Daniel Messroghli

Modified Look-Locker inversion recovery (MOLLI) for high-resolution T1 mapping of the heart.

A novel pulse sequence scheme is presented that allows the measurement and mapping of myocardial T1 in vivo on a 1.5 Tesla MR system within a single breath‐hold. Two major modifications of conventional Look‐Locker (LL) imaging are introduced: 1) selective data acquisition, and 2) merging of data from multiple LL experiments into one data set. Each modified LL inversion recovery (MOLLI) study consisted of three successive LL inversion recovery (IR) experiments with different inversion times. We acquired images in late diastole using a single‐shot steady‐state free‐precession (SSFP) technique, combined with sensitivity encoding to achieve a data acquisition window of <200 ms duration. We calculated T1 using signal intensities from regions of interest and pixel by pixel. T1 accuracy at different heart rates derived from simulated ECG signals was tested in phantoms. T1 estimates showed small systematic error for T1 values from 191 to 1196 ms. In vivo T1 mapping was performed in two healthy volunteers and in one patient with acute myocardial infarction before and after administration of Gd‐DTPA. T1 values for myocardium and noncardiac structures were in good agreement with values available from the literature. The region of infarction was clearly visualized. MOLLI provides high‐resolution T1 maps of human myocardium in native and post‐contrast situations within a single breath‐hold. Magn Reson Med 52:141–146, 2004.

Delayed Enhancement and T2-Weighted Cardiovascular Magnetic Resonance Imaging Differentiate Acute From Chronic Myocardial Infarction

Background—Delayed enhancement (DE) cardiovascular magnetic resonance (CMR) detects acute and chronic myocardial infarction (MI) by visualizing contrast media accumulation in infarcted segments. T2-weighted CMR depicts infarct-related myocardial edema as a marker of acute but not chronic myocardial injury. We investigated the clinical utility of an approach combining both techniques to differentiate acute from chronic MI. Methods and Results—Seventy-three MI patients were studied in 2 groups. Group A consisted of 15 acute MI patients who were studied twice, on day 1 and 3 months after MI. In group B, 58 patients with acute or chronic MI underwent 1 CMR scan. T2-weighted and DE images of matched slices were acquired on a 1.5-T system. In group A, quantitative segmental and region of interest–based analyses were performed to observe signal changes between the acute and chronic phases. In group B, T2-weighted and DE images were examined visually by 2 blinded observers for the presence or absence of hyperintense areas in corresponding segments. For infarct localization, coronary angiography and/or ECG changes served as the reference standard. In group A, the contrast-to-noise ratio on T2-weighted images dropped in the infarcted segments from 2.7±1.1 on day 1 to 0.1±1.2 after 3 months (P <0.0001). There was no significant change in contrast-to-noise ratio in DE images (1.9±1.5 versus 1.3±1.0; P =NS). The qualitative assessment of T2-weighted and DE images in group B yielded a specificity of 96% to differentiate acute from chronic lesions. Conclusions—An imaging approach combining DE and T2-weighted CMR accurately differentiates acute from chronic MI.

Myocardial T1 mapping and extracellular volume quantification: a Society for Cardiovascular Magnetic Resonance (SCMR) and CMR Working Group of the European Society of Cardiology consensus statement

Rapid innovations in cardiovascular magnetic resonance (CMR) now permit the routine acquisition of quantitative measures of myocardial and blood T1 which are key tissue characteristics. These capabilities introduce a new frontier in cardiology, enabling the practitioner/investigator to quantify biologically important myocardial properties that otherwise can be difficult to ascertain clinically. CMR may be able to track biologically important changes in the myocardium by: a) native T1 that reflects myocardial disease involving the myocyte and interstitium without use of gadolinium based contrast agents (GBCA), or b) the extracellular volume fraction (ECV)–a direct GBCA-based measurement of the size of the extracellular space, reflecting interstitial disease. The latter technique attempts to dichotomize the myocardium into its cellular and interstitial components with estimates expressed as volume fractions. This document provides recommendations for clinical and research T1 and ECV measurement, based on published evidence when available and expert consensus when not. We address site preparation, scan type, scan planning and acquisition, quality control, visualisation and analysis, technical development. We also address controversies in the field. While ECV and native T1 mapping appear destined to affect clinical decision making, they lack multi-centre application and face significant challenges, which demand a community-wide approach among stakeholders. At present, ECV and native T1 mapping appear sufficiently robust for many diseases; yet more research is required before a large-scale application for clinical decision-making can be recommended.

Myocardial T1 mapping: Application to patients with acute and chronic myocardial infarction

T1 maps obtained with modified Look‐Locker inversion recovery (MOLLI) can be used to measure myocardial T1. We aimed to evaluate the potential of MOLLI T1 mapping for the assessment of acute and chronic myocardial infarction (MI). A total of 24 patients with a first MI underwent MRI within 8 days and after 6 months. T1 mapping was performed at baseline and at selected intervals between 2–20 min following administration of gadopentetate dimeglumine (Gd‐DTPA). Delayed‐enhancement (DE) imaging served as the reference standard for delineation of the infarct zone. On T1 maps the myocardial T1 relaxation time was assessed in hyperenhanced areas, hypoenhanced infarct cores, and remote myocardium. The planimetric size of myocardial areas with standardized T1 threshold values was measured. Acute and chronic MI exhibited different T1 changes. Precontrast threshold T1 maps detected segmental abnormalities caused by acute MI with 96% sensitivity and 91% specificity. Agreement between measurements of infarct size from T1 mapping and DE imaging was higher in chronic than in acute infarcts. Precontrast T1 maps enable the detection of acute MI. Acute and chronic MI show different patterns of T1 changes. Standardized T1 thresholds provide the potential to dichotomously identify areas of infarction. Magn Reson Med 58:34–40, 2007.

Optimization and validation of a fully-integrated pulse sequence for modified look-locker inversion-recovery (MOLLI) T1 mapping of the heart.

To optimize and validate a fully‐integrated version of modified Look‐Locker inversion‐recovery (MOLLI) for clinical single‐breathhold cardiac T1 mapping.

Detection of Acutely Impaired Microvascular Reperfusion After Infarct Angioplasty With Magnetic Resonance Imaging

Background—Despite the reopening of the infarct-related artery (IRA) with infarct angioplasty, complete microvascular reperfusion does not always ensue. Methods and Results—We performed cardiovascular MRI (CMR) in 20 acute myocardial infarction (AMI) patients within 24 hours of successful infarct angioplasty and 10 control patients without obstructive coronary artery disease on a clinical 1.5-T CMR scanner. Three-month follow-up CMR in AMI patients evaluated the impact of abnormal reperfusion on recovery of function. Infarction was localized by delayed contrast hyperenhancement and impaired systolic thickening. Microvascular perfusion was assessed at rest by first-pass perfusion CMR after a bolus of gadolinium-DTPA by use of the time to 50% maximum myocardial enhancement. Whereas contrast wash-in was homogeneous in control patients, AMI patients exhibited delays in the hypokinetic region subtended by the IRA compared with remote segments in 19 of 20 patients, with a mean contrast delay of 0.9±0.1 seconds (95% CI, 0.6 to 1.2 seconds). At follow-up, the mean recovery of systolic thickening was lower in segments with a contrast delay of 2 seconds or more (10±7% versus 39±4%, P =0.001). A contrast delay ≥2 seconds and infarction >75% transmurally were independent predictors of impaired left ventricular systolic thickening at 3 months (P =0.002 for severe contrast delay, P =0.048 for >75% for transmural infarction). Conclusions—CMR detects impaired microvascular reperfusion in AMI patients despite successful infarct angioplasty, which when severe is associated with a lack of recovery of wall motion.

Cardiac magnetic resonance monitors reversible and irreversible myocardial injury in myocarditis

OBJECTIVES We sought to assess the value of cardiac magnetic resonance (CMR) to monitor the spectrum of myocarditis-related injuries over the course of the disease. BACKGROUND Myocarditis is associated with a wide range of myocardial tissue injuries, both reversible and irreversible. Differentiating these types of injuries is a clinical demand. METHODS We studied 36 patients (31 males, age 33 +/- 14 years) hospitalized with myocarditis during the acute phase and 18 +/- 10 months thereafter. CMR was performed on 2 1.5T scanners and included the following techniques: steady-state free precession (to assess left ventricular function and volumes), T2-weighted (myocardial edema), early (global relative enhancement [gRE], reflecting increased capillary leakage) and late T1-weighted after gadolinium-DTPA injection (late gadolinium enhancement [LGE], reflecting irreversible injury). RESULTS In the acute phase, T2 ratio was elevated in 86%, gRE in 80%, and LGE was present in 63%. At follow-up, ejection fraction increased from 56 +/- 8% to 62 +/- 7% (p < 0.0001) while both T2 ratio (2.4 +/- 0.5 to 1.9 +/- 0.2; p < 0.0001) and gRE (7.6 +/- 8 to 4.4 +/- 4; p = 0.018) significantly decreased. LGE persisted in all but 1 patient in whom LGE completely resolved. No patient had simultaneous elevation of T2 and gRE during the convalescent phase, resulting in a negative predictive value of 100% to differentiate the 2 phases of the disease. The acute phase T2 ratio correlated significantly with the change of end-diastolic volume over time (beta = 0.47; p = 0.008). This relation remained significant in a stepwise regression analysis model including T2 ratio, gRE, LGE extent, baseline ejection fraction, age, and creatine kinase, in which only T2 emerged as an independent predictor of the change in end-diastolic volume. CONCLUSIONS A comprehensive CMR approach is a useful tool to monitor the reversible and irreversible myocardial tissue injuries over the course of myocarditis and to differentiate acute from healed myocarditis in patients with still-preserved ejection fraction.

T1 Mapping in Patients with Acute Myocardial Infarction

Pixel-by-pixel calculation of T1 values (T1 mapping) has been used in different tissues to focus on T1 changes in a quantitative fashion. The aim of this study was to establish T1 mapping of human myocardium on a 1.5 Tesla system and to examine its diagnostic potential in patients with acute myocardial infarction (AMI). 8 patients with reperfused AMI (day 3 +/- 1) underwent multi-breath-hold MRI in a 1.5 Tesla system. Sets of five images with varying T1 weighting were acquired prior to and after the administration of contrast agent to generate images from calculated T1 values (T1 mapping). Prior to the contrast agent administration, all patients showed T1 prolongation in the area of infarction, which was identified in separate measurements using the delayed enhancement approach. Compared to noninfarcted areas, T1 values in the infarcted areas were increased by 18 +/- 7% (SE, p < 0.05). The spatial extent of the area of T1 prolongation was larger than that of the hyper-enhanced areas in conventional contrast-enhanced images. T1 maps obtained after the application of Gadolinium-DTPA revealed a T1 reduction of 27 +/- 4% in infarcted tissue compared to noninfarcted areas (p < 0.05). The areas showing T1 reduction were in agreement with the hyper-enhanced regions in conventional T1-weighted images. T1 mapping visualizes changes in the longitudinal relaxation time induced by AMI. T1 mapping can detect myocardial necrosis without the use of contrast media. Information that can be extracted from a combination of pre- and postcontrast T1 maps exceeds that from conventional contrast studies.

Assessment of Diffuse Myocardial Fibrosis in Rats Using Small-Animal Look-Locker Inversion Recovery T1 Mapping

Background— The concentration of gadopentetate dimeglumine in myocardium and blood can be assessed from T1 measurements and can be used to calculate the extracellular volume (ECV) of the myocardium. We hypothesized that diffuse myocardial fibrosis in a small-animal model could be quantitatively assessed by measuring myocardial ECV using small-animal Look-Locker inversion recovery T1 mapping. Methods and Results— Sprague-Dawley rats (n=10) were subjected to continuous angiotensin-2 (AT2) infusion for 2 weeks via a subcutaneously implanted minipump system. Magnetic resonance imaging (MRI) was performed both before and after AT2 infusion. The MRI protocol included multislice cine imaging and before-and-after contrast small-animal Look-Locker inversion recovery T1 mapping and late gadolinium enhancement imaging. Myocardial ECV was calculated from hematocrit and T1 values of blood and myocardium. During the course of AT2 infusion, the mean±SD systolic blood pressure increased from 122±10.9 to 152±27.5 mm Hg (P=0.003). Normalized heart weight was significantly higher in AT2-treated animals than in control littermates (P=0.033). Cine MRI documented concentric left ventricular hypertrophy. Postcontrast myocardial T1 times were shortened after treatment (median [interquartile range], 712 [63] versus 820 [131] ms; P=0.002). Myocardial ECV increased from 17.2% (4.3%) before to 23.0% (6.2%) after AT2 treatment (P=0.031), which was accompanied by perivascular fibrosis and microscarring on myocardial histological analysis. There was a moderate level of correlation between ECV and collagen volume fraction, as assessed by histological analysis (r=0.69, P=0.013). Conclusions— In a small-animal model of left ventricular hypertrophy, contrast-enhanced T1 mapping can be used to detect diffuse myocardial fibrosis by quantification of myocardial ECV.

Cardiovascular magnetic resonance of acute myocardial infarction at a very early stage.

OBJECTIVES Very early changes in myocardial tissue composition during acute myocardial infarction (AMI) are difficult to assess in vivo. Cardiovascular magnetic resonance (CMR) imaging provides techniques for visualizing tissue pathology. BACKGROUND The diagnostic role of CMR in very acute stages of myocardial infarction is uncertain. We investigated signal intensity changes beginning within 60 min after acute coronary occlusion in patients undergoing therapeutic septal artery embolization. METHODS We investigated eight patients with hypertrophic obstructive cardiomyopathy undergoing interventional septal artery embolization by applying microparticles to reduce left ventricular outflow tract obstruction. In a clinical 1.5-tesla (T) CMR system, we visualized infarct-related myocardial signal by T(1)-weighted sequences before and 20 min after administration of contrast media (delayed enhancement) and edema-related signal by T(2)-weighted spin-echo sequences before and 58 +/- 14 min after the intervention as well as on days 1, 3, 7, 14, 28, 90, and 180 during follow-up. RESULTS Infarct-related changes as defined by contrast enhancement were observed as early as 1 h after the intervention and during six months of follow-up. In contrast, infarct-related myocardial edema, as visualized by high signal intensity in T(2)-weighted spin-echo sequences, was not consistently detectable 1 h after acute arterial occlusion; this was possible in all subsequent studies until day 28. CONCLUSIONS Contrast-enhanced magnetic resonance imaging detected infarct-related signal changes as early as 1 h after AMI in humans, whereas the sensitivity of edema-related signal changes was not sufficient during this very early stage.