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1 LGE and ECV were significant predictors of FA, in line w
2 LGE burden was the best predictor of death/VT (area unde
3 LGE CMR of both atria was performed, and NEEES-based ana
4 LGE disappeared completely in 18 (10%) patients, the num
5 LGE extent (per 10% increase) corresponded to a 79% incr
6 LGE extent was analyzed with the software GT Volume.
7 LGE heterogeneity was defined as SD of LGE in the local
8 LGE imaging and left atrial activation mapping were perf
9 LGE imaging was typical in all patients with cardiac ATT
10 LGE is associated with future cardiovascular death and v
11 LGE located subepicardial basal inferolateral was detect
12 LGE significantly improved in 16 patients (67%); however
13 LGE was detected in 182 (96%) patients at CMR-I and in 1
14 LGE without edema could represent definite fibrosis wher
15 LGE+ regions were defined as signal intensity >2 SD than
16 LGE-dispersion mapping is a marker of scar heterogeneity
17 hythmia occurred in 41 LGE-positive versus 0 LGE-negative subjects (annualized incidence, 5.9% versus
19 tality occurred in 19 LGE-positive versus 17 LGE-negative subjects (annualized incidence, 3.1% versus
20 ythmia occurred in 64 LGE-positive versus 18 LGE-negative subjects (annualized incidence, 8.8% versus
22 rtality occurred in 10 LGE-positive versus 2 LGE-negative subjects (annualized incidence, 1.9% versus
27 ath or ventricular arrhythmia occurred in 64 LGE-positive versus 18 LGE-negative subjects (annualized
31 emain significantly associated with advanced LGE following DRS stratification was stroke or TIA (haza
32 r the primary end point for patients with an LGE extent of 0% to 2.5%, 2.5% to 5%, and >5% compared w
34 ation (SI-Z: coefficient, 0.004; P<0.001 and LGE: coefficient, 0.04; P<0.001) but not in ablation-nai
35 d with SI-Z (coefficient, 0.012; P=0.03) and LGE (coefficient, 0.035; P<0.001) only in ablation-naive
39 stress and rest myocardial perfusion CMR and LGE imaging had high diagnostic accuracy for CAD in 2 ph
43 presented a complete recovery from edema and LGE, 30 (16%) patients had edema with LGE, and 137 (73%)
45 s of left and right ventricular function and LGE burden were measured in 205 patients with left ventr
46 ndings of ventricular fatty infiltration and LGE were frequent and were most often found in those who
51 and projection of cardiac MRI perfusion and LGE values onto the high spatial resolution LV from CT.
53 examine the relationship between rotors and LGE signal intensity in patients with persistent atrial
57 f scar volume (r = 0.82-0.99, P < .001) and %LGE (r = 0.90-0.97, P < .001) for all sites and vendors.
64 ortantly, in ablation-naive patients, atrial LGE is associated with electrogram fractionation even in
68 models, we evaluated the association between LGE and the composite primary end point of all-cause mor
70 retrospectively studied associations between LGE presence and adverse cardiovascular events in patien
74 hrombotic treatment, LV thrombus detected by LGE CMR is associated with a 4-fold higher long-term inc
76 among patients with LV thrombus detected by LGE CMR stratified by whether the LV thrombus was also d
77 adult patients with LV thrombus detected by LGE CMR who were matched on the date of CMR, age, and LV
82 ormed to estimate the mean difference of CV (LGE+/-, wall thinning+/-), or the change of the mean of
83 ormalized variable, as well as a dichotomous LGE variable based on previously validated methodology.
85 lidated our methods on a large 3-dimensional LGE-cardiac magnetic resonance data set from 207 labeled
87 extraorbital and intraorbital glands (double LGE) was performed in male and female C57BL/6J mice to i
89 identity in the lateral ganglionic eminence (LGE), despite upregulating the neurogenic factor Ascl1.
91 Patients with late gadolinium enhancement (LGE) and low lateral MAPSE had significantly reduced sur
92 local CV versus late gadolinium enhancement (LGE) and myocardial wall thickness in a swine model of h
93 nce (CMR), with late gadolinium enhancement (LGE) and T1 mapping, is emerging as a reference standard
94 dict dynamic of late gadolinium enhancement (LGE) as persistent LGE has been shown to be a risk marke
95 ve analysis and late gadolinium enhancement (LGE) assessments and analyzed the following LVNC diagnos
96 replacement and late gadolinium enhancement (LGE) at cardiac magnetic resonance (MR) imaging in patie
98 the ability of late gadolinium enhancement (LGE) by cardiac magnetic resonance imaging (MRI) to pred
99 no ischemia or late gadolinium enhancement (LGE) by CMR, observed in 1,583 patients (67%), experienc
103 ly defined with late gadolinium enhancement (LGE) cardiovascular magnetic resonance but whether this
104 tigated whether late gadolinium enhancement (LGE) cardiovascular magnetic resonance identified patien
105 rction (STEMI), late gadolinium enhancement (LGE) has been demonstrated to overestimate MI size and T
106 nance (CMR) and late gadolinium enhancement (LGE) has not been clarified in acute myocarditis (AM) wi
112 was detected by late gadolinium enhancement (LGE) MRI, and myocardial perfusion/metabolism was evalua
113 l/midmyocardial late gadolinium enhancement (LGE) on contrast-enhanced cardiac magnetic resonance (gr
114 t CMR including late gadolinium enhancement (LGE) parameters between 2002 and 2015 and were included
115 Currently, late gadolinium enhancement (LGE) scans provide the only noninvasive estimate of atri
116 und Cardiac MRI late gadolinium enhancement (LGE) scar volume is an important marker for outcome pred
117 rophy (LVH) and late gadolinium enhancement (LGE) were independent predictors of the composite end po
118 eft atrial (LA) late gadolinium enhancement (LGE) with atrial voltage in patients with atrial fibrill
119 the presence of late gadolinium enhancement (LGE), (2) quantify their risk of death/ventricular tachy
120 T1 map, T2 map, late gadolinium enhancement (LGE), and automated extracellular volume fraction (ECV)
121 diastole, cine, late gadolinium enhancement (LGE), and extracellular volume (ECV) imaging at 3-T.
123 ibrosis through late gadolinium enhancement (LGE), extracellular volume fraction (ECV) measures by ca
125 F who underwent late gadolinium enhancement (LGE)-cardiac magnetic resonance imaging to quantify LA f
127 enhancement on late gadolinium enhancement [LGE] images >20%, n = 72) or small (enhanced volume </=2
128 brosis imaging (late gadolinium enhancement [LGE]), and (1)H magnetic resonance spectroscopy were per
129 and myocardial late gadolinium enhancement [LGE]), and metabolic parameters (hepatic proton-density
131 footprint ($1.38/liter gasoline equivalent (LGE) and 12.9 gCO(2e)/MJ) relative to facilities that co
137 r stiffness was an independent predictor for LGE (odds ratio, 1.6; 95% confidence interval: 1.2%, 2.1
140 automatic estimation of fibrosis burden from LGE-cardiac magnetic resonance scans that is comparable
147 sence of LGE, myocardial wall thinning, high LGE heterogeneity, and a high wall thickness gradient.
148 ICM patients with primary prophylactic ICD, LGE border zone predicted ICD therapy in univariable and
149 ls and Methods We retrospectively identified LGE MRI data in a multicenter (n = 7) and multivendor (n
151 Among the 374 patients with suitable images, LGE involved the subepicardial layer inferior and latera
152 maging, late gadolinium enhancement imaging (LGE) (replacement fibrosis), and T1 mapping for measurem
159 Significantly slower CV was observed in LGE+ (0.33+/-0.25 versus 0.54+/-0.36 m/s; P<0.001) and w
161 After adjustments for covariates including LGE, the relationship persisted for death (HR, 1.82 [95%
164 ex, diabetes, LV end-diastolic volume index, LGE, EF) (hazard ratio = 2.051 per mm decrease; 95% conf
169 sought to examine the association between LA LGE on cardiac magnetic resonance and electrogram abnorm
171 ing patients with stage IV versus stage I LA LGE was 1.67 (95% confidence interval: 1.01 to 2.76) for
172 ere stratified according to Utah stage of LA LGE criteria, and observed for the occurrence of MACCE,
174 ve analysis demonstrated that more severe LA LGE is associated with increased MACCE risk, driven prim
175 tained using a reference 3D left atrial (LA) LGE sequence with 1.3 mm x 1.3 mm x 2.5-mm spatial resol
179 .001 per cm(3)), increased nonapical vent LV LGE (OR, 1.09; P=0.008 per cm(3)), older age (OR, 1.6; P
180 In patients with AM and preserved LVEF, LGE in the midwall layer of the AS myocardial segment is
183 ing location and pattern, septal and midwall LGE showed strongest associations with MACE (HR: 2.55; 9
184 investigated the association between midwall LGE and the prespecified primary composite outcome of SC
190 LV) in cardiac MRI perfusion and cardiac MRI LGE, co-registration of cardiac MRI to CT data, and proj
191 risk was increased in patients with multiple LGE patterns, although arrhythmic risk was higher among
192 sity ratio defined as left atrial myocardial LGE signal intensity divided by the mean left atrial blo
193 e detection and quantification of myocardial LGE in patients with previous myocardial infarction was
194 tly different from one another in myocardial-LGE interface length, number of components and entropy,
195 athletes with ventricular arrhythmias and no LGE (group B) and 40 healthy control athletes (group C).
200 d with the McNemar test, and the accuracy of LGE quantification was calculated with the paired t test
203 /VT were associated with a greater burden of LGE (14+/-11 versus 5+/-5%, P<0.01) and right ventricula
204 c thickness >= 1.2 cm had a higher burden of LGE (4.1% vs 0.5% per segment), reduced MPRI (2.6 +/- 1.
205 -sensitive IR techniques in the detection of LGE were 90% and 95%, respectively, with patient-based a
210 determine whether size and heterogeneity of LGE predict appropriate implantable cardioverter defibri
211 stics curve, 0.80); for every 1% increase of LGE burden, the hazard of death/VT increased by 8%.
213 mpletely in 18 (10%) patients, the number of LGE segments decreased in 87 (46%), unchanged in 58 (31%
214 sion analysis, the midwall septal pattern of LGE and the presence of LGE without edema at CMR-II were
215 oup C; P<0.001), whereas a spotty pattern of LGE localized at the junction of the right ventricle to
216 nts with cardiac amyloidosis, the pattern of LGE was always typical for amyloidosis (29% subendocardi
217 ndependently associated with the presence of LGE (OR: 0.140, 95% CI: 0.035-0.567), perfusion abnormal
218 with dilated cardiomyopathy, the presence of LGE showed strong prognostic value for identification of
220 ll septal pattern of LGE and the presence of LGE without edema at CMR-II were independent predictors
221 Slower CV is observed in the presence of LGE, myocardial wall thinning, high LGE heterogeneity, a
224 ment for the detection and quantification of LGE was analyzed with kappa and Bland-Altman statistics,
226 corneal damage in female mice, yet signs of LGE-induced ocular pain and anxiety in male and female m
227 ter agreement with final IS than acute IS on LGE (ECV maps: bias, 1.9; 95% CI, 0.4-3.4 versus LGE ima
232 nd other segments in 59 patients (16%; other-LGE group), and it was absent in 26 patients (no-LGE gro
235 e gadolinium enhancement (LGE) as persistent LGE has been shown to be a risk marker in myocarditis.
238 men) were imaged at 1.5 T using the proposed LGE sequence with 1.3 mm x 1.3 mm x 2-mm spatial resolut
240 ; P = .004) and correlated with quantitative LGE (r = 0.67; P < .001), myocardial T1 relaxation times
246 ictors of inducible VT included increased RV LGE (odds ratio [OR], 1.15; P=0.001 per cm(3)), increase
247 or ruling-out and ruling-in inducible VT, RV LGE >10 cm(3) was 100% sensitive and >36 cm(3) was 100%
248 fferences in the per-patient and per-segment LGE detection rates between the synthetic and convention
250 wo hundred ninety-four (44%) patients showed LGE presence, which was associated with a more than doub
253 ion of either the extraorbital gland (single LGE), or both the extraorbital and intraorbital glands (
254 The majority of athletes with no or spotty LGE pattern had ventricular arrhythmias with a predomina
256 The use of T1 mapping to derive synthetic LGE images may reduce imaging times and operator depende
257 te of death/VT per year was >20x higher than LGE- (4.9 versus 0.2%, P<0.01); (2) death/VT were associ
258 d provides a better risk stratification than LGE presence and its extent in patients with hypertrophi
264 death/VT in the entire group and within the LGE+ group was determined using Cox proportional hazard
265 CE rates were 4.8% and 2.1% corresponding to LGE presence and absence, respectively (p < 0.001).
270 n deriving ECV, coronary artery disease type LGE, but not non-coronary artery disease type LGE, has b
274 HODS AND ICM and NICM patients who underwent LGE cardiac magnetic resonance imaging prior to ICD impl
283 ovement was 0.39 (95% CI: 0.10 to 0.67) when LGE presence was added to the multivariable model for MA
284 volunteers 48.9+/-2.5 ms, P<0.001), but when LGE was present there was also global T2 elevation (53.1
285 an age 50 years, median LVEF 50%, 25.3% with LGE) followed for a median of 4.6 years, 18 of 101 (17.8
289 c involvement who underwent cardiac MRI with LGE with at least 12 months of either prospective or ret
292 f 4.6 years, 18 of 101 (17.8%) patients with LGE reached the prespecified end point, compared with 7
294 f FT3, decreased percentage of segments with LGE and perfusion/metabolism abnormalities were found.
296 Ascl1-Gsx2 interactions are enriched within LGE VZ progenitors, whereas Ascl1-Tcf3 (E-protein) inter
300 % to 5%, and >5% compared with those without LGE were 10.6 (95% CI, 3.9-29.4), 4.9 (95% CI, 1.3-18.9)