Shinshu M ed J, 59 ⑷ :259 〜263, 2011

Spontaneous Resolution of Left Ventricular Outﬂow Tract
Obstruction in the Course of Newly‑Developed Mitral Valve
Prolapse in a Hypertrophic Cardiomyopathy Patient
Takahisa MARUYAMA , Takahiro SAKAI and Toshio KASAIDivision of Cardiology, Nagano Municipal Hospital

A 63‑year‑old man was diagnosed with hypertrophic obstructive cardiomyopathy. Echocardiography
revealed asymmetrical left ventricular hypertrophy, systolic anterior movement (SAM ) of mitral leaﬂets
causing an outﬂow tract pressure gradient of 52 mmHg, and moderate mitral regurgitation (MR) directed
posteriorlyin the left atrium.Four years later,when the patient was admitted for mild congestive heart failure,
SAM and left ventricular outﬂow obstruction were absent, and prolapse of the posterior mitral leaﬂet wascausing anteriorly‑directed severe M R. Rupture of the chordae tendineae was responsible for the mitralprolapse and for the abolition of the outﬂow obstruction. Shinshu Med J 59 : 259 ―263, 2011
(Received for publication March 9, 2011;accepted in revised form April 6, 2011)
Key words:systolic anterior movement, hypertrophic cardiomyopathy, mitral valve prolapse

Introduction

edematous. Electrocardiography showed a normal
sinus rhythm and a complete right bundle branch

Among the various features of hypertrophic car-block.On chest X‑ray study,pulmonary congestion

diomyopathy (HCM ), left ventricular outﬂow

was not seen, and the cardiothoracic ratio wasobstruction with systolic anterior movement (SAM)

51%. Echocardiography revealed that the size andof the mitral leaﬂets signiﬁcantly inﬂuences thecontraction of the left ventricle were normal (end‑clinical outcome. Although infrequent, rupture ofdiastolic dimension, 36 mm ; ejection fraction,

the chordae tendineae is reported to complicate73%), but that asymmetrical hypertrophy (inter‑obstructive HCM . We report a case of HCM withventricular septal thickness,17 mm)and SAM were

spontaneous disappearance of SAM, presumably

causing obstruction of the left ventricular outﬂow

caused by mitral valve prolapse with ruptured chor-

tract with a peak ﬂow velocity of 3.6 m/sec ondae tendineae.

continuous wave Doppler (i.e. calculated pressureCase Reportgradient,52 mmHg).M oderate mitral regurgitation(M R)was observed with the jet directed posteriorly

Our patient ﬁrst came to our hospital at the age ofin the dilated left atrium (dimension,54 mm)(Fig.1,63, seeking a consultation because of mild dyspnea

Table 1).A left‑sided cardiac catheterization study

on exertion. The pulse rate was 66 beats/min andrevealed that the coronary arteries were normalregular; blood pressure was 104/80 mmHg. Thereand that the intra‑ventricular pressure gradient waswere no rales. A systolic ejection murmur of grade

about 30 to 40 mmHg.The patient was accordingly

3/6 was heard. The extremities were notdiagnosed with hypertrophic obstructive cardiomyopathy.

Corresponding author:Takahisa M aruyama
Division of Cardiology, Nagano Municipal Hospital,

Several months later, he experienced a single

1333‑1 Tomitake, Nagano‑city, Nagano‑prefecture

episode of paroxysmal atrial ﬁbrillation ac-381‑8551, Japan

companied by a considerable decrease in blood

No. 4, 2011259

M aruyama.Sakai.KasaiFig.1 Echocardiographic images in transthoracic apical long axis view at the ﬁrst presentation. A,
Two‑dimensional image on diastole. Asymmetrical left ventricular hypertrophy was seen. B,
Two‑dimensional image on systole. Systolic anterior movement of the anterior mitral leaﬂet(arrow)caused outﬂow obstruction.C,Color Doppler ﬂow image on systole.Mitral regurgitation
jet was oriented posteriorly in the left atrium.AO＝aorta ;LA＝left atrium ;LV＝left ventricle;
M R＝mitral regurgitation.

Table 1 Echocardiographic ﬁndings
At the ﬁrst presentation

Four years later

LVDd (mm)LVDs (mm)36164018IVST (mm)EF (%)LAD (mm)
LVOT obstruction
SAM

177352(＋)(＋)(−)

177055(−)(−)(＋)

PML prolapse
M R grade

moderatesevere

M R direction

poteriorlyanteriorly

EF＝ejection fraction of left ventricle;IVST＝inter‑ventricular septal thickness; LAD＝left atrial dimension ; LVDd＝left ventricular diastolic dimension ; LVDs＝left ventricular systolic dimension ; LVOT＝left ventricular
outﬂow tract ; MR＝mitral regurgitation ; PML＝posterior mitral leaﬂet ;SAM ＝systolic anterior movement of mitral leaﬂet260

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Resolution of left ventricular outﬂow obstruction

Fig.2 Echocardiographic images in transthoracic apical long axis view four years after the ﬁrst
presentation. A, Two‑dimensional image on diastole. B, Two‑dimensional image on systole.
There was no systolic anterior movement of the anterior mitral leaﬂet,and the outﬂow tract was
not obstructive. The posterior mitral leaﬂet bulged into the left atrium. C, Color Doppler ﬂow
image on systole. The jet of severe mitral regurgitation was oriented anteriorly. AO＝aorta ;LA＝left atrium ;LV＝left ventricle;M R＝mitral regurgitation.

pressure by 20 to 30 mmHg. Disopyramide andchordae tendineae was responsible for the prolapse

atenolol were prescribed, and he subsequentlyof the posterior mitral leaﬂet (Fig. 3).

remained in NYHA class

towith no furtherevents.

The patient chose to continue with medical therapy for the following two years, until he experi-

At age 67, however, four years after the ﬁrst

enced another episode of congestive heart failure.

presentation,overexertion brought on an episode ofThen, his mitral valve was repaired surgically.

nocturnal dyspnea, and the patient was admitted

Replacement by the mechanical prosthetic valve

under a diagnosis of congestive heart failure. Pul-abolished the mitral regurgitation, and the left

monary congestion improved promptly in response

ventricular outﬂow obstruction no longer occurred.

to vasodilators and diuretics. Although change inleft ventricle size had been mild since the ﬁrst

Discussion

presentation, as seen in an echocardiogram, SAM

HCM patients exhibit structural diversity of theand outﬂow obstruction had disappeared ; instead,mitral valve apparatus;some formations can cause

severe MR was noted,in the form of a jet along theSAM and left ventricular outﬂow obstruction .

anterior wall of the left atrium, caused by theSAM often accompanies M R without prolapse of

prolapse of the central and medial portions of theleaﬂets; in such cases the degree of MR depends on

posterior leaﬂet (Fig. 2, Table 1). Transesophageal

the coaptation of leaﬂets,especiallyon the abilityof

echocardiography conﬁrmed that rupture of thethe posterior leaﬂet to follow the anterior leaﬂet ,No. 4, 2011261

M aruyama.Sakai.Kasai

Fig.3 Transesophageal echocardiogram on systole four years after the ﬁrst presentation. A torn
chorda (arrow) is attached to the tip of the prolapsed posterior mitral leaﬂet. AM L＝anterior
mitral leaﬂet ;LA＝left atrium ;LV＝left ventricle;OT＝outﬂow tract of left ventricle;PM L＝posterior mitral leaﬂet.

and the regurgitation jet is oriented posteriorly inpatients.

the left atrium . Thus, at our patientʼs ﬁrst presen-In most of the reported cases, left ventriculartation,his MR had been considered to be secondary

outﬂow obstruction persisted at the occurrence ofto SAM and outﬂow obstruction.

rupture of the chordae tendineae.On the other

Four years later,however,our patientʼs SAM hadhand, our case and that reported by Araujo et al.

disappeared and the severity and direction of his

are unique as the pressure gradient and SAM

MR had markedly changed. His MR, clearly in-disappeared after rupture of the chordae tendineae.

dependent of SAM , was caused by prolapse of theIn these patients, the rupture of the chordae ten-posterior leaﬂet due to rupture of the chordae ten-dineae may have inﬂuenced the behavior of mitral

dineae.

structures leading the disappearance of SAM,and aPetrone et al.reported that mitral valve prolapse

subtle dilatation of outﬂow tract through volume

was identiﬁed in only 3% of consecutive HCM

overload might have diminished the ﬂow velocity,patients ; however, there are several reports de-thereby abolishing the suction eﬀect.

scribing obstructive HCM cases complicated withrupture of the chordae tendineae

In treating HCM patients with SAM , the origin.Although it isand inﬂuences of accompanying M R should be deter-

controversial whether rupture of the chordae ten-mined, and the possibility of spontaneous improve-dineae may be secondary to HCM or may be ament in the extent of outﬂow obstruction should be

separate primaryentity,one speculation is that long‑

kept in mind.

term mechanical stress might result in degenerationof the chordae tendineae in obstructive HCM
262

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Resolution of left ventricular outﬂow obstruction

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