ライフサイエンスコーパス: ACS

1 ACS models as well as centralized units and hospitals wi

2 ACS NSQIP data (2006-2013) were used to create predictio

3 ACS patients with recurrent (hazard ratio (HR) = 1.62, 9

4 ACS TQIP database study including patients with blunt se

5 ACS-NSQIP risk estimates used for benchmarking and share

6 In total, 19,520 (20.0%) ACS patients experienced depression within 2 years after

7 During 12 years of follow-up, 39,523 (40.4%) ACS patients and 27,931 (28.6%) of the reference populat

8 ene amplicon sequencing of pH 7.2 and pH 5.5 ACS enrichments revealed distinct microbial communities,

9 bstructive coronary artery disease (1%-64%), ACS (1%-44%), downstream testing (4%-72%), and total (23

10 que rupture has dominated our thinking about ACS pathophysiology for decades.

11 added, thereby converting inactive to active ACS.

12 n were separated into 2 documents addressing ACS and stable ischemic heart disease individually.

13 opulation-based cohort study on 49 556 adult ACS or stable angina patients with angiographic evidence

14 After ACS, patients vary considerably in their risk for recurr

15 were performed during the first 7 days after ACS (n=2866) and repeated for another 7 days at day 30 (

16 s between patients with and without FH after ACS.

17 significant by approximately 5 months after ACS.

18 risk markers and at later time points after ACS remains uncertain.

19 tatin therapy for secondary prevention after ACS.

20 the risk of coronary event recurrence after ACS was similar in patients with FH in unadjusted analys

21 ts presenting with symptoms suggestive of an ACS at the ED of 5 community and 2 university hospitals

22 n treatments in adults within 3 months of an ACS event.

23 Patients with an ACS and histories of hypersensitivity reactions to ASA,

24 trial in which smokers hospitalized with an ACS were randomized to varenicline or placebo for 12 wee

25 causing shortness of breath (P = .002), and ACS at less than 4 years of age (P < .001).

26 ause obstructive coronary artery disease and ACS were more prevalent in patients with high CAC.

27 Patients with FH and ACS have a >2-fold adjusted risk of coronary event recur

28 Heterodimerization between ACS isoforms from distinct subclades results in increase

29 of long-term MACCE relative to PCI for both ACS and SIHD.

30 into four age- and sex-matched groups: both ACS and CP, ACS only, CP only, and healthy controls.

31 e significantly higher in patients with both ACS and CP than in those with only ACS or only CP and he

32 The nickel-bound ACS-AcsFCh complex remains inactive until MgATP is added

33 apy respectively, in subgroups with pre-CABG ACSs (15.2% vs. 16.5%; HR: 1.06; 95% CI: 0.53 to 2.10; p

34 nmatched cohorts, across all FFR categories, ACS patients had a significantly higher annualized myoca

35 In studies comparing ACS with traditional practice, mortality and morbidity w

36 We studied 206 consecutive ACS patients with 262 intermediate lesions and 370 patie

37 d a novel regulatory mechanism that controls ACS protein stability through a heterodimerization of AC

38 traoperative factors along with conventional ACS-NSQIP preoperative variables.

39 ge- and sex-matched groups: both ACS and CP, ACS only, CP only, and healthy controls.

40 deline-adherent antibiotics had lower 30-day ACS-related (odds ratio [OR], 0.71; 95% CI, 0.50-1.00) a

41 with a discharge diagnosis of SCD and either ACS or pneumonia.

42 n the management of non-ST-segment elevation ACS were published in the last 2 years, as well as scien

43 lica's measure specifications to established ACS-NSQIP outcome measure performance (eg, death/serious

44 efficacious for smoking cessation following ACS.

45 irin plus prasugrel or clopidogrel following ACS.

46 Varenicline, initiated in-hospital following ACS, is efficacious for smoking cessation.

47 t predictive accuracy for MACE) of <0.84 for ACS (MACE 21% vs. 36%; p = 0.007) and <0.81 for SIHD (MA

48 ticipants were enrolled during admission for ACS and underwent assessments at baseline (2 weeks post-

49 This document presents the AUC for ACS.

50 ccurring after the index hospitalization for ACS, SCD was associated with recurrent myocardial infarc

51 vided in 10654 of 14480 hospitalizations for ACS (73.6%).

52 All first-time hospitalizations for ACS (n = 97,793) identified in the Danish Patient Regist

53 c use for children with SCD hospitalized for ACS and to determine whether receipt of guideline-adhere

54 onal cohort study, who were hospitalized for ACS between January 2009 and April 2013.

55 At 30-days post-revascularization, for ACS patients the odds ratio for MACCE favored CABG 0.49

56 s indicate that endothelial-derived MPs from ACS patients induce premature endothelial senescence und

57 m senescent P3 cells or circulating MPs from ACS patients induced increased senescence-associated bet

58 Depletion of endothelial-derived MPs from ACS patients reduced the induction of senescence.

59 prosenescent effect of circulating MPs from ACS patients was evidenced only under conditions of low

60 arkers of atopy and increased risk of future ACS events.

61 d major adverse cardiac events (MACE) (e.g., ACS, cardiac mortality, revascularization) over 12 month

62 blind, multicentre, randomised trial (GEMINI-ACS-1) done at 371 clinical centres in 21 countries, eli

63 tion based on the concept of the generalized ACS approach.

64 disease (>/=70% stenosis) and 68 (5.5%) had ACS.

65 For patients presumed to have ACS, the CHL thickness was significantly greater in the

66 r multivariable adjustments in a heterogenic ACS population for the first time.

67 /group), MACE remained significantly higher (ACS 25% vs. SIHD 12%; p < 0.0001).

68 sus on the elements that constitute an ideal ACS model and how it can be implemented into current sur

69 The subsequent genetic analysis identified ACS-4, an acyl-CoA synthetase and its FA-CoA product, as

70 n Cancer Society Cancer Prevention Study II (ACS CPS-II) cohort have been used to estimate global O3-

71 In ACS patients who underwent invasive management, RA was a

72 In ACS, 1-year outcome of patients reclassified based on FF

73 In ACS, FFR was performed in 1.4 lesions per patient, mostl

74 Depression is common in ACS patients and is associated with increased mortality

75 These findings were confirmed in ACS explored at the culprit lesion.

76 The adjusted rate ratio for depression in ACS patients compared with the reference population was

77 I to assign risk of spontaneous MI events in ACS populations.

78 he clinical and prognostic utility of FFR in ACS patients with percutaneous coronary intervention def

79 Indications of cardiac MR imaging in ACS patients will be reviewed and specific cardiac MR pr

80 These adjustments are included in ACS NSQIP reports, where hospital odds ratios (OR) are e

81 ciated with depression seemed to be lower in ACS patients than in the reference population.

82 esentation, with a hazard ratio for MACCE in ACS patients of 0.67 (95% CI: 0.55 to 0.81) and the haza

83 ts with SIHD for clinical decision making in ACS patients.

84 levels have a direct effect on mortality in ACS patients.

85 level I or II trauma center participating in ACS TQIP (2012-2015) were included.

86 Participation in ACS NSQIP is associated with reductions in adverse event

87 al outcomes associated with participation in ACS NSQIP.

88 uding revascularization deferral, is safe in ACS.

89 pport adoption of the BARC bleeding scale in ACS clinical trials.

90 AcsFCh and inactive ACS form a stable 2:1 complex that binds two nickel ions

91 The 2007 to 2012 institutional ACS-NSQIP and administrative databases for abdominal sur

92 Cox proportional hazards analysis for MACE, ACS had a hazard ratio of 2.8 (95% confidence interval:

93 ar death, MI, or stroke in medically managed ACS patients treated with clopidogrel or prasugrel.

94 between the model NiAz system and the native ACS enzyme, highlighting the potential for related react

95 patients presenting with biomarker-negative ACS and undergoing ad hoc PCI, on a background of aspiri

96 ri-procedural period among troponin-negative ACS patients undergoing ad hoc PCI.

97 ared with the unstable angina (2.7%) and non-ACS (2.6%) groups (P < .001).

98 rocedures, unstable angina in 33.8%, and non-ACS in 33.4%.

99 associated with acute coronary syndrome (non-ACS).

100 higher in the MI group compared with the non-ACS group (odds ratio [OR] = 5.25; 95% CI, 4.08-6.75).

101 gina group were similar to those for the non-ACS group when surgery was performed within 3 months (OR

102 y FFR was high and similar to those with non-ACS (38% versus 39%; P=NS).

103 in patients with ACS as in patients with non-ACS (major cardiovascular event, 8.0% versus 8.5%; P=0.8

104 dical treatment compared with those with non-ACS (P=0.01).

105 nts, 37555 patients were enrolled after NSTE ACS (67.4% men; 32.6% women; median [interquartile range

106 ent that were associated with SCD after NSTE ACS were identified.

107 th was examined according to time after NSTE ACS.

108 ne-third of cardiovascular deaths after NSTE ACS.

109 ment elevation acute coronary syndrome (NSTE ACS) has not been characterized completely.

110 o guide clinicians in the management of NSTE-ACS, most recently in in 2014 and 2015, respectively.

111 o initial presentation and diagnosis of NSTE-ACS, risk assessment, treatments, and systems of care.

112 not differ between patients with AIS or NSTE-ACS (95 versus 94 ng/L; P=0.70).

113 ment elevation acute coronary syndrome (NSTE-ACS) and an elevated cardiac troponin T.

114 ment-elevation acute coronary syndrome (NSTE-ACS).

115 ent elevation acute coronary syndromes (NSTE-ACS) are the leading cause of morbidity and mortality fr

116 tive invasive strategy in patients with NSTE-ACS and an elevated cardiac troponin T.

117 trial that included 1,200 patients with NSTE-ACS and an elevated cardiac troponin T.

118 In patients with NSTE-ACS and elevated cardiac troponin T levels, an early inv

119 with age- and sex-matched patients with NSTE-ACS despite similar baseline cTn levels.

120 with age- and sex-matched patients with NSTE-ACS.

121 (CPT) and year, we compared the accuracy of ACS-NSQIP predicted mortality probabilities using the ob

122 Factor analysis of ACS NSQIP postoperative complication data provides 6 cli

123 echanistic approach to the categorization of ACS to provide a framework for future tailoring, triage,

124 kewise apply selectively to this category of ACS.

125 The elements of ACS models varied but included senior clinicians present

126 post-reperfusion and follow-up evaluation of ACS to identify patients at high risk of further cardiac

127 in stability through a heterodimerization of ACS isoforms.

128 rgent cardiac catheterization and history of ACS or coronary revascularization.

129 ing and cost were lower than the increase of ACS rate in patients with CAC>400, cost to diagnose one

130 ies have shed new light on the mechanisms of ACS.

131 immunity contributes to the pathogenesis of ACS and the clinical implications that arise from these

132 during the acute and convalescent phases of ACS.

133 in patients with an initial presentation of ACS is associated with significantly worse outcomes than

134 n of FFR into the decision-making process of ACS patients with obstructive coronary artery disease is

135 logy, diagnosis, treatment, and prognosis of ACS.

136 nalyses identified that the incident rate of ACS was associated with ln(Feno) levels (P = .03), as we

137 This is mainly because recurrence of ACS eventually leads to the pandemics of heart failure a

138 These findings, including a similar role of ACS-4 in a male/female species, uncover a likely conserv

139 Coronary Events) risk score for severity of ACS.

140 cid differentially regulate the stability of ACS proteins, with distinct effects on various isoforms.

141 biosynthesis by increasing the stability of ACS proteins.

142 terodimerization influences the stability of ACS proteins.

143 d those with clinical findings suggestive of ACS (nine men, 11 women aged 41-70 years).

144 Identification of patients with of ACS resulting from erosion may permit a less invasive ap

145 2 years, as well as scientific documents on ACS in understudied populations, such as women and patie

146 ing of the roles of various phytohormones on ACS protein stability, which brings new insights into cr

147 patients with CAC>400, cost to diagnose one ACS was lowest in this group (19 283 US$ versus 464 399

148 with both ACS and CP than in those with only ACS or only CP and healthy controls (P <0.05).

149 ritical feature for achieving organometallic ACS activity, and binds CO and -CH3 groups with biologic

150 Post-ACS optimism, but not gratitude, was prospectively and i

151 plied this tool prospectively to 17,717 post-ACS patients randomized either to ezetimibe and simvasta

152 velopment of an endothelial dysfunction post-ACS.

153 tratification may be useful to identify post-ACS patients who have the greatest potential for benefit

154 ic accuracy metrics that are similar in post-ACS patients and other clinical populations.

155 m or improve cardiovascular outcomes in post-ACS patients is not yet known, but can be tested in futu

156 kers, and cardiac rehospitalizations in post-ACS patients.

157 English-language studies of post-ACS patients that evaluated the diagnostic accuracy of d

158 le sex was not associated with outcomes post-ACS.

159 erwent assessments at baseline (2 weeks post-ACS) and follow-up (6 months later).

160 Gratitude was minimally associated with post-ACS outcomes.

161 mentation of clinical pathways for potential ACS in disparate hospitals.

162 rgeons National Quality Improvement Program (ACS NSQIP database).

163 rgeons National Quality Improvement Program (ACS NSQIP) database from 2005 to 2011.

164 tional Surgical Quality Improvement Program (ACS NSQIP) surgical quality feedback models are recalibr

165 tional Surgical Quality Improvement Program (ACS NSQIP), thus only hospitals participating in the ACS

166 tional Surgical Quality Improvement Program (ACS-NSQIP) Database, a total of 3,727 patients (0.9%) ex

167 geons' National Quality Improvement Program (ACS-NSQIP) database.

168 We also now recognize ACS that occur without apparent epicardial coronary arte

169 the association between gender and recurrent ACS nonstatistically significant (hazard ratio: 3.56; 95

170 153 had no association with either recurrent ACS or composite of recurrent ACS or death.

171 Outcomes included recurrent ACS and MACE over 12 months.

172 re associated with higher rates of recurrent ACS and MACE compared with masculine characteristics.

173 ther recurrent ACS or composite of recurrent ACS or death.

174 gender are at an increased risk of recurrent ACS over 12 months, independent of female sex.

175 polymorphisms were associated with recurrent ACS after multivariable adjustments in a heterogenic ACS

176 ations between gender and sex with recurrent ACS and major adverse cardiac events (MACE) (e.g., ACS,

177 GRS47 showed association with recurrent ACS independent of clinical factors (P=0.037; hazard rat

178 veral additional phytohormones also regulate ACS protein turnover.

179 In low-risk ACS patients undergoing ad hoc PCI, ticagrelor LD provid

180 onal Surgical Quality Improvement Program's (ACS-NSQIP) surgical risk calculator for predicting outco

181 The American Cancer Society (ACS) HNC Survivorship Care Guideline was reviewed for de

182 ne equivalent of the atomic collapse states (ACSs) predicted to occur at supercritically charged nucl

183 2-18 years from the adolescent cohort study (ACS) who were infected with M tuberculosis for 2 years.

184 applications, the average common substring (ACS) approach is emerging as one of the prominent alignm

185 ures derived from the Axton Cross Superfund (ACS) microcosms sustained PCE dechlorination to cDCE as

186 ipating in the American College of Surgeons (ACS) Trauma Quality Improvement Program (TQIP) and measu

187 Acute Care Surgery (ACS) is a health care model combining emergency general

188 rom the 2006-2010 American Community Survey (ACS) included race/ethnicity, education, income, poverty

189 each year on the American Community Survey (ACS), a labor-intensive door-to-door study that measures

190 mentation of clinical pathways for suspected ACS reduced the length of stay and increased the proport

191 h 31 332 patients investigated for suspected ACS with serial troponin measurements.

192 A, applied early in the work-up of suspected ACS, is safe and associated with less outpatient testing

193 or the assessment of patients with suspected ACS that included a clinical pathway document in paper o

194 sk stratification of patients with suspected ACS.

195 ively used to guide treatment, 533 sustained ACS (excluding acute ST-segment-elevation myocardial inf

196 ith increased rates of acute chest syndrome (ACS) and pain.

197 Acute chest syndrome (ACS) is a common, serious complication of sickle cell di

198 for the development of Acute Chest Syndrome (ACS), a major cause of morbidity and mortality in SCD pa

199 VT) is common after acute coronary syndrome (ACS) and a marker of increased risk of arrhythmogenic de

200 FH in patients with acute coronary syndrome (ACS) and compared the diagnostic performance of FH clini

201 iodontitis (CP) and acute coronary syndrome (ACS) and establish their correlation with periodontal cl

202 of depression after acute coronary syndrome (ACS) and whether the timing of depression onset influenc

203 P) in patients post-acute coronary syndrome (ACS) compared to placebo/simvastatin.

204 KI in patients with acute coronary syndrome (ACS) enrolled in the MATRIX-Access (Minimizing Adverse H

205 nts who have had an acute coronary syndrome (ACS) event have an increased risk for depression.

206 he early outcome of acute coronary syndrome (ACS) has considerably improved in the last decade, cardi

207 ptoms suggestive of acute coronary syndrome (ACS) have had mixed success.

208 tients suspected of acute coronary syndrome (ACS) in the emergency department (ED).

209 Acute coronary syndrome (ACS) is a frequent cause of hospitalization and coronary

210 ary angiography for acute coronary syndrome (ACS) or stable angina, in whom there is angiographic evi

211 Many low-risk acute coronary syndrome (ACS) patients are not pre-treated with a P2Y12 receptor

212 decision making in acute coronary syndrome (ACS) patients with intermediate lesions, its effect on l

213 ospitalized with an acute coronary syndrome (ACS) remain abstinent following discharge.

214 from patients with acute coronary syndrome (ACS) to promote premature EC aging and thrombogenicity.

215 ts stabilized after acute coronary syndrome (ACS) when added to statin therapy.

216 ubjects, 138 had an acute coronary syndrome (ACS), 101 of whom underwent desensitizations, whereas 17

217 on of recurrence of acute coronary syndrome (ACS), but the value of genetic risk scores (GRSs) remain

218 Patients with acute coronary syndrome (ACS), especially those receiving medical management with

219 Acute coronary syndrome (ACS), the acute manifestation of ischemic heart disease,

220 prescription after acute coronary syndrome (ACS), the risk of recurrent coronary and cardiovascular

221 8 624 patients with acute coronary syndrome (ACS).

222 l outcomes after an acute coronary syndrome (ACS).

223 ents with suspected acute coronary syndrome (ACS).

224 care for premature acute coronary syndrome (ACS); whether they are associated with cardiovascular ou

225 CAD ( n = 184), and acute coronary syndrome (ACS; n = 169).

226 rhythm), status in acute coronary syndromes (ACS) (1C), the presence of pericardial effusion (1C), ca

227 vascularization in acute coronary syndromes (ACS) and stable ischemic heart disease were combined int

228 and mechanisms of acute coronary syndromes (ACS) at the clinical, pathological, cellular, and molecu

229 aged patients with acute coronary syndromes (ACS) is not known.

230 disease (SIHD) and acute coronary syndromes (ACS) is unknown.

231 g (CABG) following acute coronary syndromes (ACS).

232 t in patients with acute coronary syndromes (ACS).

233 The acetyl coenzyme A synthase (ACS) enzyme plays a central role in the metabolism of an

234 Acetyl-CoA synthase (ACS) catalyzes the reversible condensation of CO, CoA, a

235 lopropane-1-carboxylic acid (ACC) synthases (ACS), generally the rate-limiting step in ethylene biosy

236 We show that the acyl-CoA synthetase ACS-7, which localizes to lysosome-related organelles, i

237 Further tests indicated that ACS-4-dependent protein myristoylation perceives and tra

238 The ACS NSQIP collects and reports on eighteen 30-day postop

239 The ACS-NSQIP surgical risk calculator has been proposed as

240 ASCO endorsed the ACS HNC Survivorship Care Guideline, adding qualifying s

241 age using updated effect estimates from the ACS CPS-II cohort.

242 Additionally general surgery cases from the ACS NSQIP 2008 PUF data were used to create risk models

243 CE-dechlorinating isolates obtained from the ACS pH 5.5 enrichment shared 98.6%, and 98.5% 16S rRNA g

244 2007, we enrolled 6363 participants from the ACS study and 4466 from independent South African and Ga

245 dy was performed using data derived from the ACS TQIP database.

246 From the ACS-NSQIP 2011-2012 patient user files, we selected core

247 ographic changes and their appearance in the ACS can exceed several years.

248 107 matched controls were identified in the ACS cohort.

249 4 +/- 1.6 years) MACE rate was higher in the ACS group than in the SIHD group (23% vs. 11%, p < 0.000

250 P), thus only hospitals participating in the ACS NSQIP were included.

251 ude of the sex difference was greater in the ACS patients (P(interaction) for sex and clinical presen

252 d randomized trial of CABG versus PCI in the ACS population is warranted because these patients have

253 implications for clinical management of the ACS for the future.

254 ts The ASCO Expert Panel determined that the ACS HNC Survivorship Care Guideline, published in 2016,

255 an increasingly practical supplement to the ACS.

256 This ACS approach has been further generalized by some recent

257 y within 30 days of surgery measured through ACS NSQIP, as well as resident satisfaction and well-bei

258 ls visited by patients enrolled in TRANSLATE-ACS.

259 Pri therapy from 233 United States TRANSLATE-ACS study (Treatment With Adenosine Diphosphate Receptor

260 nts After Acute Coronary Syndrome (TRANSLATE-ACS) study between April 1, 2010, and October 31, 2012.

261 nts After Acute Coronary Syndrome (TRANSLATE-ACS) study from 2010 to 2012.

262 nts After Acute Coronary Syndrome (TRANSLATE-ACS) study.

263 Using TRANSLATE-ACS (Treatment With Adenosine Diphosphate Receptor Inhib

264 We analyzed data from the randomized TRILOGY ACS (TaRgeted platelet Inhibition to cLarify the Optimal

265 in Acute Coronary Syndrome Subjects [TRILOGY ACS]; NCT00699998).

266 lly Manage Acute Coronary Syndromes (TRILOGY ACS) trials.

267 Using ACS-NSQIP data (2012-2014) for 8 ProPublica procedures a

268 variably grouped in published analyses using ACS NSQIP data.

269 Younger adults with ACS with feminine gender are at an increased risk of rec

270 6) and highest EL score were associated with ACS (OR = 2.46, 95% CI = 1.09 to 5.54, P = 0.030).

271 hes to antibiotic treatment in children with ACS vary widely, but guideline-adherent therapy appears

272 s for the care of children hospitalized with ACS.

273 y associated with CAD and in particular with ACS.

274 cluded 786 (31.7%) consecutive patients with ACS (mean [SD] age, 67.1 [9.3] years; range, 32-88 years

275 from ECs and venous blood from patients with ACS (n=30) and from healthy volunteers (n=4) by sequenti

276 of genetically confirmed FH in patients with ACS age </=65 years and with LDL-C levels >/=160 mg/dl i

277 g should be advocated in young patients with ACS and high LDL-C levels to allow prompt identification

278 ug-eluting stents) in diabetic patients with ACS and MV-CAD.

279 stigate salivary MDA levels in patients with ACS and their correlations with serum hsCRP and plasma f

280 dical treatment was as safe in patients with ACS as in patients with non-ACS (major cardiovascular ev

281 We studied 4534 patients with ACS enrolled in a multicenter, prospective cohort study

282 , diagnosis, and management of patients with ACS has been accomplished in recent years.

283 notype on ischemic outcomes in patients with ACS initially managed medically without revascularizatio

284 different, however, with less patients with ACS reclassified from revascularization to medical treat

285 become the standard of care in patients with ACS undergoing angiography.

286 y score-matched analyses among patients with ACS undergoing CABG, the use of preoperative ticagrelor

287 ons and on clinical outcome of patients with ACS undergoing coronary angiography, as compared with pa

288 Participants were patients with ACS undergoing isolated CABG from the European Multicent

289 A cohort of 2090 consecutive patients with ACS who underwent coronary angiography between July 2006

290 ion, and treatment options for patients with ACS will be introduced.

291 007 and 2014 (n = 4,661, 2,947 patients with ACS).

292 terolemia was performed in 103 patients with ACS, age </=65 years, and LDL-C levels >/=160 mg/dl.

293 In patients with ACS, reclassification by FFR was high and similar to tho

294 ay merit further evaluation in patients with ACS.

295 ularization) over 12 months in patients with ACS.

296 ent and improve the outcome of patients with ACS.

297 e associated with NT-proBNP in patients with ACS.

298 3.0% were Chinese, and 65.9% presented with ACS.

299 ups with the exception of Chinese women with ACS.

300 In patients without ACS, the median length of hospital stays decreased by 2.