Circulation. 2000;101:e107-e108
(Circulation. 2000;101:e107.)
© 2000 American Heart Association, Inc.
Circulation Electronic Pages |
Prinzmetals Angina
Etienne Delacretaz, MD;
James M. Kirshenbaum, MD;
Peter L. Friedman, MD, PhD
From the Department of Medicine, Cardiovascular Division, Brigham and
Womens Hospital, Harvard Medical School, Boston, Mass.
Correspondence to Peter L. Friedman, MD, PhD, Cape Cod Cardiovascular Associates, 14 Yellow Brick Rd, Hyannis, MA 02601.
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Introduction
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Top
Introduction
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A67-year-old woman
with a history of arterial hypertension,
peripheral
vascular disease, and chronic atrial
fibrillation presented
with atypical chest pain for 1 year. The
episodes occurred at
rest and lasted 5 to 30 minutes, occasionally
waking her from
sleep. During the week before her admission, she
developed recurrent
short episodes of lightheadedness associated with
the episodes
of chest pain. She was referred to an outside hospital to
undergo
a stress test with nuclear imaging. The day of the test, she
had
several episodes of chest pain and 2 episodes of lightheadedness.
However,
she drove to the hospital. She was again feeling chest pain
at
the time she entered the testing room. While lying down awaiting
the
arrival of a physician, she had a cardiac arrest. She received
cardiopulmonary
resuscitation; ventricular
fibrillation was present on the external
defibrillator monitor <1
minute after the loss of consciousness.
A 300-J shock restored sinus
rhythm. The 12-lead ECG immediately
after ventricular
defibrillation (Figure 1

A)
shows rapid atrial
fibrillation, absence of R-wave progression from
V
1 to V
3, and
ST-segment
elevation in anterolateral and inferior leads. ST-segment
elevation
persisted in leads V
1 through
V
3 5 minutes later (B) but completely
resolved 2
hours after the event (C). There was no elevation
of creatine kinase or
troponin I. Cardiac catheterization performed
the same
day revealed irregularities of the middle portion of
the left anterior
descending coronary artery (LAD) without significant
stenosis,
as well as normal left ventricular size
and function. The patient
was then referred for further evaluation. A
repeat coronary
angiogram was performed in the basal state
(Figure 2

A) and after
intracoronary
injection of ergonovine maleate 0.1 (not shown),
0.2 (B), and
0.3 (C) mg. Intracoronary injection of 0.2 mg of
ergonovine
(B) caused moderate spasm of the LAD at the level of the
bifurcation
of the second diagonal branch. After injection of 0.3 mg of
ergonovine,
complete occlusion of the LAD was demonstrated (C). The
patient
complained of chest pressure and lightheadedness, and the ECG
showed
ST-segment elevation and severe ventricular ectopy.
Immediate
intracoronary injection of
nitroglycerin promptly relieved the
symptoms and the
spasm. The patient was treated with nitrates,
verapamil at
a dose progressively increased up to 480 mg/d,
and coumarin. In
addition, she received a small dose of ß-blocker
(atenolol 25 mg/d)
to achieve a better control of the ventricular
rate during
atrial fibrillation. The patient has not experienced
any further
episodes of chest pain or lightheadedness during
a 12-month follow-up
period.
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Acknowledgments
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Dr Delacretaz is supported by a grant from the Swiss Foundation
for
Grants in Medicine and Biology.
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Footnotes
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The editor of Images in Cardiovascular Medicine is Hugh A. McAllister,
Jr, MD, Chief, Department of Pathology, St Lukes Episcopal
Hospital and Texas Heart Institute, and Clinical Professor of
Pathology, University of Texas Medical School and Baylor College
of Medicine.
Circulation encourages readers to submit cardiovascular images to Dr Hugh A. McAllister, Jr, St Lukes Episcopal Hospital and Texas Heart Institute, 6720 Bertner Ave, MC1-267, Houston, TX 77030.
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T. O. Cheng
Ergonovine Maleate and {{beta}}-Blockers for Prinzmetal's Angina
Circulation,
February 13, 2001;
103
(6):
e30 - e30.
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