Document Detail


ST segment elevation at the surface of a healed transmural myocardial infarction in pigs. Conditions for passive transmission from the ischemic peri-infarction zone.
MedLine Citation:
PMID:  7867198     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Ischemia of the myocardium surviving an infarction induces ST segment elevation in infarct-related ECG leads. In cases with no viable tissues, ischemia adjacent to the infarction could induce a similar ECG pattern if there is ST segment potential transmission through the necrotic scar. We analyzed whether acute ischemia adjacent to a healed infarction with no viable tissue may induce ST segment elevation on the surface of the necrotic scar. METHODS AND RESULTS: Epicardial ST segment changes elicited during 30 minutes of acute reocclusion of the left anterior descending (LAD) coronary artery 2 cm above the first diagonal branch were analyzed by 32-channel mapping in 18 chloralose-anesthetized open-chest pigs with 1-month-old anterior infarctions induced by permanent ligature below the first diagonal branch (group 1). The effect of a previous infarction on the magnitude of ischemic ST segment changes was assessed by similar mapping in 21 control pigs submitted to a LAD ligature 2 cm above the first diagonal branch (group 2, n = 11) or just below this branch (group 3, n = 10). Myocardial perfusion after coronary ligature was estimated in 7 pigs with chronic infarction and in 3 control pigs by mapping of myocardial technetium-99m-methoxyisobutyl isonitrile (99mTc-MIBI) activity in transmural samples underlying each epicardial electrode. The width of cell layers surviving the infarction was measured and their viability after 60 minutes of coronary reocclusion was assessed by intracellular glycogen staining. Reocclusion of the LAD induced parallel ST segment elevation at the periinfarction zone and at the necrotic scar, although in the latter region the changes were less marked (maximal ST segment, 8.4 +/- 3.0 mV versus 2.7 +/- 1.8 mV, ANOVA, P < .001). ST segment elevation inside the scar was greater at the margins (3.9 +/- 1.8 mV) than at sites 20 mm toward the center (2.8 +/- 1.7 mV, P = .003). The necrotic area was virtually devoid of surviving cells except for a 0.22 +/- 0.04-mm-wide subendocardial band that continued to show a positive intracellular glycogen reaction after the second LAD ligature. Acute ischemia adjacent to the infarction (group 1) induced lower ST segment elevation than acute ischemia at a comparable cardiac region in noninfarcted pigs (group 2) (ANOVA, P = .02), despite the fact that these areas developed similar underperfusion after coronary occlusion (percent MIBI activity of that in normal myocardium, 7 +/- 8 versus 7 +/- 6, P = NS). ST segment changes in group 2 pigs were comparable to those induced in group 3 pigs with a 2-cm-lower coronary occlusion. CONCLUSIONS: Acute ischemia adjacent to a chronic infarction induces ST segment elevation at the surface of the scar despite the virtual absence of viable tissue within the infarction. Data suggest a passive ST segment potential transmission through the infarction. Moreover, ischemia adjacent to a chronic infarction induces lower ST segment elevation than ischemia not adjacent to a necrosis. The mechanisms accounting for these regional differences are probably independent of collateral myocardial perfusion and ischemia extension.
Authors:
J Cinca; A Bardají; A Carreño; L Mont; R Bosch; A Soldevilla; A Tapias; J Soler-Soler
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Circulation     Volume:  91     ISSN:  0009-7322     ISO Abbreviation:  Circulation     Publication Date:  1995 Mar 
Date Detail:
Created Date:  1995-03-24     Completed Date:  1995-03-24     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  1552-9     Citation Subset:  AIM; IM    
Affiliation:
Laboratorio de Cardiologia Experimental, Hospital General Universitari Vall d'Hebron, Barcelona, Spain.
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MeSH Terms
Descriptor/Qualifier:
Animals
Electrocardiography*
Electrophysiology
Heart / radionuclide imaging
Heart Conduction System / physiopathology*
Myocardial Infarction / diagnosis,  pathology,  physiopathology*
Myocardial Ischemia / diagnosis,  pathology,  physiopathology*
Myocardium / pathology
Necrosis
Signal Processing, Computer-Assisted
Swine
Technetium Tc 99m Sestamibi / diagnostic use
Chemical
Reg. No./Substance:
109581-73-9/Technetium Tc 99m Sestamibi

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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