Distinctive changes in end-diastolic wall thickness and postsystolic thickening in viable and infarcted myocardium

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Abstract

Objectives In this study, we sought to compare the magnitude of changes in end-diastolic wall thickness (WTed) and postsystolic thickening (PST) in a swine model of stunning and reperfused acute myocardial infarction, and to explore the relationship between WTed and PST. Methods Twenty-six pigs were subjected to left anterior descending coronary artery occlusion followed by reperfusion to induce stunning (n = 6), nontransmural (n = 8), or transmural (n = 12) myocardial infarction. Myocardial wall thickness was measured using intracardiac echocardiography. Transmural extent of necrosis (TEN) was quantified by triphenyltetrazolium chloride technique. Results During the first minutes of reperfusion, a marked increase in WTed occurred in the myocardial walls with nontransmural and transmural infarct (42% and 102%, respectively) but less in those with stunning (19%). PST persisted at reperfusion in walls with stunning and nontransmural infarct (23% and 26%, respectively). In transmurally infarcted walls, PST progressively decreased either during occlusion (5/12 pigs) or shortly after reperfusion (7/12 pigs). PST at reperfusion was virtually absent when TEN was >70%. Both PST and the increase in WTed at reperfusion correlated well with TEN (P < .0001 for both). Changes in PST at reperfusion were weakly correlated with changes in WTed. Conclusions A marked increase in WTed after reperfusion and absence of PST indicate transmural myocardial infarction. Presence of PST at reperfusion indicates viable tissue in more than 30% of wall thickness. The results suggest that amplitude of PST is modulated predominately by factors related to the severity of ischemia and, to a smaller extent, by changes in wall thickness.

Original languageEnglish (US)
Pages (from-to)855-862
Number of pages8
JournalJournal of the American Society of Echocardiography
Volume17
Issue number8
DOIs
StatePublished - Aug 2004

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Reperfusion
Myocardium
Swine
Necrosis
Myocardial Infarction
Coronary Occlusion
Echocardiography
Coronary Vessels
Ischemia

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Radiology Nuclear Medicine and imaging

Cite this

@article{1b2da1e62eb34e08886942014112a2ff,
title = "Distinctive changes in end-diastolic wall thickness and postsystolic thickening in viable and infarcted myocardium",
abstract = "Objectives In this study, we sought to compare the magnitude of changes in end-diastolic wall thickness (WTed) and postsystolic thickening (PST) in a swine model of stunning and reperfused acute myocardial infarction, and to explore the relationship between WTed and PST. Methods Twenty-six pigs were subjected to left anterior descending coronary artery occlusion followed by reperfusion to induce stunning (n = 6), nontransmural (n = 8), or transmural (n = 12) myocardial infarction. Myocardial wall thickness was measured using intracardiac echocardiography. Transmural extent of necrosis (TEN) was quantified by triphenyltetrazolium chloride technique. Results During the first minutes of reperfusion, a marked increase in WTed occurred in the myocardial walls with nontransmural and transmural infarct (42{\%} and 102{\%}, respectively) but less in those with stunning (19{\%}). PST persisted at reperfusion in walls with stunning and nontransmural infarct (23{\%} and 26{\%}, respectively). In transmurally infarcted walls, PST progressively decreased either during occlusion (5/12 pigs) or shortly after reperfusion (7/12 pigs). PST at reperfusion was virtually absent when TEN was >70{\%}. Both PST and the increase in WTed at reperfusion correlated well with TEN (P < .0001 for both). Changes in PST at reperfusion were weakly correlated with changes in WTed. Conclusions A marked increase in WTed after reperfusion and absence of PST indicate transmural myocardial infarction. Presence of PST at reperfusion indicates viable tissue in more than 30{\%} of wall thickness. The results suggest that amplitude of PST is modulated predominately by factors related to the severity of ischemia and, to a smaller extent, by changes in wall thickness.",
author = "Pislaru, {Cristina D} and Bruce, {Charles J} and Seward, {James B.} and Greenleaf, {James F}",
year = "2004",
month = "8",
doi = "10.1016/j.echo.2004.04.038",
language = "English (US)",
volume = "17",
pages = "855--862",
journal = "Journal of the American Society of Echocardiography",
issn = "0894-7317",
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TY - JOUR

T1 - Distinctive changes in end-diastolic wall thickness and postsystolic thickening in viable and infarcted myocardium

AU - Pislaru, Cristina D

AU - Bruce, Charles J

AU - Seward, James B.

AU - Greenleaf, James F

PY - 2004/8

Y1 - 2004/8

N2 - Objectives In this study, we sought to compare the magnitude of changes in end-diastolic wall thickness (WTed) and postsystolic thickening (PST) in a swine model of stunning and reperfused acute myocardial infarction, and to explore the relationship between WTed and PST. Methods Twenty-six pigs were subjected to left anterior descending coronary artery occlusion followed by reperfusion to induce stunning (n = 6), nontransmural (n = 8), or transmural (n = 12) myocardial infarction. Myocardial wall thickness was measured using intracardiac echocardiography. Transmural extent of necrosis (TEN) was quantified by triphenyltetrazolium chloride technique. Results During the first minutes of reperfusion, a marked increase in WTed occurred in the myocardial walls with nontransmural and transmural infarct (42% and 102%, respectively) but less in those with stunning (19%). PST persisted at reperfusion in walls with stunning and nontransmural infarct (23% and 26%, respectively). In transmurally infarcted walls, PST progressively decreased either during occlusion (5/12 pigs) or shortly after reperfusion (7/12 pigs). PST at reperfusion was virtually absent when TEN was >70%. Both PST and the increase in WTed at reperfusion correlated well with TEN (P < .0001 for both). Changes in PST at reperfusion were weakly correlated with changes in WTed. Conclusions A marked increase in WTed after reperfusion and absence of PST indicate transmural myocardial infarction. Presence of PST at reperfusion indicates viable tissue in more than 30% of wall thickness. The results suggest that amplitude of PST is modulated predominately by factors related to the severity of ischemia and, to a smaller extent, by changes in wall thickness.

AB - Objectives In this study, we sought to compare the magnitude of changes in end-diastolic wall thickness (WTed) and postsystolic thickening (PST) in a swine model of stunning and reperfused acute myocardial infarction, and to explore the relationship between WTed and PST. Methods Twenty-six pigs were subjected to left anterior descending coronary artery occlusion followed by reperfusion to induce stunning (n = 6), nontransmural (n = 8), or transmural (n = 12) myocardial infarction. Myocardial wall thickness was measured using intracardiac echocardiography. Transmural extent of necrosis (TEN) was quantified by triphenyltetrazolium chloride technique. Results During the first minutes of reperfusion, a marked increase in WTed occurred in the myocardial walls with nontransmural and transmural infarct (42% and 102%, respectively) but less in those with stunning (19%). PST persisted at reperfusion in walls with stunning and nontransmural infarct (23% and 26%, respectively). In transmurally infarcted walls, PST progressively decreased either during occlusion (5/12 pigs) or shortly after reperfusion (7/12 pigs). PST at reperfusion was virtually absent when TEN was >70%. Both PST and the increase in WTed at reperfusion correlated well with TEN (P < .0001 for both). Changes in PST at reperfusion were weakly correlated with changes in WTed. Conclusions A marked increase in WTed after reperfusion and absence of PST indicate transmural myocardial infarction. Presence of PST at reperfusion indicates viable tissue in more than 30% of wall thickness. The results suggest that amplitude of PST is modulated predominately by factors related to the severity of ischemia and, to a smaller extent, by changes in wall thickness.

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U2 - 10.1016/j.echo.2004.04.038

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JO - Journal of the American Society of Echocardiography

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