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Comparative Study
. 1996 Aug 15;94(4):660-6.
doi: 10.1161/01.cir.94.4.660.

Remote noninfarcted region dysfunction soon after first anterior myocardial infarction. A magnetic resonance tagging study

Affiliations
Comparative Study

Remote noninfarcted region dysfunction soon after first anterior myocardial infarction. A magnetic resonance tagging study

C M Kramer et al. Circulation. .

Abstract

Background: Previous studies have demonstrated hyperkinetic endocardial motion of noninfarcted myocardium early after myocardial infarction (MI). We wished to substantiate the findings of increased function of remote noninfarcted regions using magnetic resonance (MR) myocardial tagging in patients soon after anterior MI.

Methods and results: Twenty-eight patients (25 male; mean age, 52 years) were studied on day 5 +/- 2 after first anterior MI. All had single-vessel left anterior descending coronary artery (LAD) disease and had received reperfusion therapy but had evidence of regional left ventricular (LV) dysfunction and an ejection fraction (EF) < or = 50%. Breath-hold, segmented k-space, gradient-echo MR tagging was performed with short-axis imaging spanning the LV. Percent circumferential shortening (%S) on a topographic basis, LV mass, and EF were measured. Regional %S was compared with that in 10 normal subjects (7 male; mean age, 43 years). We found reduced intramyocardial %S throughout the LV in the patient group. Percent shortening was lower in patients compared with control subjects at all sites along the long axis of the ventricle (9 +/- 5% versus 23 +/- 3% at the apex, P < .0001; 11 +/- 5% versus 21 +/- 3% at the midventricle, P < .0001; 14 +/- 3% versus 17 +/- 5% at the base, P < .02). The basal lateral and midinferior regions, remote from LAD territory, demonstrated reduced %S and a strong trend toward reduced %S, respectively.

Conclusions: Patients on day 5 after first anterior MI with single-vessel disease demonstrate reduced intramyocardial circumferential shortening throughout the LV, including remote noninfarcted regions. Potential mechanisms include altered coronary vasodilatory properties, changes in regional mechanical load, or mechanical tethering to infarcted regions.

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