ライフサイエンスコーパス: AF

1 AF ablation should be performed at early stages of the p

2 AF contained all the essential amino acids (EAA) except

3 AF genetic susceptibility was measured using a previousl

4 AF risk scores were strongly associated with 5-year inci

5 AF terminated in a majority of patients, with a high fre

6 AF terminated with ablation in 35 patients (55%) overall

7 AF upregulated nuclear protein expression of IP(3)R1 (IP

8 The study included 1546 AF cases and 41 593 controls.

9 ctors use a conserved activation function-2 (AF-2) helix 12 mechanism for agonist-induced coactivator

10 ponse was seen at 54 AFDs (77.1% of AFDs; 21 AF termination and 33 cycle length slowing) and occurred

11 VEF improvement (>35%) and recovery (>=50%), AF recurrence, and AF ablation were determined.

12 In the subset receiving targeted ablation, AF complexity showed lower values in those in whom AF te

13 ncluding 4-hydroxytamoxifen (4OHT), activate AF-1 preferentially rather than AF-2.

14 We developed algorithms to identify acute AF precipitants (surgery, sepsis, pneumonia, pneumothora

15 o develop an approach to identify additional AF-related genes by integrating multiple omics data.

16 chaemic and haemorrhagic complications after AF-associated ischaemic stroke.

17 ld only be detected very occasionally in all AF subgroups and were not locatable in patients with SR.

18 or men; and as a continuous variable) and an AF polygenic risk score for association with incident AF

19 In subgroup analyses, AF discrimination using EHR-AF was lower in individuals

20 transactivation functional domains, AF-1 and AF-2.

21 ation increased significantly in AF+AFLs and AF, but not AFL.

22 ardiomyocytes were isolated from control and AF dogs (kept in AF by atrial tachypacing [600 bpm x 1 w

23 rt, how RYR2 becomes dysfunctional in HF and AF, and its potential as a therapeutic target.

24 es suggested a link between inflammation and AF by findings of increased inflammatory markers in AF p

25 he vein of Marshall contains innervation and AF triggers that can be ablated by retrograde ethanol in

26 < 0.01) when compared to absence of NASH and AF (reference).

27 NASH and AF were associated with a greater risk of outcomes compa

28 The results showed notochordal NP and AF cells responded differently to changes of oxygen and

29 istinct genetic architecture of human NP and AF compartments and identified 2,196 differentially expr

30 5%) and recovery (>=50%), AF recurrence, and AF ablation were determined.

31 In patients with ischaemic stroke and AF, predictors of d-sICH are different than those of rec

32 to assess associations of asthma subtype and AF.

33 he underuse of OAC in patients with T2DM and AF.

34 was effective in reducing recurrence of any AF by 48% and symptomatic AF by 51% compared with drug t

35 classification of electrograms recordings as AF driver or nondriver compared with the NIOM gold-stand

36 a, prior MI and IHD (all P<0.001) as well as AF, stroke and HF (all P=0.01) were more often seen in m

37 alysis using a random effects model assessed AF recurrence stratified by DAT <=1 year versus >1 year.

38 ased side population (SP), autofluorescence (AF+) and Alde-red assays for CSCs, and Seahorse-based ox

39 ation patients, regardless of their baseline AF type.

40 carriers, a significant association between AF and rare LOF variants was observed in a single gene,

41 l evidence supporting an association between AF and SCD.

42 We assessed association between AF risk scores and 5-year incident AF, stroke, and heart

43 y and heart failure admissions in the CASTLE-AF study (Catheter Ablation for Atrial Fibrillation With

44 ke (1.61 using C(2)HEST to 1.92 using CHARGE-AF), and heart failure (1.91 using CHA(2)DS(2)-VASc to 2

45 (50 000 grids), CNN reproducibly classified AF image grids into those with/without rotational sites

46 ng and had follow-up for clinically detected AF since cohort entry.

47 ear clinical significance of device-detected AF, potential challenges in integrating patient-generate

48 umer electronic devices capable of detecting AF.

49 % male, mean age 56.9 years), 6293 developed AF during a median of 6.9 years of follow-up.

50 asthmatics are at higher risk for developing AF and that this association would be attenuated by adju

51 cantly higher risks of subsequent documented AF (incidence rate 136.4 vs 21.6 per 1000 person-years;

52 ning two transactivation functional domains, AF-1 and AF-2.

53 method are feasible and reproducible during AF.

54 alidated an electronic health record AF (EHR-AF) score in IBM Explorys Life Sciences, a multi-institu

55 bgroup analyses, AF discrimination using EHR-AF was lower in individuals with stroke (C index, 0.696

56 .85 using CHA(2)DS(2)-VASc to 2.88 using EHR-AF), stroke (1.61 using C(2)HEST to 1.92 using CHARGE-AF

57 .91 using CHA(2)DS(2)-VASc to 2.58 using EHR-AF).

58 Background The ENGAGE AF-TIMI 48 trial (Effective Anticoagulation With Factor

59 to Eliminate Atrial Fibrillation (ERADICATE-AF) trial was an investigator-initiated, multicenter, si

60 gion of Klk1b21 gene responded as an ERalpha AF-1-dependent estrogen-responsive promoter.

61 trial fibrillation (AF), but many experience AF recurrence and require repeat ablation procedures.

62 Between the 1990s and 2010s, adult female (AF) seasonal ranges more than doubled in spring and summ

63 CLOSE-guided atrial fibrillation (AF) ablation is based on contiguous (intertag distance <

64 tients with nonvalvular atrial fibrillation (AF) after percutaneous coronary intervention (PCI) is un

65 pendent risk factor for atrial fibrillation (AF) and is associated with a higher AF burden.

66 dence and prevalence of atrial fibrillation (AF) are rising, justifying the term global epidemic.

67 ablation of persistent atrial fibrillation (AF) has limited success.

68 h on atrial fibrosis in atrial fibrillation (AF) has mainly focused on quantitative or molecular feat

69 rhagic complications in atrial fibrillation (AF) have been studied, but there are limited data on pre

70 mic agents approved for atrial fibrillation (AF) in patients with reduced left ventricular ejection f

71 f catheter ablation for atrial fibrillation (AF) in reference to the time of diagnosis is unknown.

72 Growing prevalence of atrial fibrillation (AF) in the ageing population and its associated life-cha

73 Atrial fibrillation (AF) is a highly prevalent cardiac arrhythmia and cause o

74 Atrial fibrillation (AF) is associated with a risk of ischemic stroke, and fu

75 ticoagulants (DOACs) in atrial fibrillation (AF) is dependent on adherence and persistence in the rea

76 Susceptibility to atrial fibrillation (AF) is determined by well-recognized risk factors such a

77 The incidence of atrial fibrillation (AF) is higher in patients with diabetes.

78 Atrial fibrillation (AF) is the most common clinical arrhythmia and is associ

79 Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia in c

80 evidence suggests that atrial fibrillation (AF) may be associated with an increased risk of sudden c

81 ssociated with incident atrial fibrillation (AF) may improve the understanding of the pathophysiology

82 Atrial fibrillation (AF) may occur after an acute precipitant and subsequentl

83 Atrial fibrillation (AF) often arises from structural abnormalities in the le

84 Asthma and atrial fibrillation (AF) share an underlying inflammatory pathophysiology.

85 of clinically detected atrial fibrillation (AF) than whites, despite a higher prevalence of major AF

86 zed 2,204 patients with atrial fibrillation (AF) to catheter ablation or drug therapy.

87 ong-standing persistent atrial fibrillation (AF) treatment led to the development of a minimally inva

88 rces, the management of atrial fibrillation (AF), a common chronic disease with significant associate

89 se, hypertension (HTN), atrial fibrillation (AF), and chronic obstructive pulmonary disease (COPD).

90 ategy for patients with atrial fibrillation (AF), but many experience AF recurrence and require repea

91 pendent risk factor for atrial fibrillation (AF), but the underlying pathophysiological mechanisms re

92 D), heart failure (HF), atrial fibrillation (AF), stroke, peripheral artery disease, cancer, liver-,

93 ic loci associated with atrial fibrillation (AF), the most common arrhythmia.

94 Atrial fibrillation (AF), the most common sustained cardiac arrhythmia, is as

95 ic loci associated with atrial fibrillation (AF).

96 eatment for symptomatic atrial fibrillation (AF).

97 e of NASH and concomitant advanced fibrosis (AF) was significantly associated with clinical outcomes

98 gger ablation in patients undergoing a first AF ablation procedure in a small randomized study.

99 oxin secreting strain of Aspergillus flavus (AF-LHP-S1) and 12 other food borne moulds as well as AFB

100 4% for AF = 2 and reaching MNAD of 13.1% for AF = 8.

101 e best method starting with MNAD of 7.4% for AF = 2 and reaching MNAD of 13.1% for AF = 8.

102 negative predictive value) of 1.5% (66%) for AF detection, increasing to 8.3% (67%) for twice-daily 3

103 this review, we argue that current drugs for AF are inadequate because of an oversimplified system fo

104 The area of molecular intervention for AF management presents exciting new opportunities, along

105 transcriptional regulatory network model for AF defined by effector genes in Genome-wide association

106 ved histological findings in goat models for AF and AV block (AVB) using JavaCyte.

107 ty of approaches to facilitate screening for AF using both medical-prescribed devices as well as cons

108 ion, and development of new therapeutics for AF.

109 ead to a novel, mechanism-guided therapy for AF.

110 a complementary risk communication tool for AF in clinical practice.

111 In Brazil's Atlantic Forest (AF) biodiversity conservation is of key importance since

112 y Osborne procedure and the alkali fraction (AF, 45.82%) was found to be the predominant fraction.

113 ed pathogen-specific attributable fractions (AFs) of diarrhea.

114 Ultrarare variants (allele frequency [AF] < 0.0001) of 35 genes responsible for autosomal domi

115 are needed to ensure long-term freedom from AF recurrences in these high-risk patients.

116 the proportion of patients with freedom from AF/atrial tachycardia after a single procedure was 49.2%

117 jority of patients, with a high freedom from AF/atrial tachycardia off antiarrhythmic drugs at long-t

118 s has been identified in atrial samples from AF patients.

119 ealed histological characteristics of fundus AF abnormalities.

120 Furthermore, AF burden was also significantly reduced in catheter abl

121 glioside species were associated with future AF.

122 Forty-six had AF episodes during the overnight sleep study.

123 llation (AF) and is associated with a higher AF burden.

124 gies have been used to successfully identify AF in a variety of clinical and community settings, and

125 cyte function and ionic currents that impact AF risk.

126 ctive analysis of intracardiac activation in AF, which could be applied clinically if CNN classificat

127 acuity lagged behind central RPE atrophy in AF images.

128 erated the accumulation of storage bodies in AF(+) cells and led to impaired microglia physiology and

129 e isolated from control and AF dogs (kept in AF by atrial tachypacing [600 bpm x 1 week]).

130 indings of increased inflammatory markers in AF patients.

131 el expression is a known causal mechanism in AF.

132 Despite substantial unmet needs in AF prevention and treatment, drug developments hitherto

133 likely contributes to electric remodeling in AF by upregulating I(KACh) by a mechanism involving freq

134 nd the maintenance of electric remodeling in AF, as well, and (2) can be successfully prevented with

135 duced AF duration increased significantly in AF+AFLs and AF, but not AFL.

136 atrial repolarization changes like those in AF but, unlike AF or AF+AFLs, does not induce structural

137 athophysiology and prognosis, but its use in AF-related stroke remains limited.

138 polygenic predisposition to AF, and incident AF in the UK Biobank, a prospective cohort study.

139 were associated with higher risk of incident AF.

140 nic risk score for association with incident AF.

141 ere strongly associated with 5-year incident AF (hazard ratio per SD increase 1.85 using CHA(2)DS(2)-

142 n between AF risk scores and 5-year incident AF, stroke, and heart failure using Cox proportional haz

143 Induced AF duration increased significantly in AF+AFLs and AF, b

144 he strongest candidate for ibrutinib-induced AF.

145 whites, despite a higher prevalence of major AF risk factors and higher risk of ischemic stroke.

146 Many AF-associated genetic variants reside in noncoding regio

147 ocardial interface by fragmentation mapping (AF-Nests) using the velocity fractionation software, con

148 tions for the management of obesity-mediated AF in patients.

149 on of EBE and TIE is essential for mediating AF-1-dependent transactivation.

150 tes tachypaced at 3 Hz for 24 hours mimicked AF-type [Ca(2+)](Nuc) changes and L-type calcium current

151 At 12 months, AF burden in ablation patients averaged 6.3%, and in dru

152 Although "natural" AF is nearly nonexistent in most species, animal models

153 The NEW-AF study has been designed as a pragmatic, prospective,

154 Cardiac Surgery Atrial Fibrillation: The NEW-AF Trial.

155 ive analysis of non-normalized SW-AF and NIR-AF images; signal intensities were significantly lower i

156 , reduced 11-cis-retinal levels, qAF and NIR-AF intensities, and photoreceptor loss were consistent w

157 ecreased near-infrared autofluorescence (NIR-AF) provided evidence for retinal pigment epithelial cel

158 Postoperative AF vs no AF after noncardiac surgery.

159 ere blocked by atropine or DAU 5884, but not AF-DX 116.

160 dentified patients who had undergone de novo AF ablation.

161 calibration of predicted AF risk to observed AF incidence.

162 The laser was invisible (OCT, AF, Fundoscopy) in 91,3% (21/23) of eyes.

163 More than 98% of AF ablations among participating sites are performed for

164 Ablation of AF drivers holds promise, but current technologies to id

165 been proposed to explain the association of AF and dementia.

166 nistic treatments directed at root causes of AF.

167 regulator of a functionally related class of AF-miRNAs.

168 lmonary vein isolation is the cornerstone of AF ablation, and methods to improve ablation safety and

169 d stroke prophylaxis are the cornerstones of AF therapy.

170 al networks, have enabled the development of AF screening pathways using the ubiquitous 12-lead ECG t

171 reased the incidence of reported episodes of AF/AFL adverse events in high-risk patients with type 2

172 d KDM4E as signature transcription factor of AF and NP respectively, which might be involved in the r

173 PFA beyond paroxysmal to persistent forms of AF.

174 nd estimated the predicted mean time free of AF and alive over a time horizon of 10 years.

175 ded to predicted mean time alive and free of AF of 9.9, 9.6, and 8.8 years, respectively.

176 involved in the regulation of core genes of AF and NP transcriptome.

177 Family history of AF was defined as the presence of AF in a first-degree r

178 AF progression: 181 (65%) had no history of AF, 49 (18%) had paroxysmal AF, and 48 (17%) had permane

179 ardless of the patient's previous history of AF, atherosclerotic cardiovascular disease, or HF.

180 real-time, high-resolution identification of AF drivers in persistent AF.

181 ns in pacing rate upon the implementation of AF-induced electrical remodelling associated with SND ag

182 k prediction, and prognostic implications of AF and its complications.

183 ts to understand the molecular mechanisms of AF and cardiac conduction phenotypes.

184 ch in a canine, rapid atrial pacing model of AF, we demonstrate that NADPH oxidase 2 (NOX2) generated

185 research to optimize the use and outcomes of AF ablation.

186 ing key pathways driving the pathogenesis of AF.

187 ere not sensitive to the baseline pattern of AF.

188 ystem in the development and perpetuation of AF.

189 ors of LVEF improvement included presence of AF during echocardiogram (odds ratio, 4.22 [95% CI, 1.71

190 history of AF was defined as the presence of AF in a first-degree relative: mother, father, sibling,

191 Total prevalence of AF was 4.3%.

192 At the molecular level, the proteome of AF(+) microglia showed overrepresentation of endolysosom

193 with cryptogenic stroke), the refinement of AF and stroke prediction schemes through comprehensive d

194 actor to be associated with a higher risk of AF as a single factor (adjusted hazard ratio 1.11, 95% c

195 ), and high (>15%) 10-year predicted risk of AF corresponded to predicted mean time alive and free of

196 was associated with a lower relative risk of AF recurrence compared with DAT >1 year (relative risk,

197 and estimated the 10-year predicted risk of AF.

198 the relative contributions of simulations of AF induction and raw images to the predictive capability

199 that when only features from simulations of AF induction were used to train the ML classifier, its p

200 s with HFpEF were categorized into stages of AF progression: 181 (65%) had no history of AF, 49 (18%)

201 AS (Transcriptome-Wide Association Study) of AF.

202 d EWAS (Epigenome-Wide Association Study) of AF; and (3) a whole blood TWAS (Transcriptome-Wide Assoc

203 amine the annual prevalence and treatment of AF in T2DM.

204 ibuted significantly to our understanding of AF and some therapeutic options.

205 A better biological understanding of AF is needed to spearhead novel therapeutic avenues.

206 , we sought to determine the impact of BS on AF type.

207 hat flecainide has antiarrhythmic effects on AF due to impaired Pitx2 by preventing spontaneous calci

208 3 data sets from patients with at least one AF billing code from 2010 to 2017: a training set (n=886

209 New-onset AF lasting >=6 minutes was adjudicated by senior cardiol

210 n changes like those in AF but, unlike AF or AF+AFLs, does not induce structural remodeling.

211 0 years; 116 [62%] men; 102 [54%] paroxysmal AF; CHA(2)DS(2)-VASc, 2.6+/-1.7).

212 2-lead ECG to detect asymptomatic paroxysmal AF in at-risk populations (such as those with cryptogeni

213 ad no history of AF, 49 (18%) had paroxysmal AF, and 48 (17%) had permanent AF.

214 Drug refractory, paroxysmal AF was the most common ablation indication (class I, 53.

215 r CLOSE protocol in patients with paroxysmal AF significantly increases the global procedural efficie

216 ric study including patients with paroxysmal AF, planned for first CLOSE-guided pulmonary vein isolat

217 comorbidities than patients with paroxysmal AF.

218 ad paroxysmal AF, and 48 (17%) had permanent AF.

219 ans and conduction alternans that perpetuate AF.

220 phase mapping of prolonged human persistent AF recordings shows significant Endocardial-epicardial d

221 n identification of AF drivers in persistent AF.

222 ents with persistent/long-lasting persistent AF (group 1; 59 males; 60+/-11 years; 91 mitral disease-

223 utive patients with paroxysmal or persistent AF who underwent cryoballoon pulmonary vein isolation an

224 .6%) followed by drug refractory, persistent AF (class I, 41.8%).

225 of Marshall Ethanol for Untreated Persistent AF (VENUS) trial was an investigator-initiated, National

226 bidity (67.6%), and patients with persistent AF had more comorbidities than patients with paroxysmal

227 Patients (N = 350) with persistent AF referred for first ablation were enrolled from Octobe

228 Patients with persistent AF<2 years were included.

229 Postoperative AF vs no AF after noncardiac surgery.

230 ith precipitants occurred with postoperative AF (5-year incidence 32% in cardiac surgery and 39% in n

231 Patients with postoperative AF had statistically significantly higher risks of subse

232 for patients with and without postoperative AF (incidence rate, 42.5 vs 25.0 per 1000 person-years;

233 The POWER-AF study is a prospective, randomized controlled monocen

234 sing C indices, and calibration of predicted AF risk to observed AF incidence.

235 The control group received AF ablation using the standard CLOSE protocol (35 W), wh

236 rnally validated an electronic health record AF (EHR-AF) score in IBM Explorys Life Sciences, a multi

237 A mitochondrial antioxidant reduced AF burden, restored I(Na), I(Ca,L), I(Kur), action poten

238 ase-related AF, 30 nonmitral disease-related AF) and from 39 patients in sinus rhythm with mitral val

239 es; 60+/-11 years; 91 mitral disease-related AF, 30 nonmitral disease-related AF) and from 39 patient

240 omics approach identified many more relevant AF-related genes than using AFGen 2018 GWAS alone (1931

241 gies offer great promise for revolutionizing AF detection and screening, several major barriers may i

242 In cancer patient samples, RITA, AF, and Onc-1 sensitized to poly(ADP-ribose) polymerase

243 s may be effective for primary and secondary AF prevention.

244 sociated with maximum PWD, including several AF loci (TTN, CAND2, SCN10A, PITX2, CAV1, SYNPO2L, SOX5,

245 The wines produced by simultaneous AF/MLF showed the highest contents of some volatile comp

246 Yet since AF is often asymptomatic, many individuals with AF may b

247 Complexity, defined as the number of stable AF reentrant sites, was concordant between noninvasive a

248 m to enhance the competencies of early-stage AF basic, clinical, and population health researchers th

249 We studied AF type before and after BS in 220 morbidly obese patien

250 rare TTN(LOF) variants confer a substantial AF penetrance, the additive effect of many common varian

251 acing); AF superimposed on an AFL substrate (AF+AFLs); sinus rhythm (SR) with an AFL substrate (SR+AF

252 llowed for 3 weeks: sustained AFL; sustained AF (600 beats/min atrial tachypacing); AF superimposed o

253 y quantitative analysis of non-normalized SW-AF and NIR-AF images; signal intensities were significan

254 eir asymptomatic carrier parents, reduced SW-AF intensities, measured as quantitative fundus autofluo

255 ritance and disease-causing gene by using SW-AF imaging and spectral-domain optical coherence tomogra

256 recurrence of any AF by 48% and symptomatic AF by 51% compared with drug therapy over 5 years of fol

257 ained AF (600 beats/min atrial tachypacing); AF superimposed on an AFL substrate (AF+AFLs); sinus rhy

258 In each patient, ablation terminated AF.

259 T), activate AF-1 preferentially rather than AF-2.

260 yrosine kinase inhibitor, demonstrating that AF is an off-target side effect.

261 Ten centers from the AF Genetics Consortium identified patients who had under

262 ographic measures for ischemic stroke in the AF population but not incremental to global longitudinal

263 Moreover, the vast majority of the AF-associated variants lie within noncoding regions of t

264 e may be a desirable choice in reversing the AF-induced SND phenotype.

265 Fortunately, many of these AF drivers are potentially reversible, and emerging evid

266 with a greater risk of outcomes compared to AF (P = 0.01) or NASH alone (P < 0.01).

267 alcohol intake, polygenic predisposition to AF, and incident AF in the UK Biobank, a prospective coh

268 rger proportion of genetic susceptibility to AF.

269 Akita mice were highly susceptible to AF in association with increased P-wave duration and slo

270 nsulin-resistant heart and is susceptible to AF.

271 The increased risk was unrelated to AF and inserted mechanical valves.

272 Compared with pharmacological treatment, AF ablation was associated with a significant improvemen

273 onitors provide the opportunity for unbiased AF detection.

274 However, unbiased AF detection by ambulatory monitoring in the same indivi

275 Patients undergoing AF ablation were predominantly male (63.9%) and White (9

276 , and safety outcomes of patients undergoing AF ablation.

277 he electrophysiological mechanism underlying AF prevention was prolongation of atrial effective refra

278 s (P = 0.001); half were previously unknown (AF < 0.000002).

279 ization changes like those in AF but, unlike AF or AF+AFLs, does not induce structural remodeling.

280 We designed and implemented a virtual AF Strategically Focused Research Network Cross-Center F

281 pathophysiological mechanisms through which AF may promote or lead to SCD, as well as the existing e

282 ose in whom AF terminated than those in whom AF did not terminate (P<0.01).

283 plexity showed lower values in those in whom AF terminated than those in whom AF did not terminate (P

284 ters, and phospholipids were associated with AF prevalence, whereas two monosialodihexosylganglioside

285 The association with AF was more significant (odds ratio, 6.15, P=3.26x10(-14

286 included 2,694 veterans with cirrhosis with AF (n = 1,694 and n = 704 in the warfarin and DOAC cohor

287 Dogs with AF+AFLs had shorter cycle lengths and substantial irregu

288 is often asymptomatic, many individuals with AF may be unaware and do not receive treatment that coul

289 apping), including a subset of patients with AF (n = 28) with low CHA(2)DS(2)-VASc score (0/1 for men

290 OAC utilization was low in patients with AF and ESRD.

291 be patterns of OAC use in ESRD patients with AF and their associations with cardiovascular outcomes.

292 scanned using MOLLI, 99.3% of patients with AF had ECV below the fibrosis cutoff point (32.8% when c

293 ocessing algorithm to identify patients with AF using text alone, with >90% F-score at 2 separate sit

294 MDCT was performed in 89 patients with AF, analyzing the number of PVs, accessory variants and

295 ion of LA scar and fibrosis in patients with AF.

296 leeding and ischemic stroke in patients with AF.

297 All consecutive patients presenting with AF or atrial flutter on DOAC were included.

298 led little difference in the proportion with AF by race/ethnicity.

299 viduals with stroke risk factors but without AF were recruited from the general population to undergo

300 Patients without AF undergoing coronary artery bypass surgery were recrui

301 ng Cox proportional hazards modeling, 5-year AF discrimination using C indices, and calibration of pr