| Visualization of subendocardial myocardial ischemia with myocardial contrast echocardiography in humans. | |
| | |
MedLine Citation:
|
PMID: 2914344 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
Previous studies indicate the degree of myocardial echo contrast enhancement may be related to regional myocardial perfusion. In this study, myocardial contrast echocardiography was used to characterize changes in the transmural myocardial blood flow distribution that were provoked by rapid atrial pacing in 11 patients with one-vessel coronary artery disease. Ten patients without coronary artery disease served as controls. Myocardial contrast echocardiography was performed by intracoronary injection of 2 ml hand-agitated amidotrizoate sodium meglumine (Urografin-76) and by imaging a short-axis view of the left ventricle with two-dimensional echocardiography before and during injection of the contrast agent. The two-dimensional echocardiographic images at end diastole, before and after injection of the contrast agent, were digitized off-line into a 512 x 512 pixel matrix with 256 gray levels/pixel to quantify the degree of the enhancement of the peak gray level after injection. Transmural myocardial blood flow distribution was evaluated by measuring the ratio of the enhanced gray level in the endocardial half (endo) to that in the epicardial half (epi) (endo:epi gray level ratio) in the anteroseptal, posterolateral, and inferior segments before and just after rapid atrial pacing in each patient. In patients without coronary artery disease, there were no differences in the endo:epi gray level ratio between any of the three segments both before and after pacing. Mean values of the three segments were 0.95 +/- 0.08 before pacing and 0.90 +/- 0.13 after pacing, respectively. In contrast, in patients with coronary artery disease, the endo:epi gray level ratio for the segment supplied with stenotic coronary artery decreased after pacing (0.40 +/- 0.21 vs. 0.93 +/- 0.18, p less than 0.01), probably reflecting subendocardial myocardial ischemia, whereas that for the segment supplied with nonstenotic coronary artery remained unchanged (0.88 +/- 0.20 vs. 0.99 +/- 0.23, NS). Thus, changes in transmural myocardial blood flow distribution with rapid pacing, which may be due to transient subendocardial ischemia, are visualized with myocardial contrast echocardiography. |
| | |
Authors:
|
Y J Lim; S Nanto; T Masuyama; K Kodama; T Ikeda; A Kitabatake; T Kamada |
Related Documents
:
|
16438224 - A novel ex vivo heart model for the assessment of cardiac pacing systems. 19659634 - Direct his bundle pacing post avn ablation. 322484 - Simultaneous left ventricular echocardiography and aortic blood velocity during rapid r... 10856734 - Left ventricular-based pacing in patients with chronic heart failure: comparison of acu... 16327014 - Modulation of contractility by myocyte-derived arginase in normal and hypertrophied fel... 15226874 - Risk of combined coronary artery bypass and mitral valve replacement. |
Publication Detail:
|
Type: Journal Article |
Journal Detail:
|
Title: Circulation Volume: 79 ISSN: 0009-7322 ISO Abbreviation: Circulation Publication Date: 1989 Feb |
Date Detail:
|
Created Date: 1989-03-15 Completed Date: 1989-03-15 Revised Date: 2004-11-17 |
Medline Journal Info:
|
Nlm Unique ID: 0147763 Medline TA: Circulation Country: UNITED STATES |
Other Details:
|
Languages: eng Pagination: 233-44 Citation Subset: AIM; IM |
Affiliation:
|
Cardiovascular Division, Kawachi General Hospital, Osaka, Japan. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Adult Aged Cardiac Pacing, Artificial Coronary Circulation* Coronary Disease / physiopathology* Echocardiography* Endocardium / physiopathology* Female Heart / physiopathology* Humans Male Middle Aged Reference Values |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Development of coronary heart disease in familial hypercholesterolemia.
Next Document: Sustained bundle branch reentry as a mechanism of clinical tachycardia.