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To compare the image quality of coronary CT angiography (CTA) studies between standard filtered back projection (FBP) and adaptive iterative dose reduction in three-dimensions (AIDR3D) reconstruction using CT noise additional software to simulate reduced radiation exposure. Images from 93 consecutive clinical coronary CTA studies were processed utilizing standard FBP, FBP with 50 % simulated dose reduction (FBP50 %), and AIDR3D with simulated 50 % dose reduction (AIDR50 %). Signal-to-noise ratio (SNR) and contrast-to-noise ratio (CNR) were measured within 5 regions-of-interest, and image quality for each reconstruction strategy was assessed by two independent readers using a 4-point scale. Compared to FBP, the SNR measured from the AIDR50 % images was similar or higher (airway: 38.3 ± 12.7 vs. 38.5 ± 14.5, p = 0.81, fat: 5.5 ± 1.9 vs. 5.4 ± 2.0, p = 0.20, muscle: 3.2 ± 1.2 vs. 3.1 ± 1.3, p = 0.38, aorta: 22.6 ± 9.4 vs. 20.2 ± 9.7, p

Background The Systemic Capillary Leak Syndrome (SCLS) is a rare disorder of unknown etiology presenting as recurrent episodes of shock and peripheral edema due to leakage of fluid into soft tissues. Insights into SCLS pathogenesis are few due to the scarcity of cases, and the etiology of vascular barrier disruption in SCLS is unknown. Recent advances in cardiovascular magnetic resonance (CMR) allow for the quantitative assessment of the myocardial extracellular volume (ECV), which can be increased in conditions causing myocardial edema. We hypothesized that measurement of myocardial ECV may detect myocardial vascular leak in patients with SCLS. Methods Fifty-six subjects underwent a standard CMR examination at the NIH Clinical Center from 2009 until 2014: 20 patients with acute intermittent SCLS, six subjects with chronic SCLS, and 30 unaffected controls. Standard volumetric measurements; late gadolinium enhancement imaging and pre- and post-contrast T1 mapping were performed. ECV was calculated by calibration of pre- and post-contrast T1 values with blood hematocrit. Results Demographics and cardiac parameters were similar in both groups. There was no significant valvular disorder in either group. Subjects with chronic SCLS had higher pre-contrast myocardial T1 compared to healthy controls (T1: 1027 ± 44 v. 971 ± 41, respectively; p = 0.03) and higher myocardial ECV than patients with acute intermittent SCLS or controls: 33.8 ± 4.6, 26.9 ± 2.6, 26 ± 2.4, respectively; p = 0.007 v. acute intermittent; P = 0.0005 v. controls). When patients with chronic disease were analyzed together with five patients with acute intermittent disease who had just experienced an acute SCLS flare, ECV values were significantly higher than in subjects with acute intermittent SCLS in remission or age-matched controls and (31.2 ± 4.6 %, 26.5 ± 2.7 %, 26 ± 2.4 %, respectively; p = 0.01 v. remission, p = 0.001 v. controls). By contrast, T1 values did not distinguish these three subgroups (1008 ± 40, 978 ± 40, 971 ± 41, respectively, p = 0.2, active v. remission; p = 0.06 active v. controls). Abundant myocardial edema without evidence of acute inflammation was detected in cardiac tissue postmortem in one patient. Conclusions Patients with active SCLS have significantly higher myocardial ECV than age-matched controls or SCLS patients in remission, which correlated with histopathological findings in one patient.

Author(s): Liu, Songtao; Liu, Chia-Ying; Han, Jing; Turkbey, Evrim B; Liu, Yuan; Bild, Diane; Arai, Andrew E; McClelland, Robyn; Hundley, W; Gomes, Antoinette S; Tracy, Russell; Kronmal, Richard; Lima, Joao A; Bluemke, David A

Background Duchenne muscular dystrophy (DMD) cardiomyopathy is a progressive disease for which there is no cure. Disease-specific therapies are needed that can be initiated before irreversible myocardial damage ensues. In order to evaluate therapeutic efficacy, surrogate endpoints other than ejection fraction must be found. The hypothesis of this study is that T1 and extracellular volume fraction (ECV) mapping using cardiovascular magnetic resonance (CMR) can detect diffuse extracellular matrix expansion in DMD patients with normal left ventricular ejection fraction (LVEF) and without myocardial late gadolinium enhancement (LGE). Methods Thirty-one DMD and 11 healthy control participants were prospectively enrolled. CMR using a modified Look-Locker (MOLLI) sequence was performed in all participants before and after contrast administration. T1 and ECV maps of the mid left ventricular myocardium were generated and regions of interest were contoured using the standard 6-segment AHA model. Global and segmental values were compared between DMD and controls using a Wilcoxon rank-sum test. Results The DMD participants had significantly higher mean native T1 compared with controls (1045 ms vs 988 ms, p = 0.001). DMD participants with normal LVEF and without evidence of LGE also demonstrated elevated mean native T1 (1039 ms vs 988 ms, p = 0.002, and 1038 ms vs 988 ms, p = 0.011). DMD participants had a significantly greater mean ECV than controls (0.31 vs 0.24, p

Since 1948, epidemiology studies played an important role in understanding cardiovascular disease and afforded an opportunity to learn about newer diagnostic tests. In 2000, the MESA Study incorporated several advanced cardiovascular imaging modalities including cardiac magnetic resonance imaging (MRI) and coronary artery calcium scans. The decade of follow-up enabled prognosis studies, an important step beyond association studies. In brief, left ventricular hypertrophy by cardiac MRI predicted incident heart failure and stroke. In the MESA Study, coronary artery calcium was a better predictor of coronary artery disease end points than the non-contrast-enhanced MRI scan. In the ICELAND MI substudy of the AGES-Reykjavik Study, a contrast-enhanced MRI scan detected many more unrecognized myocardial infarctions (MIs) (UMIs) than detected by electrocardiography and documented these UMI had adverse prognostic significance. Thus, cardiac MRI has been successfully incorporated into large population studies and shown added value over conventional measurements of cardiovascular disease.

Background T2-weighted enhancement depicts the myocardial area at risk (AAR) associated with coronary occlusion. However, the severity of blood flow abnormality required to cause a detectable elevation in myocardial T2 is unknown. The aim of this study was to use microspheres to determine the severity of reduction in myocardial blood flow that results in visually detectable T2 weighted enhancement. Methods Surface coil intensity corrected T2 prepared SSFP at 1.5T was performed after 2 hours of coronary occlusion followed by 4 hours of reperfusion in a canine model. Myocardial blood flow during ischemia was determined by administering microspheres. A mid-ventricular short axis slice of the heart was divided into 16 transmural sectors for microsphere analysis. MR images were matched to the pathological slices at the sector level using papillary muscles and RV insertion as landmarks. ROIs delineated T2-enhanced and remote regions of the MR images and measurements were compared with microsphere blood flows. Results were reported as median (interquartile range [IQ]) and compared using the signed Wilcoxon rank test. Each T2-prepared sector was classified as bright (AAR) or normal (remote) by 2 independent readers and compared with absolute microsphere blood

Methods ICELAND-MI is a nested cohort of the Age, Gene/ Environment Susceptibility-Reykjavik Study of community-dwelling older adults that intentionally oversampled diabetic subjects. After excluding subjects with pre-existing heart failure, the cohort size was 900. CMR was used to detect myocardial infarction (MI), major patterns of non-ischemic patterns of LGE as defined by Vohringer (Herz 2007;32:129-37), and minor patterns of non-ischemic LGE including LGE near the aortic root, mitral annulus, or right ventricular insertion points. The composite end-point was adjudicated hospitalization for heart failure and death.

Methods Forty-seven patients had 1.5T steady state free precession, regadenoson stress perfusion CMR and either a ≤ 30% coronary narrowing by CT angiography (CTA) or a ≥70% stenosis by invasive coronary angiography (ICA). CMR perfusion pixel maps were generated by a modelconstrained deconvolution with and without the myocardial segmentation. The two independent observers were blinded to clinical information.

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

Summary The Food and Drug Administration (FDA) has recently recommended that the label dose of Gadolinium (Gd)based contrast agents (GBCA) not be exceeded. The primary concern for high dose GBCAs application is nephrogenic systemic fibrosis (NSF). For the majority of conventional GBCA, the label dose is 0.1 mmol/kg. GBCA use for evaluation of myocardial disease is currently considered off-label use in the United States. Little information is present in the literature regarding optimal GBCA dose for CMR. Therefore, we evaluated the current status of GBCA use for CMR of the myocardium as presented in the peer-reviewed literature, emphasizing trends before and after nephrogenic fibrosis guidelines were issued in 2008. This meta-analysis showed that the median GBCA dose for English peer reviewed publications on CMR (19,934 patients) was 0.2 mmol/kg. Further, no change in mean or median gadolinium dose was present before, versus after the FDA issued GBCA black box warnings (p>0.05). This appears surprising, given the amount of attention and many publications regarding NSF. It remains to be seen if future CMR studies will incorporate and report lower gadolinium doses. Clinical trials should be supported to determine the appropriate doses of gadolinium enhancement of the myocardium. Background Myocardial delayed enhancement MRI was originally validated using higher than label-recommended doses of gadolinium chelate. The objective of this study was to evaluate available evidence for various gadolinium dosing regimens used for cardiac MRI. The relationship of gadolinium dose warnings (due to nephrogenic systemic fibrosis) announced in 2008 to gadolinium dosing regimens was also examined. Methods

Background Isolated anomalous pulmonary venous return of one pulmonary vein is relatively rare (~1/1000) and has an unclear natural history. Patients with Turner syndrome (TS) have a relatively high incidence of partial anomalous pulmonary venous return (PAPVR). Our aim is to describe the natural history of unrepaired isolated anomalous pulmonary venous return and its hemodynamic consequences through analysis of cardiac volumetric data and Qp:Qs ratios in asymptomatic volunteers with TS.

Background Patients with sickle cell disease (SCD) and pulmonary hypertension (PH) have increased mortality. SCD-PH is often complicated by high cardiac output (CO) related to anemia. The transpulmonary gradient (TPG) reflects a pressure differential across the pulmonary vascular bed without the confounding effect of CO (PVR=TPG/CO). Based on the cardiac transplant literature, a TPG ≥ 12 mmHg indicates significant pulmonary arterial hypertension (PAH). With PH, there is often morphologic adaptation by the right ventricle (RV). In idiopathic PAH, RV dilation and decreased function have been correlated with poor prognosis. We hypothesize that patients with SCD and a TPG ≥ 12 mmHg would have lower functional capacity, increased mortality, and evidence of RV dysfunction on cardiac MRI (CMR).

Background Quantitative first pass cardiac magnetic resonance (CMR) perfusion imaging has shown excellent interobserver agreement at a sector level in healthy volunteers and patients. In this study, we compare the myocardial blood flow (MBF) estimates in sector-wise and pixel-wise analysis. We also study the interobserver variability in pixel-wise MBF estimates from patients with coronary artery disease (CAD). Methods

Background We have previously proposed an automatic solution to calculate semi-quantitative measurbes of myocardial perfusion and to present them to the user as parametric maps. Such maps have high spatial resolution which can potentially be an advantage when evaluating small regions of myocardium. On the other hand, per-segment analyses potentially benefit from higher SNR and improved clarity of presentation.

MOCO, a non-rigid image registration algorithm, can minimize myocardial motion and shape changes caused by respiration, arrhythmia, or imperfect gating. A potential benefit of this technique is to enable automated quantitative analysis. On the other hand, MOCO could introduce artifacts and adversely impact diagnostic image quality.

Background A low excitation flip angle (α

Background Pixel-wise quantitative analysis of cardiovascular magnetic resonance (CMR) perfusion images allows myocardial blood flow (MBF) to be measured at the level of approximately 30 μL of myocardium. However B1-field inhomogeneity, induced by phased array surface receiver coils, potentially confounds MBF measurements. The aim of this study was to compare the effect of: 1. no surface coil intensity correction (No-SCIC); 2. SCIC performed using saturation recovery steady-state free precession images (SSFP-SCIC); and 3. SCIC performed using proton density-weighted images (PD-SCIC); on pixel-wise measurements of MBF in patients with confirmed significant coronary artery disease (CAD) and healthy volunteers. Methods 26 subjects, comprising 18 patients (11 male; age 58 ± 12 years) with significant CAD (> 70% stenosis on invasive coronary angiography) in 1 (56%) or 2 (44%) major epicardial arteries (78% LAD, 50% RCA, 17% Cx) and 8 healthy volunteers (7 male; age 24 ± 10 years), were included. Perfusion imaging was performed using a motion-corrected saturation recovery steady-state free precession, dual sequence method at 1.5T (Espree, Siemens Medical Solutions) during Regadenoson vasodilator stress and at rest, using 0.05 mmol/kg Gadolinium-DTPA. A proton density-weighted image was acquired at the beginning of the perfusion sequence. B1-field inhomogeneity was approximated using a third-order surface fit to myocardial and body signal intensities on the PD image or the first SSFP image. The estimated intensity bias field was

Aims Cardiovascular magnetic resonance (CMR) imaging can measure the myocardial area at risk (AAR), but the technique has received criticism for inadequate validation. CMR commonly depicts an AAR that is wider than the infarct, which in turn would require a lateral perfusion gradient within the AAR. We investigated the presence of a lateral perfusion gradient within the AAR and validated CMR measures of AAR against three independent reference standards of high quality. Methods and results Computed tomography (CT) perfusion imaging, microsphere blood flow analysis, T1-weighted 3T CMR and fluorescent microparticle pathology were used to investigate the AAR in a canine model ( n = 10) of ischaemia and reperfusion. AAR size by CMR correlated well with CT ( R 2 = 0.80), microsphere blood flow ( R 2 = 0.80), and pathology ( R 2 = 0.74) with good limits of agreement [−0.79 ± 4.02% of the left ventricular mass (LVM) vs. CT; −1.49 ± 4.04% LVM vs. blood flow and −1.01 ± 4.18% LVM vs. pathology]. The lateral portion of the AAR had higher perfusion than the core of the AAR by CT perfusion imaging (40.7 ± 11.8 vs. 25.2 ± 17.7 Hounsfield units, P = 0.0008) and microsphere blood flow (0.11 ± 0.04 vs. 0.05 ± 0.02 mL/g/min, lateral vs. core, P = 0.001). The transmural extent of MI was lower in the lateral portion of the AAR than the core (28.2 ± 10.2 vs. 17.4 ± 8.4% of the wall, P = 0.001). Conclusion T1-weighted CMR accurately quantifies size of the AAR with excellent agreement compared with three independent reference standards. A lateral perfusion gradient results in lower transmural extent of infarction at the edges of the AAR compared with the core.

Methods Patients underwent regadenoson CMR that included 3 (basal, mid, apical) slices of rest and peak stress real-time cines, with matching stress and rest first-pass perfusion, and late gadolinium enhancement (LGE) imaging. The reference standard for presence or absence of CAD was derived from invasive coronary angiography or coronary CT angiography (CTA). Invasive angiography established significant CAD based on a threshold of ≥70% stenosis and could rule-in or exclude CAD. CTA was only used to exclude CAD if the calcium score was 30%; CT was not used to diagnose CAD. Two blinded, readers qualitatively scored RWM of pre and post-regadenoson.

Methods Patients referred for assessment of ARVD/C were evaluated. Using 2010 ARVD/C Task Force criteria, clinical history, family history, ECG and other test results were evaluated with and without CMR findings to determine definite, borderline or possible ARVD/C. CMR included assessment of right ventricular(RV) size, function, and regional wall motion(RWM). For alternative diagnoses, tissue characterization and late gadolinium enhancement were routinely performed. Qp:Qs was performed when intracardiac shunt was suspected by the supervising physician.

T2-weighted cardiac magnetic resonance (CMR) can visualize myocardial edema in salvaged myocardium which appears non-infarcted by late gadolinium enhancement (LGE) CMR. However, the mechanisms governing why LGE does not visualize edema in noninfarcted myocardium remain unclear. The objective of the study was to evaluate the extracellular volume fraction (ECV) of edematous salvaged myocardium using quantitative T1-mapping techniques in order to better understand why this tissue may be difficult to detect by LGE imaging. Methods Dogs (n=10) underwent coronary occlusion and reperfusion, followed by 1.5T CMR. Salvaged myocardium was defined as having bright signal intensity on T2-prepared steady-state free precession (T2-prep) images and the absence of infarction by LGE, and signal intensities were quantified SD units brighter than remote myocardium. Myocardial extracellular volume fraction (ECV) was measured by T1 quantification before and after GdDTPA contrast administration and calibration by blood hematocrit. Results LGE signal intensity of salvaged and infarcted myocardium were 1.7±0.4 and 8.1±1.5 SD from remote, respectively. T2-prep signal intensity of salvaged and infarcted myocardium were 2.8±0.2 and 4.9±1.0 SD from remote, respectively. Compared to remote myocardium, T1 of salvaged myocardium was 14% higher before contrast (1050±114ms vs 919±66ms, p