(Circulation. 2003;108:504.)
© 2003 American Heart Association, Inc.
Special Review: Clinician Update |
From the TIMI Study Group, Harvard Medical School.
Correspondence to C. Michael Gibson, MS, MD, Director TIMI Data Coordinating Center and Angiographic Core Laboratory, 350 Longwood Ave, First Floor, Boston MA 02115. E-mail mgibson@timi.org
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
For two decades, the goal of reperfusion has been restoration of normal epicardial blood flow.14 It has, however, become increasingly apparent that not all TIMI grade 3 flow is created equally, and attention has shifted downstream to the restoration of normal myocardial perfusion to fully optimize clinical outcomes.3,4 The goal of this Clinician Update is to provide clinicians with a better understanding of myocardial perfusion in terms of its importance, assessment, and treatment in clinical practice.
Case Presentation
A 59-year-old man presented to the emergency room with 2.5 hours of crushing substernal chest pain. The ECG showed 4 mm of ST-segment elevation in precordial leads V1 through V4, which was consistent with the diagnosis of acute anterior myocardial infarction. Primary angioplasty/stenting of a totally occluded left anterior descending artery was performed 90 minutes after presentation to the emergency room, resulting in restoration of normal Thrombolysis In Myocardial Infarction (TIMI) grade 3 flow. The myocardium, however, appeared pale, which is consistent with TIMI myocardial perfusion grade (TMPG) 0 flow3 (Figure, A). Although improved, the patients ST segments remained elevated. Multiple doses of 100 µg of intracoronary adenosine were administered through the central lumen of the balloon catheter, resulting in restoration of TMPG 3 flow (Figure, B). After adenosine administration, the corrected TIMI frame count (CTFC)2 improved from 50 frames to 35 frames. There was >70% resolution of ST-segment elevation, and the patient was free of chest pain.
| |||||||||||
This article has been cited by other articles:
![]() |
P L Van Herck, S G Carlier, M J Claeys, S E Haine, P Gorissen, H Miljoen, J M Bosmans, and C J Vrints Coronary microvascular dysfunction after myocardial infarction: increased coronary zero flow pressure both in the infarcted and in the remote myocardium is mainly related to left ventricular filling pressure Heart, October 1, 2007; 93(10): 1231 - 1237. [Abstract] [Full Text] [PDF] |
||||
![]() |
M. Mariani, R. Fetiveau, E. Rossetti, A. Poli, F. Poletti, P. Vandoni, M. D'Urbano, F. Cafiero, G. Mariani, C. Klersy, et al. Significance of total and differential leucocyte count in patients with acute myocardial infarction treated with primary coronary angioplasty Eur. Heart J., November 1, 2006; 27(21): 2511 - 2515. [Abstract] [Full Text] [PDF] |
||||
![]() |
The American Heart Association's Acute Myocardial, A. K. Jacobs, E. M. Antman, G. Ellrodt, D. P. Faxon, T. Gregory, G. A. Mensah, P. Moyer, J. Ornato, E. D. Peterson, et al. Recommendation to Develop Strategies to Increase the Number of ST-Segment-Elevation Myocardial Infarction Patients With Timely Access to Primary Percutaneous Coronary Intervention Circulation, May 2, 2006; 113(17): 2152 - 2163. [Abstract] [Full Text] [PDF] |
||||
![]() |
C. M. Gibson and A. Schomig Coronary and Myocardial Angiography: Angiographic Assessment of Both Epicardial and Myocardial Perfusion Circulation, June 29, 2004; 109(25): 3096 - 3105. [Full Text] [PDF] |
||||
|
Circulation Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2003 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |