Modified Look-Locker Inversion Recovery Sequence Research Articles

Evaluation of Age-Related Interstitial Myocardial Fibrosis With Cardiac Magnetic Resonance Contrast-Enhanced T1 Mapping: MESA (Multi-Ethnic Study of Atherosclerosis)

This study sought to determine the relationship of cardiovascular magnetic resonance (CMR) measures of tissue composition to age in the Multi-Ethnic Study of Atherosclerosis (MESA).Animal and human studies have demonstrated increased collagen deposition in senescent hearts. New CMR indices of tissue composition by using T1 mapping are sensitive to the presence of myocardial fibrosis.A total of 1,231 study participants (51% women; age range 54 to 93 years) of the MESA cohort were evaluated with T1 mapping by using 1.5-T CMR scanners. None of the participants had focal scar on delayed enhancement CMR. Single-slice T1 mapping was performed at the midventricular level before and at 12- and 25-min delay after administration of gadolinium contrast by using a modified Look-Locker inversion recovery sequence. The partition coefficient was determined by the slope of the linear relationship of (1/T1myo vs. 1/T1blood). The extracellular volume fraction (ECV) was derived accounting for the hematocrit level. Multivariable regression analyses were performed, adjusting for traditional risk factors and left ventricular structure.Women had significantly greater partition coefficient, ECV, and precontrast T1 than men, as well as lower post-contrast T1 values (all p < 0.05). In general, linear regression analyses demonstrated that greater partition coefficient, pre-contrast T1 values, and ECV were associated with older age in men (multivariate regression coefficients = 0.01; 5.9 ms; and 1.04% per 10 years' change; all p < 0.05). ECV was also significantly associated with age in women after multivariable adjustments.CMR parameters that have been associated with myocardial fibrosis were related to older age in the MESA study. Women had higher ECV than men but less ECV change over time.

Comprehensive Validation of Cardiovascular Magnetic Resonance Techniques for the Assessment of Myocardial Extracellular Volume

Extracellular matrix expansion is a key element of ventricular remodeling and a potential therapeutic target. Cardiovascular magnetic resonance (CMR) T1-mapping techniques are increasingly used to evaluate myocardial extracellular volume (ECV); however, the most widely applied methods are without histological validation. Our aim was to perform comprehensive validation of (1) dynamic-equilibrium CMR (DynEq-CMR), where ECV is quantified using hematocrit-adjusted myocardial and blood T1 values measured before and after gadolinium bolus; and (2) isolated measurement of myocardial T1, used as an ECV surrogate. Whole-heart histological validation was performed using 96 tissue samples, analyzed for picrosirius red collagen volume fraction, obtained from each of 16 segments of the explanted hearts of 6 patients undergoing heart transplantation who had prospectively undergone CMR before transplantation (median interval between CMR and transplantation, 29 days). DynEq-CMR-derived ECV was calculated from T1 measurements made using a modified Look-Locker inversion recovery sequence before and 10 and 15 minutes post contrast. In addition, ECV was measured 2 to 20 minutes post contrast in 30 healthy volunteers. There was a strong linear relationship between DynEq-CMR-derived ECV and histological collagen volume fraction (P<0.001; within-subject: r=0.745; P<0.001; r(2)=0.555 and between-subject: r=0.945; P<0.01; r(2)=0.893; for ECV calculated using 15-minute postcontrast T1). Correlation was maintained throughout the entire heart. Isolated postcontrast T1 measurement showed significant within-subject correlation with histological collagen volume fraction (r=-0.741; P<0.001; r(2)=0.550 for 15-minute postcontrast T1), but between-subject correlations were not significant. DynEq-CMR-derived ECV varied significantly according to contrast dose, myocardial region, and sex. DynEq-CMR-derived ECV shows a good correlation with histological collagen volume fraction throughout the whole heart. Isolated postcontrast T1 measurement is insufficient for ECV assessment.

Extracellular Volume Fractions in Chronic Myocardial Infarction

The aim of this study was to assess and delineate chronic myocardial infarction (CMI) using precontrast and postcontrast T1 mapping techniques including quantification of extracellular volume fractions (ECVs). A total of 26 patients with CMI were examined at 1.5 T applying a modified Look-Locker Inversion Recovery sequence before and 10 minutes after contrast at 3 short-axis slice positions. An inversion recovery gradient recalled echo sequence (standard of reference) was used for imaging late gadolinium enhancement. Precontrast and postcontrast T1 maps were calculated, and CMI was defined as areas with T1 values more than 3 SDs different compared with normal myocardium (MYO). T1 values of CMI, MYO, and blood pool were measured, and ECVs of CMI and MYO were calculated. Two-tailed Student t test was used for statistical analysis of T1 values and ECVs. Sensitivities and specificities for detection of CMI on precontrast and postcontrast T1 maps were calculated. Receiver operating characteristic (ROC) analysis was performed for postcontrast T1 values and ECV for discrimination of CMI. The comparison of T1 values of CMI and MYO revealed significant differences in precontrast and postcontrast scans (1159 ± 64 vs 1001 ± 47 milliseconds, P < 0.001, and 238 ± 74 vs 379 ± 59 milliseconds, P < 0.001). Sensitivities and specificities for detection of CMI on T1 mapping were 41.7% and 100% in precontrast Look-Locker Inversion Recovery scans and 95.8% and 99.3% in postcontrast images, respectively. Average ECV for MYO and CMI were 28% ± 5% and 53% ± 10% (P < 0.001). ROC analysis revealed nonsignificantly different areas under the curve of 0.937 and 0.997 for T1 values and ECV, respectively (P = 0.137). Sensitivities and specificities were 92.3% and 92.3% for detecting CMI by postcontrast T1 values and 95.5% and 100% for ECV, with cutoff values being 305 milliseconds or less and greater than 42%. Combined criteria did not result in any further improvement of sensitivity for CMI detection. Postcontrast T1 values and ECV of chronically infarcted MYO are significantly different compared with respective values of normal MYO. Both parameters allow for accurate detection of CMI with ECV showing marginally higher sensitivity and specificity. Precontrast T1 values lack accuracy in delineation of CMI.

Anti-Inflammatory Drug Evaluation in ApoE−/− Mice by Ultrasmall Superparamagnetic Iron Oxide–Enhanced Magnetic Resonance Imaging

The renin-angiotensin system and local phagocytic activity play a major role in atherosclerotic plaque development. Treatment with irbesartan, an antagonist of angiotensin II receptor, can decrease atherosclerotic lesion formation. Iron oxide-enhanced magnetic resonance imaging (MRI) can be successfully used to evaluate the phagocytic activity in the atherosclerotic plaque in mice. In this study, we used 2 iron oxide-enhanced MRI strategies, in vivo labeling by injection of iron oxide particles and injection of in vitro labeled macrophages, to investigate the effect of irbesartan on both atherosclerotic plaque size and macrophage content in apolipoprotein (Apo) E-deficient mice. ApoE-/- female mice (C57BL/6 background; Charles-River, France) were divided into 2 groups (irbesartan treated [TG] or not treated [NTG]) and started on a high-fat diet (Harlan TD88137 Western Diet, 21% fat, 0.2% cholesterol). Animals underwent magnetic resonance examinations on a 7-T scanner at baseline and at 14 and 28 weeks of treatment. At each time point, 2 MRI sessions were performed, before and 48 hours after administration of an iron oxide agent (P904; Guerbet, France) or magnetically labeled macrophages (MФΦ). At the end of the follow-up, blood samples were taken for plasma lipid dosing and aorta samples for histology. The study was approved by the animal experimentation ethic committee of our institution.Vessel wall area measurements were performed on high-resolution spin echo transverse images. Multiecho gradient echo images acquired with the same geometry were used to calculate T2* maps of the vessel wall using a pixel-by-pixel monoexponential fit. Irbesartan effect on vessel wall area over time was assessed using a factorial analysis of variance test. T2* values of the vessel wall at pre- and post-ultrasmall superparamagnetic iron oxide (USPIO) administration were analyzed with a 1-way analysis of variance test with Bonferroni post hoc. Irbesartan treatment resulted in significantly smaller vessel wall areas at 28 weeks of treatment (P = 0.04). Postinjection values varied significantly over time for both the NTG-P904 (P = 0.02) and the TG-P904 (P = 0.01) groups. Furthermore, when comparing the TG-P904 with the NTG-P904 group at 28 weeks of treatment, a significant difference was obtained for both pre- and post-USPIO administration values (P = 0.01). In the labeled-macrophage group, postinjection T2* values were smaller than the preinjection ones for the NTG animals at 14 weeks of treatment. No T2* changes were observed in the TG-MΦ group.The difference between pre- and post-USPIO administration T2* values (ΔT2*) was significantly smaller in the TG-P904 group compared with the NTG-P904 group at 28 weeks of treatment. At this point, a good correlation (R = 0.7, P = 0.03) was found between the ΔT2* values in the P904 imaging group and the macrophage-covered area by immunohistological analysis. The present study illustrates an MRI follow-up of intraplaque macrophages using in vivo labeling by iron oxide particle injection and macrophage injection after in vitro USPIO labeling in the assessment of a therapeutic effect in a mouse model of atherosclerosis. Even though in vivo labeling is not fully specific of macrophage uptake, it enabled the detection of a treatment-related reduction in the macrophage content of atherosclerotic plaques in ApoE-/- mice.

The relationship between interstitial fibrosis and contractile function in HCM: a combined T1-mapping and CSPAMM tagging study

Background Interstitial fibrosis is a pathological hallmark of hypertrophic cardiomyopathy (HCM) and is thought to contribute to the abnormal myocardial mechanics seen in this patient group. T1-mapping now allows interstitial fibrosis to be detected non-invasively. Replacement fibrosis as identified by late gadolinium enhancement imaging has been associated with abnormal cardiac mechanics in HCM. However, the relationship between interstitial fibrosis and contractile function in HCM has not been previously explored. We assessed the association between interstitial fibrosis as assessed by T1-mapping and contractile function as determined by continuous spatial modulation of magnetisation (CSPAMM) tagging, hypothesising that increased fibrosis would correlate with abnormal myocardial strain. Methods Twelve HCM patients free of significant comorbidity and 16 controls were studied. CMR was undertaken on a 1.5T Siemens Avanto (Siemens, Erlangen, Germany). Tagged images were acquired at the mid-ventricle using aC SPAMM sequence (Field of View: 300mm, slice thickness 6mm, tag separation 7mm, typical TR/TE 30/ 1.26ms, Flip Angle 20°, 20 phases). Peak circumferential (Ecc) and radial (Err) strains were determined using inTag (Creatis, Lyon, France). Mid-ventricular short-axis T1 maps were acquired using the Modified Look-Locker Inversion Recovery sequence pre-gadolinium bolus and then at 5, 7, 9, 11, 15, 20 and 25 minutes. Signal intensity-time curves for myocardial and blood pool regions of interest were used to determine T1 relaxation times through a non-linear curve-fit (CMR42, Circle Cardiovascular Imaging, Calgary, Canada). The partition coefficient at equilibrium, an index of fibrosis, was determined by plotting the reciprocal of myocardial T1 times at equilibrium against those for the blood pool and calculating the slope of the resultant linear regression line. Results HCM patients were older than the controls and there was a preponderance of men. In keeping with their diagnosis, HCM patients had significantly higher indexed LV mass and wall thickness than controls (Table 1). The partition coefficient was significantly higher in HCM patients than controls (mean ±SD: 0.439 ±0.230 for HCM vs 0.281 ±0.071 for controls, P=0.02). Whilst peak global Ecc was significantly lower in the HCM group relative to the controls (0.173 ±0.041 vs 0.226 ±0.025, P<0.001), there was no significant difference with respect to peak global Err (0.154 ±0.06 vs 0.134 ±0.051, P=0.25). No significant association was found between the partition coefficient and either circumferential or radial strain. Conclusions The partition coefficient for gadolinium was significantly raised in patients with HCM relative to controls, however, no association was found between this and local contractile function. This implies that interstitial fibrosis alone may not account for the perturbations in myocardial mechanics seen in patients with HCM and that alternative mechanisms should be explored.

Phantom validation of 17 and 11 heartbeat MOLLI T1 mapping sequence at 3T

Background and objective The Modified Look-Locker Inversion-Recovery (MOLLI) sequence (Messroghli, et al, JMRI, 2007) was optimized for myocardial T1 mapping on 1.5T. However, little data exists on T1 mapping at 3T. The standard MOLLI sequence uses three inversion-recovery blocks to acquire 11 images over 17 heartbeats (HB). The long breath hold could limit its clinical application in patients with cardiorespiratory compromise. A new 11 HB MOLLI protocol with two inversion-recovery blocks was introduced recently, which reduces scan time by 35%. This aim of this study is to verify both 17 HB and 11 HB MOLLI sequences at 3T.

Quantitative T1-maps delineate myocardium at risk as accurately as T2-maps - experimental validation with microspheres

Methods Dogs (n=12) underwent coronary occlusion (2 hours), during which microspheres were injected into the left atrium, followed by reperfusion (4 hours). The entire left ventricle was imaged at 1.5T (Siemens) in contiguous short-axis slices with a Modified Look-Locker Inversion-recovery sequence for T1 mapping (Messroghli, JMRI, 2007), and a T2-prepared SSFP sequence for T2 mapping (Giri, JCMR, 2009). Myocardium at risk was defined as regions in the left ventricle which had a T1 or T2 value greater than 2SD from remote. In four dogs, hearts were excised and blood flow (ml/min/g) was determined by microsphere analysis in 16 sectors per short-axis slice for all short-axis slices in the left ventricle. Myocardium at risk was defined as regions in the left ventricle with a blood flow at occlusion less than 2SD from remote. Results Global myocardium at risk, expressed as percent of left ventricular mass (%LVM), showed similar results for T1 mapping compared to T2 mapping (n=12, mean+/SD difference 1.5+/-4.0 %LVM, R2=0.86, p<0.001). On a slice-by-slice basis (n=4 dogs, 34 slices), myocardium at risk was also similar for T1 and T2 mapping (difference 0.4+/-7.6 % of slice, R2=0.96, p<0.001), T1 mapping corresponded to microsphere analysis (mean difference 2.0+/-12.8 % of slice, R2=0.90, p<0.001), and T2 mapping corresponded to microsphere analysis (mean difference 1.6+/-13.8 % of slice, R2=0.86, p<0.001). Figure 1. Conclusions When it comes to determining myocardium at risk after coronary ischemia and reperfusion, clinical non-contrast T1 mapping and T2 mapping sequences yield similar results, and both correspond excellently to microspheres. It appears that the relaxation properties T1 and T2 both change in a way which is consistent with the myocardial edema which occurs following myocardial ischemia/reperfusion.