Time course of 23Na signal intensity after myocardial infarction in humans
✍ Scribed by Joern J.W. Sandstede; Hanns Hillenbrand; Meinrad Beer; Thomas Pabst; Felix Butter; Wolfram Machann; Wolfgang Bauer; Dietbert Hahn; Stefan Neubauer
- Book ID
- 102531886
- Publisher
- John Wiley and Sons
- Year
- 2004
- Tongue
- English
- Weight
- 275 KB
- Volume
- 52
- Category
- Article
- ISSN
- 0740-3194
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Experimental studies demonstrated persistently increased ^23^Na content in nonviable myocardium post‐myocardial infarction (MI). We hypothesized that nonviable myocardium in humans would show elevated ^23^Na content at all stages of infarct development, and therefore could be imaged with ^23^Na MRI. Ten patients were examined on days 4, 14, and 90 after infarction, and five of these patients participated in a 12‐month follow‐up. Double angulated short‐axis cardiac ^23^Na images were obtained with the use of a ^23^Na surface coil and an ECG‐triggered, 3D gradient‐echo sequence. ^1^H T~2~‐weighted imaging (N = 9) was performed on days 4, 14, and 90. Wall motion was assessed by cine MRI, and the infarct size was determined by late enhancement on day 90. The ^23^Na signal intensity (SI) of infarcted myocardium was expressed as the percentage increase over ^23^Na SI of noninfarcted myocardium. All of the patients showed an area of elevated SI on ^23^Na and ^1^H T~2~‐weighted images that correlated with wall motion abnormalities and late enhancement. ^23^Na SI was highest on day 4. It then decreased until day 90, but remained elevated (39% ± 18%, 31% ± 17%, 28% ± 13% on days 4, 14, and 90, respectively, P = 0.001). No further decrease was found 1 year after infarction (25% ± 7%, P = 0.89 vs. day 90). ^1^H T~2~‐weighted SI decreased between days 4 and 14, but on day 90 only six of nine patients had a residual elevated SI. Thus, ^23^Na SI is elevated in nonviable infarction at all time points following MI, and ^23^Na MRI may become a suitable technique for imaging nonviable myocardium in humans. Magn Reson Med 52:545–551, 2004. © 2004 Wiley‐Liss, Inc.
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