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J Am Coll Cardiol, 2006; 48:1961-1968, doi:10.1016/j.jacc.2006.03.071 (Published online 31 October 2006).
© 2006 by the American College of Cardiology Foundation
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Discrimination of Myocardial Acute and Chronic (Scar) Infarctions on Delayed Contrast Enhanced Magnetic Resonance Imaging With Intravascular Magnetic Resonance Contrast Media

Maythem Saeed, DVM, PhD*,*, Oliver Weber, PhD*, Randall Lee, MD, PhD{dagger}, Loi Do, BS*, Alastair Martin, PhD*, David Saloner, PhD*, Philip Ursell, MD{ddagger}, Philippe Robert, PhD§, Claire Corot, PhD§ and Charles B. Higgins, MD, FACC*

* Radiology
{dagger} Medicine/Cardiology
{ddagger} Pathology, University of California San Francisco, San Francisco, California
§ Guerbet-Group, Paris, France


Figure 1
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Figure 1 Long- and short-axis views T2-turbo spin echo. Magnetic resonance images acquired from 2 animals (top and bottom rows). Acute (left) but not chronic (center) infarctions showed differential enhancement (arrows). The bright signal in the left ventricular chambers (arrowheads) represents slow flowing blood adjacent to infarction. Triphenyltetrazolium chloride staining (right) shows the extent and location of infarction.

 

Figure 2
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Figure 2 Long- (rows A and D) and short-axis (rows B and E) views of inversion recovery gradient echo images acquired from 2 animals (top and bottom sets of images). The extracellular and intravascular gadolinium-chelates produced enhancement of acute infarctions (left blocks, arrows). In the long-axis view (rows A and D), the cores of acute infarctions show small patchy hypoenhanced regions, an indication of the presence of microvascular obstruction. In chronic infarctions (center blocks, arrows) the extracellular agent produced differential enhancement. Triphenyltetrazolium chloride staining (right slices C and F) confirmed the extent and location of infarction (arrows).

 

Figure 3
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Figure 3 Long-axis view T1-turbo spin echo images acquired at 3 days (left panels) and 8 weeks (right panels) from 2 animals (top and bottom rows). As in the inversion recovery gradient echo sequence, both extracellular and intravascular gadolinium-chelates produced differential enhancement (arrows) in acute infarctions (left panels). In chronic infarctions, the extracellular agent produced differential enhancement (far right panels, arrows), but not the intravascular agent (middle right panels). Accordingly, intravascular gadolinium-chelate discriminates acute myocardial infarction from scar tissue.

 

Figure 4
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Figure 4 Plots show average changes in signal intensity (SI) ratio after administration of the intravascular agent in acute and chronic infarctions with inversion recovery gradient echo (top) and T1–turbo spin echo (bottom) magnetic resonance imaging. On both sequences, the intravascular agent significantly increased the SI ratio in acute but not chronic infarctions. *p < 0.01 compared with baseline SI ratio in acute infarctions; +p < 0.01 compared with SI ratio at 10 min; #p < 0.01 SI ratio of chronic compared with acute infarctions.

 

Figure 5
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Figure 5 Histograms show the signal intensity (SI) ratios after administration of the intravascular (top) and extracellular (bottom) gadolinium-chelates. T2–turbo spin echo (TSE) and the intravascular agent provided differential enhancement of acute (black bars) but not chronic (white bars) infarctions on T1-TSE and sequences. The extracellular agent provided the same magnitude of enhancement in acute and chronic infarctions on T1-TSE and inversion recovery gradient echo (IR-GRE) sequences. Note that contrast enhanced IR-GRE sequence provides better contrast than both T1-TSE and T2-TSE sequences. *p < 0.01 SI ratios compared with acute infarctions. +p < 0.01 SI ratios compared with contrast enhanced magnetic resonance imaging (MRI).

 

Figure 6
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Figure 6 Histopathology of swine myocardial infarction at 8 weeks. (A) Irregular but clear interface between scar (S) and viable myocardium (VM). The infarct contains scattered, remodeled vessels (arrows) (100x, Masson's trichrome). At high magnification (B, 400x, Masson's trichrome), the scar comprises dense collagen that signifies a completely healed infarct. At the peri-infarction zone, the collagen interdigitates with viable myofibers. (C) Numerous uniformly distributed microvessels localized by brown reaction product between the non-stained myofibers in remote myocardium. In this transversely cut section, there is at least 1 vessel/myofiber (400x, biotinylated Baneiria simplicifolia isolectin B4). (D) Demonstrates the paucity of vessels in scarred myocardium. Brown reaction product localizes a haphazard array of sparse microvessels within the fibrous tissue (400x).

 




 
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