Purpose:To determine the utility of cardiac magnetic resonance (MR) T1 mapping for quantification of diffuse myocardial fibrosis compared with the standard of endomyocardial biopsy. Materials and Methods:This HIPAA-compliant study was approved by the institutional review board. Cardiomyopathy patients were retrospectively identified who had undergone endomyocardial biopsy and cardiac MR at one institution during a 5-year period. Forty-seven patients (53% male; mean age, 46.8 years) had undergone diagnostic cardiac MR and endomyocardial biopsy. Thirteen healthy volunteers (54% male; mean age, 38.1 years) underwent cardiac MR as a reference. Myocardial T1 mapping was performed 10.7 minutes 6 2.7 (standard deviation) after bolus injection of 0.2 mmol/kg gadolinium chelate by using an inversion-recovery Look-Locker sequence on a 1.5-T MR imager. Late gadolinium enhancement was assessed by using gradientecho inversion-recovery sequences. Cardiac MR results were the consensus of two radiologists who were blinded to histopathologic findings. Endomyocardial biopsy fibrosis was quantitatively measured by using automated image analysis software with digital images of specimens stained with Masson trichrome. Histopathologic findings were reported by two pathologists blinded to cardiac MR findings. Statistical analyses included Mann-Whitney U test, analysis of variance, and linear regression. Results:Median myocardial fibrosis was 8.5% (interquartile range, 5.7-14.4). T1 times were greater in control subjects than in patients without and in patients with evident late gadolinium enhancement (466 msec 6 14, 406 msec 6 59, and 303 msec 6 53, respectively; P , .001). T1 time and histologic fibrosis were inversely correlated (r = 20.57; 95% confidence interval: 20.74, 20.34; P , .0001). The area under the curve for myocardial T1 time to detect fibrosis of greater than 5% was 0.84 at a cutoff of 383 msec. Conclusion:Cardiac MR with T1 mapping can provide noninvasive evidence of diffuse myocardial fibrosis in patients referred for evaluation of cardiomyopathy.q RSNA, 2012

Hypertrophic cardiomyopathy (HCM) is the most common genetic disease of the heart. HCM is characterized by a wide range of clinical expression, ranging from asymptomatic mutation carriers to sudden cardiac death as the first manifestation of the disease. Over 1000 mutations have been identified, classically in genes encoding sarcomeric proteins. Noninvasive imaging is central to the diagnosis of HCM and cardiovascular magnetic resonance (CMR) is increasingly used to characterize morphologic, functional and tissue abnormalities associated with HCM. The purpose of this review is to provide an overview of the clinical, pathological and imaging features relevant to understanding the diagnosis of HCM. The early and overt phenotypic expression of disease that may be identified by CMR is reviewed. Diastolic dysfunction may be an early marker of the disease, present in mutation carriers prior to the development of left ventricular hypertrophy (LVH). Late gadolinium enhancement by CMR is present in approximately 60% of HCM patients with LVH and may provide novel information regarding risk stratification in HCM. It is likely that integrating genetic advances with enhanced phenotypic characterization of HCM with novel CMR techniques will importantly improve our understanding of this complex disease.

PURPOSE To evaluate the relationship between “Look-Locker” (LL) and modified Look-Locker Inversion recovery (MOLLI) approaches for T1 mapping of the myocardium. MATERIALS AND METHODS 168 myocardial T1 maps using MOLLI and 165 maps using LL were obtained in human subjects at 1.5 Tesla. The T1 values of the myocardium were calculated before and at five time points after gadolinium administration. All time and heart rate normalizations were done. The T1 values obtained were compared to determine the absolute and bias agreement. RESULTS The pre-contrast global T1 values were similar when measured by the LL and by MOLLI technique (mean 1004.9 ms +/- 120.3 vs. 1034.1 ms +/- 53.1, respectively, p = 0.26). Post-contrast myocardial T1 time from LL was significantly longer than MOLLI from 5 to 25 minutes (mean difference, LL - MOLLI was +61.8 +/- 46.4 ms, p < 0.001). No significant differences in T1 values were noted between long and short axis measurements for either MOLLI or LL. CONCLUSION Post-contrast LL and MOLLI showed very good agreement, although LL vaules are higher than MOLLI. Pre-contrast T1 values showed good agreement, however LL has greater limits of agreement. Short and long axis planes can reliably assess T1 values.

ABSTRACT. Delayed enhancement cardiac magnetic resonance (DE-CMR) imaging is used increasingly to identify and quantify focal myocardial scar. Our objective is to describe factors used in the interpretation of DE-CMR images and to highlight potential pitfalls and artefacts that mimic myocardial scar. Inversion recovery gradient recalled echo sequence is commonly accepted as the standard of reference for DE-CMR. There are also alternative sequences that can be performed in a single breath-hold or with free breathing. Radiologists need to be aware of factors affecting image quality, and potential pitfalls and artefacts that may generate focal hyperintense areas that mimic myocardial scar. Delayed enhancement cardiac magnetic resonance (DE-CMR) imaging can identify the presence, location and extent of myocardial scar (dense myocardial fibrosis) due to ischaemic and non-ischaemic heart diseases. This technique is also called late gadolinium-enhanced MRI (LGE-MRI), myocardial delayed enhanced (MDE) MRI and delayed hyperenhanced MRI (DHE-MRI) in the literature. DE-CMR has been shown to be more sensitive than other imaging methods in detecting small subendocardial infarctions [1] and has recently been used in population-based studies to assess the presence of myocardial scar [2,3]. The technique is relatively straightforward to implement, and images can be interpreted visually for the presence of myocardial scar (hyperenhanced region) without the need for post-processing.This article is intended to describe quality control procedures, factors affecting image quality, assessment of myocardial scar, and potential pitfalls and artefacts causing focal hyperintensities that mimic myocardial scar in delayed enhancement imaging.

Myocardial steatosis is unrelated to hepatic, adipocyte, or peripheral insulin sensitivity. Although it is frequently observed in insulin-resistant subjects, further studies are necessary to identify and delineate pathogenic mechanisms that differentially affect cardiac and hepatic steatosis.

Background: Current guidelines for the primary prevention of atherosclerotic cardiovascular disease are based on the estimation of a predicted 10-year cardiovascular disease risk and the average relative risk reduction estimates from statin trials. In the clinical setting, however, decision-making is better informed by the expected benefit for the individual patient, which is typically lacking. Consequently, a personalized statin benefit approach based on absolute risk reduction over 10 years (ARR₁₀ benefit threshold ≥2.3%) has been proposed as a novel approach. However, how this benefit threshold relates with coronary plaque burden in asymptomatic individuals with low/intermediate cardiovascular disease risk is unknown. Aims: In this study, we compared the predicted ARR₁₀ obtained in each individual with plaque burden detected by coronary computed tomography angiography. Methods and Results: Plaque burden (segment volume score, segment stenosis score, and segment involvement score) was assessed in prospectively recruited asymptomatic subjects (n = 70; 52% male; median age 56 years [interquartile range 51–64 years]) with low/intermediate Framingham risk score (< 20%). The expected ARR₁₀ with statin in the entire cohort was 2.7% (1.5–4.6%) with a corresponding number needed to treat over 10 years of 36 (22–63). In subjects with an ARR₁₀ benefit threshold ≥2.3% (vs. < 2.3%), plaque burden was significantly higher (p = 0.02). Conclusion: These findings suggest that individuals with higher coronary plaque burden are more likely to get greater benefit from statin therapy even among asymptomatic individuals with low cardiovascular risk.

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