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Updated: Jun 4, 2026

Brain Infarct Segmentation and Registration on MRI or CT for Lesion-symptom Mapping
Published on: September 25, 2019
Acute infarct selective MRI contrast agent
Robert Kirschner1, Akos Varga-Szemes, Tamas Simor
1Department of Biochemistry and Molecular Genetics, University of Alabama at Birmingham, MCLM 556, Birmingham, AL 35294-0005, USA.
Abstract:
To determine the infarct affinity of a low molecular weight contrast agent, Gd(ABE-DTTA), during the subacute phase of myocardial infarct (MI). Dogs (n = 7) were examined, using a closed-chest, reperfused MI model. MI was generated by occluding for 180 min the left anterior descending (LAD) coronary artery with an angioplasty balloon. DE-MRI images with Gd(ABE-DTTA) were obtained on days 4, 14, and 28 after MI. Control DE-MRI by Gd(DTPA) was carried out on day 27. T2-TSE images were acquired on day 3, 13 and 27. Triphenyltetrazolium chloride (TTC) histomorphometry validated postmortem the existence of infarct. Gd(ABE-DTTA) highlighted the infarct on day 4, but not at all on day 14 or on day 28, following MI. On day 4, the mean ± SD signal intensity (SI) of infarcted myocardium in the presence of Gd(ABE-DTTA) significantly differed from that of healthy myocardium (45 ± 6.0 vs. 10 ± 5.0, P < 0.05), but it did not on day 14 (11 ± 9.4 vs. 10 ± 5.7, P = NS), nor on day 28 (7 ± 1.5 vs. 7 ± 2.4, P = NS). The mean ± SD signal intensity enhancement (SIE) induced by Gd(ABE-DTTA) was 386 ± 165% on day 4, significantly different from mean SIE on day 14 (9 ± 20%), and from mean SIE on day 28 (12 ± 18%), following MI (P < 0.05). The last two mean values did not differ significantly (P = NS) from each other. As control, Gd(DTPA) was used and it did highlight the infarct on day 27, inducing a mean SIE value of 312 ± 40%. The mean SIE on day 3, 13, or 27 did not vary significantly (P = NS) on the T2-TSE images (114 ± 41%, 123 ± 41%, and 150 ± 79%, respectively). Post mortem, the existence of infarcts was confirmed by TTC staining. The infarct affinity of Gd(ABE-DTTA) vanishes in the subacute phase of scar healing, allowing its use for infarct age differentiation early on, immediately following the acute phase.
Insights
The contrast agent Gd(ABE-DTTA) effectively highlights myocardial infarcts in the early subacute phase but loses affinity as the infarct heals. This allows for early differentiation of infarct age using MRI imaging.
Area of Science:
- Cardiovascular Imaging
- Radiology
- Medical Contrast Agents
Background:
- Myocardial infarction (MI) diagnosis and age assessment are crucial for patient management.
- Assessing infarct healing and scar formation requires advanced imaging techniques.
- Contrast agents play a vital role in enhancing MRI visualization of cardiac tissue.
Purpose of the Study:
- To evaluate the infarct affinity of the low molecular weight contrast agent Gd(ABE-DTTA) during the subacute phase of myocardial infarction (MI).
- To determine if Gd(ABE-DTTA) can differentiate infarct age in the subacute healing phase.
- To compare the performance of Gd(ABE-DTTA) with a conventional contrast agent, Gd(DTPA).
Main Methods:
- A canine closed-chest, reperfused MI model was utilized.
- Delayed-enhancement MRI (DE-MRI) with Gd(ABE-DTTA) was performed on days 4, 14, and 28 post-MI.
- Control DE-MRI with Gd(DTPA) and T2-TSE imaging were also acquired.
- Triphenyltetrazolium chloride (TTC) histomorphometry validated infarct presence postmortem.
Main Results:
- Gd(ABE-DTTA) significantly highlighted infarcts on day 4 post-MI (signal intensity difference P < 0.05).
- Infarct visualization by Gd(ABE-DTTA) diminished significantly by day 14 and was absent by day 28 (P < 0.05).
- Gd(DTPA) effectively visualized the infarct on day 27, indicating sustained contrast enhancement.
Conclusions:
- The infarct affinity of Gd(ABE-DTTA) diminishes during subacute scar healing.
- Gd(ABE-DTTA) shows potential for early infarct age differentiation, immediately following the acute phase.
- This characteristic allows for distinguishing recent MIs from older ones based on contrast agent uptake patterns.
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