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Circulation. 1999;99:e15

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(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@t-online.de


*    Introduction
 
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, FigureDown, 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 . . . [Full Text of this Article]