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J Am Coll Cardiol, 1999; 34:974-982
© 1999 by the American College of Cardiology Foundation
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Impaired coronary blood flow in nonculprit arteries in the setting of acute myocardial infarction

C. Michael Gibson, MD, MS, FACCa, Kathryn A. Ryan, BSa, Sabina A. Murphy, MPHa, Rebecca Mesley, BSa, Susan J. Marble, RN, MSa, Robert P. Giugliano, MD, SM{dagger}, Christopher P. Cannon, MD, FACC{dagger}, Elliott M. Antman, MD, FACC{dagger}, Eugene Braunwald, MD, FACC{dagger} for the TIMI Study Group

a Cardiovascular Divisions of the Departments of Medicine, the University of California at San Francisco, San Francisco, California, USA
{dagger} Brigham & Women’s Hospital, Boston, Massachusetts, USA



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Figure 1 Distribution of the CTFC in nonculprit arteries at 90 min after thrombolytic administration. Nonculprit CTFC was unimodally distributed with a single peak and a long tail, similar to previously published data for the CTFC in culprit arteries (8).

 


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Figure 2 Relationship between culprit artery flow and nonculprit artery flow for the LAD versus other locations. If the LAD was the culprit artery, then nonculprit artery flow was slower by approximately 3.5 frames.

 


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Figure 3 Relationship between the presence of abnormal flow (CTFC ≥ 28) in nonculprit arteries and a wall motion abnormality within the distribution of the nonculprit artery. Patients with abnormal nonculprit artery flow had a greater frequency of regional wall motion abnormalities within the distribution of the nonculprit artery (p < 0.001). When the analysis was restricted to patients without a prior MI, similar findings were observed (p = 0.038).

 


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Figure 4 Paired analysis of the change in the nonculprit artery CTFC over time. Flow improved by 1.4 frames between 60 and 75 min (p = 0.007, median = 1), by 1.0 frame between 75 and 90 min (p = 0.02, median = 0.59) and by a total of 3.3 frames between 60 and 90 min after thrombolytic administration (p = 0.0001, median = 2).

 


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Figure 5 Relationship between improved nonculprit artery flow and improved culprit artery flow between 60 and 90 min after thrombolytic administration. When flow improved in the culprit artery, flow in the associated nonculprit artery improved by 7.4 frames (p = 0.0003), but when flow in the culprit artery did not improve, there was no significant improvement in nonculprit artery flow (1.0 frame, p = NS).

 


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Figure 6 Relationship between the global CTFC (the average CTFC in all three arteries) and adverse outcomes. Patients who sustained adverse events had slower global frame counts.

 




 
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