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Anesth Analg 1999;88:973-979
© 1999 International Anesthesia Research Society


CARDIOVASCULAR ANESTHESIA

Tachycardia-Induced Subendocardial Necrosis in Acutely Instrumented Dogs with Fixed Coronary Stenosis

Giora Landesburg, MD, DSc*, Wei Zhou, MD{dagger}, and Thomas Aversano, MD*

*Department of Anesthesiology and Critical Care Medicine, Hebrew University-Hadassah Hospital, Jerusalem, Israel; and {dagger}Department of Medicine, Division of Cardiology, Johns Hopkins Hospital, Baltimore, Maryland

Address correspondence and reprint requests to Giora Landesberg, MD, DSc, Department of Anesthesiology and C. C. M., Hebrew University-Hadassah Hospital, Ein-Kerem, Jerusalem, Israel 91120. Address e-mail to gio{at}cc.huji.ac.il

It has been speculated but never proven that tachycardia-induced ischemia per se may lead to myocardial infarction. In 17 anesthetized dogs, the proximal left anterior descending (LAD) artery was cannulated and perfused via bypass from the left subclavian artery. Distal LAD pressure was reduced by a screw clamp to cause >=20% decrease in wall thickening during pacing tachycardia but no decrease in resting heart rate (approximately 90 bpm). Dogs were randomly assigned to three groups: 1) control (n = 6) maintained at resting heart rate (approximately 90 bpm) and mean coronary pressure of 49 ± 5 mm Hg for 4 h; 2) 4-h ischemia (n = 6), paced at 150 bpm and mean coronary pressure maintained at 59 ± 6 mm Hg for 4 h; and 3) 1-h ischemia (n = 5), paced at 150 bpm and mean coronary pressure of 54 ± 8 mm Hg for 1 h. Myocardial blood flow and infarct area were measured by radiolabeled microspheres and triphenyl-tetrazolium chloride staining, respectively. Despite the higher coronary pressure in the 4-h ischemia group (P = 0.02), patchy subendocardial necrosis occurred in all these dogs and in two of the 1-h ischemia dogs, and one control dog had minimal papillary muscle necrosis. Infarct area was largest in the 4-h ischemic group (15.5% ± 9.1%) compared with control and 1-h ischemia groups (0.09% ± 0.2% and 1.6% ± 2.1%, respectively) (P < 0.002). Relative (risk/nonrisk areas) subendocardial flow was lower at the end of ischemia in the 4- and 1-h ischemia groups compared with the control group (0.3 ± 0.1 and 0.4 ± 0.1 vs 0.9 ± 0.2; P = 0.008 and 0.01, respectively). Prolonged tachycardia-induced ischemia, in the face of fixed coronary stenosis causing no ischemia at the resting heart rate, leads to patchy subendocardial necrosis, despite anticoagulation and antiplatelet treatment.

Implications: Prolonged tachycardia-induced ischemia, in the face of fixed coronary stenosis causing no ischemia at the resting heart rate, leads to subendocardial infarction in dogs. These findings suggest a possible mechanism for postoperative myocardial infarction.




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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins with the assistance of Stanford University Libraries' HighWire Press®. Copyright 2006 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press
Copyright © 1999 by the International Anesthesia Research Society.