Clin. Cardiol.
8, 306-308 (1985)
0 Clinical Cardiology Publishing Co., Inc.
Case Reports
Mitral Valve Prolapse Syndrome with Coronary Artery Spasm: A Possible
Cause of Recurrent Ventricular Tachyarrhythmia
T. SAKUMA, M.D., M. KAKIHANA,M.D., T. TOGO,M.D., M. MATSUDA,M.D., T. OGAWA, M.D., Y.SUGISHITA, M.D.,
I. ITO, M.D.,* T. KURUSU,M.D.
Division of Cardiology, Department of Medicine, University of Tsukuba, *OgawamachiHospital, Ibaraki, Japan
Summary: A 54-year-old man with mitral valve prolapse
syndrome diagnosed by echochardiography complained
of anginal pain associated with ventricular tachyarrhyth-
mia. One day he suddenly lost consciousness, and ECG
at that time revealed ventricular fibrillation. Thereafter,
he developed ST elevation, sporadic premature ventricu-
lar contractions, and R on T phenomenon leading to ven-
tricular fibrillation during the attack of anginal pain. His
coronary arteriogram was normal. This case implies that
coronary artery spasm may be one of the causes of chest
pain and ventricular tachyarrhythmias in patients with
mitral valve prolapse syndrome.
Key words: mitral valve prolapse, coronary artery spasm,
ventricular arrhythmia, angina pectoris
Introduction
Some patients with mitral valve prolapse (MVP) syn-
drome complain of chest pain, palpitation, and syncope
(Barlow and Pocock, 1975; Devereux et al., 1976; Fon-
tana et al., 1976; Hancock and Cohn, 1966). Many
authors have reported that MVP is associated with vari-
Address for reprints:
Tohuru Sakuma, M.D.
University of Tsukuba, Ogawamachi Hospital
1-1 - 1 Tennodai, Sakurarnura, Niiharigun, Ibaraki 305, Japan
Received: October 3, 1984
Accepted: November 28, 1984
ous kinds of arrhythmias, including ventricular tachyar-
rhythmias (Aradana et al., 1976; Barlow and Pocock,
1975; Devereux et al., 1976; Fontana et af., 1976; Han-
cock and Cohn, 1966; Paul and Douglas, 1979; Winkle
et af., 1975, 1976). However, the mechanisms of chest
pain and arrhythmias experienced in MVP have not been
clearly identified. We report a patient with MVP suffer-
ing from chest pain and ventricular fibrillation (VF), which
was preceded by ST-segment elevation on ECG. This case
implies that coronary artery spasm may be a cause of ches:
pain and ventricular fibrillation complicating MVP.
Case Report
The patient was a 54-year-old farmer suffering from
chest pain and syncopal attack. Hypertension and prostate
hypertrophy were detected at the age of 33 and 52, respec-
tively. Since 1980 he has occasionally complained of chest
pain during his daily work, lasting for 2-3 minutes. In
January 1982 he suddenly lost consciousness while drink-
ing alcohol, and was referred to a local hospital. He be-
came conscious in a short time, and neither abnormal
neurological nor abnormal ECG findings were detected
at that time. Before his discharge from the hospital, it was
found that he had prostate hypertrophy. In July 1982 he
was admitted to the Department of Urology of Tsukuba
University Hospital for surgical therapy of the prostate
hypertrophy. On physical examination, the heart rhythm
was irregular at the rate of 82 beatdmin, and blood pres-
sure was 126/96 mmHg. A grade 4/6 holosystolic mur-
mur was heard at the apex. Routine laboratory
examinations including hematological tests, urinalysis,
blood chemistry, and serological tests were unremarka-
ble. On chest x-ray film, cardiothoracic ratio was 50%
and no congestion was found. At rest, ECG showed atri-
al fibrillation and left ventricular high voltage (Fig. 1A).
 T. Sakuma et al.: MVP with coronary artery spasm 307

aVR V2V4
. ”
-‘-J--4.

aVL ’/2V5
-..-

aVF %VS

---
FIG. 1 (A) ECG at rest showed atrial fibrillation and high voltage. (B) ECG showed ventricular fibrillation when the patient lost con-
sciousness. (C) ECG recorded during chest pain on a different day from the day for Fig. 1A. Lead I was shifted to lead 11, then lead I1
was shifted to lead In sequentially. ST elevation was seen in lead I, then ST depression and ventricular tachycardia after R on T phenomenon
in lead 11, and finally ventricular fibrillation appeared in lead 111. Calibration was 10 mm = 1 mV in limo leads and VI-3. 5 m m = 1
mV in v4-6.

On July 2 he was t r a n s f e d from the Department of Uml-
ogy to the Division of Cardiology, Department of Medi-
cine in order to evaluate his cardiac state. That day, he
suddenly lost consciousness while talking with a family
member. At that time, ECG showed ventricular fibrilla-
tion (Fig. 1B). Cardioversion was performed immediate-
ly and sinus rhythm was restored. Prolapsed posterior
mitral valve leaflet into the left atrium was revealed by
two-dimensional echocardiography (Fig. 2), and no ab-
normal left ventricular wall motion was detected.
Thallium-201 myocardial scintigraphy and technetium-
99m radionuclide ventriculogramwere performed and no
abnormalities were detected.
The next day, when the patient complained of chest
pain, ECG sequentially revealed ST elevation, premature
ventricular contmction with R on T phenomenon, and tran-
sient VF (Fig. 1C). A 20 mg dose of isosorbide dinitrate
and 40 mg of nifedipine per day were given orally.
However, chest pain with ST-segment elevation occurred
as frequently as before. However, after nifedipine was in-
creased to 80 mg/day, he no longer experienced chest pain
or ventricular arrhythmia.
After abolishment of the chest pain, cardiac catheteri-
zation was performed. Left ventriculography showed
moderate mitral regurgitation. Coronary angiography
showed no significant stenosis. The provocation test for

FIG.2 Two-dimensional echocardiography . Posterior rnitral valve leaflet was prolapsed into left atrium. The arrow indicates prolapsed
leatlet.
308 Clin. Cardiol. Vol. 8, May 1985
coronary artery spasm was performed by injecting 0.05
mg of ergonovine maleate every 5 minutes up to a cu-
mulative dose of 0.2 mg. However, neither chest pain nor
ST elevation was provoked at that time.
Discussion
Various kinds of arrhythmias are not infrequently found
in association with MVP. According to Swarts et al.
(1977), among 589 cases of MVP, premature ventricular
contraction and ventricular tachycardia were seen in 265
(44.5%) and 37 cases (6.3%), respectively. Sudden death
was found in 8 cases (1.4%). Almost all of them were
thought to have died from arrhythmias. Some hypotheses
as to the mechanisms of anthymias in MVP have been
presented elsewhere (Aradena er al., 1976; Winkle er a f . ,
1975; Zeilenga and Criley, 1973). Hancock et al. (1966)
suggested that pathological changes in papillary muscles
and some partial neuropsychiatric disturbance may en-
hance ventricular arrhythmias. Zeilenga and Criley (1973)
postulated two mechanisms by which mitral valve dys-
function and ectopic impulse formation might be related:
(1) by mechanical stimulus of the left ventricle or left atri-
um excessive movement of the distended blood-laden
valve leaflet; and (2) by ectopic impulse formation from
stretching of the valve leaflet myocardium. However,
these still remain speculative.
Chest pain is one of the most common symptoms in
MVP. There have been various explanations as to the gen-
esis of chest pain (Aradena et al. 1976; Barlow et al. 1968;
LeWinter et al., 1974; Pocock and Barlow, 1974; Steel-
man et a f . , 197 1). LeWinter et af. (1974) considered that
pain in MVP might be due to localized ischemia associated
with increased wall tension at the area of the base of the
papillary muscle.
Elliot et a f . (1976) reported 4 patients with MVP who
suffered from myocardial infarction in spite of normal
coronary arteriograms. They speculated that coronary ar-
tery spasm might play a significant role in the myocardi-
al infarction in patients with MVP. Buda et al. (1978)
reported that among 10 cases of coronary spasm seen at
coronary angiography, 9 had mitral valve prolapse. They
also speculated that coronary artery spasm might occur
in patients with MVP.
In our present case, we could record ST-segment ele-
vation concomitant with premature ventricular contractions
(PVCs) and fatal ventricular arrhythmias several times
when the patient complained of chest pain. These episodes
could no longer be seen after the intake of 80 mg/day of
nifedipine. We could not provocate coronary artery spasm
with ergonovine, however, this was probably due to the
fact that the patient had not been able to stop taking nifedi-
pine even 8 hours before coronary arteriography because
of the fear for his chest pain. Consequently, remaining
vasodilator effects of the drug might eliminate the spas-
modic effect of ergonovine.
We conclude that our case suggests that coronary ar-
tery spasm may play a significant role in the genesis of
chest pain and ventricular arrhythmia complications as-
sociated with MVP.
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