation of the anterior mitral leaflet to the ventricular septum) was reported to correlate with the presence and the degree of left ventricular outflow obstruction.4 More recently, SAM has been reported without asymmetric septal hypertrophy both in the presence"8 and in the absenceg of associated subaortic obstruction. Conditions other than hypertrophic cardiomyopathy known to be associated with SAM include membranous subaortic stenosis,10 dextraposition of the great vessels with subpulmonic obstruction,1' pulmonary hypertension,'2 concentric left ventricular hypertrophy, 13 14 hyperkinetic states14' 1 ' (including aortic insufficiency and hypovolemia), mitral valve prolapse (MVP)16-'8 and the absence of detectable heart disease. 8,15,19 Fifteen patients who demonstrated SAM in the

Symbolism in Early Russian Cinema and the Ghostwriter Aleksandr Kursinskii

“…Furthermore, in his memoirs Gardin himself wrote about The Mask of Death as "an absurdly mystical film"; he does not seem to have in mind a story that he wrote himself. 69 On the other hand, The Mask of Death does correspond closely to the Kursinskii texts we already have discussed, as well as to many of his poems:…”

Hypertrophic Cardiomyopathy and the Athlete

“…33 The systolic anterior motion may reflect buckling of mitral valve chordae in normal persons and in patients with mitral 118 valve prolapse. 34 Theories regarding the mechanism of systolic anterior motion in hypertrophic cardiomyopathy include ( 1) mitral chordal buckling; (2) vigorous posterobasal LV wall contraction, forcing the mitral leaflets into the nearly empty LV outflow tract; (3) a hypertrophied septum, leading to malalignment ofthe anterolateral papillary muscle; and (4) a Venturi effect, wherein blood is ejected through a narrowed LV outflow tract, drawing the anterior mitral leaflet toward it.…”

An evaluation of two‐dimensional echocardiography in the diagnosis of hypertrophic cardiomyopathy

“…When seen in pericardial effusion or with mitral valve prolapse it has been interpreted as an artifact (Mintz et al, 1978;Nanda and Gramiak, 1978). In one 2-D echo study SAM was observed both in normal individuals and in mitral valve prolapse, the suggestion being that it was due to buckling of the chordae tendineae (Gardin et al, 1981). We studied 16 patients with SAM but without hypertrophic cardiomyopathy ; 40 % had evidence of left ventricular hypertrophy, left ventricular contraction was increased with an ejection fraction of 75% or more in 40 % , and in 47 % there appeared to be asymmetry of contraction.…”