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JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
Tissue Doppler imaging differentiates transmural from nontransmural acute myocardial infarction after reperfusion therapy.
Circulation 2001 January 31
BACKGROUND: The evaluation of transmural extent of necrosis after acute myocardial infarction remains a major problem in clinical practice. We sought to determine whether color M-mode tissue Doppler imaging (TDI) could differentiate transmural from nontransmural myocardial infarction.
METHODS AND RESULTS: Twenty-one anesthetized open-chest dogs underwent 90 or 120 minutes of left anterior descending coronary artery occlusion followed by 180 minutes of reperfusion. The transmural extension of infarct was measured by triphenyltetrazolium chloride (TTC) staining. Segment shortening in the endocardium and epicardium of the anterior and posterior walls was assessed by sonomicrometry. Regional myocardial blood flow was measured by radioactive microspheres. TDI was obtained from an epicardial short-axis view. We calculated systolic and diastolic velocities within the endocardium and epicardium of myocardial walls and the subsequent myocardial velocity gradient (MVG). TTC staining could identify 2 groups according to the transmural extent of necrosis: 15 dogs had a nontransmural (NT) necrosis (42+/-3% of wall thickness), and 6 dogs developed a transmural (T) infarct (81+/-4% of wall thickness). In both groups, ischemia resulted in a significant and similar reduction in endocardial and epicardial velocities, with a resulting low systolic MVG in the anterior wall (0.10+/-0.07 in NT and 0.10+/-0.08 s(-1) in T). At 60 minutes of reperfusion, systolic MVG failed to change significantly in the transmural group (-0.20+/-0.09 s(-1)). In contrast, it increased significantly after reflow in the NT group compared with ischemic values (-0.99+/-0.20 versus 0.10+/-0.07 s(-1), P:<0.05).
CONCLUSIONS: TDI can differentiate transmural from nontransmural myocardial infarction early after reperfusion.
METHODS AND RESULTS: Twenty-one anesthetized open-chest dogs underwent 90 or 120 minutes of left anterior descending coronary artery occlusion followed by 180 minutes of reperfusion. The transmural extension of infarct was measured by triphenyltetrazolium chloride (TTC) staining. Segment shortening in the endocardium and epicardium of the anterior and posterior walls was assessed by sonomicrometry. Regional myocardial blood flow was measured by radioactive microspheres. TDI was obtained from an epicardial short-axis view. We calculated systolic and diastolic velocities within the endocardium and epicardium of myocardial walls and the subsequent myocardial velocity gradient (MVG). TTC staining could identify 2 groups according to the transmural extent of necrosis: 15 dogs had a nontransmural (NT) necrosis (42+/-3% of wall thickness), and 6 dogs developed a transmural (T) infarct (81+/-4% of wall thickness). In both groups, ischemia resulted in a significant and similar reduction in endocardial and epicardial velocities, with a resulting low systolic MVG in the anterior wall (0.10+/-0.07 in NT and 0.10+/-0.08 s(-1) in T). At 60 minutes of reperfusion, systolic MVG failed to change significantly in the transmural group (-0.20+/-0.09 s(-1)). In contrast, it increased significantly after reflow in the NT group compared with ischemic values (-0.99+/-0.20 versus 0.10+/-0.07 s(-1), P:<0.05).
CONCLUSIONS: TDI can differentiate transmural from nontransmural myocardial infarction early after reperfusion.
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