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The aim of this study was to measure the myocardial area at risk in rat, using MRI and manganese injection during a coronary occlusion/reperfusion model at 1.5T. A sequential protocol with occlusion and MnCl2 injection immediately followed by MRI was used with the assumption that MnCl2-induced contrast persistence is enough to accurately image the area at risk 90 min after occlusion. A total of 15 adult rats underwent a single 30-min episode of coronary occlusion followed by reperfusion. MnCl2 was injected (25 micromol/kg) at the beginning of the occlusion for 11 rats (group 1) and 6 h after reperfusion for four animals (group 2). A deficit of signal enhancement was observed in all rats. Hypoenhancement area in group 1 was correlated to the area at risk delineated by methylene blue (r=0.96, P<0.0001) whereas in group 2 it was correlated to the infarct area given by triphenyltetrazolium chloride (TTC) solution (r=0.98, P=0.003). The area at risk size was significantly correlated with left ventricle ejection fraction (LVEF), end-systolic volume and anterolateral wall thickening. This work demonstrates that hypoenhanced zone obtained after manganese injection during occlusion represents the area at risk and not only the infarct zone., (Copyright (c) 2008 Wiley-Liss, Inc.)

It has been shown that manganese-enhanced MRI (MEMRI) can safely depict the myocardial area at risk in models of coronary occlusion-reperfusion for at least 2 h after reperfusion. To achieve this, a solution of MnCl(2) is injected during coronary occlusion. In this model, the regional function quantification deficit of the stunning phase cannot be assessed before contrast injection using MR tagging. The relaxation effects of manganese (which remains in normal cardiac myocytes for several hours) may alter the tags by increasing tag fading and hence the quality of strain measurement. Therefore, we evaluated the feasibility of cardiac MR tagging after manganese injection in normal rats. Six normal Sprague-Dawley rats were imaged in vivo using complementary spatial modulation of magnetization (C-SPAMM) at 1.5 T, before and 15 min after intraperitoneal injection of MnCl(2) solution (~17.5 micromol kg(-1)). The contrast-to-noise ratio of the tag pattern increased significantly (P < 0.001) after injection and remained comparable to the control scan in spite of the higher myocardial relaxation rate caused by the presence of manganese. The measurements of circumferential strain obtained from harmonic phase imaging analysis of the tagged images after MnCl(2) injection did not differ significantly from the measurements before injection in the endocardial, mid-wall, and epicardial regions. In particular, the transmural strain gradient was preserved. Thus, our study suggests that MR tagging could be used in combination with MEMRI to study the acute phase of coronary artery disease.

The objectives of this study were to define the relationship between the first order constant of Gd-DTPA transfer (K1) and the myocardial blood flow (MBF) at rest and to compare it with an equivalent relationship obtained for positron emission tomography (PET). In a canine model of permanent coronary occlusion (n = 4), myocardial and blood time concentration curves obtained by 13N-ammonia PET and Gd-DTPA-enhanced MRI were fitted by a one-compartment model to determine K1. A linear relationship was observed between MRI-derived K1 and MBF measured by microspheres (K1 = 0.88 x flow -0.015, R = 0.95), which compares favorably with the equivalent relationship derived from PET (K1 = 0.74 x flow +0.16, R = 0.88). The results of this preliminary study suggest that, at rest and distal to a permanently occluded coronary artery, myocardial perfusion quantification by MRI is possible and can challenge PET.

K1 (first-order transfer constant from arterial plasma to myocardium for Gd-DTPA) and Vd (distribution volume of Gd-DTPA in myocardium) were measured in vivo in a canine model (n = 5) using MRI-derived myocardial perfusion curves and a compartmental model. Perfusion curves were obtained after a bolus injection of Gd-DTPA (0.04 mM/kg) with an inversion-prepared fast gradient echo sequence. Myocardium and blood signal intensity were converted to a concentration of Gd-DTPA, according to a model appropriate for short (<1 s) interimage intervals characteristic of cardiac-triggered acquisitions. Before dipyridamole-induced stress, K1 and Vd, obtained from the fit of the MRI-derived perfusion curves, were 6.2 +/- 1.4 (mHz) and 17.5 +/- 4.2%, respectively. After dipyridamole infusion, a K1 increase of a factor of 2.82 +/- 0.72 was measured (P = 0.003). No change was observed in Vd (P = 0.98). These results suggest that the K1 increase after dipyridamole reflects a flow-related effect that can be useful to quantify the MRI-derived perfusion curves.