Title of article :
Temporal changes in regional end-diastolic wall thickness early after reperfusion in acute anterior myocardial infarction: Relation to myocardial viability and vascular damage
Author/Authors :
Hidemasa Oh، نويسنده , , Hiroshi Ito، نويسنده , , Katsuomi Iwakura، نويسنده , , Tohru Masuyama، نويسنده , , Shin Takiuchi MD، نويسنده , , Atsushi Maruyama، نويسنده , , Yorihiko Higashino، نويسنده , , Kenshi Fujii، نويسنده , , Junichi Azuma، نويسنده , , Takazo Minamino، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 1996
Pages :
8
From page :
1113
To page :
1120
Abstract :
We investigated early temporal changes in end-diastolic wall thickness (EDWT) of the infarcted myocardium in 46 patients with reperfused anterior acute myocardial infarction in relation to myocardial viability. Two-dimensional echocardiography was performed on days 1 and 2 of acute myocardial infarction, and the EDWT of the anterior segment was measured in the short-axis view. Patients were divided into three groups on the basis of day 1 to day 2 ratio of EDWT: the ratio ≤0.85 as group A (n = 13), >0.85 but <1.15 as group B (n = 23), and>1.15 as group C (n = 10). Left ventricular functional improvement was significantly better in group B than in groups A and C. Substantial size of “no reflow” phenomenon was observed only in groups A (n = 9, 69%) and C (n = 6, 60%). The frequency of transient ST re-elevation after reperfusion was the highest in group C (70%), and left ventricular expansion was observed at day 2 only in group A. We conclude that changes in the EDWT of the infarct segment early after reperfusion, either decreases or increases, are related to irreversibly damaged myocardium. A decrease in EDWT and concomitant ventricular expansion may be related to impaired myocardial perfusion. An increase in EDWT after reperfusion may be caused by accelerated myocardial and microvascular damage after reperfusion.
Journal title :
American Heart Journal
Serial Year :
1996
Journal title :
American Heart Journal
Record number :
526980
Link To Document :
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