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Relationship between edema and wall thickness in acute myocardial infarction
© Mikami et al; licensee BioMed Central Ltd. 2010
Published: 21 January 2010
Experimental studies using echocardiography have shown that reperfusion of acutely infarcted myocardium induces changes in end-diastolic wall thickness (EDWT), likely caused by myocardial edema. However, the relationship between edema and EDWT has not been described.
The purpose of this study is to assess the relationship between regional EDWT and myocardial edema as defined by T2-weighted CMR in patients with reperfused acute myocardial infarction (MI).
972 segments (81 slices) from 19 patients and 372 segments (31 slices) from healthy subjects were analyzed. Segmental EDWT of regions without edema was not significantly different from that of healthy subjects (6.32 +/- 2.22 mm and 6.26 +/- 1.73 mm, p = N.S.). Edema was observed in 358 segments and infarction was observed in 95 segments. The salvaged area at risk had significantly increased EDWT compared with regions without edema (7.31 ± 2.39 mm and 6.32 ± 2.22 mm, p < 0.05, respectively). The infarction area also had significantly increased EDWT compared with area without edema (7.97 ± 2.48 mm, p < 0.05). The infarcted segments had a significantly increased EDWT compared to the salvaged area at risk (p < 0.05, Figure 2). In healthy subjects, EDWT in the LCX area was less than in the RCA area (5.89 +/- 1.72 mm and 6.63 +/- 1.71 mm, p < 0.05). In an additional analysis excluding LCX area (648 segments), the salvaged area at risk had an increased EDWT compared with regions without edema (7.46 +/- 2.46 mm and 6.93 +/- 2.46 mm, p < 0.05, respectively) and also had less EDWT when compared to infarcted myocardium (8.24 +/- 2.40 mm, p < 0.05).
Myocardial edema as defined by T2-weighted CMR is strongly associated with regionally increased EDWT. Within the area at risk, infarcted segments have a significantly increased EDWT compared to edematous, yet salvaged myocardium.
This article is published under license to BioMed Central Ltd.