ライフサイエンスコーパス: coronary event

1 (median follow-up 17.2 years; 1070 incident coronary events).

2 in TRACE (Transitions, Risks and Actions in Coronary Events).

3 , 130 subjects developed a fatal or nonfatal coronary event.

4 d sudden cardiac death (SCD) during an acute coronary event.

5 y medicolegal autopsy to be because of acute coronary event.

6 r high-risk individual prior to a subsequent coronary event.

7 women, and 24 980 experienced a first major coronary event.

8 g the platelet gene expression preceding the coronary event.

9 ACS grew larger in the 16 weeks following a coronary event.

10 h type 2 diabetes who had had a recent acute coronary event.

11 y identify patients with high risk of future coronary events.

12 yme are associated with an increased risk of coronary events.

13 iation of AKI with long-term risk of adverse coronary events.

14 lular adhesion molecule-1 (ICAM-1) and acute coronary events.

15 patients at a high risk of sustaining acute coronary events.

16 helial function are recognized predictors of coronary events.

17 ted with dose-dependent lower risks of major coronary events.

18 ar events, 162 heart failure events, and 142 coronary events.

19 89; 95% CI: 0.74 to 0.90) although not major coronary events.

20 lop coronary arterial lesions and subsequent coronary events.

21 ut was associated with a lower risk of major coronary events.

22 ociated with each end point (P<0.001) except coronary events.

23 erms and when compared with the reduction in coronary events.

24 cted by CT and has been suggested to predict coronary events.

25 Findings were similar for coronary events.

26 s, but was not found for patients with acute coronary events.

27 urden and with the development of subsequent coronary events.

28 pattern reduced risks of diabetes and major coronary events.

29 h heart failure and outcomes associated with coronary events.

30 719Arg (rs20455) in KIF6 was associated with coronary events.

31 savings, while avoiding a negative impact on coronary events.

32 y of the Framingham equations for predicting coronary events.

33 el window on gene expression preceding acute coronary events.

34 /- 1.4 y were followed over 5 more years for coronary events.

35 coronary atherosclerosis that precede acute coronary events.

36 ntral in risk-stratifying patients for acute coronary events.

37 in treatment for the secondary prevention of coronary events.

38 rganism have been linked to a higher risk of coronary events.

39 also lead to occlusive thrombosis and acute coronary events.

40 do not have a correspondingly higher rate of coronary events.

41 There have been no late coronary events.

42 genetic effects on loge(CAC+1) and incident coronary events.

43 fected patients may be at increased risk for coronary events.

44 RP) levels are independently associated with coronary events.

45 spontaneous fibrinolytic activity with acute coronary events.

46 cation, that underlies the majority of acute coronary events.

47 r therapeutic potential for reducing adverse coronary events.

48 ation is the major determinant of most acute coronary events.

49 lar health and dysfunction is a predictor of coronary events.

50 thogenic sequelae of atherogenesis and acute coronary events.

51 ls were associated with lower rates of major coronary events.

52 atients for decades, hoping to prevent acute coronary events.

53 y studies have been associated with clinical coronary events.

54 italization did not reduce the risk of major coronary events.

55 94) for strokes, 0.91 (CI, 0.74 to 1.12) for coronary events, 0.80 (CI, 0.57 to 1.12) for heart failu

56 ed them as having the lowest risk for future coronary events (1.4% over 5 years).

57 associated risk was only observed for major coronary events (1.64 [1.35, 2.00]) and ischemic stroke

58 ex quintile were 2.15 [1.72, 2.69] for major coronary events, 1.65 [1.50, 1.80] for ischemic stroke,

59 y associated with the absolute rate of major coronary events (11301 events, including coronary death

60 90; 95% CI, 0.82 to 1.00; P=0.045) and total coronary events (14.6% vs. 16.1%; hazard ratio, 0.91; 95

61 There were significant excess risks of major coronary event (2.44, 95% CI 2.18-2.73), ischaemic strok

62 sociated with an increase in the risk of any coronary event (2091 events; hazard ratio, 1.04; 95% con

63 oke (2.08%vs 2.54% per year, p=0.002) and in coronary events (4.3%vs 5.3% per year, p<0.0001).

64 ifferences in terms of 4-month major adverse coronary events (5.4% vs. 2.6%; p = 0.25).

65 no significant effect on the risk of primary coronary events (533 vs. 553 events; hazard ratio, 0.95;

66 ared with placebo, reduced the rate of major coronary events (9.3% vs. 10.3%; hazard ratio, 0.90; 95%

67 was associated with an OR of 0.22 for major coronary events (95% CI, 0.17-0.26; P < .001), and 0.32

68 mm Hg lower SBP, and an OR of 0.61 for major coronary events (95% CI, 0.59-0.64; P < .001).

69 wer LDL-C levels and an OR of 0.73 for major coronary events (95% CI, 0.70-0.75; P < .001).

70 -mm Hg lower SBP and an OR of 0.82 for major coronary events (95% CI, 0.79-0.85, P < .001).

71 The primary outcome was any coronary event (a composite of death from coronary heart

72 vy drinkers had a 74% higher risk of a major coronary event, a 133% higher risk of stroke, and a 127%

73 any cardiovascular event (a composite of any coronary event, a cerebrovascular event, peripheral vasc

74 The primary outcome was the first major coronary event, a composite of coronary death, myocardia

75 ship between mean heart dose (MHD) and acute coronary event (ACE) rate was reported in a study of pat

76 verse associations were found for HDL-C with coronary events across a range of LDL-C values, includin

77 OR 0.64, 95% CI 0.37-1.11; p=0.11) or acute coronary events (adjusted hazard ratio [HR] 0.76, 95% CI

78 CAC and hsCRP independently predicted 91 coronary events (adjusted hazard ratios [HRs]: log(2)(CA

79 have an excellent prognosis for survival and coronary events after 3 years compared with patients wit

80 The risk levels of de novo coronary events after hospital discharge were similar in

81 ess the association of Lp-PLA(2) with future coronary events among diabetic men and women.

82 r are independently associated with incident coronary events among postmenopausal women.

83 ociations were found for HDL-C with incident coronary events among women with a range of LDL-C values

84 consecutive victims of SCD because of acute coronary event and 532 survivors of such an event, in wh

85 ark; the study included 963 women with major coronary events and 1205 controls.

86 mg/l) were 5.92 (95% CI: 3.14 to 11.16) for coronary events and 3.02 (95% CI: 1.82 to 5.01) for all-

87 es discrimination and stratification of hard coronary events and all-cause mortality in the general p

88 The risk of coronary events and all-cause mortality that is mediated

89 stic curves for the prediction of both major coronary events and any coronary event were higher when

90 ry associated with higher long-term risks of coronary events and death in this cohort, suggesting tha

91 the assessment of plaque burden and risk of coronary events and evaluation of therapeutic interventi

92 counted for about half of the differences in coronary events and for about 40% of the differences in

93 rotein 6, is associated with greater risk of coronary events and greater benefit from pravastatin ver

94 meta-analysis has confirmed benefit on major coronary events and ischaemic stroke in many diabetic pa

95 larization) and major vascular events (major coronary events and ischemic stroke).

96 f postprandial hypotension on a high risk of coronary events and mortality in aging, we hypothesized

97 istent association of Trp719Arg with risk of coronary events and statin benefit.

98 6 to 2.89; p = 0.029), the composite of hard coronary events and stroke (HR: 1.72; 95% CI: 1.16 to 2.

99 HRs for coronary events and stroke adjusted for blood pressure r

100 Most acute coronary events and sudden death are believed to arise f

101 the assessment of plaque burden and risk of coronary events and the evaluation of therapeutic interv

102 ave increased risk of recurrent severe acute coronary events and unfavorable prognosis.

103 patients at increased risk of posttransplant coronary events and was also useful to define a low-risk

104 carotid stenosis, and 10-year risk of acute coronary events) and of cardioembolism (ie, risk of card

105 Primary outcome was any coronary event, and secondary outcomes were any cardiova

106 tion is associated with an increased odds of coronary events, and inflammation, as assessed by higher

107 n cardiovascular resource utilization, major coronary events, and insurer spending.

108 KIF6 719Arg allele had an increased risk of coronary events, and pravastatin treatment substantially

109 te end point was cardiovascular death, major coronary events, and stroke.

110 ues is responsible for the majority of acute coronary events, and the culprit lesions demonstrate dis

111 now inclusive of stroke in addition to hard coronary events, and there are now separate equations to

112 who experience major bleeding after an acute coronary event are at higher risk of death in the months

113 infarction (MI), but changes after an acute coronary event are unknown.

114 Mortality and coronary events are dramatically reduced in coronary art

115 In contrast, coronary events are extremely rare even in closely relat

116 in the cardiology community that most acute coronary events arise from ruptures of mildly stenotic p

117 The mean body size of children who had coronary events as adults was below average at birth.

118 However, it is unclear whether the risk of coronary events associated with decreased kidney functio

119 whether troponin concentration could predict coronary events, be modified by statins, and reflect res

120 rticipants with either missing data or had a coronary event before CACS was performed.

121 disease (defined as 12 months from an acute coronary event) between 2002 and 2011 were identified.

122 als have shown that fibrates reduce nonfatal coronary events but do not confer any benefit on mortali

123 evels were inversely associated with CVD and coronary events but not stroke.

124 s have been used for determining the risk of coronary events, but the exact role of this marker for c

125 Psychosocial factors have been linked to coronary events, but the mechanisms underlying these ass

126 ular calcification are at increased risk for coronary events, but the relationship between calcium co

127 calcium score increased the risk of a major coronary event by 15 to 35% and the risk of any coronary

128 riability (by ASV) increased the risk of any coronary event by 16% (hazard ratio [HR]: 1.16; 95% conf

129 onary event by 15 to 35% and the risk of any coronary event by 18 to 39%.

130 ollow-up, there were 434 deaths overall, 472 coronary events (CE), 213 myocardial infarctions (MI), a

131 The Transitions, Risks, and Actions in Coronary Events Center for Outcomes Research and Educati

132 lprit lesion had a higher mortality and more coronary events compared with those without (p < 0.0005,

133 management of coronary artery disease, acute coronary events continue to occur in many patients.

134 duction in LDL-C level; 5-year rate of major coronary events (coronary death or MI) associated with a

135 Outcomes consisted of major coronary events (coronary heart death, myocardial infarc

136 nts with coronary artery disease but without coronary event), coronary artery disease was evaluated u

137 ole of vulnerable plaque in the causation of coronary events, coupled with novel diagnostic and thera

138 ts of the primary end point as well as major coronary events (death from coronary heart disease, myoc

139 arization for myocardial ischemia) and total coronary events (death from coronary heart disease, myoc

140 Mean annual rates for major adverse coronary events declined from 0.41 for 2 years before LA

141 to assess the 1-year risk of first recurrent coronary events defined as coronary death or myocardial

142 disease received a diagnosis of an incident coronary event (defined as nonfatal myocardial infarctio

143 Odds ratio (OR) for major coronary events, defined as coronary death, nonfatal myo

144 The effect of raloxifene on the incidence of coronary events differed significantly by age (interacti

145 status, and GRACE (Global Registry of Acute Coronary Events) discharge risk scores (hazard ratio: 1.

146 iovascular risk factors and age at the first coronary event displayed significant heritable component

147 Twenty-three patients developed coronary events during a median of 6.5 years of follow-u

148 nt was also a strong predictor of stroke and coronary events (eg, top-decile HR for stroke: 3.25, 2.3

149 m particulate exposures contributed to acute coronary events, especially among patients with underlyi

150 a substantial reduction in the incidence of coronary events, even in populations with a high prevale

151 Scarce data exist on coronary events following transcatheter aortic valve rep

152 ion in the standardized 10-year incidence of coronary events from 10.7% for an unfavorable lifestyle

153 nd imaging at unstented sites and subsequent coronary events from new culprit lesions.

154 fied post-discharge Global Registry of Acute Coronary Events (GRACE) score was used to calculate an i

155 iuretic peptide and Global Registry of Acute Coronary Events (GRACE) scores as comparators and to ide

156 ta derived from the Global Registry of Acute Coronary Events (GRACE) we trained a logistic regression

157 nd PATIENTS: In the Global Registry of Acute Coronary Events (GRACE), a multinational cohort study, 4

158 risk measures (eg, Global Registry of Acute Coronary Events [GRACE] score) for death, death/myocardi

159 On average, adults who had a coronary event had been small at birth and thin at two y

160 lerotic plaques that are precursors of acute coronary events harbor abundant macrophage infiltration,

161 ve demonstrated that plaques which result in coronary events have larger plaque volume and necrotic c

162 AKI recovery associated with higher risk of coronary events (hazard ratio [HR], 1.67; 95% confidence

163 and additional risk allele) and for incident coronary events (hazard ratiogxincome=0.69 [95% confiden

164 adjustment gave HRs of 0.94 (0.81-1.08) for coronary events (HDL cholesterol being the largest contr

165 The two primary outcomes were coronary events (i.e., death from coronary causes, myoca

166 population-based case-control study of major coronary events (i.e., myocardial infarction, coronary r

167 disease (CAD) could be at increased risk for coronary events if diastolic pressure falls below critic

168 ure (IH-CHF) and interim hospitalization for coronary events (IH-CE), were examined with proportional

169 ivariate analyses, the odds ratio (OR) for a coronary event in women with an estimated CrCl <60 ml/mi

170 evels of LDL cholesterol on the incidence of coronary events in a large population.

171 eract with SES to influence CAC and incident coronary events in a population-based cohort.

172 c status (SES) to influence CAC and incident coronary events in a population-based cohort.

173 Raloxifene had no effect on the incidence of coronary events in any subgroup except in the case of a

174 PIbalpha subunit predicts risk for recurrent coronary events in diabetic postinfarction patients, but

175 The adjusted HR for coronary events in intermediate risk subjects was 6.98 (

176 not reduce mortality but may reduce nonfatal coronary events in patients at risk for cardiovascular d

177 t fluctuation is a risk factor for death and coronary events in patients without cardiovascular disea

178 There was a 68% increased risk of coronary events in subjects with ASc (hazard ratio [HR]:

179 the usefulness of Lp PLA2 as a predictor of coronary events in the general population and in those w

180 al fat is associated with fatal and nonfatal coronary events in the general population independent of

181 rmine whether epicardial fat volume predicts coronary events in the general population.

182 Sixty-two percent (95% CI: 49%, 74%) of coronary events in this cohort may have been prevented w

183 between treatment groups in the incidence of coronary events in women > or =60 and <70 or > or =70 ye

184 The incidence of coronary events in women <60 years of age was significan

185 icantly associated with an increased odds of coronary events in women with an estimated CrCl < or =74

186 r, had no overall effect on the incidence of coronary events in women with established coronary heart

187 does provide benefit in reducing the risk of coronary events in women; however, women remain undertre

188 er in patients with CP for all major adverse coronary events, including stroke, bleeding, and mortali

189 Incidence of coronary events increased by quartile of EAT (0.9% vs. 4

190 h coronary artery calcification, the risk of coronary events increased incrementally across tertiles

191 Rates of major coronary events increased linearly with the mean dose to

192 Acute coronary events induce a dynamic increase of PCSK9 level

193 enoses, that patients who experience a fatal coronary event invariably had antecedent exposure to one

194 d coronary inflammation for predicting acute coronary events is a currently a source of considerable

195 e use of aspirin for secondary prevention of coronary events is controversial in patients with HF.

196 ociation between inflammatory biomarkers and coronary events is influenced by level of kidney functio

197 Troponin concentration predicts coronary events, is reduced by statin therapy, and chang

198 Notably, in individuals with prior coronary events, living in a home with a dog was associa

199 points included patient-oriented major acute coronary events (MACE) (death, myocardial infarction [MI

200 unadjusted rates of death and major adverse coronary events (MACEs; defined as death, readmission fo

201 Managing patients at risk of acute coronary events mandates a greater focus on the atherosc

202 ntifying patients who have a high risk for a coronary event may decrease morbidity and mortality.

203 olesterolemia, 57% (95% CI: 32%, 79%) of all coronary events may have been prevented with a low-risk

204 n (CRP), in addition to being a predictor of coronary events, may have direct actions on the vessel w

205 and fibrinogen with risks of incident major coronary events (MCE), ischemic stroke (IS) and intracer

206 or major vascular events (MVEs) (i.e., major coronary events [MCE] [nonfatal myocardial infarction or

207 ascular events (MVEs), including 7,326 major coronary events (MCEs), 37,992 ischemic heart disease (I

208 on was higher with versus without subsequent coronary events (median, 115 [Q1-Q3, 23-360] versus 8 [0

209 Coronary events, MI, HF, and overall hospital stays occu

210 ndently conferred an increased risk for hard coronary events (myocardial infarction or death from cor

211 follow-up, we documented 1744 and 1430 major coronary events (myocardial infarction plus fatal ischem

212 Outcomes were incident total CVD (n = 929), coronary events (n = 602), and stroke (n = 319).

213 ) and 3 registries (Global Registry of Acute Coronary Events, National Registry of Myocardial Infarct

214 For coronary events, net reclassification improvement (NRI)

215 some pediatric disease states, with clinical coronary events occurring in childhood and very early ad

216 oronary artery dissection (SCAD) is an acute coronary event of uncertain origin.

217 There were 162 coronary events, of which 89 were major events (myocardi

218 was a composite of initial fatal or nonfatal coronary event or stroke or revascularization.

219 ing to heart failure cases without preceding coronary events or developed diabetes during follow-up.

220 Participants who experienced coronary events or died were followed for a median of 7.

221 o be due primarily to a reduction in interim coronary events or differences in blood pressure.

222 ciated with a reduction in risk of recurrent coronary events or thromboembolism, whereas risk of blee

223 ary end point of cardiovascular death, major coronary event, or nonfatal stroke, the relative risk re

224 neither target (cardiovascular death, major coronary event, or stroke; 38.9% versus 28.0%; adjusted

225 acy composite of cardiovascular death, major coronary events, or stroke was significantly lower in pa

226 er in the statin-treated arm: by 18% for any coronary event (P=0.002), by 24% for myocardial infarcti

227 ntion cohort resulted in an 11% reduction in coronary events (P = 0.16), a similar but significant re

228 r vascular events (P(trend)=0.005) and major coronary events (P(trend)<0.0001).

229 nts) at baseline were not at higher risk for coronary events (P=0.91 for interaction) or stroke (P=0.

230 umber, the hazard ratios for major occlusive coronary event per 1-SD-higher level were 0.91 (95% CI,

231 e interval, 1.01-2.07; P=0.049) for incident coronary events per additional risk allele.

232 e proportional increase in the rate of major coronary events per gray was similar in women with and w

233 ajor vascular event was pre-defined as major coronary event plus revascularization or stroke.

234 ncidence, characteristics, and management of coronary events post-TAVR, and increasing interest exist

235 ts of the Thrombogenic Factors and Recurrent Coronary Events postinfarction study.

236 We compared coronary event rates between patients with and without F

237 s that statins substantially reduce not only coronary event rates but also total stroke rates in pati

238 ngle years revealed increasing major adverse coronary event rates from 0.30 to 0.54 (P=0.001) for y-2

239 onary angiography was associated with higher coronary event rates than was undergoing the procedure.

240 s and test-positive angina, age-standardized coronary event rates were 9.9 per 100 person-years in wo

241 mpared with patients without FH, the risk of coronary event recurrence after ACS was similar in patie

242 h FH and ACS have a >2-fold adjusted risk of coronary event recurrence within the first year after di

243 ons (or deaths) for all 4 diagnostic groups: coronary events (relative risk, 0.848; 95% confidence in

244 diovascular disease (CVD) and, specifically, coronary events remains unclear.

245 23- and 1.65-fold increased hazard for major coronary events, respectively.

246 It has been believed that most acute coronary events result from the rupture of mildly stenot

247 r lack of interaction was observed for major coronary events, revascularizations, and strokes conside

248 sks of incident major vascular events, major coronary events, revascularizations, or strokes.

249 plore altered platelet function in recurrent coronary event risk among diabetic postinfarction patien

250 In a population at 2% average coronary event risk per year, cholesterol, apolipoprotei

251 elationship between plaque rupture and acute coronary event risk suggested by pathology studies and c

252 mplementary to global CAC measures to assess coronary event risk.

253 sus 72), had higher Global Registry of Acute Coronary Events risk score (129 versus 127), and were wi

254 association between Global Registry of Acute Coronary Events risk score variables and optimal in-hosp

255 o assessed were the Global Registry of Acute Coronary Events risk score, Charlson comorbidity index,

256 ility of the GRACE (Global Registry of Acute Coronary Events) risk score for both all-cause mortality

257 ion, and the GRACE (Global Registry of Acute Coronary Events) risk score for severity of ACS.

258 (RR=0.86; 95% CI, 0.75-0.99; P=0.03) but not coronary events (RR=0.86; 95% CI, 0.67-1.11; P=0.24).

259 (NSTEMI) and GRACE (Global Registry of Acute Coronary Events) score >140, coronary angiography (CAG)

260 ere made for GRACE (Global Registry of Acute Coronary Events) score, left ventricular ejection fracti

261 GRACE (Global Registry of Acute Coronary Events) scores were compared with ProSP for dea

262 nts (including myocardial infarctions, fatal coronary events, silent infarctions, revascularization p

263 The main cause of acute coronary events, such as thrombosis, is the rupture of a

264 victims of SCD than in survivors of an acute coronary event suggests that the presence of ER increase

265 ssociated with a substantially lower risk of coronary events than an unfavorable lifestyle (defined a

266 associated with a 46% lower relative risk of coronary events than an unfavorable lifestyle (hazard ra

267 e more relevant to systemic atherothrombotic coronary events than clinical measures.

268 th 70% or greater narrowing experienced more coronary events than patients with less significant lesi

269 rapib resulted in a lower incidence of major coronary events than the use of placebo.

270 In postmenopausal women at increased risk of coronary events, the overall lack of benefit of raloxife

271 in treating conditions that range from acute coronary events to traumatic injury.

272 ciated with increased risk of acute ischemic coronary events (unstable angina and myocardial infarcti

273 ll validated GRACE (Global Registry of Acute Coronary Events) variables together with troponin I and

274 hest variation in body weight, the risk of a coronary event was 64% higher, the risk of a cardiovascu

275 no coronary calcium, the adjusted risk of a coronary event was increased by a factor of 7.73 among p

276 Major coronary event was pre-defined as coronary death or nonf

277 ence of cerebrovascular events compared with coronary events was 1.19 (95% CI 1.06-1.33) overall; 1.4

278 The relative risk of incident coronary events was 91% higher among participants at hig

279 rs, coronary artery calcification (CAC), and coronary events was assessed using regression analysis.

280 relationship between diastolic pressure and coronary events was documented in treated patients with

281 The risk of coronary events was more strongly related to the tempo o

282 clopidogrel), no increased risk of recurrent coronary events was seen for OAC plus clopidogrel (hazar

283 function, inflammatory biomarker levels, and coronary events was studied.

284 The primary end point (major coronary events) was the composite of coronary heart dis

285 tes that has a known association with future coronary events, we divided individuals from the Malmo D

286 iction of both major coronary events and any coronary event were higher when the calcium score was ad

287 The incidence rates of coronary events were 19.8 and 10.3 per 1000 person-years

288 Incident coronary events were ascertained over a median follow-up

289 Incident coronary events were assessed during a follow-up period

290 Major occlusive coronary events were equally strongly associated with th

291 74% of all coronary events were in the 239 (25%) of participants wi

292 parable negative predictive values for major coronary events were obtained in studies considering the

293 centile, 11; 75th percentile, 24 months), no coronary events were recorded.

294 f EAT was associated with a 1.5-fold risk of coronary events when adjusting for cardiovascular risk f

295 There was a 5-fold greater reduction in coronary events when troponin concentrations decreased b

296 the entire coronary vascular tree predicted coronary events, whereas changes in the worst flow-limit

297 (respiratory failure, myositis, and an acute coronary event), which could have been precipitated by t

298 (FRANCIS [Fewer Recurrent Acute Coronary Events With Near-Term Cardiovascular Inflammati

299 A total of 922 men had a major coronary event within 20 years, 352 men had a stroke, an

300 dard glycaemic control significantly reduces coronary events without an increased risk of death.