ライフサイエンスコーパス: infarction

1 interval, 1.92-2.81 versus type 1 myocardial infarction).

2 luding acute ST-segment-elevation myocardial infarction).

3 eous coronary occlusion to induce myocardial infarction.

4 n, but also in the case of healed myocardial infarction.

5 ctively, in the risk of death and myocardial infarction.

6 aemic neuronal injury, consistent with acute infarction.

7 ll thickness and cardiac contractility after infarction.

8 st risk after discharge for acute myocardial infarction.

9 with lower specificity for type 1 myocardial infarction.

10 s on the shape of the growth dynamics of the infarction.

11 tandardized mortality after acute myocardial infarction.

12 cretome of CPCs in the setting of myocardial infarction.

13 gen delivery increasing the risk of cerebral infarction.

14 were monitored for 3 weeks after myocardial infarction.

15 cular events as those with type 1 myocardial infarction.

16 and 1-year readmission rates for myocardial infarction.

17 ncidence of late rupture after nonreperfused infarction.

18 sion of those who died from acute myocardial infarction.

19 (QIs) for the management of acute myocardial infarction.

20 on is useful for the treatment of myocardial infarction.

21 blood flow to the heart and cause myocardial infarction.

22 th in normal conditions and after myocardial infarction.

23 t revascularization, and nonfatal myocardial infarction.

24 c and dilated cardiomyopathy, and myocardial infarction.

25 inating between acute and chronic myocardial infarction.

26 ty statin use and adherence after myocardial infarction.

27 atients with ST-segment-elevation myocardial infarction.

28 rmed 84 weeks (15-111 weeks) post-myocardial infarction.

29 ricular systolic dysfunction, and myocardial infarction.

30 s per the universal definition of myocardial infarction.

31 rct size in rat and pig models of myocardial infarction.

32 ed with increased risk of CAD and myocardial infarction.

33 erior wall thinning 28 days after myocardial infarction.

34 ng to the universal definition of myocardial infarction.

35 arterial damage and thrombosis-induced organ infarction.

36 emodeling in ST-segment-elevation myocardial infarction.

37 terol, and extended to stroke and myocardial infarction.

38 licated by intracranial haemorrhage or brain infarction.

39 osclerosis and its progression to myocardial infarction.

40 come (HR 1.31, 95% CI 1.20-1.42), myocardial infarction (1.55, 1.33-1.80), hospital admission for hea

41 atrial fibrillation, 89 (8%) with myocardial infarction, 11 (0.9%) with ischemic stroke, and 1 (0.1%)

42 had 502 ischemic events (306 with myocardial infarction, 113 with stent thrombosis, and 83 with ische

43 follow-up, 62 strokes or TIAs, 42 myocardial infarctions, 156 HF events, and 38 cardiovascular deaths

44 ed decreases in PAC use for acute myocardial infarction (20.0 PACs placed per 1000 admissions in 1999

45 more likely to have a history of myocardial infarction (28% versus 22%), higher body mass index (31

46 ia required for spontaneous acute myocardial infarction (280/397, 71%) versus those with at least 1 a

47 rial Fibrillation-Thrombolysis in Myocardial Infarction 48), the factor Xa inhibitor edoxaban was non

48 ground of Aspirin-Thrombolysis in Myocardial Infarction 54) (ticagrelor) were blinded, randomized pla

49 ground of Aspirin-Thrombolysis In Myocardial Infarction 54) trial, which randomized 21,162 patients t

50 After myocardial infarction, A2b receptor (A2bR) transcription was induce

51 nt CHD included fatal or nonfatal myocardial infarction, acute coronary syndrome without myocardial i

52 evaluated: (i) CVD events/deaths (myocardial infarction, acute coronary syndrome, stroke, congestive

53 Of 199 162 myocardial infarction admissions, 9466 consecutive unique patients

54 entricular function at 35 d after myocardial infarction, albeit iPSC-EVs rendered greater improvement

55 regeneration in adult mice after myocardial infarction, although the degree of cardiomyocyte prolife

56 in treatment, mortality in acute myocardial infarction (AMI) complicated by cardiogenic shock (CS) r

57 ment patients with possible acute myocardial infarction (AMI) has been shown to effectively identify

58 evealed that mortality from acute myocardial infarction (AMI) has decreased, whereas the prevalence o

59 ma samples of patients with acute myocardial infarction (AMI) was carried out with screen-printed ele

60 For acute myocardial infarction (AMI) without heart failure (HF), it is uncle

61 tention to young women with acute myocardial infarction (AMI), who represent an extreme phenotype.

62 released more rapidly after acute myocardial infarction (AMI).

63 (NSAIDs) use could trigger acute myocardial infarction (AMI).

64 The excess risk of cerebral infarction among CNS tumor survivors increases with atta

65 a composite outcome of stroke or myocardial infarction among nondiabetic patients with insulin resis

66 rtery disease had higher rates of myocardial infarction and acute limb ischemia, with similar composi

67 Patients with suspected myocardial infarction and an oxygen saturation of 90% or higher wer

68 eviously showed associations with myocardial infarction and arterial stiffness, as well as coronary a

69 s associated with future risk for myocardial infarction and can be modulated with short-term therapie

70 Subsequent type 1 myocardial infarction and cardiac death were reported at 1 year.

71 rest is only a surrogate of acute myocardial infarction and confounded by the choice of anesthesia, h

72 entuated adverse remodeling after reperfused infarction and exhibited an increased incidence of late

73 0(6)) were injected 24 hours post-myocardial infarction and homed to regions of myocardial injury; ho

74 ification in patients with type 2 myocardial infarction and myocardial injury.

75 treating more patients with acute myocardial infarction and performing more PCIs than nonoutlier hosp

76 s driven mainly by differences in myocardial infarction and repeat revascularization.

77 ST-elevation myocardial infarction and sinus venous tract thrombosis occurred as

78 nts with non-ST-segment-elevation myocardial infarction and stable angina pectoris , similar patterns

79 Rates of myocardial infarction and stroke did not differ between the 2 group

80 n regarding an increased risk for myocardial infarction and stroke.

81 ardiac events (fatal and nonfatal myocardial infarction and sudden cardiac death), and harms.

82 buted to both the acute unilateral choroidal infarction and to the chronic development of bilateral g

83 d cases (individuals with CAD and myocardial infarction) and noncases, with baseline data collected f

84 sel disease, ST-segment-elevation myocardial infarction, and cardiogenic shock were included.

85 ction for cardiovascular disease, myocardial infarction, and heart failure over use of established an

86 rdiovascular mortality, non-fatal myocardial infarction, and non-fatal stroke.

87 izations for heart failure, acute myocardial infarction, and pneumonia, respectively.

88 oriasis have an increased risk of myocardial infarction, and psoriasis is now recognized as an indepe

89 te rates of cardiovascular death, myocardial infarction, and stroke when compared with patients enrol

90 diac death, target vessel-related myocardial infarction, and target lesion revascularization) was 5.4

91 s the composite of cardiac death, myocardial infarction, and target vessel revascularization.

92 ciated with hypertension, stroke, myocardial infarction, and vascular diseases.

93 tin or fibrate, had no history of myocardial infarction, and were not being treated for angina were r

94 CAD cases [approximately 70% with myocardial infarction] and 123504 noncases), the 6 SNPs related to

95 rted incident CVD, defined as new myocardial infarction, angina pectoris, or stroke, which developed

96 Secondary outcomes were myocardial infarction, angina, heart failure, hypertension, arrhyth

97 ion (CTP) ischemic core threshold to predict infarction as thrombolysis patients with complete reperf

98 ted the trial), the rate of freedom from CNS infarction at 7 days was 32.0% with suction-based extrac

99 rest without ST-segment-elevation myocardial infarction at the point of care.

100 ously administered MSCs for acute myocardial infarction attenuate the progressive deterioration in LV

101 mes of patients treated for acute myocardial infarction before and after a hospital had been publicly

102 ears (n = 27956) hospitalized for myocardial infarction between 2007 and 2012 who filled a high-inten

103 ted with increased risk of death, myocardial infarction, bleeding, and recurrent renal injury after d

104 rge anterior ST-segment-elevation myocardial infarctions, bone marrow mononuclear cells administratio

105 nting with symptoms suggestive of myocardial infarction by 2 independent cardiologists by 2 1 method

106 d the overall management of acute myocardial infarction can be reviewed for simplicity.

107 Myocardial infarction, cardiovascular death, and repeat revasculari

108 ff-the-shelf early after an acute myocardial infarction, comply with stringent criteria for product h

109 for five medical diagnoses (acute myocardial infarction, congestive heart failure, stroke, pneumonia,

110 on how primary and comorbid acute myocardial infarction contribute to the mortality burden of acute m

111 th or major cardiovascular event (myocardial infarction, coronary angioplasty, coronary artery bypass

112 verse events comprised CVD death, myocardial infarction, coronary insufficiency, index admission for

113 e cardiovascular outcomes (death, myocardial infarction, coronary revascularization, or cerebrovascul

114 , acute coronary syndrome without myocardial infarction, coronary revascularization, or CHD death.

115 ent of Patients With ST-elevation Myocardial Infarction [DANAMI-3]; NCT01435408).

116 y or other medical complications (myocardial infarction, deep vein thrombosis, pulmonary embolism, an

117 ring PCI for ST-segment-elevation myocardial infarction did not improve clinical outcomes.

118 ST-Elevation or Non-ST-Elevation Myocardial Infarction (FAST-MI) 2005 (n=3670) and FAST-MI 2010 (n=4

119 ascular causes, fatal or nonfatal myocardial infarction, fatal or nonfatal stroke, hospitalization fo

120 s, and modern management of acute myocardial infarction, focusing on the recent advances in reperfusi

121 ratory diseases, hypertension and myocardial infarction from the life-course perspective, and the ris

122 tients (53% female, 74% anterior circulation infarction) fulfilled the inclusion criteria and were in

123 diagnosis of ST-segment elevation myocardial infarction (group by PCI or ST-segment elevation myocard

124 Acute myocardial infarction has traditionally been divided into ST elevat

125 age of the HRRP, 30-day RSRRs for myocardial infarction, heart failure, and pneumonia decreased more

126 cardiovascular disease (including myocardial infarction, heart failure, and stroke) and all-cause mor

127 dmitted to the hospital for acute myocardial infarction, heart failure, or pneumonia.

128 18-fold higher risk of dying from myocardial infarction, heart failure, or stroke, respectively, than

129 In the 182 days after myocardial infarction hospital discharge, 15.4% of beneficiaries di

130 ST elevation or non-ST elevation myocardial infarction; however, therapies are similar between the t

131 CI: 1.35 to 1.42; p < 0.0001) and myocardial infarction (HR: 1.03; 95% CI: 1.00 to 1.05; p < 0.04).

132 (HR: 1.45; 95% CI: 1.21 to 1.74), myocardial infarction (HR: 1.47; 95% CI: 1.23 to 1.78), and repeat

133 % CI: 1.34 to 2.21), and nonfatal myocardial infarction (HR: 1.58; 95% CI: 1.42 to 1.76).

134 rhage, extracranial bleeding, and myocardial infarction identified from hospital claims among propens

135 l blood RNA and PCTP and death or myocardial infarction in 2 separate patient cohorts (587 total pati

136 o induce spreading depolarizations and acute infarction in adjacent cortex.

137 s in evidence-based treatment for myocardial infarction in China have largely been eliminated, substa

138 Rates of myocardial infarction in firefighters are increased during fire sup

139 re suppression activity and acute myocardial infarction in firefighters.

140 pression is associated with death/myocardial infarction in patients with cardiovascular disease.

141 e to that of ST-segment-elevation myocardial infarction in the era of primary percutaneous coronary i

142 artery disease had to have had a myocardial infarction in the past 20 years, multi-vessel coronary a

143 issions with a diagnosis of acute myocardial infarction, in the second or later physician encounter i

144 Both heart failure and myocardial infarction increase risk of AF and vice versa creating a

145 up by PCI or ST-segment elevation myocardial infarction interaction effect; p = 0.86 and p = 0.71, re

146 composite of all-cause mortality, myocardial infarction, ischemia-driven revascularization, or stent

147 composite of all-cause mortality, myocardial infarction, ischemia-driven revascularization, or stent

148 Cardiovascular events including myocardial infarction, ischemic stroke and cardiovascular death, qu

149 VEs, including fatal and nonfatal myocardial infarction, ischemic stroke, and cardiovascular death.

150 se mortality, hospitalization for myocardial infarction, ischemic stroke, and heart failure.

151 V) dysfunction, ischemic MR, and left atrial infarction (LAI); and 2) to analyze how LA remodeling in

152 d that clinical reperfusion after myocardial infarction led to significant elevation of the soluble f

153 ass graft-related Thrombolysis In Myocardial Infarction major and minor bleeding.

154 ystemic embolism, vascular death, myocardial infarction, major bleeding, or intracranial hemorrhage a

155 Negative control outcomes of myocardial infarction (MI) and herpes zoster were also studied.

156 of coronary artery disease (CAD), myocardial infarction (MI) and their risk factors.

157 following hospital discharge for myocardial infarction (MI) between 2011 and 2014.

158 higher risk for future stroke or myocardial infarction (MI) derive more benefit from the insulin-sen

159 vity but face an elevated risk of myocardial infarction (MI) due to common MI risk factors and HIV-sp

160 Myocardial infarction (MI) elicits inflammation, but the dominant m

161 d outcomes of patients with acute myocardial infarction (MI) have been described, but little is known

162 cell-based therapies after acute myocardial infarction (MI) have produced mostly neutral results.

163 Myocardial infarction (MI) is a leading cause of heart failure and

164 emic heart disease resulting from myocardial infarction (MI) is the most prevalent form of heart dise

165 within 1 year of the index acute myocardial infarction (MI) of 12365 patients enrolled in the Treatm

166 In the DAPT Study, combined myocardial infarction (MI) or stent thrombosis and moderate/severe

167 Myocardial infarction (MI) results in the generation of dead cells

168 etoprolol (Meto) may improve post-myocardial infarction (MI) structural and functional outcomes via r

169 on (r-I/R) injury without ensuing myocardial infarction (MI) to elaborate a spatial- and chronologic

170 otal of 1,230 patients with acute myocardial infarction (MI) treated with primary percutaneous corona

171 ferences in early mortality after myocardial infarction (MI) vary by age.

172 s been identified for early onset myocardial infarction (MI), modified the association of LC n-3 PUFA

173 of periprocedural death, stroke, myocardial infarction (MI), or nonperiprocedural ipsilateral stroke

174 or adverse cardiovascular events, myocardial infarction (MI), or target vessel revascularization in S

175 In chronic myocardial infarction (MI), segments with a transmural extent of in

176 ological effects, but its role in myocardial infarction (MI)-induced cardiac remodeling remains uncle

177 biomarker levels in patients with myocardial infarction (MI)-to test whether ANGPTL3 deficiency is as

178 ardiac recovery process following myocardial infarction (MI).

179 hronic periodontitis (CP); and 3) myocardial infarction (MI).

180 ring cardiac remodeling following myocardial infarction (MI).

181 tcomes of (1) death; (2) death or myocardial infarction (MI); (3) death, MI, or repeat revascularizat

182 site of all-cause death, nonfatal myocardial infarction [MI], heart failure, stroke, transient ischem

183 Acute CHD events included myocardial infarctions (MIs; nonfatal and fatal) and acute CHD deat

184 CELF1 overexpression models and a myocardial infarction model.

185 In healing myocardial infarction, myofibroblast- and cardiomyocyte-specific ac

186 ated in patients with spontaneous myocardial infarction (n=63; P<6.17E-04).

187 ent regional ST-segment-elevation myocardial infarction networks focused on prehospital catheterizati

188 Study endpoints included myocardial infarction, new or worsening heart failure, atrial fibri

189 cose-lowering drugs for non-fatal myocardial infarction, non-fatal stroke, or atrial fibrillation.

190 scular events, including nonfatal myocardial infarction, nonfatal stroke, and CVD mortality.

191 f the primary end point (nonfatal myocardial infarction, nonfatal stroke, or death from cardiovascula

192 ng patients with non-ST elevation myocardial infarction (NSTEMI).

193 t proportion of deaths from acute myocardial infarction occurred in people who had been in hospital o

194 ed with a lower risk of death and myocardial infarction (odds ratio, 0.71; 95% confidence interval, 0

195 ed with a lower risk of death and myocardial infarction (odds ratio, 0.76; 95% confidence interval, 0

196 PCAs resulted in the development of ischemic infarction of the choroid, retinal pigment epithelium, o

197 tion, venous thromboembolism, and myocardial infarction, on these outcomes was comparatively small.

198 myocardial infarction, or type 1 myocardial infarction or cardiac death at 30 days.

199 rdiovascular events (eg, nonfatal myocardial infarction or cardiovascular death) and noncardiovascula

200 se, defined as the first incident myocardial infarction or death owing to coronary heart disease, and

201 cular death, patients with type 2 myocardial infarction or myocardial injury have a similar crude rat

202 xcess deaths in those with type 2 myocardial infarction or myocardial injury were because of noncardi

203 in imaging in patients with acute myocardial infarction or stable ischemic heart disease.

204 3.2%) had PAD (1505 with no prior myocardial infarction or stroke).

205 cs of patients suffering an acute myocardial infarction or undergoing cardiovascular surgery.

206 derate evidence of a reduction of myocardial infarction (OR, 0.62; 95% credible intervals, 0.39-1.05)

207 r post-discharge hazard of death, myocardial infarction, or bleeding (AKIN 1: hazard ratio [HR], 1.53

208 ary efficacy outcomes were death, myocardial infarction, or cerebrovascular accident.

209 the time to occurrence of stroke, myocardial infarction, or death within 90 days.

210 adjudicated cardiovascular death, myocardial infarction, or ischemic stroke.

211 omposite of death from any cause, myocardial infarction, or major bleeding was not lower among those

212 s the composite of cardiac death, myocardial infarction, or stent thrombosis.

213 was a composite of cardiac death, myocardial infarction, or stent thrombosis.

214 endpoint of cardiovascular death, myocardial infarction, or stroke (126 [5%] of 2492 vs 174 [7%] of 2

215 sed risk of cardiovascular death, myocardial infarction, or stroke compared with patients with hsTnI

216 ear incidence of all-cause death, myocardial infarction, or stroke of 18.3% (319 events) in patients

217 omposite of cardiovascular death, myocardial infarction, or stroke.

218 e trial was cardiovascular death, myocardial infarction, or stroke.

219 omposite of cardiovascular death, myocardial infarction, or stroke.

220 diac death, target vessel-related myocardial infarction, or target vessel revascularization.

221 e of cardiac death, target-vessel myocardial infarction, or target-vessel revascularization).

222 a primary outcome of index type 1 myocardial infarction, or type 1 myocardial infarction or cardiac d

223 The primary end point was death, myocardial infarction, or unstable angina hospitalizations over a m

224 (LVEF) less than 50% (P < .001) and anterior infarction (P = .008) independently helped predict LV th

225 e with global cognitive performance (lacunar infarctions, P = .060; acute lesions, P = .088; chronic

226 for the evaluation of early-onset myocardial infarction, participants with CHIP had a risk of myocard

227 Consecutive ST-segment-elevation myocardial infarction patients from a defined health region were cl

228 ification of ST-segment-elevation myocardial infarction patients treated with primary percutaneous co

229 consecutive ST-segment-elevation myocardial infarction patients were enrolled within 12 hours from s

230 g Underlying Disparities in Acute Myocardial Infarction Patients' Health Status) is an observational

231 with 23 498 ST-segment-elevation myocardial infarction patients) were surveyed before (March 2012) a

232 k factors in ST-segment-elevation myocardial infarction patients.

233 failing myocardium and in a post-myocardial infarction (PMI) HF model evaluated in wild-type (wt-PMI

234 ith anterior ST-segment-elevation myocardial infarctions resulting in LV dysfunction.

235 However, for myocardial infarction, results for CEE+MPA were in the direction of

236 outcome was all-cause mortality; myocardial infarction, revascularization, and stroke were also anal

237 and a 40% increased risk of acute myocardial infarction (RR 1.40; 95% CI, 1.23 to 1.59).

238 ty (RR, 0.84; 95% CI, 0.59-1.18), myocardial infarction (RR, 0.47; 95% CI, 0.20-1.11), and stroke (RR

239 fined as a modified Thrombolysis in Cerebral Infarction score of 2b or 3 at the end of all endovascul

240 cell depletion 24 hours pre-acute myocardial infarction significantly improved infarct size, LV eject

241 Myocardial infarction size was larger in aged hearts (P < 0.05 vs.

242 treatment of ST-segment-elevation myocardial infarction (STEMI) has been widely used; however, recent

243 erfusion for ST-segment elevation myocardial infarction (STEMI) in settings where health-care resourc

244 on (PCI) for ST-segment elevation myocardial infarction (STEMI) may not be uniform over time, which m

245 and therapy, ST-segment-elevation myocardial infarction (STEMI) victims remain at risk for infarct ex

246 atients with ST-segment elevation myocardial infarction (STEMI), the use of percutaneous coronary int

247 rvention for ST-segment elevation myocardial infarction (STEMI).

248 ter an acute ST-segment-elevation myocardial infarction (STEMI).

249 nificant differences in recurrent myocardial infarction, stent thrombosis, heart failure, or target v

250 imary endpoint was a composite of myocardial infarction, stroke, and death from cardiovascular causes

251 se cardiovascular events, such as myocardial infarction, stroke, and death.

252 dverse clinical events, including myocardial infarction, stroke, and heart failure hospitalization, w

253 ted cardiovascular events such as myocardial infarction, stroke, and heart failure.

254 Cardiovascular outcomes were myocardial infarction, stroke, congestive heart failure, and cardio

255 ortant outcomes including risk of myocardial infarction, stroke, heart failure, and major cardiovascu

256 n risk score validated to predict myocardial infarction, stroke, heart failure, or death.

257 ral adverse events such as death, myocardial infarction, stroke, or cardiac tamponade, and feasibilit

258 trated to reduce the composite of myocardial infarction, stroke, or cardiovascular death in patients

259 ipid species and the risk of CVD (myocardial infarction, stroke, or cardiovascular death); 2) a MedDi

260 harm or benefit was observed for myocardial infarction, stroke, or hospital admission for heart fail

261 d a composite of all-cause death, myocardial infarction, stroke, or repeat revascularization at long-

262 We also identified potential myocardial infarctions, strokes, and heart failure events in Health

263 ticipants with CHIP had a risk of myocardial infarction that was 4.0 times as great as in noncarriers

264 Among patients undergoing PCI for myocardial infarction, the rate of the composite of death from any

265 to the mortality burden of acute myocardial infarction, the share of these deaths that occur during

266 complicating ST-segment-elevation myocardial infarction, there may be no significant benefit with sin

267 ailure (one [<1%] vs three [2%]), myocardial infarction (three [1%] vs none), lung infection (three [

268 the active surveillance group was myocardial infarction (three patients).

269 apy through day 30, perioperative myocardial infarction through day 5, or use of a mechanical cardiac

270 of out-of-hospital Thrombosis in Myocardial Infarction (TIMI) major or minor bleeding stratified by

271 Arteries [GUSTO], Thrombolysis in Myocardial Infarction [TIMI], and Acute Catheterization and Urgent

272 among patients admitted for acute myocardial infarction to 2615 for mortality among patients admitted

273 ty cardiac troponin assays enable myocardial infarction to be ruled out earlier, but the optimal appr

274 1 men and women with a history of myocardial infarction to placebo or one of three doses of canakinum

275 nrollment of patients with recent myocardial infarction, total occlusions, bifurcations lesions, and

276 emic attack, ischaemic stroke, or myocardial infarction treated with antiplatelet drugs (mainly aspir

277 atients with ST-segment-elevation myocardial infarction treated with primary percutaneous coronary in

278 ure (cardiac death, target vessel myocardial infarction [TVMI], or ischemia-driven target lesion reva

279 atients with ST-segment-elevation myocardial infarction undergoing percutaneous coronary intervention

280 , or MESA, who were free of prior myocardial infarction underwent both ECG and cardiac magnetic reson

281 ent cardiovascular disease (CVD) (myocardial infarction, unstable angina, arterial revascularization,

282 le-in of non-ST-segment elevation myocardial infarction using high-sensitivity cardiac troponin (hs-c

283 for very early rule-out of acute myocardial infarction using high-sensitivity cardiac troponin I (hs

284 iation between dabigatran use and myocardial infarction varied in sensitivity analyses and by exposur

285 y, obesity, major bleeding, acute myocardial infarction, vascular complications, and sepsis were iden

286 ia required for spontaneous acute myocardial infarction versus those patients who do.

287 r survivors were hospitalized for a cerebral infarction (versus 0.06% expected).

288 r survivors were hospitalized for a cerebral infarction (versus 0.1% expected), whereas at any age, e

289 The prediction of infarction volume after stroke onset depends on the shap

290 c Ischemic Events-Thrombolysis in Myocardial Infarction) (vorapaxar) and PEGASUS-TIMI 54 (Prevention

291 ) data were available, the OR for myocardial infarction was 0.93 (95% CI 0.90-0.97; p<0.0001) per 1-S

292 Acute myocardial infarction was diagnosed in the first physician encounte

293 METHODS AND Acute infarction was induced by cardiac catheterization of dom

294 receding death, and whether acute myocardial infarction was one of the recorded diagnoses in such adm

295 e, including ST-segment-elevation myocardial infarction were enrolled.

296 rtality and combined death/stroke/myocardial infarction were observed.

297 the neonatal proliferative network following infarction, which was associated with loss of chromatin

298 en increased bleeding and reduced myocardial infarctions with prolonged dual antiplatelet therapy, fi

299 ratory diseases, hypertension and myocardial infarction, with a particular focus from a life-course p

300 of HSPC mobilisation 8 days post-myocardial infarction, with increased circulating neutrophils and p