(Circulation. 1999;99:E15.)
© 1999 American Heart Association, Inc.
Circulation Electronic Pages |
From the 1. Medizinische Klinik, Klinikum rechts der Isar und Deutsches Herzzentrum, Technische Universität München, Germany.
Correspondence to Christian Firschke, MD, Deutsches Herzzentrum, Technische Universität München, Lazarettstraße 36, 80636 München, Germany. E-mail cfirschke@t-online.de
| Introduction |
|---|
A 68-year-old man with known single-vessel coronary artery
disease presented with 6 hours of moderate chest pain typical
of unstable angina. Four years earlier, a percutaneous
transluminal coronary angioplasty of the left anterior
descending coronary artery had been performed; the patient was
asymptomatic throughout the following years. On admission,
the 12-lead ECG showed atrial fibrillation and descending ST-segment
depression up to 0.25 mV in leads V3 through
V6. Cardiac enzymes, including troponin I, were
normal at that time. After medical treatment with heparin,
nitroglycerin, ß-blocker, and aspirin, the chest pain
and ECG changes resolved completely. Eight hours later, the patient
reported reoccurrence of mild chest pain; by then, troponin I was
elevated, at 0.8 ng/mL. Cardiac imaging at rest with venous myocardial
contrast echocardiography (digitally processed and
color-coded echocardiographic images,
Figure
, A) and
99mTc-sestamibi single photon emission computed
tomography (SPECT; B) showed perfusion defects of the basal
inferior left ventricular wall. On cardiac
catheterization, a subtotal occlusion of the left
circumflex coronary artery (C) was seen, and uncomplicated
stenting of the lesion was performed (F). Creatine kinase reached a
maximum of 256 U/L (MB fraction, 34 U/L) during the next day. After
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