127 research outputs found
Variability and homogeneity of cardiovascular magnetic resonance myocardial T2-mapping in volunteers compared to patients with edema
BACKGROUND: The aim of the study was to test the reproducibility and variability of myocardial T2 mapping in relation to sequence type and spatial orientation in a large group of healthy volunteers. For control T2 mapping was also applied in patients with true edema. Cardiovascular magnetic resonance (CMR) T2-mapping has potential for the detection and quantification of myocardial edema. Clinical experience is limited so far. The variability and potential pitfalls in broad application are unknown. METHODS: Healthy volunteers (n = 73, 35 +/- 13 years) and patients with edema (n = 28, 55 +/- 17 years) underwent CMR at 1.5 T. Steady state free precession (SSFP) cine loops and T2-weighted spin echo images were obtained. In patients, additionally late gadolinium enhancement images were acquired. We obtained T2 maps in midventricular short axis (SAX) and four-chamber view (4CV) based on images with T2 preparation times of 0, 24, 55 ms and compared fast low angle shot (FLASH) and SSFP readout. 10 volunteers were scanned twice on separate days. Two observers analysed segmental and global T2 per slice. RESULTS: In volunteers global myocardial T2 systematically differed depending on image orientation and sequence (FLASH 52 +/- 5 vs. SSFP 55 +/- 5 ms in SAX and 57 +/- 6 vs. 59 +/- 6 ms in 4CV; p /= 70 ms. Mean intraobserver variability was 1.07 +/- 1.03 ms (r = 0.94); interobserver variability was 1.6 +/- 1.5 ms (r = 0.87). The coefficient of variation for repeated scans was 7.6% for SAX and 6.6% for 4CV. Mapping revealed focally increased T2 (73 +/- 9 vs. 51 +/- 3 ms in remote myocardium; p < 0.0001) in all patients with edema. CONCLUSIONS: Myocardial T2 mapping is technically feasible and highly reproducible. It can detect focal edema und differentiate it from normal myocardium. Increased T2 was found in some volunteers most likely due to partial volume and residual motion
Myocardial T(1) and T(2) mapping at 3 T: reference values, influencing factors and implications
BACKGROUND: Myocardial T1 and T2 mapping using cardiovascular magnetic resonance (CMR) are promising to improve tissue characterization and early disease detection. This study aimed at analyzing the feasibility of T1 and T2 mapping at 3 T and providing reference values. METHODS: Sixty healthy volunteers (30 males/females, each 20 from 20--39 years, 40--59 years, 60--80 years) underwent left-ventricular T1 and T2 mapping in 3 short-axis slices at 3 T. For T2 mapping, 3 single-shot steady-state free precession (SSFP) images with different T2 preparation times were acquired. For T1 mapping, modified Look-Locker inversion recovery technique with 11 single shot SSFP images was used before and after injection of gadolinium contrast. T1 and T2 relaxation times were quantified for each slice and each myocardial segment. RESULTS: Mean T2 and T1 (pre-/post-contrast) times were: 44.1 ms/1157.1 ms/427.3 ms (base), 45.1 ms/1158.7 ms/411.2 ms (middle), 46.9 ms/1180.6 ms/399.7 ms (apex). T2 and pre-contrast T1 increased from base to apex, post-contrast T1 decreased. Relevant inter-subject variability was apparent (scatter factor 1.08/1.05/1.11 for T2/pre-contrast T1/post-contrast T1). T2 and post-contrast T1 were influenced by heart rate (p < 0.0001, p = 0.0020), pre-contrast T1 by age (p < 0.0001). Inter- and intra-observer agreement of T2 (r = 0.95; r = 0.95) and T1 (r = 0.91; r = 0.93) were high. T2 maps: 97.7% of all segments were diagnostic and 2.3% were excluded (susceptibility artifact). T1 maps (pre-/post-contrast): 91.6%/93.9% were diagnostic, 8.4%/6.1% were excluded (predominantly susceptibility artifact 7.7%/3.2%). CONCLUSIONS: Myocardial T2 and T1 reference values for the specific CMR setting are provided. The diagnostic impact of the high inter-subject variability of T2 and T1 relaxation times requires further investigation
Current T(1) and T(2) mapping techniques applied with simple thresholds cannot discriminate acute from chronic myocadial infarction on an individual patient basis: a pilot study
BACKGROUND: Studying T1- and T2-mapping for discrimination of acute from chronic myocardial infarction (AMI, CMI). METHODS: Eight patients with AMI underwent CMR at 3 T acutely and after >3 months. Imaging techniques included: T2-weighted imaging, late enhancement (LGE), T2-mapping, native and post-contrast T1-mapping. Myocardial T2- and T1-relaxation times were determined for every voxel. Abnormal voxels as defined by having T2- and T1-values beyond a predefined threshold (T2 > 50 ms, native T1 > 1250 ms and post-contrast T1 delete acute infarction; unfortunately this is not possible in your web interface) acute infarction only in half of the subjects. Abnormal T2-values were also present in subjects with CMI, thereby matching the chronically infarcted territory in some. Abnormal native T1 times were present in voxels with AMI in 5/8 subjects, but also remote from the infarcted territory in four. In CMI, abnormal native T1 values corresponded with infarcted voxels, but were also abnormal remote from the infarcted territory. Voxels with abnormal post-contrast T1-relaxation times agreed well with LGE in AMI and CMI. CONCLUSIONS: In this pilot-study, T2- and T1-mapping with simple thresholds did not facilitate the discrimination of AMI and CMI
Study of the decays B->D_s1(2536)+ anti-D(*)
We report a study of the decays B -> D_s1(2536)+ anti-D(*), where anti-D(*)
is anti-D0, D- or D*-, using a sample of 657 x 10^6 B anti-B pairs collected at
the Upsilon(4S) resonance with the Belle detector at the KEKB asymmetric-energy
e+e- collider. The branching fractions of the decays B+ -> D_s1(2536)+ anti-D0,
B0 -> D_s1(2536)+ D- and B0 -> D_s1(2536)+ D*- multiplied by that of
D_s1(2536)+ -> (D*0K+ + D*+K0) are found to be (3.97+-0.85+-0.56) x 10^-4,
(2.75+-0.62+-0.36) x 10^-4 and (5.01+-1.21+-0.70) x 10^-4, respectively.Comment: 6 pages, 2 figues, submitted to PRD (RC
Evidence for the Suppressed Decay B- -> DK-, D -> K+pi-
The suppressed decay chain B- -> DK-, D -> K+pi-, where D indicates a anti-D0
or D0 state, provides important information on the CP-violating angle phi_3. We
measure the ratio R_{DK} of the decay rates to the favored mode B- -> DK-, D ->
K-pi+ to be R_{DK} = [1.63^{+0.44}_{-0.41}(stat)^{+0.07}_{-0.13}(syst)] x
10^{-2}, which indicates the first evidence of the signal with a significance
of 4.1sigma. We also measure the asymmetry A_{DK} between the charge-conjugate
decays to be A_{DK} = -0.39^{+0.26}_{-0.28}(stat)^{+0.04}_{-0.03}(syst). The
results are based on the full 772 x 10^6 B anti-B pair data sample collected at
the Upsilon(4S) resonance with the Belle detector.Comment: 6 pages, 2 figures, 2 tables, accepted by Physical Review Letter
Search for CP Violation in the Decay
We search for CP violation in the decay using a
data sample with an integrated luminosity of 977 fb collected with the
Belle detector at the KEKB asymmetric-energy collider. No CP violation
has been observed and the CP asymmetry in decay is
measured to be , which is the most sensitive
measurement to date. After subtracting CP violation due to
mixing, the CP asymmetry in decay is found to be
.Comment: 15 pages, 4 figures, 1 table. Published in JHE
Observation of and Evidence for
We report the first observation of and first
evidence for , which are CP eigenstate decay modes.
These results are obtained from of data collected at
the resonance with the Belle detector at the KEKB
collider. We measure the branching fractions with a significance of , and
with a significance of . The last error
listed is due to uncertainty in the number of produced pairs.Comment: 5 pages, 2 figures, 2 tables, published in PR
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