ライフサイエンスコーパス: CAD

1 raphic diagnoses of coronary artery disease (CAD).

2 ly in patients with coronary artery disease (CAD).

3 to as having stable coronary artery disease (CAD).

4 al causal effect on coronary artery disease (CAD).

5 th of patients with coronary artery disease (CAD).

6 ble risk factor for coronary artery disease (CAD).

7 ed lifetime risk of coronary artery disease (CAD).

8 isk factors causing coronary artery disease (CAD).

9 unctional group characterization compared to CAD.

10 f CTRPs (CTRP1, CTRP5, CTRP7, and CTRP15) in CAD.

11 rt equations, and both combined for incident CAD.

12 (CAD) loci and find molecular biomarkers for CAD.

13 diac death, and MI in patients with unstable CAD.

14 genomic regions known to be associated with CAD.

15 and the prevalence and extent of subclinical CAD.

16 represent novel therapeutic targets against CAD.

17 tithrombotic therapy in patients with DM and CAD.

18 as a marker for the single-vessel lesion of CAD.

19 or individuals at different genetic risk for CAD.

20 ronary angiography could exclude significant CAD.

21 ls (ECFCs) contribute to vascular repair and CAD.

22 GE in adult patients with known or suspected CAD.

23 to be men (78% vs. 73%) and had more severe CAD.

24 on studies revealed 163 loci associated with CAD.

25 ther they have nonobstructive or obstructive CAD.

26 ean age was 60 years, and 11,020 (23.4%) had CAD.

27 to affect a number of treatment choices for CAD.

28 at were causally associated with the risk of CAD.

29 AR duration were associated with low BDNF in CAD.

30 higher risk than presence of nonobstructive CAD.

31 ure television watching is a risk factor for CAD.

32 P5 may serve as an independent predictor for CAD.

33 suggesting it as one of the risk factors for CAD.

34 community to reconsider the role of T2DM in CAD.

35 ation of patients with suspected obstructive CAD.

36 applications of genetic risk score (GRS) of CAD.

37 is not reliable in screening LT patients for CAD.

38 SNPs showed that TG is not a risk factor for CAD.

39 ing that dads need not necessarily eliminate cads.

40 es, thus altering the fitness of dads versus cads.

41 .4% versus 10.2%, P<0.0001), have high-grade CAD (0.5% versus 6.5%, P<0.0001), and receive revascular

42 in the placebo group was related to PRS for CAD: 17.0% for high PRS patients (>90th percentile) and

43 was significantly lower in individuals with CAD (30.69 +/- 5.45 ng/ml) than controls (46.58 +/- 7.95

44 m BDNF concentration and blood parameters of CAD achieved significant improvement from 90.95 to 98.19

45 to explore associations between subclinical CAD and cumulative exposure to the 10 most frequently us

46 deeper insights into the genetic etiology of CAD and demonstrate knowledge gaps where further researc

47 In patients with multivessel CAD and diabetes, CABG was associated with improved long

48 rotic cardiovascular events in patients with CAD and DM.

49 Patients, without a history of CAD and no elevation in troponin, referred for PET/CT at

50 mandible expressed the epithelial markers E-Cad and P63.

51 redictive factors for the vascular lesion of CAD and represent novel therapeutic targets against CAD.

52 ssociation between CAC and 90-day high-grade CAD and revascularization were assessed.

53 a 201-variant polygenic risk score (PRS) for CAD and tested for interaction with diabetes prevention

54 sence of AGE-autoantibodies in patients with CAD and that in parallel to the AGEs themselves, they ma

55 ciated with risk of coronary artery disease (CAD) and cancer, whereas the Prudent dietary pattern (PD

56 eated patients with coronary artery disease (CAD) and concomitant type 2 diabetes mellitus (T2DM), T2

57 y autonomous downregulation of E-cadherin (E-cad) and consequent activity of p120-catenin.

58 ients with unstable coronary artery disease (CAD), and their recruitment to inflamed arteries is impl

59 For 27 genes we infer they are causal for CAD, and for 10 further genes we judge them most likely

60 on should be considered in future studies of CAD, and GRSs should not be assumed to perform equally w

61 Because Rho, EGF receptor (EGFR), and E-cad are associated with colorectal cancer in humans [10-

62 ts with obstructive coronary artery disease (CAD) are at high risk for cardiovascular disease (CVD) e

63 Because rates of coronary artery disease (CAD) are substantially higher among South Asians, a GPS

64 ption of guideline recommended therapies for CAD as well as clinical outcomes (emergency department p

65 isease-associated TGFB1-SMAD3 pathway to the CAD-associated FN1 gene through a response QTL that modu

66 loci, existing evidence suggested additional CAD-associated genes.

67 Functional analysis of non-CAD-associated loci implicate genes involved in cardiac

68 w systematized information for a total of 51 CAD-associated loci.

69 Identification of typical features of CAD-associated lymphoproliferative disorder in the bone

70 ulatory variants that mediate binding of the CAD-associated transcription factor TCF21 with ChIPseq s

71 The TL-CAD association remained significant when adjusting only

72 ied a sex-interaction whereby the inverse Mg-CAD association was much stronger among women than men.

73 s (ARIC) Study article that evaluated the Mg-CAD association, based on 319 events occurring over 4-7

74 are fee-for-service patients >=65 years with CAD at outpatient practices participating in the the Pra

75 d 232 patients with cold agglutinin disease (CAD) at 24 centers in 5 countries.

76 linder PAHs decreased following a peak at 10 CAD ATDC but subsequently increased significantly during

77 e associations with coronary artery disease (CAD), atrial fibrillation, or reduced left ventricular f

78 ve performance of a polygenic risk score for CAD based on summary statistics from published genome-wi

79 as strongly associated with reduced risk for CAD (beta = -0.315, OR = 0.729 per 1 SD (equivalent to 1

80 ing the full datasets, an increased risk for CAD (beta = 0.184, OR = 1.2 per 1 SD (equivalent to 89 m

81 strongly associated with increased risk for CAD (beta = 0.396,OR = 1.486 per 1 SD (equivalent to 38

82 tic associations with prevalent and incident CAD between men and women were investigated among 317 50

83 at TG itself is not a causal risk factor for CAD, but it's shown as a risk factor due to pleiotropic

84 d specificity of gadobutrol for detection of CAD by assessing myocardial perfusion and late gadoliniu

85 estimation of the likelihood of obstructive CAD by combining a pre-test probability (PTP) model (Dia

86 ysis demonstrated superior discrimination of CAD by flurpiridaz PET versus SPECT in the overall popul

87 t for 18 out of these loci, association with CAD can be explained by changes in gene expression in on

88 utes to the risk of coronary artery disease (CAD) can be evaluated as a risk score of multiple varian

89 .80 * 10(-84)), and the corresponding motif "CAD" captured the risk association of DQ2.5 (OR 2.10, P

90 baseline subsamples of UK Biobank: prevalent CAD cases (N = 10 287) and individuals without CAD (N =

91 er a median follow-up of 27 y, 2131 incident CAD cases accrued.

92 GPS(CAD) reference distribution using 1,800 CAD cases and 1,163 control subjects newly recruited in

93 A case-control sample of 15 947 prevalent CAD cases and equal number of age and sex frequency-matc

94 Additionally, among prevalent CAD cases, we found an evidence of an inverse associatio

95 Coronary artery disease (CAD) causes mortality and morbidity worldwide.

96 Through our CAD-centered multiomics data analysis approach, we ident

97 we observed a 2.4x higher risk for incident CAD comparing men with high genetic risk to men with low

98 A genome-wide PRS for CAD comprising 6 579 025 genetic variants was evaluated

99 n/Brain Stem, CNS, Computer Aided Diagnosis (CAD), Computer Applications-General (Informatics), Image

100 The GPS(CAD), containing 6,630,150 common DNA variants, had an o

101 CAD delineations of the area of neoplasm overlapped with

102 on imaging shows promise as a new tracer for CAD detection and assessment of women, obese patients, a

103 the role of non-obstructive CAD patients in CAD diagnostics.

104 and may help with comprehensive noninvasive CAD diagnostics.Supplemental material is available for t

105 Testing for CAD differed by LVEF: 53% in HF with reduced EF (LVEF <=

106 CAD discrimination for polygenic risk score, pooled coho

107 ronounced for those in the top 5% of the GPS(CAD) distribution-ORs of 4.16, 2.46, and 3.22 in the Sou

108 d miRNAs, down-regulation of miR-548aq-3p in CAD ECFCs after FIR treatment was observed in FIR-respon

109 FIR treatment was observed in FIR-responsive CAD ECFCs by RT-qPCR.

110 rrelated with the tube formation activity of CAD ECFCs enhanced by FIR.

111 n-regulated, respectively, in FIR-responsive CAD ECFCs in both genders.

112 he down-regulation of miR-548aq-3p by FIR in CAD ECFCs, we demonstrated through overexpression and kn

113 ube length) capacities in a subpopulation of CAD ECFCs.

114 for new-onset HF did not receive testing for CAD either during the hospitalization or in the 90 days

115 e of p120-catenin (p120) and VE-cadherin (VE-cad) endocytosis in vascular development using mouse mut

116 The following subclinical CAD endpoints were analyzed separately: CAC score >0, an

117 Cases had a first CAD event during 01.01.2000-31.12.2017.

118 L quintile had univariable and multivariable CAD event OR=0.56 (95% confidence interval, 0.35-0.91) a

119 easurement was 9.4 (5.9-13.8) years prior to CAD event.

120 ars before, is independently associated with CAD events after adjusting for multiple traditional and

121 More than 1700 additional ARIC CAD events have since accrued.

122 We matched 1-3 PLWH controls without CAD events on sex, age, and observation time.

123 he examined models, there were 6272 incident CAD events over a median of 8 years of follow-up.

124 CAD events were defined by myocardial infarction or CAD

125 Coronary artery disease (CAD) events have been associated with certain antiretrov

126 is associated with coronary artery disease (CAD) events in the general population.

127 their structures were examined using further CAD experiments (MS(n) experiments wherein n = 2-5).

128 e-wide association study to derive a new GPS(CAD) for South Asians.

129 erating characteristic curves of obstructive CAD: for the PTP model, 72 (95% confidence intervals [CI

130 iable and multivariable odds ratios (OR) for CAD from conditional logistic regression analyses.

131 mprovement from 90.95 to 98.19% in detecting CAD from healthy controls.

132 sure the BDNF level in the classification of CAD from healthy controls.

133 cal utility of CCTA across various stages of CAD, from the detection of early subclinical disease to

134 ive interventions improve CRFs regardless of CAD genetic risk and delivers hypothesis-generating data

135 ascular risk factors depending on individual CAD genetic risk profile.

136 ecreased in CAD patients compared to the non-CAD group.

137 g data from the UK Biobank, we constructed a CAD-GRS based on all known loci, 3 mediating trait-based

138 w that these QTLs are highly associated with CAD GWAS loci and correlate to lead SNPs where they show

139 The new GPS(CAD) has been developed and tested using 3 distinct Sout

140 icare patients with coronary artery disease (CAD) have been a significant focus of value-based paymen

141 In other forms of coronary artery disease (CAD), however, it has been controversial whether PCI red

142 l [CI], 0.79-2.33; P = 0.298; nonobstructive CAD, HR, 1.53; 95% CI, 0.84-2.77; P = 0.161; and signifi

143 5% CI, 0.84-2.77; P = 0.161; and significant CAD, HR, 1.96; 95% CI, 0.93-4.15; P = 0.080). Post-LT ou

144 c analyses to determine whether high PRS for CAD identifies higher-risk individuals, independent of b

145 sk scores (PRS) for coronary artery disease (CAD) identify high-risk individuals more likely to benef

146 sk scores (PRS) for coronary artery disease (CAD) identify individuals at higher risk who derive incr

147 Disrupt CAD III (NCT03595176) was a prospective, single-arm mult

148 LGE imaging had high diagnostic accuracy for CAD in 2 phase 3 clinical trials.

149 use of CAC in PET/CT patients without known CAD in identifying patients unlikely to need revasculari

150 is especially important in the evaluation of CAD in immune-driven conditions with increased cardiovas

151 thermore, by integrating the risk factors of CAD in our analysis, we were able to investigate the cli

152 of effective, patient-centered management of CAD in patients with T2DM, with emphasis on the emerging

153 It is unknown whether TL is associated with CAD in PLWH.

154 entifying patients with ACP with significant CAD in the ED setting and reduce unnecessary downstream

155 luding 5 studies, the pooled RR (95% CI) for CAD in the lowest compared with the highest circulating

156 ment in severity of coronary artery disease (CAD) in 52% (82 of 159) of all cases.

157 5 as a biomarker of coronary artery disease (CAD) in a real-world clinical practice setting.

158 Applied to coronary artery disease (CAD) in both the WGHS and in JUPITER (N = 8,749), a rand

159 each of the three potential risk factors for CAD including low density lipoprotein cholesterol (LDL-c

160 amples from patients treated for symptomatic CAD including non-ST elevation MI, along with healthy ag

161 ew-onset HF, 6672 (39%) received testing for CAD, including 3997 (23%) during the index hospitalizati

162 or several HF risk factors, and demonstrates CAD-independent effects for atrial fibrillation, body ma

163 e, termed SIC, that demarcates patients with CAD independently and more effectively than conventional

164 A total of 60 patients with CAD indicated for coronary artery bypass graft surgery (

165 and platelets were significantly elevated in CAD individuals compared to controls.

166 Herein, we leverage CAD-induced oxocarbenium ion generation to trigger ultra

167 ss age strata), ESRD (IRR range, 3.30-9.02), CAD (IRR range, 2.77-10.7), and COPD (IRR range, 5.89-8.

168 A high PRS for CAD is associated with elevated risk for recurrent MACE

169 The concept of 'stable' CAD is misleading for two important reasons: the continu

170 Coronary artery disease (CAD) is a major cause of morbidity and mortality worldwi

171 th before and after coronary artery disease (CAD) is established.

172 hing a diagnosis of coronary artery disease (CAD) is more difficult than it would seem.

173 Coronary artery disease (CAD) is more frequent among individuals with dysglycemia

174 ediction models for coronary artery disease (CAD) is uncertain.

175 atients with stable coronary artery disease (CAD) is unknown.

176 unravel the functional mechanisms underlying CAD loci and to identify novel molecular biomarkers.

177 chanisms underlying coronary artery disease (CAD) loci and find molecular biomarkers for CAD.

178 ed were enriched in coronary artery disease (CAD) loci, and this result has specific implications for

179 revealed that CTRP7 and CTRP15 may serve as CAD markers, while CTRP1 may serve as a marker for the s

180 athways were determined by comparison of the CAD mass spectra measured for undeuterated and deuterate

181 -for-service patients >=65 years of age with CAD (mean [SD] age, 75.3 [7.7] years; 39.7% female) care

182 entifying appropriate candidates for optimal CAD medical therapy and revascularization.

183 dels predicted the prevalence of obstructive CAD more accurately in the validation cohorts than the P

184 nts were defined by myocardial infarction or CAD mortality.

185 bjected to collision-activated dissociation (CAD; MS(2) experiments).

186 CAD (myocardial infarction and its related sequelae).

187 giogram examination as control (n = 105) and CAD (n = 116).

188 D cases (N = 10 287) and individuals without CAD (N = 393 108), we evaluated associations between a C

189 Flurpiridaz F 18 Injection in Patients with CAD; NCT01347710).

190 e primary endpoint (MACE) comprised death of CAD, nonfatal myocardial infarction, ischemic stroke, or

191 the highest 5% of the PRS to the lowest 95%, CAD odds ratio was 1.36 (95% CI, 1.24-1.49) for the LDL-

192 e CAD PRS strongly associated with prevalent CAD (odds ratio: 1.4 per SD increase in PRS; p < 0.0001)

193 red to collisionally activated dissociation (CAD) on a series of agrochemicals.

194 05) in the cardiac samples of the CAD+P than CAD only (25% and 47.2%, respectively).

195 PET/CT patients unlikely to have high-grade CAD or require revascularization within 90 days and unli

196 on was found for ischaemic stroke [prevalent CAD (OR 0.78; 95% CI 0.67, 0.90); without CAD (OR 1.09;

197 % CI 0.85, 0.98) compared with those without CAD (OR 1.01; 95% CI 0.99, 1.03) and heterogeneity P = 0

198 nt CAD (OR 0.78; 95% CI 0.67, 0.90); without CAD (OR 1.09; 95% CI 1.04, 1.15), heterogeneity P < 0.00

199 ted the association of smoking behavior with CAD (OR 1.24, 95% CI: 1.12-1.37, P = 2 x 10-5), but not

200 1.5 hour increase in television watching and CAD (OR 1.44, 95%CI 1.25-1.66, P = 5.63 x 10(-07)), that

201 mically disadvantaged populations have worse CAD outcomes, and if this reflects the delivery of lower

202 f PRS) conferred 1.9-fold odds of developing CAD (p < 0.0001).

203 ng age, male gender, and personal history of CAD (P < 0.05 for all).

204 vely, P <0.05) in the cardiac samples of the CAD+P than CAD only (25% and 47.2%, respectively).

205 10(-36), OR = 0.95 [95% CI: 0.94-0.96], for CAD; P = 3.35 x 10(-6), OR = 0.96 [95% CI: 0.95-0.98] fo

206 as CTRP7 and CTRP15 levels were decreased in CAD patients compared to the non-CAD group.

207 c profile that distinguishes non-obstructive CAD patients from no CAD patients is associated with hig

208 goal to identify the role of non-obstructive CAD patients in CAD diagnostics.

209 guishes non-obstructive CAD patients from no CAD patients is associated with higher precision, sugges

210 ECFCs from CAD patients that smoke did not respond to FIR in most c

211 f periodontal viruses such as EBV and CMV in CAD patients with periodontitis suggesting it as one of

212 more suitable biomarker for the diagnosis of CAD patients, whereas CTRP5 may serve as an independent

213 el biomarker for therapeutic usage of FIR in CAD patients.

214 or diagnosis of severity of vessel-lesion of CAD patients.

215 in non-ST elevation MI compared with stable CAD patients.

216 biomarkers for indication of FIR therapy in CAD patients.

217 In unstable CAD, PCI also reduced cardiac death (RR, 0.69 [95% CI, 0

218 For stable CAD, PCI did not reduce mortality (RR, 0.98 [95% CI, 0.8

219 For patients with stable CAD, PCI shows no evidence of an effect on any of these

220 ocioeconomically disadvantaged patients with CAD perform worse on some clinical outcomes, despite pro

221 Polygenic risk score for CAD, pooled cohort equations, and both combined.

222 ulticenter cohort of patients with suspected CAD, presence of UMI or RMI portended an equally signifi

223 An opportunity may exist to improve CAD prevention efforts by integrating both genetic and c

224 thin healthy limits is a useful strategy for CAD prevention remains to be seen.

225 In patients with DM without established CAD, primary prevention with aspirin is not routinely ad

226 tates for detecting coronary artery disease (CAD) prior to the current studies.

227 d search approach, applied to two phenotypic CAD profiles.

228 rd an inflammatory phenotype associated with CAD progression is unknown.

229 of this study was to evaluate if obstructive CAD provides predictive value beyond its association wit

230 nly slightly attenuated when adjusting for a CAD PRS (odds ratio, 1.26 [95% CI, 1.16-1.38] for LDL-C

231 93 108), we evaluated associations between a CAD PRS and incident cardiovascular and fatal outcomes.

232 idence of an inverse association between the CAD PRS and risk of all-cause death (OR 0.91; 95% CI 0.8

233 The CAD PRS strongly associated with prevalent CAD (odds rat

234 A genome-wide CAD PRS was applied to 47,108 individuals across 3 U.S.

235 ay be recommended for statin therapy if high CAD PRS were considered a guideline-based risk-enhancing

236 ipid levels and partially overlapping with a CAD PRS.

237 the hands of nonprovisioning, mate-seeking "cads." Recent models require exacting interplay between

238 ndividuals onto this static ancestry and GPS(CAD) reference distribution using 1,800 CAD cases and 1,

239 Next, a static ancestry and GPS(CAD) reference distribution was built using whole-genome

240 In the present study, we aimed to prioritize CAD-relevant genes based on cumulative evidence from the

241 by changes in gene expression in one or more CAD-relevant tissues.

242 essing the risks of coronary artery disease (CAD) remains controversial.

243 nd 559 underwent CATH (69%), of whom 10% had CAD requiring PCI.

244 sess for high-grade coronary artery disease (CAD) requiring revascularization.

245 all, low serum Mg was associated with higher CAD risk after adjustment for demographics, lifestyle fa

246 for future clinical detection and improving CAD risk assessment.

247 The CAD risk associated with a high polygenic load for lipid

248 r demographics, lifestyle factors, and other CAD risk factors than was higher serum Mg (HR Q1 compare

249 and independently associated with long-term CAD risk in ARIC and in a meta-analysis with other prosp

250 We generated a novel sphingolipid-inclusive CAD risk score, termed SIC, that demarcates patients wit

251 ow circulating Mg was associated with higher CAD risk than was higher Mg.

252 terolemia associates with severely increased CAD risk, it remains less clear to what extent a high po

253 to stop smoking to limit type 2 diabetes and CAD risk.

254 ncreasing variants associates with increased CAD risk.

255 ional mechanisms of coronary artery disease (CAD) risk, as well as the functional regulation of chrom

256 omic loci affecting coronary artery disease (CAD) risk.

257 ociated with higher coronary artery disease (CAD) risk.

258 eir Combined Annotation Dependent Depletion (CADD) scores.

259 the design of tandem mass spectrometry-based CAD sequencing strategies for mixtures of lignin degrada

260 zard rates (HR) for mortality increased with CAD severity (normal CATH, HR, 1.35; 95% confidence inte

261 tases in lungs, and functional deletion of N-cad significantly reduced metastasis.

262 The CAD system achieved higher accuracy than any of the indi

263 The CAD system classified images as containing neoplasms or

264 The CAD system identified the optimal site for biopsy of det

265 of experience from 4 countries to benchmark CAD system performance.

266 We developed a hybrid ResNet-UNet model CAD system using 5 independent endoscopy data sets.

267 et 5 (80 patients and images) values for the CAD system vs those of the general endoscopists were 88%

268 rams to gauge the performance of emerging AI CAD systems.

269 ligence (AI)-based computer-aided detection (CAD) systems for use in screening mammography.

270 e of BDNF as a potential diagnostic value in CAD that might lead to clinical application.

271 pathophysiology in coronary artery disease (CAD) that may shed light upon potential diagnostic bioma

272 For both prevalent and incident CAD, the associations of comprehensive and genome-wide G

273 as the first-line test for the evaluation of CAD, the ISCHEMIA trial also resulted in some interestin

274 In contrast with a PRS for CAD, the lipid PRSs point to known and directly modifiab

275 sive risk factor management in patients with CAD, there is mounting evidence that the mechanism by wh

276 African American) were followed for incident CAD through 2017.

277 6514 within the BSN gene exert its effect on CAD through central nervous system-lifestyle risk factor

278 A3, ILF3, and N4BP2L2) exert their effect on CAD through height.

279 obstructive disease: 6.1 per 1,000 PY for no CAD to 34.7 per 1,000 PY for 3-vessel disease).

280 s periprocedural management of patients with CAD undergoing non-cardiac surgery, including those trea

281 ation between eQTLs and loci associated with CAD using SMR/HEIDI approach.

282 Evaluation of coronary artery disease (CAD) using coronary computed tomography angiography (CCT

283 In symptomatic patients with CAD, very low hs-cTn concentrations, including hs-cTnI c

284 The prevalence of CAD was 27.8% defined by a >=70% QCA stenosis.

285 ss echocardiography in detecting significant CAD was 37%.

286 sensitivity and specificity for multivessel CAD was 87.4% and 73.0%.

287 The optimal threshold for detecting CAD was a >=67% QCA stenosis in GadaCAD1 and >=63% QCA s

288 CAD was defined by quantitative coronary angiography (QC

289 Compared with the middle quintile, risk for CAD was most pronounced for those in the top 5% of the G

290 00, and >1,000), the presence of obstructive CAD was not associated with higher risk than presence of

291 This GPS(CAD) was validated in 7,244 South Asian UK Biobank parti

292 viously in mostly asymptomatic patients with CAD, was assessed.

293 In dispelling the myth of 'stable' CAD, we explore the pathophysiology of the disease and t

294 years of age, 53% were male) with suspected CAD were assessed by stress CMR and followed over a medi

295 0 consecutive patients with suspected stable CAD who had undergone coronary computed tomographic angi

296 with angiographic evidence of 2- or 3-vessel CAD who were treated with either PCI or isolated CABG fr

297 ssification of patients to low likelihood of CAD, who need no further testing.

298 Charged aerosol detection (CAD), whose response is proportional to the amount of no

299 syndrome; and (4) patients with truly stable CAD with no recent infarct.

300 markers causally associated with the risk of CAD within genomic regions known to be associated with C