Prevalence of systolic anterior motion of the mural (posterior) leaflet of the mitral valve in hypertrophic cardiomyopathy: an echocardiographic study

Prevalence of systolic anterior motion of the mural (posterior) leaflet of the mitral valve in hypertrophic cardiomyopathy: an echocardiographic study

InternatIonal Journal of Cardiology, 17 (1987) 197-206 Elsevier 197 IJC 00596 Prevalence of systolic anterior motion of the mural (posterior) leafl...

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InternatIonal Journal of Cardiology, 17 (1987) 197-206 Elsevier

197

IJC 00596

Prevalence of systolic anterior motion of the mural (posterior) leaflet of the mitral valve in hypertrophic cardiomyopathy: an echocardiographic study Eugenio

Moro l. * , Folkert

J. ten Cate I, James J. Leonard

*, Jos Roelandt



’ Thoraxcenter, Erasmus University and Academic Hospital Dijkzigt-Rotterdam, Rotterdam, The Netherlands; ’ Department of Medicine, Uniformed Services, lJniversit,v of Health Sciences. Bethesda. Maryland, U.S.A. (Received

10 March

1987; revision

accepted

2 June 1987)

Moro E, Ten Cate FJ, Leonard JJ, Roelandt J. Prevalence of systolic anterior motion of the mural (posterior) leaflet of the mitral valve in hypertrophic cardiomyopathy: an echocardiographic study. Int J Cardiol 1987;17:197-206. Cross-sectional echocardiography was used to identify systolic anterior motion of the mural (posterior) leaflet of the mitral valve from a group of 53 patients with hypertrophic cardiomyopathy. This type of systolic anterior motion was identified in parastemal long axis, apical four-chamber and/or long-axis cross-sections and was characterized by an elongation of the mural leaflet and an abnormal coaptation with the aortic (anterior) leaflet. At end-diastole, the aortic leaflet coapted at the basal or mid portion of the mural leaflet, leaving its distal “residual” segment in the left ventricle. Subsequently, during systole this “residual” segment approached or touched the ventricular septum. Systolic anterior motion of the mural leaflet was present in 6 (12%) of our patients with hypertrophic cardiomyopathy. Lengthening of the leaflet and an abnormal coaptation were associated with increased thickening of the posterior wall of the left ventricle and narrowing of the left ventricular outflow tract. All these elements contribute to the occurrence of systolic anterior motion and left ventricular tract obstruction.

Key words: Mural leaflet of the mitral valve; Hypertrophic

cardiomyopathy

Correspondence to: Jos Roelandt. M.D., Thoraxcenter. Erasmus University, P.O. Box 1738. Rotterdam, The Netherlands. * Present address: Laboratorio di Ecocardiografia, Servizio di Emodinamica, Pordenohe. Italy. Dr. Moro is supported by a fellowship in Cardiology from Italian Government (grant A-15550).

0167-5273/87/$03.50

0 1987 Elsevier Science Publishers

B.V. (Biomedical

Division)

198

Introduction Systolic anterior motion of the mitral valve is an echocardiographic hallmark in many patients with hypertrophic cardiomyopathy when outflow tract obstruction is present. Cross-sectional echocardiographic studies have indicated that systolic anterior motion has many varied morphologic expressions [1,2]. Furthermore, the mural leaflet of the mitral valve alone can demonstrate systolic anterior motion and be responsible for the outflow tract obstruction [3]. Therefore the present echocardiographic study was undertaken to investigate the prevalence and possible mechanism that produce systolic anterior motion of mural leaflet of the mitral valve in patients with hypertrophic obstructive cardiomyopathy. Methods Selection of Patients

Fifty-three consecutive patients with hypertrophic cardiomyopathy were analysed by cross-sectional and M-mode echocardiography. Diagnosis of hypertrophic cardiomyopathy was based on the combined characteristic clinical and echocardiographic findings [4,5]. Echocardiography demonstrated a hypertrophied and nondilated left ventricle with a disproportionate increase of thickness of the interventricular septum (interventricular septum/left ventricular posterior wall > 1.5). No other cardiac or systemic disease was present in these patients that could produce left ventricular hypertrophy [5]. The patients ranged in age from 14 to 68 years (mean 48 years). Thirty-eight were men, 15 were women. Eighteen age-matched controls were analysed for reference values of the left ventricular outflow tract area and the percentage of thickening of the left ventricular posterior wall. The age of these patients ranged from 34 to 61 years (mean 46) 10 were men and 8 women. Echocardiographic

Examinations

Cross-Sectional Echocardiography. A phased-array sector scanner with a 3.5 and/or 5 MHz transducer was used to perform the cross-sectional echocardiograms. The examinations were carried out in the standard fashion including the following cross-sections: (a) parastemal long axis, (b) parasternal short axis (at multiple levels), (c) apical long axis, and (d) apical four-chamber [6]. The images so obtained were recorded on video-tape and later analysed on a video cassette system capable of bidirectional play-back at normal speed, slow motion speed, frame by frame and stop frame. M-Mode Echocardiography. M-mode echocardiograms were selected from the parasternal long-axis cross-section and standard criteria were applied for measuring all echocardiographic parameters [7].

199

Echocardiographic

Analysis

Cross-Sectional Echocardiographic Data. The distribution of the hypertrophy in the left ventricle was identified applying a previously described method which divides the left ventricle in segments [8,9]. In order to avoid problems due to lateral resolution of the sector, the segments of the left ventricle visualized in the lateral regions of the sector (in the short axis cross-section) were considered hypertrophied if the wall was judged to be at least 17 mm in thickness. The cross-sectional area of the left ventricular outflow tract was assessed from a short-axis cross-section at the level of mitral valve at end-diastole when both mitral leaflets could be visualized in the closed position [lo]. The leaflet motion on cross-sectional echocardiography was best appreciated by analysis of real-time video recordings. The distinction of the leaflet from its tendinous cords was performed by analysis of the motion patterns and of the continuity of both structures throughout the cardiac cycle. M-Mode Echocardiographic Data. Systolic anterior motion of the mitral valve was evaluated semiquantitatively using a modification of the classification proposed by Gilbert et al. [ll]: mild if the minimal mitral-septal distance was greater than 10 mm, moderate if this distance was 10 mm or less but there was no mitral-septal contact and severe if there was either brief or prolonged mitral-septal contact. Thickening of the posterior wall of the left ventricle was calculated in percent as follows:

ES-ED ___ ED

X 100% = %LVPW thickening,

where ES = end-systolic thickness and ED = end-diastolic thickness. Hemodynamic

Studies

Cardiac catheterization was performed in all patients with systolic anterior motion of mural mitral leaflet. Left ventricular outflow tract gradients of 35 to 60 mm Hg were present under basal conditions. No provocative maneuvers were carried

out in these patients. Results

Control Subjects

The percentage of left ventricular posterior wall thickening ranged from 38 to 55% (mean + SD = 42 + 12%). The cross-sectional area of the left ventricular outflow tract ranged from 8.6 to 11.2 cm* (9.4 5 1.6 cm2).

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Cross-Sectional

Echocardiographic

Findings

In 4 patients, cross-sectional images adequate for analysis and appropriate identification of the mitral apparatus were not obtained. Systolic anterior motion of the mural leaflet was present in 6 of the remaining 49 patients studied (12%). The apical cross-sections of the left ventricle were more advantageous for identification of patterns of motion of the valve. It was also possible to obtain pictures suitable for analysis from the parasternal views (Fig. 1). All 6 patients with systolic anterior motion of the mural leaflet had an abnormal coaptation of the distal leaflet margins at end-diastole. Subsequently, at the onset of systole the aortic leaflet contacted the mural one near its base or its mid portion. In this way, the distal segment of the mural leaflet passed caudal to the aortic leaflet, leaving a “residual” free edge (Fig.

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Fig. 1. Sequential cross-sectional echocardiographic stop-frame images obtained during the same cardiac cycle in the parastemal long axis view in a patient with hypertrophic cardiomyopathy and systolic anterior motion of the mural leaflet of the mitral valve. Each stop frame is accompanied by schematic illustrations. A and C during diastole: A. the mitral valve is wide open; B. the mitral leaflets approach each other; D and C during the subsequent systole: the free residual portion of the mural leaflet approaches and makes contact with the interventricular septum. aML = aortic mitral leaflet; Ao = aorta: IVS = interventricular septum; LA = left atrium; LV = left ventricle; pML = mural (posterior) leaflet.

2A). During mid-systole, the residual segment continued its anterior movement and closely approached or contacted the interventricular septum (Fig. 2B, C). Consequently, in all these patients, the length of the mural leaflet was longer than that of the aortic leaflet. These peculiar findings were not observed in the other patients with hypertrophic obstructive cardiomyopathy.

202

M-Mode Echocardiographic

Findings

All 6 patients showed systolic anterior motion of the mitral valve on M-mode echocardiography, although its duration and extent were variable: moderate in 3 and severe in the other 3 patients. Premature systolic closure of the aortic valve was identified in 4 patients, was absent in 1 and could not be assessed in the last patient. Ventricular septal thickness ranged from 18 to 34 mm (mean 23.5) and ventricular septal to free wall thickness ratio from 1.6-2.5 (mean 2). Left ventricular outflow tract cross-sectional areas ranged from 1.6 to 3.7 cm2 (mean 3). The percentage of posterior wall thickening ranged from 72 to 111% (mean IfI SD = 86 + 19). The

203

Fig. 2. Sequential cross-sectional echocardiographic stop-frame images obtained during the same cardiac cycle in the long-axis apical view in a patient with hypertrophic cardiomyopathy and systolic anterior motion of the mural leaflet. Each stop frame is a accompanied by schematic illustration. A, during diastole before mitral valve coaptation: the anterior leaflet (AML) and the mural (posterior) leaflet (PML) approach each other. B, at the end of diastole: the aortic leaflet comes into opposition with the base of the mural leaflet. C, during systole: the ‘I residual” free portion of the mural leaflet shows anterior motion and approaches the ventricular septum. RV = right ventricle; other abbreviations as in Fig. 1.

TABLE

1

Echocardiographic and hemodynamic of the mitral valve. Patient

IVS thickness

findings

in patients

2 3 4 5 6

18 34 26 24 21 18

IVS = interventricular wall; SAM = systolic ventricular outflow.

anterior

motion

of mural

leaflet

IVS/ LVPW

Degree of SAM

systolic aortic notch

Hypertrophic segments

LVOT area (cm’)

LVPW-th

A-LVOT

(W)

(mm Hg)

1.6 2.5 1.8 2.2 2.1 1.9

severe moderate severe moderate severe moderate

present present present present not identifiable present

2 3 3 2 3 3

2.4 3.6 3.4 3.3 1.6 3.1

100 12 111 14 83 78

49 47 60 35 59 47

(mm) 1

with systolic

septum; anterior

LVOT = left ventricular motion: th = thickening;

relationship between systolic anterior echocardiographic findings is reported

outflow tract; LVPW = ventricular posterior A-LVOT = pressure gradient across the left

motion of the mural in Table 1.

leaflet

and

the other

Discussion Cross-sectional tures participating

echocardiography facilitates in systolic anterior motion

visualisation of the anatomical strucof the mitral valve and causing left

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ventricular outflow tract obstruction in patients with hypertrophic cardiomyopathy [1,2]. Recent investigations have proposed that the mural leaflet alone can be responsible for the occurrence of systolic anterior motion. The leaflet fails to coapt normally with the aortic one in late diastole and moves anteriorly, toward the left ventricular outflow tract, during the subsequent systole. Divergence of opinion still exists among investigators regarding the precise mechanism for subaortic obstruction and systolic anterior movement in patients with hypertrophic cardiomyopathy [12,13]. The mechanism of systolic anterior motion of the mural leaflet may be similar to that previously postulated for other patterns of systolic anterior movement, that is hemodynamic forces pull the “residual” portion of the leaflet anteriorly towards the ventricular septum. We recognize that the anatomical elongation of the leaflet is the morphological hallmark of this unusual type of systolic anterior motion. In our patients, on the other hand, there is close association between critical narrowing of the left ventricular outflow tract, increased contraction of the left ventricular posterior wall, thickness of the interventricular septum and start of systolic anterior movement. These elements can be responsible for a significant ventriculo-valvar disproportion, such that the outflow tract of the left ventricle is too small and the elongated mural leaflet is displaced abnormally close to the ventricular septum. Systolic anterior motion during systole may occur because the elongated free edge of the mural leaflet is further carried out to the restricted outflow tract by the energetic contraction of the left ventricular posterior wall. In this case, it can be postulated that a mechanical process (i.e. brisk contraction of the posterior wall) initiates systolic anterior motion of the mural leaflet and produces the increase of blood flow velocity in the left ventricular outflow tract which is responsible for the induction of the Venturi effect. In conclusion, our study indicates that systolic. anterior motion of the mural leaflet of the mitral valve is a peculiar finding present in some patients with hypertrophic obstructive cardiomyopathy (12% in our study). An integrated mechanism for its occurrence can be postulated. Anatomical and dynamic determinants cause both anterior displacement of the mural leaflet and left ventricular outflow tract obstruction.

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205 7 O’Rourke RA, Hanrath P, Henry WN, et al. Report of the Joint International Society and Federation of Cardiology/World Health Organization Task Force on Recommendations for standardization of measurements from M-mode echocardiograms. Circulation 1984;69:854A-857A. 8 Maron BJ, Gottdiener JS, Epstein SE. Patterns and significance of distribution of left ventricular hypertrophy in hypertrophic cardiomyopathy. A wide angle two-dimensional echocardiographic study in 125 patients. Am J Cardiol 1981;48:418-428. 9 Domenicucci S, Lazzeroni E, Roelandt J. Ten Cate FJ, Vletter WB. Das SK. Progression of hypertrophic cardiomyopathy. A cross-sectional echocardiographic study. Br Heart J 1985;53:405-411. 10 Spirit0 P, Maron BJ. Significance of left ventricular outflow tract cross-sectional area in hypertrophic cardiomyopathy: a two-dimensional echocardiographic assessment. Circulation 1983;65:1100-1108. 11 Gilbert BW, Pollick C. Adelman AG, Wigle ED. Hypertrophic cardiomyopathy: subclassification by M-mode echocardiography. Am J Cardiol 1980;45:861-872. 12 Caplan J, Boltwood CM, Tei C. Shah PM. Clinical improvement in hypertrophic cardiomyopathy after inferior myocardial infarction. J Am Co11 Cardiol 1985:5:797-802. 13 Criley JM, Siegel RJS. Has “obstruction” hindered our understanding of hypertrophic cardiomyopathy? Circulation 1985;72:1148-1154.