ライフサイエンスコーパス: myocardial infarction

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

2 ed ACS (excluding acute ST-segment-elevation myocardial infarction).

3 ease, respectively, in the risk of death and myocardial infarction.

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

5 re at highest risk after discharge for acute myocardial infarction.

6 risk, but with lower specificity for type 1 myocardial infarction.

7 -day risk-standardized mortality after acute myocardial infarction.

8 d by the secretome of CPCs in the setting of myocardial infarction.

9 thetic axis were monitored for 3 weeks after myocardial infarction.

10 e cardiovascular events as those with type 1 myocardial infarction.

11 ransfusion, and 1-year readmission rates for myocardial infarction.

12 pital admission of those who died from acute myocardial infarction.

13 indicators (QIs) for the management of acute myocardial infarction.

14 dministration is useful for the treatment of myocardial infarction.

15 an occlude blood flow to the heart and cause myocardial infarction.

16 he heart both in normal conditions and after myocardial infarction.

17 uses, repeat revascularization, and nonfatal myocardial infarction.

18 nt, ischemic and dilated cardiomyopathy, and myocardial infarction.

19 for discriminating between acute and chronic myocardial infarction.

20 igh-intensity statin use and adherence after myocardial infarction.

21 for older patients with ST-segment-elevation myocardial infarction.

22 g was performed 84 weeks (15-111 weeks) post-myocardial infarction.

23 , left ventricular systolic dysfunction, and myocardial infarction.

24 is of whole exome sequencing for early onset myocardial infarction.

25 ng PCI in patients with ST-segment-elevation myocardial infarction.

26 mation, and diet-induced atherosclerosis and myocardial infarction.

27 judicated as per the universal definition of myocardial infarction.

28 educes infarct size in rat and pig models of myocardial infarction.

29 as associated with increased risk of CAD and myocardial infarction.

30 erbated anterior wall thinning 28 days after myocardial infarction.

31 ted according to the universal definition of myocardial infarction.

32 ntricular remodeling in ST-segment-elevation myocardial infarction.

33 -HDL cholesterol, and extended to stroke and myocardial infarction.

34 early atherosclerosis and its progression to myocardial infarction.

35 to percutaneous coronary occlusion to induce myocardial infarction.

36 primary outcome (HR 1.31, 95% CI 1.20-1.42), myocardial infarction (1.55, 1.33-1.80), hospital admiss

37 9.2%) with atrial fibrillation, 89 (8%) with myocardial infarction, 11 (0.9%) with ischemic stroke, a

38 als (4.1%) had 502 ischemic events (306 with myocardial infarction, 113 with stent thrombosis, and 83

39 During follow-up, 62 strokes or TIAs, 42 myocardial infarctions, 156 HF events, and 38 cardiovasc

40 ere sustained decreases in PAC use for acute myocardial infarction (20.0 PACs placed per 1000 admissi

41 , they were more likely to have a history of myocardial infarction (28% versus 22%), higher body mass

42 onal criteria required for spontaneous acute myocardial infarction (280/397, 71%) versus those with a

43 ation in Atrial Fibrillation-Thrombolysis in Myocardial Infarction 48), the factor Xa inhibitor edoxa

44 o on a Background of Aspirin-Thrombolysis in Myocardial Infarction 54) (ticagrelor) were blinded, ran

45 o on a Background of Aspirin-Thrombolysis In Myocardial Infarction 54) trial, which randomized 21,162

46 After myocardial infarction, A2b receptor (A2bR) transcription

47 Incident CHD included fatal or nonfatal myocardial infarction, acute coronary syndrome without m

48 sures were evaluated: (i) CVD events/deaths (myocardial infarction, acute coronary syndrome, stroke,

49 Of 199 162 myocardial infarction admissions, 9466 consecutive uniqu

50 of cell delivery after ST-segment-elevation myocardial infarction affects recovery of left ventricul

51 ubjects and was associated with future death/myocardial infarction after adjustment for age, sex, and

52 oved left ventricular function at 35 d after myocardial infarction, albeit iPSC-EVs rendered greater

53 tes cardiac regeneration in adult mice after myocardial infarction, although the degree of cardiomyoc

54 te advances in treatment, mortality in acute myocardial infarction (AMI) complicated by cardiogenic s

55 ency department patients with possible acute myocardial infarction (AMI) has been shown to effectivel

56 dialysis revealed that mortality from acute myocardial infarction (AMI) has decreased, whereas the p

57 and 14 plasma samples of patients with acute myocardial infarction (AMI) was carried out with screen-

58 For acute myocardial infarction (AMI) without heart failure (HF),

59 creasing attention to young women with acute myocardial infarction (AMI), who represent an extreme ph

60 Tn) and is released more rapidly after acute myocardial infarction (AMI).

61 atory drugs (NSAIDs) use could trigger acute myocardial infarction (AMI).

62 he risk for a composite outcome of stroke or myocardial infarction among nondiabetic patients with in

63 eripheral artery disease had higher rates of myocardial infarction and acute limb ischemia, with simi

64 Patients with suspected myocardial infarction and an oxygen saturation of 90% or

65 hat also previously showed associations with myocardial infarction and arterial stiffness, as well as

66 lammation is associated with future risk for myocardial infarction and can be modulated with short-te

67 Subsequent type 1 myocardial infarction and cardiac death were reported at

68 ioplegic arrest is only a surrogate of acute myocardial infarction and confounded by the choice of an

69 d MSCs (1x10(6)) were injected 24 hours post-myocardial infarction and homed to regions of myocardial

70 risk stratification in patients with type 2 myocardial infarction and myocardial injury.

71 re larger, treating more patients with acute myocardial infarction and performing more PCIs than nono

72 improvements driven mainly by differences in myocardial infarction and repeat revascularization.

73 ST-elevation myocardial infarction and sinus venous tract thrombosis

74 nd in patients with non-ST-segment-elevation myocardial infarction and stable angina pectoris , simil

75 Rates of myocardial infarction and stroke did not differ between

76 e of concern regarding an increased risk for myocardial infarction and stroke.

77 ke, major cardiac events (fatal and nonfatal myocardial infarction and sudden cardiac death), and har

78 hat included cases (individuals with CAD and myocardial infarction) and noncases, with baseline data

79 th multivessel disease, ST-segment-elevation myocardial infarction, and cardiogenic shock were includ

80 risk prediction for cardiovascular disease, myocardial infarction, and heart failure over use of est

81 ited to, cardiovascular mortality, non-fatal myocardial infarction, and non-fatal stroke.

82 31 hospitalizations for heart failure, acute myocardial infarction, and pneumonia, respectively.

83 nts with psoriasis have an increased risk of myocardial infarction, and psoriasis is now recognized a

84 lar composite rates of cardiovascular death, myocardial infarction, and stroke when compared with pat

85 site of cardiac death, target vessel-related myocardial infarction, and target lesion revascularizati

86 assessed as the composite of cardiac death, myocardial infarction, and target vessel revascularizati

87 ns are associated with hypertension, stroke, myocardial infarction, and vascular diseases.

88 aking a statin or fibrate, had no history of myocardial infarction, and were not being treated for an

89 als (60801 CAD cases [approximately 70% with myocardial infarction] and 123504 noncases), the 6 SNPs

90 s self-reported incident CVD, defined as new myocardial infarction, angina pectoris, or stroke, which

91 Secondary outcomes were myocardial infarction, angina, heart failure, hypertensi

92 cardiac arrest without ST-segment-elevation myocardial infarction at the point of care.

93 Intravenously administered MSCs for acute myocardial infarction attenuate the progressive deterior

94 pital outcomes of patients treated for acute myocardial infarction before and after a hospital had be

95 r than 75 years (n = 27956) hospitalized for myocardial infarction between 2007 and 2012 who filled a

96 is associated with increased risk of death, myocardial infarction, bleeding, and recurrent renal inj

97 nts with large anterior ST-segment-elevation myocardial infarctions, bone marrow mononuclear cells ad

98 ients presenting with symptoms suggestive of myocardial infarction by 2 independent cardiologists by

99 the two, and the overall management of acute myocardial infarction can be reviewed for simplicity.

100 -risk features, such as ST-segment-elevation myocardial infarction, cardiogenic shock, and multivesse

101 Myocardial infarction, cardiovascular death, and repeat

102 inistered off-the-shelf early after an acute myocardial infarction, comply with stringent criteria fo

103 r admitted for five medical diagnoses (acute myocardial infarction, congestive heart failure, stroke,

104 available on how primary and comorbid acute myocardial infarction contribute to the mortality burden

105 nsplant death or major cardiovascular event (myocardial infarction, coronary angioplasty, coronary ar

106 Adverse events comprised CVD death, myocardial infarction, coronary insufficiency, index adm

107 cted adverse cardiovascular outcomes (death, myocardial infarction, coronary revascularization, or ce

108 infarction, acute coronary syndrome without myocardial infarction, coronary revascularization, or CH

109 cute Treatment of Patients With ST-elevation Myocardial Infarction [DANAMI-3]; NCT01435408).

110 of mortality or other medical complications (myocardial infarction, deep vein thrombosis, pulmonary e

111 piration during PCI for ST-segment-elevation myocardial infarction did not improve clinical outcomes.

112 RATIONALE: The TIME trial (Timing in Myocardial Infarction Evaluation) was the first cell the

113 ry of Acute ST-Elevation or Non-ST-Elevation Myocardial Infarction (FAST-MI) 2005 (n=3670) and FAST-M

114 rom cardiovascular causes, fatal or nonfatal myocardial infarction, fatal or nonfatal stroke, hospita

115 gical trends, and modern management of acute myocardial infarction, focusing on the recent advances i

116 ident respiratory diseases, hypertension and myocardial infarction from the life-course perspective,

117 ose with a diagnosis of ST-segment elevation myocardial infarction (group by PCI or ST-segment elevat

118 es, the holy grail in the treatment of acute myocardial infarction has been the mitigation of lethal

119 Acute myocardial infarction has traditionally been divided int

120 After passage of the HRRP, 30-day RSRRs for myocardial infarction, heart failure, and pneumonia decr

121 cidence of cardiovascular disease (including myocardial infarction, heart failure, and stroke) and al

122 who were admitted to the hospital for acute myocardial infarction, heart failure, or pneumonia.

123 old, and a 18-fold higher risk of dying from myocardial infarction, heart failure, or stroke, respect

124 In the 182 days after myocardial infarction hospital discharge, 15.4% of benef

125 ivided into ST elevation or non-ST elevation myocardial infarction; however, therapies are similar be

126 [95% CI, 0.99-1.16]; P=0.10) or spontaneous myocardial infarction (HR, 1.03 [95% CI, 0.97-1.09]; P=0

127 1.38; 95% CI: 1.35 to 1.42; p < 0.0001) and myocardial infarction (HR: 1.03; 95% CI: 1.00 to 1.05; p

128 rt disease (HR: 1.45; 95% CI: 1.21 to 1.74), myocardial infarction (HR: 1.47; 95% CI: 1.23 to 1.78),

129 R: 1.72; 95% CI: 1.34 to 2.21), and nonfatal myocardial infarction (HR: 1.58; 95% CI: 1.42 to 1.76).

130 anial hemorrhage, extracranial bleeding, and myocardial infarction identified from hospital claims am

131 n peripheral blood RNA and PCTP and death or myocardial infarction in 2 separate patient cohorts (587

132 disparities in evidence-based treatment for myocardial infarction in China have largely been elimina

133 Rates of myocardial infarction in firefighters are increased duri

134 between fire suppression activity and acute myocardial infarction in firefighters.

135 this synthetic formulation immediately after myocardial infarction in mice resulted in marked reducti

136 PCTP expression is associated with death/myocardial infarction in patients with cardiovascular di

137 e comparable to that of ST-segment-elevation myocardial infarction in the era of primary percutaneous

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

139 446 744 admissions with a diagnosis of acute myocardial infarction, in the second or later physician

140 Both heart failure and myocardial infarction increase risk of AF and vice versa

141 rction (group by PCI or ST-segment elevation myocardial infarction interaction effect; p = 0.86 and p

142 nt was the composite of all-cause mortality, myocardial infarction, ischemia-driven revascularization

143 ent effects on the primary end point (death, myocardial infarction, ischemia-driven revascularization

144 nt was the composite of all-cause mortality, myocardial infarction, ischemia-driven revascularization

145 Cardiovascular events including myocardial infarction, ischemic stroke and cardiovascula

146 to assess CVEs, including fatal and nonfatal myocardial infarction, ischemic stroke, and cardiovascul

147 as all-cause mortality, hospitalization for myocardial infarction, ischemic stroke, and heart failur

148 ortic calcium score, and incident ASCVD (ie, myocardial infarction, ischemic stroke, or fatal coronar

149 e discovered that clinical reperfusion after myocardial infarction led to significant elevation of th

150 artery bypass graft-related Thrombolysis In Myocardial Infarction major and minor bleeding.

151 stroke or systemic embolism, vascular death, myocardial infarction, major bleeding, or intracranial h

152 Negative control outcomes of myocardial infarction (MI) and herpes zoster were also s

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

154 statin use following hospital discharge for myocardial infarction (MI) between 2011 and 2014.

155 e, those at higher risk for future stroke or myocardial infarction (MI) derive more benefit from the

156 roved longevity but face an elevated risk of myocardial infarction (MI) due to common MI risk factors

157 Myocardial infarction (MI) elicits inflammation, but the

158 reatment and outcomes of patients with acute myocardial infarction (MI) have been described, but litt

159 bone marrow cell-based therapies after acute myocardial infarction (MI) have produced mostly neutral

160 Myocardial infarction (MI) is a leading cause of heart f

161 Ischemic heart disease resulting from myocardial infarction (MI) is the most prevalent form of

162 S hospitals within 1 year of the index acute myocardial infarction (MI) of 12365 patients enrolled in

163 In the DAPT Study, combined myocardial infarction (MI) or stent thrombosis and moder

164 Myocardial infarction (MI) results in the generation of

165 s such as metoprolol (Meto) may improve post-myocardial infarction (MI) structural and functional out

166 a/reperfusion (r-I/R) injury without ensuing myocardial infarction (MI) to elaborate a spatial- and c

167 A total of 1,230 patients with acute myocardial infarction (MI) treated with primary percutan

168 Sex differences in early mortality after myocardial infarction (MI) vary by age.

169 We collected 10-year follow-up of death, myocardial infarction (MI), and revascularization throug

170 ), which has been identified for early onset myocardial infarction (MI), modified the association of

171 ite outcome of periprocedural death, stroke, myocardial infarction (MI), or nonperiprocedural ipsilat

172 tality, major adverse cardiovascular events, myocardial infarction (MI), or target vessel revasculari

173 In chronic myocardial infarction (MI), segments with a transmural e

174 pathophysiological effects, but its role in myocardial infarction (MI)-induced cardiac remodeling re

175 iency, and biomarker levels in patients with myocardial infarction (MI)-to test whether ANGPTL3 defic

176 chestrate cardiac recovery process following myocardial infarction (MI).

177 trol); 2) chronic periodontitis (CP); and 3) myocardial infarction (MI).

178 arts and during cardiac remodeling following myocardial infarction (MI).

179 and the outcomes of (1) death; (2) death or myocardial infarction (MI); (3) death, MI, or repeat rev

180 CE, a composite of all-cause death, nonfatal myocardial infarction [MI], heart failure, stroke, trans

181 Acute CHD events included myocardial infarctions (MIs; nonfatal and fatal) and acu

182 type 1 and CELF1 overexpression models and a myocardial infarction model.

183 In healing myocardial infarction, myofibroblast- and cardiomyocyte-

184 ombopag recipients (arterial thrombosis n=1; myocardial infarction n=1) and no placebo recipients exp

185 e also elevated in patients with spontaneous myocardial infarction (n=63; P<6.17E-04).

186 s to implement regional ST-segment-elevation myocardial infarction networks focused on prehospital ca

187 Study endpoints included myocardial infarction, new or worsening heart failure, a

188 f other glucose-lowering drugs for non-fatal myocardial infarction, non-fatal stroke, or atrial fibri

189 or cardiovascular events, including nonfatal myocardial infarction, nonfatal stroke, and CVD mortalit

190 wer risks of the primary end point (nonfatal myocardial infarction, nonfatal stroke, or death from ca

191 cularly among patients with non-ST elevation myocardial infarction (NSTEMI).

192 culated what proportion of deaths from acute myocardial infarction occurred in people who had been in

193 as associated with a lower risk of death and myocardial infarction (odds ratio, 0.71; 95% confidence

194 so associated with a lower risk of death and myocardial infarction (odds ratio, 0.76; 95% confidence

195 tract infection, venous thromboembolism, and myocardial infarction, on these outcomes was comparative

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

197 adverse cardiovascular events (eg, nonfatal myocardial infarction or cardiovascular death) and nonca

198 heart disease, defined as the first incident myocardial infarction or death owing to coronary heart d

199 e cardiovascular events in those with type 2 myocardial infarction or myocardial injury (hazard ratio

200 oncardiovascular death, patients with type 2 myocardial infarction or myocardial injury have a simila

201 jority of excess deaths in those with type 2 myocardial infarction or myocardial injury were because

202 ardial strain imaging in patients with acute myocardial infarction or stable ischemic heart disease.

203 patients (13.2%) had PAD (1505 with no prior myocardial infarction or stroke).

204 led Cohort Equations (for fatal or non-fatal myocardial infarction or stroke, C-statistics 0.61-0.66,

205 aracteristics of patients suffering an acute myocardial infarction or undergoing cardiovascular surge

206 we found moderate evidence of a reduction of myocardial infarction (OR, 0.62; 95% credible intervals,

207 with higher post-discharge hazard of death, myocardial infarction, or bleeding (AKIN 1: hazard ratio

208 e composite of incident heart failure, acute myocardial infarction, or cardiovascular death.

209 Primary efficacy outcomes were death, myocardial infarction, or cerebrovascular accident.

210 dpoint was the time to occurrence of stroke, myocardial infarction, or death within 90 days.

211 mposite of adjudicated cardiovascular death, myocardial infarction, or ischemic stroke.

212 te of the composite of death from any cause, myocardial infarction, or major bleeding was not lower a

213 iaries hospitalized for heart failure, acute myocardial infarction, or pneumonia, reductions in hospi

214 e defined as the composite of cardiac death, myocardial infarction, or stent thrombosis.

215 y endpoint was a composite of cardiac death, myocardial infarction, or stent thrombosis.

216 composite endpoint of cardiovascular death, myocardial infarction, or stroke (126 [5%] of 2492 vs 17

217 e at increased risk of cardiovascular death, myocardial infarction, or stroke compared with patients

218 with a 5-year incidence of all-cause death, myocardial infarction, or stroke of 18.3% (319 events) i

219 t was the composite of cardiovascular death, myocardial infarction, or stroke.

220 point of the trial was cardiovascular death, myocardial infarction, or stroke.

221 t was the composite of cardiovascular death, myocardial infarction, or stroke.

222 site of cardiac death, target vessel-related myocardial infarction, or target vessel revascularizatio

223 (a composite of cardiac death, target-vessel myocardial infarction, or target-vessel revascularizatio

224 ported for a primary outcome of index type 1 myocardial infarction, or type 1 myocardial infarction o

225 The primary end point was death, myocardial infarction, or unstable angina hospitalizatio

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

227 METHODS AND Consecutive ST-segment-elevation myocardial infarction patients from a defined health reg

228 ostic stratification of ST-segment-elevation myocardial infarction patients treated with primary perc

229 e study, 88 consecutive ST-segment-elevation myocardial infarction patients were enrolled within 12 h

230 nvestigating Underlying Disparities in Acute Myocardial Infarction Patients' Health Status) is an obs

231 tals (n=167 with 23 498 ST-segment-elevation myocardial infarction patients) were surveyed before (Ma

232 linical risk factors in ST-segment-elevation myocardial infarction patients.

233 ed in human failing myocardium and in a post-myocardial infarction (PMI) HF model evaluated in wild-t

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

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

236 The primary outcome was all-cause mortality; myocardial infarction, revascularization, and stroke wer

237 6 to 1.72) and a 40% increased risk of acute myocardial infarction (RR 1.40; 95% CI, 1.23 to 1.59).

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

239 ral killer cell depletion 24 hours pre-acute myocardial infarction significantly improved infarct siz

240 Myocardial infarction size was larger in aged hearts (P

241 nd obese patients after ST-segment-elevation myocardial infarction (STEMI) has been demonstrated.

242 I) for the treatment of ST-segment-elevation myocardial infarction (STEMI) has been widely used; howe

243 hanical reperfusion for ST-segment elevation myocardial infarction (STEMI) in settings where health-c

244 intervention (PCI) for ST-segment elevation myocardial infarction (STEMI) may not be uniform over ti

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

246 In patients with ST-segment elevation myocardial infarction (STEMI), the use of percutaneous c

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

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

249 were no significant differences in recurrent myocardial infarction, stent thrombosis, heart failure,

250 The primary endpoint was a composite of myocardial infarction, stroke, and death from cardiovasc

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

252 vival and adverse clinical events, including myocardial infarction, stroke, and heart failure hospita

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

254 dence of cardiovascular events (composite of myocardial infarction, stroke, and transient ischemic at

255 Cardiovascular outcomes were myocardial infarction, stroke, congestive heart failure,

256 several important outcomes including risk of myocardial infarction, stroke, heart failure, and major

257 a 9-protein risk score validated to predict myocardial infarction, stroke, heart failure, or death.

258 periprocedural adverse events such as death, myocardial infarction, stroke, or cardiac tamponade, and

259 been demonstrated to reduce the composite of myocardial infarction, stroke, or cardiovascular death i

260 etween 1) lipid species and the risk of CVD (myocardial infarction, stroke, or cardiovascular death);

261 No harm or benefit was observed for myocardial infarction, stroke, or hospital admission for

262 rization and a composite of all-cause death, myocardial infarction, stroke, or repeat revascularizati

263 death and thrombotic complications (nonfatal myocardial infarction, stroke, pulmonary embolism, renal

264 We also identified potential myocardial infarctions, strokes, and heart failure event

265 rction, participants with CHIP had a risk of myocardial infarction that was 4.0 times as great as in

266 Among patients undergoing PCI for myocardial infarction, the rate of the composite of deat

267 contribute to the mortality burden of acute myocardial infarction, the share of these deaths that oc

268 enic shock complicating ST-segment-elevation myocardial infarction, there may be no significant benef

269 spiratory failure (one [<1%] vs three [2%]), myocardial infarction (three [1%] vs none), lung infecti

270 e event in the active surveillance group was myocardial infarction (three patients).

271 high thrombus burden (TIMI [Thrombolysis in Myocardial Infarction] thrombus grade >/=3), thrombus as

272 cement therapy through day 30, perioperative myocardial infarction through day 5, or use of a mechani

273 predictors of out-of-hospital Thrombosis in Myocardial Infarction (TIMI) major or minor bleeding str

274 d Coronary Arteries [GUSTO], Thrombolysis in Myocardial Infarction [TIMI], and Acute Catheterization

275 mortality among patients admitted for acute myocardial infarction to 2615 for mortality among patien

276 h-sensitivity cardiac troponin assays enable myocardial infarction to be ruled out earlier, but the o

277 ocate 10 061 men and women with a history of myocardial infarction to placebo or one of three doses o

278 a allowed enrollment of patients with recent myocardial infarction, total occlusions, bifurcations le

279 Secondary outcomes included myocardial infarction, total stroke, CVD mortality, and

280 sient ischaemic attack, ischaemic stroke, or myocardial infarction treated with antiplatelet drugs (m

281 nsecutive patients with ST-segment-elevation myocardial infarction treated with primary percutaneous

282 lesion failure (cardiac death, target vessel myocardial infarction [TVMI], or ischemia-driven target

283 t size in patients with ST-segment-elevation myocardial infarction undergoing percutaneous coronary i

284 rosclerosis, or MESA, who were free of prior myocardial infarction underwent both ECG and cardiac mag

285 es of incident cardiovascular disease (CVD) (myocardial infarction, unstable angina, arterial revascu

286 strategies for very early rule-out of acute myocardial infarction using high-sensitivity cardiac tro

287 -out and rule-in of non-ST-segment elevation myocardial infarction using high-sensitivity cardiac tro

288 f the association between dabigatran use and myocardial infarction varied in sensitivity analyses and

289 coagulopathy, obesity, major bleeding, acute myocardial infarction, vascular complications, and sepsi

290 onal criteria required for spontaneous acute myocardial infarction versus those patients who do.

291 rothrombotic Ischemic Events-Thrombolysis in Myocardial Infarction) (vorapaxar) and PEGASUS-TIMI 54 (

292 poprotein(a) data were available, the OR for myocardial infarction was 0.93 (95% CI 0.90-0.97; p<0.00

293 Acute myocardial infarction was diagnosed in the first physici

294 e 28 days preceding death, and whether acute myocardial infarction was one of the recorded diagnoses

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

296 rence in mortality and combined death/stroke/myocardial infarction were observed.

297 57 years +/- 12; 78% men) with a first acute myocardial infarction, who were prospectively enrolled b

298 deoff between increased bleeding and reduced myocardial infarctions with prolonged dual antiplatelet

299 ng on respiratory diseases, hypertension and myocardial infarction, with a particular focus from a li

300 red pattern of HSPC mobilisation 8 days post-myocardial infarction, with increased circulating neutro