8 research outputs found
Quantification of myocardial infarct area based on TRAFFn relaxation time maps:comparison with cardiovascular magnetic resonance late gadolinium enhancement, T1Ď and T2 in vivo
Abstract
Background: Two days after myocardial infarction (MI), the infarct consists mostly on necrotic tissue, and the myocardium is transformed through granulation tissue to scar in two weeks after the onset of ischemia in mice. In the current work, we determined and optimized cardiovascular magnetic resonance (CMR) methods for the detection of MI size during the scar formation without contrast agents in mice.
Methods: We characterized MI and remote areas with rotating frame relaxation time mapping including relaxation along fictitious field in nth rotating frame (RAFFn), T1Ď and T2 relaxation time mappings at 1, 3, 7, and 21 days after MI. These results were compared to late gadolinium enhancement (LGE) and Sirius Red-stained histology sections, which were obtained at day 21 after MI.
Results: All relaxation time maps showed significant differences in relaxation time between the MI and remote area. Areas of increased signal intensities after gadolinium injection and areas with increased TRAFF2 relaxation time were highly correlated with the MI area determined from Sirius Red-stained histology sections (LGE: R²â=â0.92, Pâ<â0.01, TRAFF2: R²â=â0.95, Pâ<â0.001). Infarct area determined based on T1Ď relaxation time correlated highly with Sirius Red histology sections (R²â=â0.97, Pâ<â0.01). The smallest overestimation of the LGE-defined MI area was obtained for TRAFF2 (5.6âÂąâ4.2%) while for T1Ď overestimation percentage was >â9% depending on T1Ď pulse power.
Conclusion: T1Ď and TRAFF2 relaxation time maps can be used to determine accurately MI area at various time points in the mouse heart. Determination of MI size based on TRAFF2 relaxation time maps could be performed without contrast agents, unlike LGE, and with lower specific absorption rate compared to on-resonance T1Ď relaxation time mapping
Lymphatic insufficiency leads to distinct myocardial infarct content assessed by magnetic resonance TRAFFn, T1Ď and Tâ relaxation times
Abstract
The role of cardiac lymphatics in the pathogenesis of myocardial infarction (MI) is unclear. Lymphatic system regulates cardiac physiological processes such as edema and tissue fluid balance, which affect MI pathogenesis. Recently, MI and fibrosis have been assessed using endogenous contrast in magnetic resonance imaging (MRI) based on the relaxation along a fictitious field with rank n (RAFFn). We extended the RAFFn applications to evaluate the effects of lymphatic insufficiency on MI with comparison to longitudinal rotating frame (T1Ď) and Tâ relaxation times. MI was induced in transgenic (TG) mice expressing soluble decoy VEGF receptor 3 that reduces lymphatic vessel formation and their wild-type (WT) control littermates for comparison. The RAFFn relaxation times with rank 2 (TRAFF2), and rank 4 (TRAFF4), T1Ď and Tâ were acquired at time points 0, 3, 7, 21 and 42 days after the MI at 9.4 T. Infarct sizes were determined based on TRAFF2, TRAFF4, T1Ď and Tâ relaxation time maps. The area of differences (AOD) was calculated based on the MI areas determined on Tâ and TRAFF2, TRAFF4 or T1Ď relaxation time maps. Hematoxylinâeosin and Sirius red stained histology sections were prepared to confirm MI locations and sizes. MI was detected as increased TRAFF2, TRAFF4, T1Ď and Tâ relaxation times. Infarct sizes were similar on all relaxation time maps during the experimental period. Significantly larger AOD values were found together with increased AOD values in the TG group compared to the WT group. Histology confirmed these findings. The lymphatic deficiency was found to increase cardiac edema in MI. The combination of TRAFF2 (or TRAFF4) and Tâ characterizes MI and edema in the myocardium in both lymphatic insufficiency and normal mice without any contrast agents