(Circulation. 1999;99:E15.)
© 1999 American Heart Association, Inc.
Circulation Electronic Pages |
Myocardial Perfusion in Acute Coronary Syndrome
Jörg Horcher, MD;
Rudolf Blasini, MD;
Stefan Martinoff, MD;
Markus Schwaiger, MD;
Albert Schömig, MD;
Christian Firschke, MD
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{at}t-online.de
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Introduction
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Top
Introduction
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Venous myocardial
contrast echocardiography is a new method
for
myocardial perfusion imaging. It has been shown to accurately
evaluate
risk area and infarct size in the experimental setting
of acute
myocardial infarction and has recently become clinically
available. We
used this method to assess myocardial salvage
after coronary
reperfusion in a patient with acute coronary
syndrome.
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 7
days, venous myocardial contrast echocardiography
(D) and 99mTc-sestamibi SPECT (E) were repeated
and demonstrated almost complete reperfusion of the
inferior left ventricular wall. The patient was
discharged 10 days after admission.

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Figure 1. A, Venous myocardial contrast
echocardiography before reperfusion; apical
2-chamber view; contrast defect (arrows) of basal inferior
left ventricular myocardium. Precontrast images
were digitally subtracted from contrast-enhanced images, and resulting
image was color-coded, with gradual transition from red to orange to
yellow and white representing increasing contrast
enhancement. B, 99mTc-sestamibi SPECT before reperfusion
(99mTc-sestamibi injected simultaneously with
A); vertical long-axis slice; reduced tracer uptake of basal
inferior left ventricular
myocardium (arrows). C, Coronary angiography; right
anterior oblique angulation; subtotal occlusion (arrow) of left
circumflex coronary artery. D, Venous myocardial contrast
echocardiography 7 days after stenting of left
circumflex coronary artery; almost normal contrast enhancement
(arrows) of inferior myocardium. E,
99mTc-sestamibi SPECT 7 days after stenting of left
circumflex coronary artery; nearly normal tracer uptake of
basal inferior left ventricular
myocardium. F, Coronary angiography; result after
successful stenting of left circumflex coronary artery.
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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 Luke's 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 Luke's Episcopal Hospital and Texas Heart Institute, 6720 Bertner Ave, MC1-267, Houston, TX 77030.