This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Lee, J. T. Articles by Reimer, K. A. Search for Related Content PubMed PubMed Citation Articles by Lee, J. T. Articles by Reimer, K. A.

Circulation, Vol 64, 526-534, Copyright © 1981 by American Heart Association

ARTICLES

Myocardial infarct size and location in relation to the coronary vascular bed at risk in man

JT Lee, RE Ideker and KA Reimer

Recent infarcts were compared with the anatomic boundaries of the involved vascular bed in human hearts to determine the amount and location of necrosis in relation to the myocardium at risk. The coronary arteries were injected with BaSO4 in 18 human hearts with 3-16- day-old infarcts. Thin (3-4 mm) slices were cut at 10-15 mm intervals, photographed, x-rayed and used for histologic analysis. Infarct outlines were traced from gross photographs using histologic confirmation of infarct boundaries, and the vascular bed was independently traced from the x-rays. Ischemic bed size and infarct size were then calculated by computerized planimetry. Infarct size ranged from 13-72% of the left ventricle (mean 30 +/- 3.6%) and was linearly related to the size of the occluded vascular bed (r = 0.93). However, the infarcts were always smaller than the occluded beds. They involved 50-88% of the ischemic bed (mean 69 +/- 3.0%) due to variation in the transmural extent of necrosis. A lateral zone of viable muscle within the ischemic bed was present but was consistently narrow (mean 1.7 +/- 0.3 mm) so that the infarcts involved 93 +/- 2.3% of the width of the bed at risk. Thus, ischemic bed size is a major determinant of infarct size in fatal human infarcts. When natural limitation of infarct size occurs, it is due primarily to limitation of the transmural extent of necrosis.

This article has been cited by other articles:

				J. Wright, T. Adriaenssens, S. Dymarkowski, W. Desmet, and J. Bogaert Quantification of Myocardial Area at Risk With T2-Weighted CMR: Comparison With Contrast-Enhanced CMR and Coronary Angiography J. Am. Coll. Cardiol. Img., July 1, 2009; 2(7): 825 - 831. [Abstract] [Full Text] [PDF]

				D. P. O'Regan, R. Ahmed, C. Neuwirth, Y. Tan, G. Durighel, J. V. Hajnal, I. Nadra, S. J. Corbett, and S. A. Cook Cardiac MRI of myocardial salvage at the peri-infarct border zones after primary coronary intervention Am J Physiol Heart Circ Physiol, July 1, 2009; 297(1): H340 - H346. [Abstract] [Full Text] [PDF]

				D. V. Cuong, M. Warda, N. Kim, W. S. Park, J. H. Ko, E. Kim, and J. Han Dynamic changes in nitric oxide and mitochondrial oxidative stress with site-dependent differential tissue response during anoxic preconditioning in rat heart Am J Physiol Heart Circ Physiol, September 1, 2007; 293(3): H1457 - H1465. [Abstract] [Full Text] [PDF]

				J. T. Ortiz-Perez, S. N. Meyers, D. C. Lee, P. Kansal, F. J. Klocke, T. A. Holly, C. J. Davidson, R. O. Bonow, and E. Wu Angiographic estimates of myocardium at risk during acute myocardial infarction: validation study using cardiac magnetic resonance imaging Eur. Heart J., July 2, 2007; 28(14): 1750 - 1758. [Abstract] [Full Text] [PDF]

				U. Sechtem Imaging myocardial area at risk and final infarct size Eur. Heart J. Suppl., June 1, 2001; 3(suppl_C): C36 - C46. [PDF]

				F. Ammarguellat, I. Larouche, and E. L. Schiffrin Myocardial Fibrosis in DOCA-Salt Hypertensive Rats : Effect of Endothelin ETA Receptor Antagonism Circulation, January 16, 2001; 103(2): 319 - 324. [Abstract] [Full Text] [PDF]

				I. Larouche and E. L. Schiffrin Cardiac Microvasculature in DOCA-Salt Hypertensive Rats : Effect of Endothelin ETA Receptor Antagonism Hypertension, October 1, 1999; 34(4): 795 - 801. [Abstract] [Full Text] [PDF]

				J. Bogaert, A. Maes, F. Van de Werf, H. Bosmans, M.-C. Herregods, J. Nuyts, W. Desmet, L. Mortelmans, G. Marchal, and F. E. Rademakers Functional Recovery of Subepicardial Myocardial Tissue in Transmural Myocardial Infarction After Successful Reperfusion : An Important Contribution to the Improvement of Regional and Global Left Ventricular Function Circulation, January 12, 1999; 99(1): 36 - 43. [Abstract] [Full Text] [PDF]

				A. Sabri, J.-L. Samuel, F. Marotte, P. Poitevin, L. Rappaport, and B. I. Levy Microvasculature in Angiotensin II–Dependent Cardiac Hypertrophy in the Rat Hypertension, August 1, 1998; 32(2): 371 - 375. [Abstract] [Full Text] [PDF]

				V. Richard, C. E. Murry, and K. A. Reimer Healing of Myocardial Infarcts in Dogs : Effects of Late Reperfusion Circulation, October 1, 1995; 92(7): 1891 - 1901. [Abstract] [Full Text]

				K. M. Choi, R. J. Kim, G. Gubernikoff, J. D. Vargas, M. Parker, and R. M. Judd Transmural Extent of Acute Myocardial Infarction Predicts Long-Term Improvement in Contractile Function Circulation, September 4, 2001; 104(10): 1101 - 1107. [Abstract] [Full Text] [PDF]