ライフサイエンスコーパス: coronary artery disease

1 in values, and have more severe angiographic coronary artery disease.

2 ic instability in the absence of obstructive coronary artery disease.

3 t ischemic attack, age >=75, and no previous coronary artery disease.

4 the risk of SCD and non-SCD in patients with coronary artery disease.

5 in patients with subclinical, nonobstructive coronary artery disease.

6 tment strategy for patients with symptomatic coronary artery disease.

7 ification in patients with clinically stable coronary artery disease.

8 nary disease, interstitial lung disease, and coronary artery disease.

9 cholesterol levels and hence development of coronary artery disease.

10 ted in female and male patients with complex coronary artery disease.

11 ar arrhythmias in patients with a history of coronary artery disease.

12 e from structurally normal vessels to severe coronary artery disease.

13 he most common mode of revascularization for coronary artery disease.

14 ed the association between CHIP and incident coronary artery disease.

15 and atherothrombotic events in patients with coronary artery disease.

16 traditional risk factors of atherosclerotic coronary artery disease.

17 ual inflammation in patients at high risk of coronary artery disease.

18 are thus key to understand the pathology of coronary artery disease.

19 aluated in a phase 2a study for treatment of coronary artery disease.

20 features, including variants associated with coronary artery disease.

21 ment, and therapy guidance for patients with coronary artery disease.

22 among persons with genetic predisposition to coronary artery disease.

23 e identified chromosome 14q32 as a locus for coronary artery disease.

24 disease, but not in patients with left main coronary artery disease.

25 that involve chronic inflammation including coronary artery disease.

26 TCFA, as well as expand our understanding of coronary artery disease.

27 e characteristics in patients with suspected coronary artery disease.

28 revascularization in patients with 3-vessel coronary artery disease.

29 -related biomarkers with type 2 diabetes and coronary artery disease.

30 hypertension and valvular heart disease) or coronary artery disease.

31 with rates highest in those with CT-defined coronary artery disease.

32 cardiovascular outcomes among patients with coronary artery disease.

33 rse cardiovascular outcomes in patients with coronary artery disease.

34 n humans, TCF21 expression inhibits risk for coronary artery disease.

35 rely performed for patients with multivessel coronary artery disease.

36 rtality at 10 years in patients with complex coronary artery disease.

37 larisation strategy in patients with complex coronary artery disease.

38 ray of applications beyond the assessment of coronary artery disease.

39 or the treatment of hypercholesterolemia and coronary artery disease.

40 n myocardial infarction (MI) and multivessel coronary artery disease.

41 ty, such as hypertension, hyperlipidemia, or coronary artery disease.

42 s correlates with angina in individuals with coronary artery disease.

43 n the workup of patients suspected of having coronary artery disease.

44 cardiovascular events in those without overt coronary artery disease.

45 chemic cause in patients with nonobstructive coronary artery disease.

46 iovascular events (MACE) in individuals with coronary artery disease.

47 95% confidence interval [CI], 1.60 to 2.41), coronary artery disease (10.2%, vs. 5.2% among those wit

48 e by age 75 years ranged from 17% to 78% for coronary artery disease, 13% to 76% for breast cancer, a

49 In patients with established coronary artery disease, (18)F-NaF PET provides powerful

50 quency of 1-vessel disease or nonobstructive coronary artery disease (39.6% versus 29.1%, P<0.0001).

51 The most common cause of SCD was coronary artery disease (40%), followed by sudden arrhyt

52 s; P<0.001), and the presence of obstructive coronary artery disease (54% versus 25%; P<0.001) were a

53 Methods: 1,160 patients without known coronary artery disease (64% male) were studied.

54 Higher rates of coronary artery disease (76.5% versus 50.6%, P<0.001), m

55 11-1.81]), and among patients with left main coronary artery disease, 95 (27%) of 357 had died after

56 In patients with 3-vessel coronary artery disease, a noninvasive physiology assess

57 developing important common diseases.(,) For coronary artery disease, about 8% of the population can

58 32 145 patients: 14 095 (43.8%) with stable coronary artery disease and 18 046 (56.1%) with acute co

59 These patients have a significant burden of coronary artery disease and acute coronary thrombotic ev

60 Coronary artery disease and aortic stenosis often coexis

61 Patients with preexisting diagnoses of coronary artery disease and arrhythmia had the highest l

62 y contribute to observed clinical effects on coronary artery disease and blood pressure regulation.

63 s without evidence of obstructive epicardial coronary artery disease and healthy left ventricular eje

64 icantly increased in cardiovascular disease (coronary artery disease and heart failure) after adjustm

65 n (STEMI) is the most acute manifestation of coronary artery disease and is associated with great mor

66 l infarction (MI) is common in patients with coronary artery disease and is associated with high mort

67 In conclusion, prediabetes likely causes coronary artery disease and its prevention is likely to

68 ed 5706 ventricular MAPs in 42 patients with coronary artery disease and left ventricular ejection fr

69 reported associations with increased risk of coronary artery disease and lower risk for multiple canc

70 3.02]) and (2) lower risk of atherosclerotic coronary artery disease and MI in the UK Biobank (P = 1.

71 evoted to understanding the genetic basis of coronary artery disease and other common, complex cardio

72 ferior to CABG in the treatment of left main coronary artery disease and reported outcomes after a me

73 ction between a previously validated PGS for coronary artery disease and the seemingly most disadvant

74 latelet count, and on disease traits such as coronary artery disease and type 2 diabetes.

75 PRSs for coronary artery disease and years of education were sign

76 iagnosis and PRP) and medical comorbidities (coronary artery disease and/or myocardial infarction, he

77 ease type (three-vessel disease or left main coronary artery disease) and anatomical SYNTAX score.

78 cohorts; p.R220W of ATG16L2 (associated with coronary artery disease) and p.V326A of POT1 (associated

79 history of cardiovascular disease, premature coronary artery disease, and a diagnosis of FH.

80 indicated genetic correlation between CAVS, coronary artery disease, and cardiovascular risk factors

81 ith glycated hemoglobin 6.5% to 10.0%, known coronary artery disease, and estimated glomerular filtra

82 , p <0.05) included end-stage renal disease, coronary artery disease, and neurologic disorders, but n

83 ents with de-novo three-vessel and left main coronary artery disease, and reported results up to 5 ye

84 Risk factors include tobacco use, coronary artery disease, and respiratory failure.

85 igh-density lipoprotein cholesterol content, coronary artery disease, and the inflammatory biomarker

86 7.2%) and was associated with age, male sex, coronary artery disease, and vasopressor use.

87 erotic cardiovascular disease-in particular, coronary artery disease-and its contribution to disease

88 ilure (aOR: 49.1; 95% CI: 37.4 to 64.3), and coronary artery disease (aOR: 31.7; 95% CI: 21.4 to 47.0

89 dial infarction in patients with established coronary artery disease are lacking.

90 grafting (CABG), in patients with left main coronary artery disease are not clearly established.

91 onic conditions were included: hypertension, coronary artery disease, arthritis, chronic kidney disea

92 anisms, further establishing a role for this coronary artery disease-associated gene in fundamental S

93 Cardiovascular disease (CVD), including coronary artery disease, atrial fibrillation, and heart

94 on cardiovascular conditions: heart failure, coronary artery disease, atrial fibrillation, and hypert

95 Selected patients with obstructive coronary artery disease benefit from revascularization w

96 For the prediction of coronary artery disease, boosting algorithms had a poole

97 That coronary artery disease, but not chronic lung disease, w

98 nic kidney disease without overt obstructive coronary artery disease, but the mechanisms remain poorl

99 mplicate the care of patients with suspected coronary artery disease, but their prevalence and impact

100 y of patients with polymorphic VT related to coronary artery disease, but without evidence of acute m

101 y revascularization (HCR) treats multivessel coronary artery disease by combining a minimally invasiv

102 sion of NBEAL1 may lead to increased risk of coronary artery disease by downregulation of LDLR levels

103 In diabetic patients with multivessel coronary artery disease, CABG was associated with a lowe

104 serum samples from individuals with familial coronary artery disease (CAD) (n = 462) and population-b

105 s) have robustly found a correlation between coronary artery disease (CAD) and an intergenic region a

106 n (WD) is positively associated with risk of coronary artery disease (CAD) and cancer, whereas the Pr

107 ardiologists have long treated patients with coronary artery disease (CAD) and concomitant type 2 dia

108 This study focused on coronary artery disease (CAD) and investigated the genet

109 Coronary artery disease (CAD) and its major complication

110 Background The severity of coronary artery disease (CAD) and of ischemia are evalua

111 Patients with obstructive coronary artery disease (CAD) are at high risk for cardi

112 Because rates of coronary artery disease (CAD) are substantially higher a

113 arction (UMI), detected during assessment of coronary artery disease (CAD) by stress CMR, beyond card

114 ic structure that contributes to the risk of coronary artery disease (CAD) can be evaluated as a risk

115 Coronary artery disease (CAD) causes mortality and morbi

116 Coronary artery disease (CAD) events have been associate

117 TL) shortens with age and is associated with coronary artery disease (CAD) events in the general popu

118 Medicare patients with coronary artery disease (CAD) have been a significant fo

119 Polygenic risk scores (PRS) for coronary artery disease (CAD) identify high-risk individ

120 ndicate high polygenic risk scores (PRS) for coronary artery disease (CAD) identify individuals at hi

121 graphy demonstrated agreement in severity of coronary artery disease (CAD) in 52% (82 of 159) of all

122 e circRNA hsa_circ_0001445 as a biomarker of coronary artery disease (CAD) in a real-world clinical p

123 Applied to coronary artery disease (CAD) in both the WGHS and in JU

124 are limited data on contemporary testing for coronary artery disease (CAD) in patients with new-onset

125 The prevalence of obstructive coronary artery disease (CAD) in symptomatic patients re

126 Coronary artery disease (CAD) is a major cause of morbid

127 n patients without DM, both before and after coronary artery disease (CAD) is established.

128 Establishing a diagnosis of coronary artery disease (CAD) is more difficult than it

129 Coronary artery disease (CAD) is more frequent among ind

130 well-established risk prediction models for coronary artery disease (CAD) is uncertain.

131 eillance in symptomatic patients with stable coronary artery disease (CAD) is unknown.

132 investigate functional mechanisms underlying coronary artery disease (CAD) loci and find molecular bi

133 Regulatory SNPs identified were enriched in coronary artery disease (CAD) loci, and this result has

134 approved in the United States for detecting coronary artery disease (CAD) prior to the current studi

135 diagnosis factors for assessing the risks of coronary artery disease (CAD) remains controversial.

136 Coronary artery disease (CAD) represents one of the lead

137 /CT), is often used to assess for high-grade coronary artery disease (CAD) requiring revascularizatio

138 Genetic variants currently known to affect coronary artery disease (CAD) risk explain less than one

139 lerosis and the influence of this process on coronary artery disease (CAD) risk have not been clearly

140 epigenetic and transcriptional mechanisms of coronary artery disease (CAD) risk, as well as the funct

141 in identification of genomic loci affecting coronary artery disease (CAD) risk.

142 centrations have been associated with higher coronary artery disease (CAD) risk.

143 low in contemporary patients with suspected coronary artery disease (CAD) selected based on American

144 ts into the BDNF mediated pathophysiology in coronary artery disease (CAD) that may shed light upon p

145 Evaluation of coronary artery disease (CAD) using coronary computed to

146 n hemostasis, we genotyped 865 patients with coronary artery disease (CAD), 915 with myocardial infar

147 in the circulation of patients with unstable coronary artery disease (CAD), and their recruitment to

148 ch demonstrate one or more associations with coronary artery disease (CAD), atrial fibrillation, or r

149 asive test to assess hemodynamic severity of coronary artery disease (CAD), but has not yet been comp

150 ntly associated with plasma lipid traits and coronary artery disease (CAD), but the biological basis

151 adults with congestive heart failure (CHF), coronary artery disease (CAD), cerebrovascular accidents

152 hy SPECT for the detection and evaluation of coronary artery disease (CAD), defined as >=50% stenosis

153 In other forms of coronary artery disease (CAD), however, it has been cont

154 For secondary prevention of coronary artery disease (CAD), oral antiplatelet therapy

155 lasma samples of 91 patients with documented coronary artery disease (CAD), who underwent coronary ar

156 erved to improve the health of patients with coronary artery disease (CAD).

157 event are often referred to as having stable coronary artery disease (CAD).

158 d to estimate the potential causal effect on coronary artery disease (CAD).

159 idemia is a highly heritable risk factor for coronary artery disease (CAD).

160 y individuals with elevated lifetime risk of coronary artery disease (CAD).

161 G) in patients with diabetes and multivessel coronary artery disease (CAD).

162 lipoproteins are strongly linked to risk for coronary artery disease (CAD).

163 yocardial infarction (STEMI) and multivessel coronary artery disease (CAD).

164 diabetes despite lower rates of obstructive coronary artery disease (CAD).

165 variables for inferring risk factors causing coronary artery disease (CAD).

166 (TPOT) to predict angiographic diagnoses of coronary artery disease (CAD).

167 rdiac surgery, particularly in patients with coronary artery disease (CAD).

168 y intervention (PCI) in cases of significant coronary artery disease (CAD; >=50% stenosis).

169 1.21, 95% CI: 1.15-1.27, P = 1 x 10-12) and coronary artery disease (CAD; OR 1.21, 95% CI: 1.16-1.26

170 Yet the role of periodontal viruses in coronary artery diseases (CAD) remains unclear.

171 estations of cardiovascular disease, such as coronary artery disease, cerebrovascular disease and per

172 with ST-segment elevation MI and multivessel coronary artery disease, complete revascularization redu

173 to medical therapy for patients with stable coronary artery disease continues to be debated in routi

174 In diabetic patients with multivessel coronary artery disease, coronary artery bypass grafting

175 le causal link between insomnia symptoms and coronary artery disease, depressive symptoms, and subjec

176 rong causal association of lipoprotein(a) in coronary artery disease development (beta, -0.13; per SD

177 ng for participating sites, age, preexisting coronary artery disease, diabetes mellitus, baseline LDL

178 hy angiography increases the sensitivity for coronary artery disease diagnoses compared with function

179 In patients with angina and nonobstructive coronary artery disease, diminished coronary flow reserv

180 We included 13 patients with coronary artery disease due to severe atherosclerosis an

181 ted with an increased risk of heart failure, coronary artery disease events, and mortality from coron

182 efforts and dynamic research in the field of coronary artery disease genetic risk prediction.

183 insic sex difference in ECs are enriched for coronary artery disease GWAS hits.

184 eir postresuscitation ECG, the prevalence of coronary artery disease has been shown to be 25% to 50%.

185 eir postresuscitation ECG, the prevalence of coronary artery disease has been shown to be 70% to 85%.

186 review, we describe how genomic analyses of coronary artery disease have been leveraged to create po

187 Clinical studies using DCB in de novo coronary artery disease have shown mixed results, with a

188 P was independently associated with incident coronary artery disease (hazard ratio associated with al

189 -cause and cardiovascular mortality, stroke, coronary artery disease, heart failure, end-stage renal

190 f the predictive ability of ML algorithms of coronary artery disease, heart failure, stroke, and card

191 actors (chest pain, ST-elevation, absence of coronary artery disease history, and shockable initial r

192 is a clinically used modality for assessing coronary artery disease, however, its use has not been v

193 d atheroprotective marker, in particular for coronary artery disease; however, HDL particle concentra

194 Smoking is a potent risk factor for coronary artery disease; however, prior studies describe

195 95% confidence interval [CI]: 1.37 to 3.76), coronary artery disease (HR: 1.89; 95% CI: 1.26 to 2.82)

196 Comorbidities included hypertension in 61%, coronary artery disease in 25%, ventricular arrhythmia h

197 Concurrent coronary artery disease in a vessel remote from a chroni

198 The poorer prognosis of coronary artery disease in females compared with males i

199 of NBEAL1 in arteries and increased risk of coronary artery disease in humans.

200 accuracy to rule out clinically significant coronary artery disease in patients with NSTEACS.

201 known prevalence and potential importance of coronary artery disease in patients with OHCA and to des

202 revascularisation of patients with left main coronary artery disease in place of the standard treatme

203 of genome-wide association study signals for coronary artery disease in RA signaling target gene loci

204 ming coronary calcium scoring, modified Duke coronary artery disease index and Reduction of Atherothr

205 y stenosis, REACH and SMART scores, the Duke coronary artery disease index, and recent myocardial inf

206 ses of sudden cardiac death: cardiomyopathy, coronary artery disease, inherited arrhythmia syndrome,

207 In the absence of obstructive coronary artery disease, intravascular imaging technique

208 cardial ischaemia resulting from obstructive coronary artery disease is a major cause of morbidity an

209 Coronary artery disease is common in patients with sever

210 ile our conventional framework of epicardial coronary artery disease is foundational in cardiology, a

211 Coronary artery disease is partly heritable.

212 Coronary artery disease is the leading cause of morbidit

213 Coronary artery disease is the main cause of burden of d

214 has been shown that in patients with chronic coronary artery disease, ischemic episodes lead to a glo

215 , and 26 biomarkers strongly associated with coronary artery disease, ischemic stroke, atrial fibrill

216 icism is associated with the genetic risk of coronary artery disease, lower intelligence, lower socio

217 We analyzed 148 individuals with coronary artery disease (mean age [SD] 62 [8] years; 69%

218 We excluded those with rejection, graft coronary artery disease, mechanical support, or hemodial

219 ions with depression and insomnia as well as coronary artery disease, mirroring findings from epidemi

220 e and function, the presence and severity of coronary artery disease, mitral regurgitation, pulmonary

221 Patients with obstructive coronary artery disease more likely have HF with reduced

222 bowel disease, psoriasis, Sjogren syndrome, coronary artery disease, multiple sclerosis, cystic fibr

223 nce athletes have an increased prevalence of coronary artery disease, myocardial fibrosis and arrhyth

224 CYP17A1 genetic variants are associated with coronary artery disease, myocardial infarction and visce

225 ents with stable angina and risk factors for coronary artery disease, myocardial-perfusion cardiovasc

226 Patients with angiographically verified coronary artery disease (n=1946) underwent a clinical ev

227 Fourteen percent of patients had preexisting coronary artery disease (n=31), 33% arterial hypertensio

228 on clinical read and no known macrovascular coronary artery disease (n=783), MPR remained independen

229 s ratio, 4.22 [95% CI, 1.71-10.4], P=0.002), coronary artery disease (odds ratio, 0.35 [95% CI, 0.16-

230 ) who presented with ACS and had evidence of coronary artery disease on coronary angiography managed

231 n between therapeutic strategy and number of coronary arteries diseased or severity of ischemia.

232 Epidemiology Atrial Fibrillation), C(2)HEST (coronary artery disease or chronic obstructive pulmonary

233 nt in many patients with complex multivessel coronary artery disease or left main disease.

234 Patients with chronic coronary artery disease or peripheral artery disease and

235 In patients with chronic coronary artery disease or peripheral artery disease and

236 Patients with established coronary artery disease or peripheral artery disease oft

237 ith education but is not strongly causal for coronary artery disease or type 2 diabetes.

238 netically predicted alcohol consumption with coronary artery disease (OR, 1.16 [95% CI, 1.00-1.36]; P

239 smoking (OR, 1.20 [95% CI, 1.09-1.32]), and coronary artery disease (OR, 1.19 [95% CI, 1.11-1.27]) w

240 nfidence interval (CI), 1.2-3.4, P = 0.009), coronary artery disease (OR, 1.9; 95% CI, 1.1-3.7; P = 0

241 therapy is secondary prevention, concomitant coronary artery disease, particularly with prior myocard

242 ean subpopulations in distinguishing between coronary artery disease patients and healthy individuals

243 Inactive coronary artery disease patients had increased risk for

244 nd the risk of sudden cardiac death (SCD) in coronary artery disease patients is not well known.

245 In the absence of epicardial coronary artery disease, patients with heart transplants

246 In revascularisation of left main coronary artery disease, PCI was associated with an infe

247 the association of APOL1 G1/G2 alleles with coronary artery disease, peripheral artery disease, and

248 e modest than, the degree of protection from coronary artery disease predicted by these same methods

249 Coronary artery disease prevalence among participants at

250 i-tissue gene expression associations to key coronary artery disease processes and clinical phenotype

251 litus and hypertension to slow and stabilize coronary artery disease progression and improve clinical

252 The primary end point was coronary artery disease progression, defined as the abso

253 erent definitions in patients with left main coronary artery disease randomized to percutaneous coron

254 ients with de novo 3-vessel and/or left main coronary artery disease randomized to treatment with PCI

255 In patients with known or suspected coronary artery disease, reduced MBF and MPR measured au

256 dy of patients with both suspected and known coronary artery disease referred clinically for perfusio

257 Residential remoteness was associated with coronary artery disease-related SCD (odds ratio, 1.44 [9

258 Incidence of coronary artery disease-related SCD decreased from 2001-

259 cidence of SCD in the young and specifically coronary artery disease-related SCD has declined in rece

260 Patients with left main coronary artery disease requiring revascularisation were

261 ing target gene loci and correlation between coronary artery disease risk alleles and repressed expre

262 III activity levels on venous thrombosis and coronary artery disease risk and plasma VWF levels on is

263 In the Coronary Artery Disease Risk Development in Young Adults

264 d phenotypic modulation of this cell type in coronary artery disease risk.

265 ular development, and has been implicated in coronary artery disease risk.

266 i were associated with birthweight and adult coronary artery disease (rs2870463 in CTRB1) and with bi

267 acute myocardial infarction and multivessel coronary artery disease should not be treated differentl

268 Among patients with coronary artery disease, statin medication rates increas

269 found a sphingolipid profile that predicted coronary artery disease status.

270 investigating the effects of prediabetes in coronary artery disease, stroke and chronic kidney disea

271 Elevated risks of arrhythmia, pericarditis, coronary artery disease, stroke, and valvular heart dise

272 oatheroma (TCFA) are the unstable lesions in coronary artery disease that are prone to rupture, resul

273 mong patients with angina and nonobstructive coronary artery disease, those with coronary microvascul

274 to improve clinical outcomes in multivessel coronary artery disease, though its impact in diabetic p

275 y angiography (CTCA) performed for suspected coronary artery disease to undergo a repeat research CTC

276 NIRS) and clinical outcomes in patients with coronary artery disease treated with contemporary drug-e

277 xtended long-term follow-up of patients with coronary artery disease treated with drug-eluting stents

278 tcomes of diabetic patients with multivessel coronary artery disease treated with fractional flow res

279 wer-risk patients who may eventually require coronary artery disease treatment.

280 population-based cohort study of adults with coronary artery disease undergoing single-vessel FFR ass

281 Patients with known coronary artery disease underwent (18)F-NaF PET computed

282 Participants with stable coronary artery disease underwent acute mental stress te

283 Individuals with stable coronary artery disease underwent acute mental stress te

284 ervational study, patients with multi-vessel coronary artery disease underwent serial (18)F-fluoride

285 Patients with angina and nonobstructive coronary artery disease underwent simultaneous acquisiti

286 Background Progression of coronary artery disease using serial coronary computed t

287 In fully adjusted models, the number of coronary arteries diseased was not associated with incre

288 utility of polygenic risk scores to stratify coronary artery disease was also assessed.

289 PRS for coronary artery disease was independently associated wit

290 the use of paclitaxel DCBs for treatment of coronary artery disease was not associated with increase

291 ntal value of polygenic risk score (PRS) for coronary artery disease, we added the score to 3 models

292 , ST-segment elevation, and absence of known coronary artery disease were independent predictors of u

293 viously underwent coronary CTA for suspected coronary artery disease were prospectively included to u

294 ents with de-novo three-vessel and left main coronary artery disease were randomly assigned (1:1) to

295 acute myocardial infarction and multivessel coronary artery disease were randomly assigned to one of

296 n diet reduces the incidence and severity of coronary artery disease, whereas supplementation with ni

297 Among patients with coronary artery disease who underwent single-vessel FFR

298 at prediabetes is only causally related with coronary artery disease, with no evidence of causal effe

299 several vascular diseases, including FMD and coronary artery disease, with the putative causal noncod

300 ng were more frequently male; more often had coronary artery disease, worse renal function, and impai