J Cardiol 2006 Jan; 47（1）: 31 – 37

Recurrent Severe Mitral Regurgitation Due to Left Ventricular
Apical Wall Motion Abnormality
Caused by Coronary Vasospastic
Angina: A Case Report
Masatoshi

SHIMIZU, MD

Yukio

KATO, MD＊1

Ritsu

MATSUKAWA, MD＊2

Hiroyuki

MASAI, MD

Takashi

SHIMA, MD

Yoichi

MIWA, MD＊1

Teruo

YAMASHITA, MD＊3

YutakaOKITA, MD＊3

Abstract ─────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────
A 76-year-old man developed congestive heart failure due to severe mitral regurgitation after episodesof vasospastic angina. Echocardiography demonstrated left ventricular apical akinesis with ballooning anddeformity of the anterior mitral leaflet becoming concave toward the left atrium. The acetylcholine provocation test induced diffuse coronary vasospasm in the distal segments of both right and left coronary arteries and reproduced severe mitral regurgitation. Follow-up echocardiography demonstrated decreased mitral
regurgitation with ameliorated apical wall motion. Coronary vasospasm remained refractory to antivasospastic medications and severe mitral regurgitation relapsed 1 month after discharge. Mitral valve annuloplasty with a Carpentier-Edwards physio ring was performed, and no recurrence of mitral regurgitation
was observed despite some episodes of vasospastic angina. We speculate that vasospastic angina and theresultant apical wall motion abnormality caused tethering of the mitral subvalvular apparatus, leading toinappropriate mitral coaptation and severe regurgitation.
──────────────────────────────────────────────────────────────────────────────────────────────────────────────────────────J Cardiol 2006 Jan ; 47（1）: 31−37

Key Words
Mitral regurgitation
Mitral valve, repair
Coronary vasospasm
Echocardiography, transthoracic
Cardiomyopathies, other ischemic

INTRODUCTION
Coronary vasospasm induces regional myocardial dysfunction, which is either transient or permanent according to the severity of coronaryvasospasm1）. The left ventricular apex is susceptible to multivessel coronary vasospasm, and dysfunction of the left ventricular apex influences thewall motion at the root of the papillary muscles. In
these circumstances, the chordae tendineae andmitral leaflets could be displaced apically and outward, resulting in mitral regurgitation due to thetethering of the mitral valve2）.
CASE REPORT
A 76-year-old man, complaining of chest dis-──────────────────────────────────────────────
国立病院機構神戸医療センター 循環器科，＊ 1 内科，＊ 2 心臓血管外科 : 〒 654−0155 神戸市須磨区西落合 3−1−1 ; ＊ 3 神戸大学医学部 呼吸循環器外科学，神戸
Departments of Cardiology, ＊ 1Internal Medicine, and ＊ 2Cardiovascular Surgery, National Hospital Organization Kobe Medical Center,Kobe ; ＊ 3Department of Cardiovascular, Thoracic and Pediatric Surgery, School of Medicine, University of Kobe, Kobe
Address for correspondence : SHIMIZU M, MD, Department of Cardiology, National Hospital Organization Kobe Medical Center,
Nishiochiai 3−1−1, Suma-ku, Kobe 654−0155
Manuscript received May 23, 2005 ; revised September 14, 2005 ; accepted September 14, 20053132Shimizu, Kato, Matsukawa et alA

BFig. 1 Initial echocardiographic examinations
A : Left ventricular apical akinesis showing ballooning and concave deformity of the anterior mitral leaflet（arrow）.
Left : Enddiastole. Right : Endsystole.
B : Severe mitral regurgitation with the electrocardiogram showing an inverted T wave.

comfort and severe dyspnea lasting for 2 hr, wasadmitted to our hospital because of congestive heart
failure on November 23, 2003. He started to experience anterior chest oppression 12 years before. At
the age of 73 years, coronary angiography revealed
spontaneous coronary vasospasm in the left anterior
descending and circumflex coronary arteries, andleft ventriculography showed normal wall motion.
Nifedipine and nitrate were administered, andechocardiography showed normal left ventricular
contraction with moderate aortic regurgitation.
However, anginal attacks occurred more frequently
in the preceding weeks.
Physical examination found his heart rate was 90
beats /min with irregularity and blood pressure was
102/62 mmHg. Fine crackles were heard over both
lower lung fields, and there was a grade Ⅳ/Ⅵholosystolic murmur at the apex of the heart.
Arterial blood gas analysis revealed Pa O 2 of
52 mmHg. Laboratory studies, including cardiac
enzymes, were unremarkable except for positive
serologic tests for syphilis. Electrocardiography
revealed atrial fibrillation and ST-segment elevationin the chest leads Ⅴ2 to Ⅴ6, and subsequent T-wave
inversion in these leads after sublingual nitroglycerin administration. Chest radiography showed cardiomegaly with a cardiothoracic ratio of 64%, pulmonary congestion, and left pleural effusion.
Echocardiography demonstrated severe mitral
regurgitation and left ventricular apical akinesis
with ballooning. The anterior mitral leaflet present-

ed a concave configuration toward the left atrium（Fig. 1）. The mitral valve coaptation depth, that isthe distance between the point of coaptation of themitral leaflets and the plane of the mitral annulus
measured at endsystole, was 11.6 mm. Left atrial
dimension was 49 mm, and left ventricular diameterwas 42 mm at enddiastole and 28 mm at endsystole.
Percentage fractional shortening was 33%. On thethird hospital day, resting thallium-201 myocardial
scintigraphy detected a perfusion defect in the apex
（Fig. 2）, and echocardiography demonstrated aless concave anterior mitral leaflet and decreased
mitral regurgitation（Fig. 3）.
He recovered from congestive heart failure after
treatment with carperitide, nitroglycerin infusion,and dobutamine. On the seventh hospital day, coronary angiography revealed no organic stenosis, but
the acetylcholine provocation test induced diffuse
coronary vasospasm in the distal segments of bothright and left coronary arteries（Fig. 4−A）accompanied by chest oppression and ST-T changes in theelectrocardiogram. Simultaneous echocardiography
showed severe mitral regurgitation. After intracoronary nitroglycerin infusion, left ventriculography
showed dyskinetic wall motion of the apex（Fig.
4−B）. Left ventricular end-diastolic and end-systolic volumes were 100 and 61 ml, respectively.
Left ventricular ejection fraction was 39%. Followup echocardiography 11 days after admission
demonstrated a non-concave anterior mitral leaflet
along with ameliorated apical wall motion（Fig. 5−J Cardiol 2006 Jan; 47（1）: 31 – 37Mitral Regurgitation Due to Coronary Vasospasm

33

APEX＞
−BASE

SEPT＞
− LAT

INF＞
−ANTFig. 2 Resting thallium-201 myocardial scintigrams showing a myocardial perfusion defect in theleft ventricular apex
ANT ＝ anterior ; SEPT ＝ septal ; LAT ＝ lateral ; INF ＝ inferior.

Fig. 3 Echocardiograms on the third hospital day
A less concave anterior mitral leaflet（arrow ; left）and decreased mitral regurgitation（right）are shown.

A）. The mitral valve coaptation depth was10.4 mm.
The patient was followed up with additional
administration of diuretic, nicorandil, andJ Cardiol 2006 Jan; 47（1）: 31 – 37

angiotensin receptor blocker. However, further
episodes of vasospastic angina occurred, and congestive heart failure recurred 1 month after discharge. Echocardiography again demonstrated left

34

Shimizu, Kato, Matsukawa et al

A

BFig. 4 Catheter examinations
A : Acetylcholine provocation test inducing diffuse multivessel coronary vasospasm（left : left coronary
artery, right : right coronary artery）.
ACH ＝ acetylcholine.
B : Left ventriculography showing dyskinetic wall motion of the apex（left : enddiastole, right :endsystole）.

ventricular apical wall motion abnormality andsevere mitral regurgitation. The concave deformityof the anterior mitral leaflet reappeared with anincrease in the mitral valve coaptation depth to12.3 mm（Fig. 5−B）. The preexisting aortic regurgitation remained unchanged throughout the clinical course. Notwithstanding the successful recovery
from congestive heart failure, severe mitral regurgitation was expected to recur because of intractablevasospastic angina. Therefore, management ofmitral regurgitation by surgical intervention wasindicated. In addition, chest computed tomographyincidentally detected an aortic arch aneurysm of asaccular type. On March 9, 2004, mitral valve
annuloplasty with a 26 mm Carpentier-Edwards
physio ring was performed concurrently with total
aortic arch replacement and aortic valve replacement. No organic lesions were found in the mitralvalve itself. The postoperative course was uneventful, and no recurrence of mitral regurgitation wasobserved despite some episodes of vasospastic
angina.

DISCUSSION
Severe mitral regurgitation occurred after recurrent episodes of vasospastic angina. The acetylcholine provocation test induced multivessel coronary vasospasm and reproduced severe mitral
regurgitation. Moreover, vasospastic anginal
attacks caused left ventricular apical akinesis withballooning. We speculate that multivessel coronary
vasospasm induced stunned myocardium in the left
ventricular apex. Although myocardial scintigraphy
showed a perfusion defect in the left ventricularapex suggesting severe myocardial damage,echocardiography demonstrated amelioration of theapical wall motion. There are very few case reportsof severe mitral regurgitation due to coronaryvasospasm. Transient severe mitral regurgitation
was observed in a patient with hypokinesis of theleft ventricular anteroseptal and anterolateral walls.
The mitral regurgitation was probably related tocoronary vasospasm of the left anterior descending
artery, but the acetylcholine provocation test did
J Cardiol 2006 Jan; 47（1）: 31 – 37

Mitral Regurgitation Due to Coronary Vasospasm

35ABFig. 5 Follow-up echocardiograms
A : A non-concave anterior mitralleaflet（arrow）with ameliorated apicalwall motion. Note the electrocardiogram showing a flattened T wave.
Left : Enddiastole. Right : Endsystole.
B : Reappearance of the concave
deformity of the anterior mitral leaflet（arrowhead ; left）when severe mitral
regurgitation recurred（ right）. Notethe electrocardiogram showing theinverted T wave.

not induce mitral regurgitation3）. Transient severe
mitral regurgitation was demonstrated during
ergonovine stress echocardiography in another
patient who had presented with acute pulmonary
edema, but regional wall motion changes were notdetected4）.
How vasospastic angina produced severe mitral
regurgitation remained unclear. No organic lesions
were found in the mitral valve itself. Left atrialenlargement due to atrial fibrillation could be associated with mitral regurgitation, but mitral annularenlargement secondary to atrial fibrillation does not
usually promote important mitral regurgitation5）.
Vasospastic angina may have caused left ventricular dysfunction and diminished mitral leaflet closing force, however, functional mitral regurgitationin the setting of acute myocardial ischemia is not
fully explained by the inadequate mitral leaflet
closing force6）.
Severe mitral regurgitation was closely associated with left ventricular apical wall motion abnorJ Cardiol 2006 Jan; 47（1）: 31 – 37mality. As the apical wall motion improved, theamount of mitral regurgitation subsequentlydecreased. On the other hand, the apical wallmotion deteriorated when vasospastic angina andsevere mitral regurgitation relapsed. It is important
to note that echocardiography demonstrated concave deformity of the anterior mitral leaflet andincreased mitral valve coaptation depth whensevere mitral regurgitation occurred. These findings
suggest that the severe mitral regurgitation derived
from dysfunction of subvalvular mitral apparatus
such as the chordae tendineae, papillary muscles,
and the adjacent myocardial wall. The impaired
apical wall motion could cause tethering of thechordae tendineae by displacing the papillary muscles outward. Then, the mitral leaflets were coapted
inappropriately, leading to severe regurgitation7）. It
is possible that the papillary muscle contraction
was preserved and the tethering force was augmented, because the coronary branches feeding the papillary muscles differ from the apical myocar-36

Shimizu, Kato, Matsukawa et aldium2,8）. The apical myocardium is perfused by thedistal left anterior descending artery, whereas theposterior papillary muscle is fed by the right coronary artery and the anterior papillary muscle is fedby the first obtuse marginal branch and the first
diagonal branch9）. These mechanisms are comparable to mitral regurgitation in ischemic heart disease.
There is growing evidence that ischemic mitral
regurgitation results from tethering of the mitralleaflets. Bulging of the ventricular segment overlying the papillary muscle displaces the mitral leaflets
outward, leading to incomplete coaptation2,7）. The
concave deformity of the anterior mitral leaflet isconsistent with tethering by intermediate chords
attached to the belly of the anterior leaflet10）. In
addition, experiments have proven that ischemic
mitral regurgitation diminishes if the tethering
force is relieved by an extracardiac patch device or
chordal cutting11,12）. Therefore, the present case represents an atypical case of ischemic mitral regurgitation, in that coronary vasospasm caused left ventricular apical wall motion abnormality, which inturn resulted in severe mitral regurgitation throughdisplacement of the mitral leaflets.
The present patient underwent mitral valve annuloplasty with a Carpentier-Edwards physio ring.
要

Although antivasospastic drugs had been administered as the first-line treatment to prevent mitral
regurgitation, coronary vasospasm remained refractory to medications and severe mitral regurgitation
recurred. Mitral valve annuloplasty increases thecoaptational surface of the mitral leaflets and counteracts the tethering force13）. These hemodynamic
effects may resemble those of takotsubo cardiomyopathy. Takotsubo cardiomyopathy has a prominent
feature of left ventricular apical akinesis and basal
hyperkinesis14）. Apical ballooning would generatepotent tethering force for the mitral leaflets, butbasal annulus narrowing would prevent inadequate
coaptation of the mitral leaflets. In fact, mitral
regurgitation is uncommon in takotsubo cardiomyopathy except for secondary regurgitation resulting
from systolic anterior motion of the mitral valvesand outflow tract obstruction. The present case differs from takotsubo cardiomyopathy in that basal
hyperkinesia was absent and apical wall motion
abnormality was partially irreversible. However,we believe that these explanations support the rationale for mitral valve annuloplasty to prevent severe
mitral regurgitation secondary to apical wallmotion abnormality in the present case.

約冠攣縮性狭心症による左室心尖部壁運動異常が原因となった再発性高度僧帽弁逆流の 1 例
清水雅俊

加藤裕生

松 川律

正井博之

島

尚 司

三輪陽一

山下輝夫

大 北裕

症例は 76 歳，男性．冠攣縮性狭心症発作時に高度僧帽弁逆流によるうっ血性心不全の合併をみた例である．心エコー図では，僧帽弁逆流とともに左室心尖部の風船様無収縮が認められ，僧帽弁前尖は左房側に対し凹状に変形して後尖との接合不全をきたしていた．冠動脈造影ではアセチルコリン負荷で左右冠動脈の末梢にび漫性冠攣縮が誘発され，僧帽弁逆流の再現が得られた．心エコー図の経過上，心尖部壁運動の改善とともに僧帽弁逆流の減少が認められた．冠攣縮性狭心症は治療抵抗性で，退院 1 ヵ月後に再び高度僧帽弁逆流を発症した．Carpentier-Edwards physio ring を用いた僧帽弁形成術後では，冠攣縮発作にもかかわらず僧帽弁逆流は再発していない．冠攣縮性狭心症による高度僧帽弁逆流の成因として，心尖部壁運動異常による僧帽弁装置の心尖方向への牽引が弁の接合不全を引き起こしていたと考えられた．

J Cardiol 2006 Jan; 47（1）: 31−37

J Cardiol 2006 Jan; 47（1）: 31 – 37

Mitral Regurgitation Due to Coronary Vasospasm

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