ライフサイエンスコーパス: CMR

1 CMR and EVM sensitivity and specificity regarding the id

2 CMR is also the preferred methodology for the identifica

3 CMR is an imaging modality integrating myocardial functi

4 CMR is often repeated after 6 months to assess the evolu

5 CMR was abnormal in 74.1% (86/116) of participants.

6 CMR was completely negative in 14 patients (10%), isolat

7 CMR was performed in 705 subjects (mean age 48 +/- 4 yea

8 CMR with multiparametric mapping is a promising tool to

9 s were "abnormal innervation only" (18.2%), "CMR scar plus abnormal innervation only" (14.9%), and "C

10 (reported as median [quartile 1-quartile 3]: CMR scar, 46.1 cm(2) [33.1-86.9 cm(2)]; abnormal innerva

11 nd inconclusive electrocardiogram compared a CMR- or CTA-first strategy with a control strategy of ro

12 ll patients (n = 32 patients) demonstrated a CMR sign on ultra-widefield fundus photography.

13 ions with incident heart failure events in a CMR referral base.

14 MACE associated with presence of a CMR diagnosis, extent of late gadolinium enhancement, an

15 Inclusion criterion was the presence of a CMR sign detected on ultra-widefield fundus photography.

16 were prospectively recruited and underwent a CMR at 4 +/- 2 days.

17 Predicted LVM calculated using a CMR-derived equation that incorporates height, weight, a

18 ceive PVI plus CMR-guided fibrosis ablation (CMR group) or PVI alone (PVI-alone group).

19 After CMR, only four areas had decreased FC compared to health

20 nced sensorimotor recovery post-stroke after CMR.

21 evascularization during the first year after CMR.

22 Although CMR is undeniably the gold standard for assessing left v

23 [95% confidence interval: 0.31 to 1.42]; and CMR vs. CTA, 1.19 [95% confidence interval: 0.53 to 2.66

24 e assigned intervention in the PVI-alone and CMR group, respectively.

25 80% and 71% of patients in the PVI-alone and CMR groups, respectively.

26 Methods Echocardiography and CMR were performed in 1119 patients discharged for ST-se

27 alve intervention 6MWT, echocardiography and CMR with 4D flow.

28 tine strategy underwent echocardiography and CMR, whereas those assigned to selective use underwent e

29 EVM and CMR together conferred a positive predictive value of 89

30 Sensitivity of pooled EVM and CMR was as high as 95%.

31 in pathological areas identified at EVM and CMR.

32 The coexistence of abnormal innervation and CMR scar may identify a particularly "proarrhythmic" ada

33 GLS was superior and incremental to LVEF and CMR markers of infarct severity.

34 Multimodality imaging with coronary OCT and CMR identified potential mechanisms in 84.5% of women wi

35 Angiography, OCT, and CMR were evaluated at blinded, independent core laborato

36 lus abnormal innervation only" (14.9%), and "CMR scar only" (14.6%).

37 The authors associated CMR findings with a primary outcome of cardiovascular de

38 At CMR-II, 20 (11%) patients presented a complete recovery

39 tients at CMR-I and persisted in 31 (16%) at CMR-II.

40 (96%) patients at CMR-I and in 164 (86%) at CMR-II.

41 LGE and the presence of LGE without edema at CMR-II were independent predictors of a cardiac event.

42 LGE was detected in 182 (96%) patients at CMR-I and in 164 (86%) at CMR-II.

43 al edema was detected in all the patients at CMR-I and persisted in 31 (16%) at CMR-II.

44 thological areas that had been undetected at CMR evaluation.

45 and PERCIST and distinguished better between CMR and non-CMR.

46 ain were not significantly different between CMR-FT and the three echocardiography gating methods (p

47 greement and stronger discrimination between CMR and non-CMR, highlighting the importance of visual a

48 the left ventricular repercussions of AS by CMR is not routinely performed in clinical practice, and

49 hesized that myocardial ischemia assessed by CMR is associated with myocardial fibrosis and reduced e

50 Elevated measures of ECV by CMR are associated with incident heart failure outcomes

51 Increased extracellular volume (ECV) by CMR is a marker of interstitial myocardial fibrosis and

52 e ischemia or late gadolinium enhancement by CMR.

53 , multivessel OCT was performed, followed by CMR (cine imaging, late gadolinium enhancement, and T2-w

54 ed 116 British families (427 individuals) by CMR and ECG, and undertook heritability analyses using v

55 Myocardial ischemia by CMR is associated with myocardial segmental dysfunction

56 emia or late gadolinium enhancement (LGE) by CMR, observed in 1,583 patients (67%), experienced low a

57 isk of large-sized infarction as measured by CMR, as well as adverse clinical outcomes.

58 ritish Caucasian families were phenotyped by CMR and genotyped for 557,124 SNPs.

59 The earliest doxorubicin-cardiotoxicity CMR parameter was T(2) relaxation-time prolongation at w

60 The all-cause CMRs during and after opioid substitution treatment with

61 From 21 studies, the pooled all-cause CMRs were 0.92 per 100 person-years (95% CI: 0.79-1.04)

62 ,604 serial patients referred for a clinical CMR with myocardial T1 maps, 331 were eligible after exc

63 Comprehensive CMR investigations were performed 3 (interquartile range

64 ve stable HD patients underwent non-contrast CMR including volumetric assessment and native T1 and T2

65 ntly analyzed by 2 blinded experts in a core CMR lab.

66 Later, coronary angiography and DE-CMR images were reviewed independently and blindly for i

67 rtery disease diagnosis was identified by DE-CMR in 14% and 13%, respectively.

68 rtery disease diagnosis was identified by DE-CMR in 60% and 19% of patients, respectively.

69 are believed to be nonculprit arteries by DE-CMR is not uncommon.

70 onary artery territories as determined by DE-CMR.

71 In nearly half, DE-CMR may lead to a new IRA diagnosis or elucidate a nonis

72 The pattern of DE-CMR hyperenhancement was also used to determine whether

73 Overall, DE-CMR led to a new IRA diagnosis in 31%, a diagnosis of no

74 d-enhancement cardiac magnetic resonance (DE-CMR) can accurately identify small MIs.

75 ventional cardiologist was blinded to the DE-CMR results.

76 Patients underwent DE-CMR followed by coronary angiography.

77 se of this study was to determine whether DE-CMR improves the ability to identify the IRA in patients

78 ) were localized to myocardium demonstrating CMR scar and abnormal innervation.

79 As per study design, CMR was performed in all the patients at enrollment.

80 Different CMR presentations of ARVC are associated with different

81 score to predict cardiac events in different CMR presentations.

82 DT-CMR assessment of left ventricular myoarchitecture match

83 DT-CMR demonstrated that failure of sheetlet relaxation in

84 Conclusions DT-CMR can characterize the microstructural effects of amyl

85 Consequently, DT-CMR offers a contrast-free tool to identify novel pathop

86 Methods DT-CMR was performed at diastole and systole in 20 CA, 11 h

87 fusion tensor cardiac magnetic resonance (DT-CMR) imaging.

88 tensor cardiovascular magnetic resonance (DT-CMR) to noninvasively assess the effects of amyloid infi

89 +/- 16 years of age, 70% male) underwent DT-CMR in diastole, cine, late gadolinium enhancement (LGE)

90 This study sought to validate in vivo DT-CMR measures of cardiac microstructure against histology

91 sis quantified by extracellular volume (ECV) CMR measures.

92 ministration approval of gadobutrol-enhanced CMR (0.1 mmol/kg) to assess myocardial perfusion and LGE

93 Finally, CMR-derived right ventricular mass showed considerable h

94 These novel 4D flow CMR derived imaging markers have future potential for RV

95 6MWT was associated with 4D flow CMR derived pressure gradient (r = -0.45, P = 0.01) and

96 4D flow CMR offers an alternative method for non-invasive assess

97 s document is to provide recommendations for CMR endpoint selection in experimental and clinical tria

98 le model adjusted for age and stratified for CMR, independent predictors of HCM development were male

99 In the entire group, CMR-LVEF (but not echocardiography-LVEF) independently p

100 However, CMR features such as fibrosis, fat infiltration, and lef

101 nderwent cardiac magnetic resonance imaging (CMR) and a complete blood cell count within 24 hours bef

102 nderwent cardiac magnetic resonance imaging (CMR) at 3.0 T.

103 Stress cardiac magnetic resonance imaging (CMR) has demonstrated excellent diagnostic and prognosti

104 r cardiovascular magnetic resonance imaging (CMR) or computed tomographic angiography (CTA) may serve

105 t cardiovascular magnetic resonance imaging (CMR) provides complementary information, especially for

106 A novel strategy of implementing CMR or CTA first in the diagnostic process in non-ST-seg

107 The decrease in CMR with population size previously observed is maintain

108 However, there is a wide heterogeneity in CMR methodologies used in experimental and clinical tria

109 le analysis, AS LGE was the best independent CMR predictor of the combined endpoint (odds ratio: 2.73

110 ntrol group was sacrificed after the initial CMR.

111 Follow-up ICA was recommended when initial CMR or CTA suggested myocardial ischemia, infarction, or

112 the presence nor extent of the investigated CMR-based tissue injury markers were predictive of our p

113 l requires invasive investigations and lacks CMR imaging to identify high-risk patients.

114 isk of embolism as that detected by both LGE CMR and echocardiography.

115 LV thrombus detected by LGE CMR but not by echocardiography is associated with a sim

116 botic treatment, LV thrombus detected by LGE CMR is associated with a 4-fold higher long-term inciden

117 ft ventricular (LV) thrombus detected by LGE CMR is unknown.

118 ng patients with LV thrombus detected by LGE CMR stratified by whether the LV thrombus was also detec

119 lt patients with LV thrombus detected by LGE CMR who were matched on the date of CMR, age, and LV eje

120 We evaluated the association between LGE-CMR intensity and CV with multilevel linear mixed models

121 Noninvasive derivation of CV maps from LGE-CMR is feasible.

122 nced cardiac magnetic resonance imaging (LGE-CMR) in patients with ICM.

123 All patients underwent LGE-CMR and electroanatomic mapping (EAM) in sinus rhythm (2

124 CV is inversely associated with LGE-CMR fibrosis density in patients with ICM.

125 Compared with echocardiography-LVEF, CMR-LVEF significantly improved MACE prediction in the g

126 erconductivity, colossal magnetoresistances (CMR), and multiferroicity.

127 edures for capture-mark-recapture modelling (CMR) for the study of animal demography include running

128 The presence of LGE without edema at 6-month CMR is associated with worse prognosis, particularly whe

129 the clinical and prognostic role of 6-month CMR is unknown.

130 m onset (CMR-I) and repeated after 6 months (CMR-II).

131 ted quality control pipeline for cardiac MR (CMR) images to the first 19,265 short-axis (SA) cine sta

132 ent late gadolinium enhancement cardiac MRI (CMR), (123)I-metaiodobenzylguanidine SPECT, and high-res

133 but none occurred in patients with negative CMR.

134 As new CMR techniques for the assessment of MR have arisen, sta

135 stronger discrimination between CMR and non-CMR, highlighting the importance of visual assessment to

136 and distinguished better between CMR and non-CMR.

137 In the non-CMR and non-CTA arms, follow-up CMR and CTA were perform

138 the selective group underwent a nonprotocol CMR.

139 d the LVM obtained from manual contouring of CMR cine images.

140 d by LGE CMR who were matched on the date of CMR, age, and LV ejection fraction to up to 3 patients w

141 ectively investigated the natural history of CMR-based myocardial injury and chamber remodeling over

142 However, the natural history of CMR-based tissue markers and their association with left

143 ach integrates the prognostic information of CMR imaging into a simple risk score that showed increme

144 An ischemic pattern of CMR abnormalities (infarction or myocardial edema in a c

145 A nonischemic pattern of CMR abnormalities (myocarditis, takotsubo syndrome, or n

146 Despite the potential of CMR for characterization of the arrhythmogenic substrate

147 review, we discuss the emerging potential of CMR for the diagnosis and prognosis of AS.

148 The prognostic power of CMR beyond echocardiography-LVEF was assessed using adju

149 A was associated with a higher prevalence of CMR-detected LVNC phenotype according to diverse establi

150 and prognostic role of 6-month repetition of CMR in patients with AM.

151 ities, and we sought to evaluate the role of CMR in determining sudden cardiac arrest pathogenesis an

152 rs sought to evaluate the prognostic role of CMR phenotype in patients with definite ARVC and to eval

153 of a >=70% QCA stenosis, the sensitivity of CMR was 78.9%, specificity was 86.8%, and area under the

154 ma highlight the need for standardization of CMR timing to retrospectively delineate MaR and quantify

155 serum samples acquired and stored at time of CMR scan, and patients were categorized into 3 groups fo

156 ) by echocardiography for a selective use of CMR after ST-segment-elevation myocardial infarction.

157 iption of the current evidence on the use of CMR for MR assessment, highlight its current clinical ut

158 forward strategy based on a selective use of CMR for risk prediction in ST-segment-elevation myocardi

159 gnostic utility and support the wider use of CMR for the clinical assessment of MR.

160 secondary hypothesis was that routine use of CMR will improve patient outcomes.

161 r primary hypothesis was that routine use of CMR will yield more specific diagnoses in nonischemic HF

162 ere was analysed before and after 6 weeks of CMR.

163 years had adequate tracking for analysis on CMR-FT and 2D-STE.

164 50 (32.0%) fulfilled diagnostic criteria on CMR but not echocardiography.

165 reserved and MF was present as determined on CMR, ACE inhibitor therapy was associated with significa

166 Patients with MF noted on CMR had a higher probability of cardiovascular events (e

167 the experimental model by showing that only CMR-MaR values for day 4 and day 7 postreperfusion, coin

168 d within the first week after symptom onset (CMR-I) and repeated after 6 months (CMR-II).

169 ing, higher than with OCT alone (P<0.001) or CMR alone (P=0.001).

170 e allocated to the PVI-alone group (N=76) or CMR group (N=79).

171 The STEM-AMI OUTCOME CMR (Stem Cells Mobilization in Acute Myocardial Infarct

172 Based on 16 studies, the pooled overdose CMRs were 0.24 (0.20-0.28) while receiving MAT, 0.68 (0.

173 Therefore, ASL perfusion CMR may be an alternative method for quantifying the AAR

174 dilator stress and rest myocardial perfusion CMR and LGE imaging had high diagnostic accuracy for CAD

175 nostic value of vasodilator stress perfusion CMR in patients with HFrEF.

176 ly referred for vasodilator stress perfusion CMR were followed for the occurrence of major adverse ca

177 andomized in a 1:1 basis to receive PVI plus CMR-guided fibrosis ablation (CMR group) or PVI alone (P

178 n and activities of daily life pre- and post-CMR, and at 1-year post-CMR.

179 Frenchay Activities Index (p = 0.03) at post-CMR and at 1-year follow-up.

180 y life pre- and post-CMR, and at 1-year post-CMR.

181 Compared to baseline (pre-CMR), participants improved on motor function (MESUPES a

182 Preoperative CMR showed late gadolinium enhancement in 70% of the pat

183 ll-cause and overdose crude mortality rates (CMRs) and relative risks (RRs) by treatment status, diff

184 tively), with similar outcome (hazard ratio: CMR vs. routine, 0.78 [95% confidence interval: 0.37 to

185 Three-dimensional reconstructed CMR/(123)I-metaiodobenzylguanidine models were coregiste

186 AMY (ITAlian study in MYocarditis) registry, CMR was performed within the first week after symptom on

187 ith a higher risk of developing HCM. Regular CMR should be considered in long-term screening.

188 Cognitive Multisensory Rehabilitation (CMR) is a promising therapy for upper limb recovery in s

189 multiparametric cardiac magnetic resonance (CMR) and its pathological correlates in a large animal m

190 sodilator stress cardiac magnetic resonance (CMR) can detect and quantitate inducible ischemia in HCM

191 Cardiovascular magnetic resonance (CMR) can detect morphological, functional, or tissue abn

192 efined in cardiovascular magnetic resonance (CMR) has been suggested to correlate with conduction cha

193 ECV) measures by cardiac magnetic resonance (CMR) have emerged as a phenotypic imaging risk marker fo

194 VNC phenotype on cardiac magnetic resonance (CMR) imaging and accelerometer-measured physical activit

195 Cardiovascular magnetic resonance (CMR) imaging is commonly used to diagnose acute myocardi

196 ent (LGE) cardiovascular magnetic resonance (CMR) imaging is more sensitive than echocardiography for

197 feature-tracking cardiac magnetic resonance (CMR) imaging qualifies this novel modality as potential

198 graphy (OCT) and cardiac magnetic resonance (CMR) imaging to assess mechanisms of MINOCA.

199 We performed cardiac magnetic resonance (CMR) imaging within 24 hours of a diagnostic right heart

200 nts using cardiovascular magnetic resonance (CMR) imaging, to find underlying factors related to pote

201 ecific data from cardiac magnetic resonance (CMR) imaging.

202 w of the role of cardiac magnetic resonance (CMR) in aortic stenosis (AS).

203 Cardiovascular magnetic resonance (CMR) included gadobutrol-enhanced first-pass vasodilator

204 Cardiac magnetic resonance (CMR) is a recommended imaging test for patients with hea

205 Cardiac magnetic resonance (CMR) is the gold-standard technique for noninvasive myoc

206 Cardiac magnetic resonance (CMR) is widely used to assess tissue and functional abno

207 Cardiac magnetic resonance (CMR) is widely used to confirm the diagnosis of acute my

208 arametric cardiovascular magnetic resonance (CMR) mapping to interrogate the myocardium following ST-

209 or stress cardiovascular magnetic resonance (CMR) may have a less optimal hemodynamic response to int

210 (4D flow) cardiovascular magnetic resonance (CMR) methods for AS assessment.

211 Background Cardiac magnetic resonance (CMR) permits robust risk stratification of discharged ST

212 Stress cardiac magnetic resonance (CMR) provides accurate assessment of both myocardial inf

213 a 4D flow cardiovascular magnetic resonance (CMR) scan on 1.5 T Philips Ingenia.

214 tients underwent cardiac magnetic resonance (CMR) to assess LVEF and late gadolinium enhancement, ind

215 by incorporating cardiac magnetic resonance (CMR), genetic, and biomarker data.

216 alidate a cardiovascular magnetic resonance (CMR)-derived equation for predicted left ventricular mas

217 cacy of ablating cardiac magnetic resonance (CMR)-detected atrial fibrosis plus pulmonary vein isolat

218 ompare it with a cardiac magnetic resonance (CMR)-guided approach.

219 50.9%) underwent cardiac magnetic resonance (CMR).

220 HD using cardiovascular magnetic resonance (CMR).

221 ons using cardiovascular magnetic resonance (CMR).

222 tively by cardiovascular magnetic resonance (CMR).

223 ted using cardiovascular magnetic resonance (CMR).

224 atients (61 G-CSF and 58 SOC, respectively), CMR was available at baseline and 6-month follow-up.

225 categorized as complete metabolic response (CMR), partial metabolic response, stable metabolic disea

226 ; there were 2 complete molecular responses (CMR) and 1 partial molecular response in CALR-positive r

227 In patients with nonischemic HF, routine CMR does not yield more specific HF causes on clinical a

228 not different between routine and selective CMR (34% versus 30%, respectively; P=0.34).

229 The routine and selective CMR strategies had similar rates of specific HF causes a

230 were randomized to routine versus selective CMR.

231 inical utility, and recommend a standardized CMR protocol and report for MR assessment.

232 assessment of MR have arisen, standardizing CMR protocols for research and clinical studies has beco

233 In specific cases, simple, uni-state CMR modeling showing transients may allow researchers to

234 Stress CMR is safe and has a good discriminative prognostic val

235 Stress CMR was well tolerated without any adverse events.

236 (Stress CMR Perfusion Imaging in the United States [SPINS]: A So

237 (Stress CMR Perfusion Imaging in the United States [SPINS]; NCT0

238 ) with suspected CAD were assessed by stress CMR and followed over a median of 5.4 years.

239 t of coronary artery disease (CAD) by stress CMR, beyond cardiac function and ischemia.

240 t pain syndrome and were referred for stress CMR were followed for a target period of 4 years.

241 o investigate the prognostic value of stress CMR and downstream costs from subsequent cardiac testing

242 In the multicenter SPINS (Stress CMR Perfusion Imaging in the United States) study, 2,349

243 ort with stable chest pain syndromes, stress CMR performed at experienced centers offers effective ca

244 A pragmatic ablation approach targeting CMR-detected atrial fibrosis plus PVI was not more effec

245 ent, being greater when measured by ECG than CMR.

246 Predicted LVM was considerably higher than CMR-derived LVM (mean+/-SD of 138.8+/-28.9 g versus 86.3

247 We hypothesised that CMR-derived measurements, being more precise than echoca

248 The CMR core laboratory identified ischemia-related and noni

249 The CMR sign seen on ultra-widefield fundus imaging may be a

250 The CMR variables were combined with the noninvasive compone

251 The CMR- and CTA-first strategies reduced ICA compared with

252 38.7% [37.2-39.0]), 1018 (97%) completed the CMR protocol and 950 (93%) completed the follow-up (medi

253 Flow metrics were derived from the CMR images to provide some local information about blood

254 I-alone group and 22 patients (27.8%) in the CMR group (odds ratio: 1.01 [95% CI, 0.50-2.04]; P=0.976

255 nces in the rate of adverse events (3 in the CMR group and 2 in the PVI-alone group; P=0.68).

256 ial infarction patients were enrolled in the CMR Substudy and assigned to standard of care (SOC) plus

257 the routine clinical care arm, in 69% in the CMR-first arm (p = 0.308 vs. routine), and in 85% in the

258 c tissue category accounted for 68.3% of the CMR scar and 31.2% of the total abnormal postischemic VT

259 These CMR thresholds should be used for patient selection in f

260 e stage shows the clinical potential of this CMR marker for tailored anthracycline therapy.

261 EVM proved to have sensitivity similar to CMR (74% versus 77%), with specificity being 70% and 47%

262 was demonstrated to have accuracy similar to CMR.

263 netic resonance myocardial feature tracking (CMR-FT) provides insight into all phases of atrial funct

264 ocardial strain measured by feature-tracking-CMR for the prediction of clinical outcome following ST-

265 ntal prognostic validity of feature-tracking-CMR over left ventricular ejection fraction (LVEF) and m

266 GLS by feature-tracking-CMR strongly and independently predicted the occurrence

267 ble for both the scientists involved in UKBB CMR acquisition and for the ones who use the dataset for

268 in 53.4% (62/116) of participants undergoing CMR.

269 VNC was evaluated in all subjects undergoing CMR.

270 All underwent CMR evaluations at baseline and 12 months, inclusive of

271 iabetes, n = 882 without diabetes) underwent CMR 3 days after AMI.

272 hout prior cardiovascular disease, underwent CMR at 3.0 T including cine, and late gadolinium enhance

273 hy volunteers (n = 41, 51% female) underwent CMR at 1.5 T.

274 Participants underwent CMR at baseline and after 6-months of standard care.

275 Forty-eight STEMI patients underwent CMR at 4 +/- 2 days.

276 Patients underwent CMR including cine imaging, late gadolinium enhancement

277 ective study, individuals with SCA underwent CMR, echocardiography and exercise test.

278 quality for analysis; 116 of these underwent CMR.

279 s old) UK Biobank participants who underwent CMR imaging in 2014 to 2015.

280 In the non-CMR and non-CTA arms, follow-up CMR and CTA were performed in 67% and 13% of patients an

281 This is the first study to use CMR to assess independent prognostic implications of fun

282 (age 14.0 +/- 4.2 y) were assessed by using CMR 11.2 +/- 5.4 years after HT.

283 strain rate between RA and LA function using CMR-FT (p > 0.05 for all).

284 We review almost 1000 papers using CMR modeling and find that almost 40% of studies fitting

285 RA strain and strain rate using CMR-FT had fair and good intra- and inter-observer repro

286 was to compare all phases of RA strain using CMR-FT and STE and also assess the relationship between

287 amined 547 patients with functional TR using CMR to quantify TRVol and TRF.

288 hnique was tested in high-resolution ex-vivo CMR images in 20 post-infarct swine models who underwent

289 All groups underwent weekly CMR examinations including anatomical and T(2) and T(1)

290 discuss different clinical situations where CMR could be useful in AS, for example, in low-flow low-

291 ial estimates of heritability (60%), whereas CMR-derived LV mass was only modestly heritable (20%).

292 ersus healthy adults to then explore whether CMR affects OP1/OP4 connectivity and sensorimotor recove

293 operculum (parts OP1/OP4) is activated with CMR exercises.

294 eight, and sex has a strong correlation with CMR LVM in large cohort of normal individuals in the Uni

295 ignificantly increased only in patients with CMR-LVEF<40% (>=50%: 7%, 40%-49%: 9%, <40%: 27%, P<0.001

296 but significantly increased in patients with CMR-LVEF<40% (55/212, 26%; P<0.001).

297 %), the MACE rate was also low in those with CMR-LVEF>=40% (24/278, 9%) but significantly increased i

298 e underwent echocardiography with or without CMR according to the clinical presentation.

299 Patients without CMR ischemia or LGE experienced a low incidence of cardi

300 bjects (65% men; mean age 48 [18-80] years), CMR contributed to the diagnosis in 80 (49%) and was dec