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CLINICAL RESEARCH: CARDIAC IMAGING

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 and Sanjiv Kaul, MD, FACC^*,*

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

Manuscript received April 27, 2004; revised manuscript received October 24, 2004, accepted November 1, 2004.

^* Reprint requests and correspondence: Dr. Sanjiv Kaul, Box 800158, Cardiovascular Division, University of Virginia, Charlottesville, Virginia 22908-0158 (Email: sk{at}virginia.edu).

Received the First Prize at the Young Investigator Award Competition at the 13th Annual Scientific Sessions of the American Society of Echocardiography, June 2002, Orlando, Florida. Dr. Leong-Poi is currently affiliated with Saint Michael's Hospital in Toronto, Ontario, Canada.

OBJECTIVES: The aim of this study was to test the hypothesis that the apparent disparity between the circumferential extent of abnormal wall thickening (WT) and that of infarct size (IS) at rest or size of ischemic zone (IZ) during demand ischemia (DI) is principally due to the effects of collateral blood flow (CollBF).

BACKGROUND: A disparity has been reported between the circumferential extent of abnormal WT and that of IS at rest or IZ size during DI.

METHODS: Wall thickening and CollBF were measured in 18 dogs: at 6 h after coronary occlusion (Group 1, n = 6), and during 40 µg·kg·min^–1 of dobutamine in the presence of either one-vessel (Group 2, n = 6) or two-vessel stenosis (Group 3, n = 6).

RESULTS: The apparent overestimation of the IS by the circumferential extent of abnormal WT was due to intermediate levels of CollBF in border zones within the risk area that had escaped necrosis. Although reduced, WT in these regions was commensurate with the level of flow. Similarly, during DI, regions within the IZ exhibiting the worst WT in Group 2 and 3 dogs were those not supplied by CollBF. The regions supplied by CollBF had intermediate WT, which was also commensurate with the level of flow. Only in two Group 3 dogs was tethering seen in small, normally perfused regions that were interspersed between two large IZ. Excluding these few tethered regions, data from different myocardial regions (infarcted, ischemic, CollBF dependent, and normal) were described by a single relation: y = 57(1 – e^{[–0.72(x – 0.06)]}) (r = 0.80, p < 0.001).

CONCLUSIONS: Myocardial regions at the margins of ischemic territories contribute to the apparent disparity between the circumferential extent of abnormal WT and IS or IZ during DI. In most circumstances, these regions are supplied by collaterals and their WT is commensurate with the degree of myocardial blood flow. The apparent disparity between the circumferential extent of WT and ischemia is rarely due to myocardial tethering, which is seen only in some instances of multi-vessel disease where a small normal region is interspersed between two large IZs.

Abbreviations and Acronyms   AI = acoustic intensity   CollBF = collateral blood flow   DI = demand ischemia   IS = infarct size   IZ = ischemic zone   LAD = left anterior descending coronary artery   LCx = left circumflex coronary artery   LV = left ventricular   MBF = myocardial blood flow   MCE = myocardial contrast echocardiography   PD = perfusion defect   RA = risk area   RM = radiolabeled microsphere   WT = wall thickening

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