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J Am Coll Cardiol, 2005; 45:565-572, doi:10.1016/j.jacc.2004.11.032
© 2005 by the American College of Cardiology Foundation
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Role of collateral blood flow in the apparent disparity between the extent of abnormal wall thickening and perfusion defect size during acute myocardial infarction and demand ischemia

Howard Leong-Poi, MD*,*, Matthew P. Coggins, MD*, Jiri Sklenar, PhD*, Ananda R. Jayaweera, PhD*, Xin-Qun Wang, MS{dagger} and Sanjiv Kaul, MD, FACC*,*

* Cardiovascular Imaging Center, Cardiovascular Division
{dagger} Division of Biostatistics and Epidemiology, Department of Health Evaluation Sciences, University of Virginia, Charlottesville, Virginia



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Figure 1 Data from a Group 1 dog with left anterior descending occlusion. (A) Region of wall thickening abnormality (defined by chords and arrows). (B) risk area (perfusion defect at 5 s after microbubble destruction). (C) Region with no flow even at 20 s after microbubble destruction (arrows), corresponding to (D) infarct size.

 


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Figure 2 Flow-function relation in Group 1 dogs. Red denotes the infarcted zone, green the collateral blood flow-supplied zone, and blue the remote normal myocardium. MBF = myocardial blood flow; WT = wall thickening.

 


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Figure 3 Data from a Group 2 dog with a non-critical left anterior descending stenosis at peak dobutamine dose where myocardial blood flow is increased. (A) Perfusion defect early (1 s) after microbubble destruction (arrows) that is similar in topology to the hypoperfused zone by radiolabeled microsphere (B). (C) Perfusion defect later (5 s) after microbubble destruction is partly filled by collateral blood flow. The region still not filled (arrows) corresponds to that with abnormal wall thickening (defined by chords and arrows) (D).

 


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Figure 4 Flow-function relation in Group 2 dogs. Red denotes the central portion of the perfusion defect corresponding to hypoperfused zone in panel C in Figure 3. Green denotes the collateral blood flow-supplied zone within the perfusion defect (that seen in lateral portions of the perfusion defect in panel A in Figure 3). Blue denotes the normal remote myocardium. MBF = myocardial blood flow; WT = wall thickening.

 


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Figure 5 Data from a Group 3 dog with non-critical left anterior descending and left circumflex artery stenoses at peak dobutamine dose when myocardial blood flow is increased. Perfusion defects (PDs) (arrows) (A) early (1 s) and (C) late (5 s) after microbubble destruction showing little filling-in because of reduced collateral blood flow. Both are similar in topology to the hypoperfused zones by radiolabeld microsphere (B). (D) End-systolic image with extent of abnormal wall thickening (defined by chords and arrows) in the latter, corresponding to the PDs. This region also includes the better perfused myocardium between the two PDs seen in (A) and (C).

 


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Figure 6 Flow-function relation in Group 3 dogs when (A) all myocardial regions are included and (B) small segments in the anterior wall supplied by the diagonal branch interspersed between two large perfusion defects are excluded. Red denotes the central portions of the perfusion defects, and green and blue denote the collateral blood flow-supplied zones and the remote normal myocardium, respectively. MBF = myocardial blood flow; WT = wall thickening.

 


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Figure 7 Flow-function relation for all regions in all three groups of dogs, excluding the tethered regions in Group 3 dogs. Red, yellow, and green denote data points from Groups 1, 2, and 3 dogs, respectively. MBF = myocardial blood flow; WT = wall thickening.

 




 
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