HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article 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 Add to Personal Folders Download to citation manager Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Beyersdorf, F. Articles by Allen, B. S. Search for Related Content PubMed PubMed Citation Articles by Beyersdorf, F. Articles by Allen, B. S.

The Journal of Thoracic and Cardiovascular Surgery, Vol 98, 368-380, Copyright © 1989 by The American Association for Thoracic Surgery and The Western Thoracic Surgical Association

ARTICLES

Studies on prolonged acute regional ischemia. III. Early natural history of simulated single and multivessel disease with emphasis on remote myocardium

F Beyersdorf, C Acar, GD Buckberg, MT Partington, F Sjostrand, HH Young, HI Bugyi, F Okamoto and BS Allen
Division of Cardiothoracic Surgery, University of California, Los Angeles Medical Center.

The early natural history of left anterior descending coronary artery occlusion was studied in 35 open-chest anesthetized dogs observed for 6 hours. Six control dogs underwent isolation of the left anterior descending without occlusion, 13 underwent isolated occlusion of the artery to simulate single-vessel disease, and 14 underwent occlusion of the left anterior descending and 50% stenosis of the circumflex coronary artery to simulate multivessel disease. Regional systolic shortening was measured by ultrasonic crystals. Control dogs had a mild fall in cardiac output (27%) and rise in aortic pressure (15 mm Hg). Ischemia produced immediate dyskinesia (-60% of control systolic shortening), and passive lengthening persisted for 6 hours. All dogs with only occlusion of the left anterior descending artery survived (0% mortality). They were less prone to ventricular fibrillation (46% versus 79%, p less than 0.05), developed compensatory hypercontractility of remote muscle (131% of control systolic shortening, p less than 0.05), mild energy and substrate depletion, and anaerobic metabolism (increased glucose-6-phosphate, p less than 0.05) despite maintenance of "normal" blood flow. In contrast, the early mortality rate was 57% (p less than 0.05) when 50% circumflex stenosis coexisted. Intractable ventricular fibrillation and/or cardiogenic shock caused the deaths. Remote muscle became progressively hypocontractile (61% of control systolic shortening, p less than 0.05), with progressive reduction in stroke work index (less than 0.5 gm-m/kg, p less than 0.05). Remote muscle showed moderate substrate and energy depletion (greater than 60% fall of adenosine triphosphate and creatine phosphate, 37% fall of glutamate) and more pronounced evidence of anaerobic metabolism (glucose-6-phosphate rose greater than 400%, p less than 0.05) despite normal blood flow. Mitochondrial ultrastructure and function remained intact in all hearts. These findings suggest that remote muscle is the principal determinant of mortality after an otherwise nonlethal ischemic event. Functional deterioration despite normal blood flow to remote muscle suggests either autoregulatory failure or substrate depletion as a cause of hypocontractility. The structural and functional integrity of mitochondria in ischemic and remote myocardium implies that salvage is possible despite hemodynamic deterioration and intractable ventricular fibrillation.

This article has been cited by other articles:

				A. Kilic, T. Li, T. D.C. Nolan, J. R. Nash, S. Li, D. J. Prastein, G. Schwartzbauer, S. L. Moainie, G. K. Yankey, C. DeFilippi, et al. Strain-related regional alterations of calcium-handling proteins in myocardial remodeling J. Thorac. Cardiovasc. Surg., October 1, 2006; 132(4): 900 - 908. [Abstract] [Full Text] [PDF]

				ReneG. Favaloro Surgical treatment of acute myocardial infarction J. Am. Coll. Cardiol., April 1, 2000; 35(5_Suppl_B): 18B - 24B. [PDF]

				B. Tomasco, A. Cappiello, R. Fiorilli, A. Leccese, R. Lupino, A. Romiti, and U. F. Tesler Surgical Revascularization for Acute Coronary Insufficiency: Analysis of Risk Factors for Hospital Mortality Ann. Thorac. Surg., September 1, 1997; 64(3): 678 - 683. [Abstract] [Full Text]

				F. Beyersdorf Protection of Evolving Myocardial Infarction and Failed PTCA Ann. Thorac. Surg., September 1, 1995; 60(3): 833 - 838. [Abstract] [Full Text]

				D. R. Spahn, L. R. Smith, R. M. Schell, R. D. Hoffman, R. Gillespie, and B. J. Leone Importance of severity of coronary artery disease for the tolerance to normovolemic hemodilutionComparison of single-vessel versus multivessel stenoses in a canine model J. Thorac. Cardiovasc. Surg., August 1, 1994; 108(2): 231 - 239. [Abstract] [Full Text]