ライフサイエンスコーパス: myocardial infarction

1 study of patients hospitalized with an acute myocardial infarction.

2 conditions, during atherosclerosis and after myocardial infarction.

3 sms to enhance myocardial regeneration after myocardial infarction.

4 ease, leading to ischaemic heart disease and myocardial infarction.

5 ochondrial function in swine models of acute myocardial infarction.

6 o regenerate functional myocardium following myocardial infarction.

7 on improves outcomes in ST-segment-elevation myocardial infarction.

8 ective use of CMR after ST-segment-elevation myocardial infarction.

9 ears of follow-up, 1,816 were diagnosed with myocardial infarction.

10 tively, fulfilled criteria for a biochemical myocardial infarction.

11 d point of all-cause mortality or new Q-wave myocardial infarction.

12 in vivo confirmed a reduction of EndMT after myocardial infarction.

13 independent prediction of fatal or nonfatal myocardial infarction.

14 2) inhibitor prescription in the 1 year post-myocardial infarction.

15 outcome was a composite of death or nonfatal myocardial infarction.

16 atients presenting with ST-segment-elevation myocardial infarction.

17 deficiency of IDO and challenged with acute myocardial infarction.

18 enrolled women with a clinical diagnosis of myocardial infarction.

19 clinical complications including stroke and myocardial infarction.

20 otential immunomodulatory treatment in acute myocardial infarction.

21 men, and 65 (69.1%) had ST-segment elevation myocardial infarction.

22 ronary intervention for ST-segment-elevation myocardial infarction.

23 type using the Third Universal Definition of Myocardial Infarction.

24 atory and the reparatory immune responses to myocardial infarction.

25 se limb events, 0.60 (95% CI, 0.48-0.74) for myocardial infarction, 0.94 (95% CI, 0.75-1.18) for isch

26 versus 3.11%; HR, 0.88 [95% CI, 0.77-1.02]), myocardial infarction (1.08% versus 1.27%; HR, 0.85 [95%

27 t failure, 1.76 (95% CI 1.51-2.05) for acute myocardial infarction, 1.78 (95% CI 1.53-2.07) for perip

28 5 [95% CI, 2.38-3.32]), or family history of myocardial infarction (2.71 [95% CI, 2.38-3.05]).

29 cardiac arrest (3.0-fold, 95% CI 2.64-3.46), myocardial infarction (2.9-fold, 95% CI 2.43-3.42) and m

30 ow-up, while preintervention Thrombolysis in Myocardial Infarction-3 flow was protective.

31 et Inhibition With Prasugrel-Thrombolysis In Myocardial Infarction 38), which randomized patients to

32 ation in Atrial Fibrillation-Thrombolysis in Myocardial Infarction 48) demonstrated noninferiority of

33 n repair was associated with higher rates of myocardial infarction (5.0% vs 3.0%, P = 0.03), acute ki

34 rophic cardiomyopathy 55.6+/-4.3 ms, chronic myocardial infarction 53.7+/-3.4 ms and healthy voluntee

35 ect on Cardiovascular Events-Thrombolysis in Myocardial Infarction 58) studied the efficacy and safet

36 ale 19.4%, diabetes mellitus 35.7%, previous myocardial infarction 74.8%, multivessel PCI 38.0%).

37 CI, 1.23-5.18]; P=0.009), and target vessel myocardial infarction (8% versus 14%; hazard ratio, 1.92

38 troponin for accelerated diagnosis of acute myocardial infarction: a systematic review and meta-anal

39 y outcome was sensitive to the definition of myocardial infarction; a secondary analysis yielded more

40 plaque burden was the strongest predictor of myocardial infarction (adjusted hazard ratio, 1.60 (95%

41 maging, adjusted for age, sex, type of acute myocardial infarction, affected coronary artery territor

42 Readmission rates after acute myocardial infarction (AMI) and heart failure (HF) hospi

43 tial green spaces and the incidence of acute myocardial infarction (AMI) and heart failure (HF), post

44 T for early diagnosis and prognosis of acute myocardial infarction (AMI) are presented.

45 recent decades, the rates of incident acute myocardial infarction (AMI) have declined in the United

46 The diagnosis of acute myocardial infarction (AMI) is missed more frequently in

47 ency department discharge diagnosis of acute myocardial infarction (AMI) or stroke using Internationa

48 In patients with shock after acute myocardial infarction (AMI), the optimal level of pharma

49 f platelet inhibition in patients with acute myocardial infarction (AMI).

50 2 diabetes predicts outcome following acute myocardial infarction (AMI).

51 pital admission for unstable angina or acute myocardial infarction [AMI], 30-day readmission after AM

52 (0.45%), which resulted in 1 peri-procedural myocardial infarction and 1 emergent coronary bypass.

53 hypertrophic cardiomyopathy, 30 with chronic myocardial infarction and 59 healthy volunteers were inc

54 ntiretroviral therapy with increased risk of myocardial infarction and endothelial dysfunction, but a

55 lications such as cardiac regeneration after myocardial infarction and gene correction for inherited

56 ap junctions have been associated with acute myocardial infarction and heart failure.

57 namics in patients with ST-segment-elevation myocardial infarction and is an independent predictor of

58 tery atheroma, cardiac hypertensive disease, myocardial infarction and ischaemic stroke.

59 increased risks, although nonsignificant, of myocardial infarction and ischemic stroke.

60 CAD (myocardial infarction and its related sequelae).

61 The coprimary end points were myocardial infarction and major bleeding, which constitu

62 nd men presenting with CS complicating acute myocardial infarction and multivessel coronary artery di

63 Shock), patients with CS complicating acute myocardial infarction and multivessel coronary artery di

64 esions in patients with ST-segment-elevation myocardial infarction and multivessel disease.

65 re important mediators of inflammation after myocardial infarction and of allograft injury after hear

66 The number of patients with myocardial infarction and severe obesity is increasing a

67 t chronic vascular disease and root cause of myocardial infarction and stroke, is leukocyte accumulat

68 to the pathogenesis of deep vein thrombosis, myocardial infarction and stroke.

69 at are active in atherosclerosis and lead to myocardial infarction and stroke.

70 are associated with coronary artery disease, myocardial infarction and visceral and subcutaneous fat

71 laque rupture is the proximate cause of most myocardial infarctions and many strokes.

72 s, 67.0% were men, 81.3% had an ST-elevation myocardial infarction, and 43.3% had cardiac arrest.

73 e of stroke/thromboembolism, major bleeding, myocardial infarction, and all-cause mortality over 2 ye

74 including fatal/nonfatal ischemic stroke and myocardial infarction, and cardiovascular death.

75 ve heart failure or non-ST-segment-elevation myocardial infarction, and had multivessel or left main

76 , HRs were adjusted for age, sex, history of myocardial infarction, and history of chronic obstructiv

77 te of all-cause mortality, all-cause stroke, myocardial infarction, and major or life-threatening ble

78 COVID-19 can have both primary (arrhythmias, myocardial infarction, and myocarditis) and secondary (m

79 e composite of all-cause mortality, nonfatal myocardial infarction, and nonfatal stroke).

80 included all-cause mortality, non-procedural myocardial infarction, and repeat revascularisation.

81 as MACE, defined as the composite of stroke, myocardial infarction, and repeat revascularization.

82 or adverse cardiovascular events, fatal CVD, myocardial infarction, and stroke.

83 dence of distal embolization, periprocedural myocardial infarction, and target lesion revascularizati

84 ent heart repair and function after neonatal myocardial infarction, and that cardiac delivery of RELN

85 Hospitalizations after acute myocardial infarction are commonly underreported in inte

86 rategies, morbidity and mortality from acute myocardial infarction are still substantial.

87 left ventricular systolic function following myocardial infarction, as demonstrated by echocardiograp

88 t overall increase in the risk of stroke and myocardial infarction associated with POAF (weighted mea

89 dverse cardiovascular outcomes, specifically myocardial infarction, associated with certain glucose-l

90 , non-procedure-related bleeding, stroke, or myocardial infarction at 12 months (secondary composite

91 subjects free of lipid-lowering therapy and myocardial infarction at study entry.

92 g stents, whereas extended-term DAPT reduces myocardial infarction at the expense of more bleeding ev

93 heart failure/cardiomyopathy, hypertension, myocardial infarction, atrial fibrillation, valvular dis

94 e myocardial infarction, particularly type 2 myocardial infarction, because of respiratory failure wi

95 return to pre-infarct activities after acute myocardial infarction, but the trial lacked statistical

96 ementation increased the diagnosis of type 1 myocardial infarction by 11% (510/4471), type 2 myocardi

97 cardial infarction by 11% (510/4471), type 2 myocardial infarction by 22% (205/916), and acute and ch

98 improves heart function in adult mice after myocardial infarction by a cardioprotective effect.

99 model the structure of the human heart after myocardial infarction (by mimicking the infarcted, borde

100 action, type 2 diabetes mellitus, history of myocardial infarction, Canadian Cardiovascular Society g

101 on how sex influences the outcomes of acute myocardial infarction-cardiogenic shock (AMI-CS) in youn

102 ng regional disparities in the care of acute myocardial infarction-cardiogenic shock (AMI-CS).

103 ary outcome was highest in those with type 1 myocardial infarction (cause-specific hazard ratio [HR]

104 Heart failure, induced via myocardial infarction, causes a decrease of the cGMP lev

105 luded cardiovascular disease (a composite of myocardial infarction, cerebrovascular accident, heart f

106 te of atherosclerotic cardiovascular events (myocardial infarction, coronary revascularization, and i

107 composite outcome was cardiovascular death, myocardial infarction, coronary revascularization, and s

108 te primary end point of all-cause death, any myocardial infarction, definite/probable stent thrombosi

109 ubstantial proportion of patients with acute myocardial infarction develop clinical heart failure, wh

110 ction of 10-year first CHD events (including myocardial infarctions, fatal coronary events, silent in

111 Myocardial infarction, following heart ischemia and repe

112 and IDL + LDL cholesterol 29% of the risk of myocardial infarction from apoB-containing lipoproteins,

113 d subgroup analysis of elderly patients with myocardial infarction (>=75 years) from the VALIDATE-SWE

114 Thus, cardiomyocyte death as occurs during myocardial infarction has very detrimental consequences

115 early 5 times more likely to have subsequent myocardial infarction (hazard ratio, 4.65; 95% CI, 2.06-

116 omorbidities (coronary artery disease and/or myocardial infarction, heart failure, chronic kidney dis

117 d by primary CR-qualifying event type (acute myocardial infarction hospitalization; coronary artery b

118 on (HR, 0.78 [95% CI, 0.63-0.95]), and fatal myocardial infarction (HR, 0.50 [95% CI, 0.26-0.97]) but

119 ociated with significant reductions in total myocardial infarction (HR, 0.72 [95% CI, 0.59-0.90]), pe

120 mparison with clopidogrel, prasugrel reduced myocardial infarction (HR, 0.81 [95% CI, 0.67-0.98]), wh

121 er 10 years, increasing risks were found for myocardial infarction (HR, 1.4; 95% CI, 1.0 to 2.0) and

122 initiation of BEP treatment were as follows: myocardial infarction (HR, 6.3; 95% CI, 2.9 to 13.9), ce

123 commendations of the Universal Definition of Myocardial Infarction identified patients at high-risk o

124 y end point occurred in 104 (4.0%) patients, myocardial infarction in 9 (0.4%), cerebrovascular accid

125 ischemic events in patients with prior acute myocardial infarction in a large phase III clinical tria

126 m DAPT was associated with a reduced risk of myocardial infarction in comparison with 12-month DAPT (

127 n in ST-Segment and Non-ST-Segment Elevation Myocardial Infarction in Patients on Modern Antiplatelet

128 Reliable methods for predicting myocardial infarction in patients with established coron

129 n used to study cardiac remodeling following myocardial infarction in small-animal models.

130 ely young women and is an important cause of myocardial infarction in young patients without traditio

131 remote zones), and recapitulate hallmarks of myocardial infarction (in particular, pathological metab

132 -cause death, non-fatal stroke, or non-fatal myocardial infarction) in patients receiving PCI or CABG

133 ents eccentric cardiac remodeling induced by myocardial infarction, in each case improving cardiac fu

134 , but with CIs including the null value, for myocardial infarction (incidence rate, 3.9 versus 1.8 pe

135 patients discharged for ST-segment-elevation myocardial infarction included in a multicenter registry

136 Patients with acute myocardial infarction including ST-segment elevation and

137 acy of current classical risk predictors for myocardial infarction, including stenosis severity.

138 Myocardial infarction is a frequent cardiovascular event

139 Scar tissue size following myocardial infarction is an independent predictor of car

140 inical hypothyroidism in patients with acute myocardial infarction is associated with poor prognosis.

141 The future risk of myocardial infarction is commonly assessed using cardiov

142 I trial (Omega-3 Fatty acids in Elderly with Myocardial Infarction) is an investigator-initiated, mul

143 nary artery disease, particularly with prior myocardial infarction, is associated with greatest risk

144 confidence intervals for the study outcomes (myocardial infarction, ischemic stroke, heart failure, a

145 oint (MACE) comprised death of CAD, nonfatal myocardial infarction, ischemic stroke, or unstable angi

146 MACE was defined as myocardial infarction, late (>180 days) revascularizatio

147 unstable angina or non-ST segment elevation myocardial infarction less than 30 days before randomisa

148 l safety end point was TIMI (Thrombolysis in Myocardial Infarction) major bleeding, with Internationa

149 reatening/moderate and TIMI (Thrombolysis in Myocardial Infarction) major/minor bleeding with time-de

150 Here we show that myocardial infarction (MI) accelerates breast cancer out

151 ular events in stable patients with previous myocardial infarction (MI) and elevated high-sensitivity

152 Secondary analysis included myocardial infarction (MI) and fatal CHD.

153 events in patients with ST-segment elevation myocardial infarction (MI) and multivessel coronary arte

154 cardiovascular event in patients with prior myocardial infarction (MI) and residual inflammatory ris

155 Genetic risk scores (GRSs) for myocardial infarction (MI) and stroke were calculated to

156 with the association between post-discharge myocardial infarction (MI) and subsequent mortality.

157 and acute coronary syndrome (ACS) including myocardial infarction (MI) are discussed.

158 , and surface area (PSC) concentrations, and myocardial infarction (MI) at an hourly timescale.

159 ve recently shown that cardiac fibrosis post-myocardial infarction (MI) can be regulated by resident

160 Adverse cardiac remodeling after myocardial infarction (MI) causes structural and functio

161 health insurance through Medicare who had a myocardial infarction (MI) hospitalization between 2008

162 e consequences of CMC administration on post myocardial infarction (MI) immune responses in vivo and

163 the studies: transverse aortic constriction/myocardial infarction (MI) in mice and post-MI remodelin

164 eart disease, although evidence on PM2.5 and myocardial infarction (MI) incidence is mixed.

165 The formation of new blood vessels after myocardial infarction (MI) is essential for the survival

166 ice exhibit natural heart regeneration after myocardial infarction (MI) on postnatal day 1 (P1), but

167 o 31.5% of deaths globally, and particularly myocardial infarction (MI) results in 7.4 million deaths

168 ventricular dilation in mice one week after myocardial infarction (MI) surgery.

169 Acute myocardial infarction (MI) triggers a local and systemic

170 Rapid diagnosis of myocardial infarction (MI) using electrocardiography (EC

171 of intravenous statin administration during myocardial infarction (MI) with oral administration imme

172 Heart disease (especially myocardial infarction (MI)) and cancer are major causes

173 s significantly reduce mortality after acute myocardial infarction (MI), a large number of patients w

174 Primary outcomes were acute myocardial infarction (MI), acute cerebrovascular diseas

175 y and outcomes (first occurrences of stroke, myocardial infarction (MI), and hospitalisation for hear

176 xtrahepatic manifestations of HCV, including myocardial infarction (MI), are a topic of active resear

177 cardiovascular diseases, particularly acute myocardial infarction (MI), is one of the leading causes

178 onic obstructive pulmonary disease, previous myocardial infarction (MI), ischemic heart disease (IHD)

179 diovascular disease (CVD) outcomes including myocardial infarction (MI), ischemic stroke (IS), and pe

180 Despite improvements in prognosis following myocardial infarction (MI), racial disparities persist.

181 Endpoints were the composite of death, myocardial infarction (MI), recurrent ischemia, or throm

182 re (DBP) lowering might increase the risk of myocardial infarction (MI), reflecting a J- or U-shaped

183 dicted five-year risk of heart failure (HF), myocardial infarction (MI), stroke (ST), cardiovascular

184 ion (SCAD) is a non-atherosclerotic cause of myocardial infarction (MI), typically in young women.

185 In a mouse model of myocardial infarction (MI), wild-type EPC-derived exosom

186 renol-, transverse aortic constriction-, and myocardial infarction (MI)-induced heart failure mouse m

187 ociated with better long-term outcomes after myocardial infarction (MI).

188 most common long-term complication of acute myocardial infarction (MI).

189 function and decreases heart dilation after myocardial infarction (MI).

190 ture is a major lethal complication of acute myocardial infarction (MI).

191 nary lesions in 898 patients presenting with myocardial infarction (MI).

192 OC)-hs-cTnI assay in patients with suspected myocardial infarction (MI).

193 , ventricular remodeling, and function after myocardial infarction (MI).

194 gina (UA) or non-ST-segment elevation (NSTE) myocardial infarction (MI).

195 biomarker of recurrence and mortality after myocardial infarction (MI).

196 ipate in cardiac repair and remodeling after myocardial infarction (MI); however, how these factors c

197 due to decompensated heart failure (50%) or myocardial infarction (MI; 35%).

198 case-control study of 55 PWH with first-time myocardial infarction (MI; cases) and 182 PWH with no CV

199 jury (troponin rise not meeting criteria for myocardial infarction [MI]) using the universal definiti

200 ary arteries (MINOCA) occurs in 6% to 15% of myocardial infarctions (MIs) and disproportionately affe

201 ion at chromosome 9p21.3 accounts for 20% of myocardial infarctions (MIs) in several populations.

202 tervention in patients presenting with acute myocardial infarction, multivessel disease, and cardioge

203 years after surgery; pneumonia (n = 21) and myocardial infarction (n = 10) were the most common caus

204 In a mouse model of myocardial infarction, nanoparticle-mediated inhibition

205 ar diagnoses such as heart failure and acute myocardial infarction, need frequently arises for advanc

206 end point was cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, coronary revascu

207 composite of cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, coronary revascu

208 Fatal or nonfatal myocardial infarction occurred only in patients with inc

209 One death possibly related to treatment (myocardial infarction) occurred after 11 days of treatme

210 PMI was classified as a myocardial infarction occurring within 48 h of the proce

211 Myocardial infarctions occurring in this short term risk

212 dial infarction (STEMI), non-STEMI (NSTEMI), myocardial infarction of unknown type, or other acute co

213 a secondary analysis yielded more procedural myocardial infarctions of uncertain clinical importance.

214 ry group had serious adverse events (1 had a myocardial infarction on postoperative day 5 and 1 was h

215 CAD events were defined by myocardial infarction or CAD mortality.

216 analysis, we compared the primary outcome of myocardial infarction or cardiovascular death and second

217 events (a composite of cardiovascular death, myocardial infarction or other acute coronary syndrome,

218 tionship between concomitant therapy and new myocardial infarction or stroke (i.e., rates were not in

219 Those who had myocardial infarction or stroke in the previous 6 months

220 rt failure hospitalization), its components, myocardial infarction or stroke, and a renal composite o

221 , defined as the composite of cardiac death, myocardial infarction, or definite-probable stent thromb

222 sequent testing, a composite outcome (death, myocardial infarction, or hospitalization for unstable a

223 intraabdominal leak, unplanned reoperation, myocardial infarction, or infectious complications.

224 events (MACE; a composite of cardiac death, myocardial infarction, or ischemia-driven target lesion

225 f death from cardiovascular causes, nonfatal myocardial infarction, or nonfatal stroke, the hazard ra

226 occurrence of cardiovascular death, nonfatal myocardial infarction, or nonfatal stroke.

227 t of cardiovascular death, all-cause stroke, myocardial infarction, or rehospitalization for heart fa

228 ed to have higher adjusted risk of CV death, myocardial infarction, or stroke (adjusted hazard ratio

229 erse cardiovascular events (all-cause death, myocardial infarction, or stroke).

230 vent (MACE) outcome of cardiovascular death, myocardial infarction, or stroke, as well as, mortality,

231 occurrence of cardiovascular death, nonfatal myocardial infarction, or stroke.

232 utcome was death from cardiovascular causes, myocardial infarction, or stroke.

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

234 he composite of cardiac death, target vessel myocardial infarction, or target vessel revascularizatio

235 y and were followed up for fatal or nonfatal myocardial infarction over 42 months (interquartile rang

236 k of stroke/thromboembolism (P(trend)=0.06), myocardial infarction (P(trend)=0.65), or all-cause mort

237 ion=0.65), irrespective of having a previous myocardial infarction (P-interaction=0.64).

238 (SCAD) has emerged as an important cause of myocardial infarction, particularly among younger women.

239 cute nonischemic myocardial injury and acute myocardial infarction, particularly type 2 myocardial in

240 Myocardial infarction patients receiving reperfusion the

241 atients presenting with ST-segment-elevation myocardial infarction, percutaneous coronary interventio

242 uded 1653 patients with ST-segment-elevation myocardial infarction randomized to receive ticagrelor o

243 mortality (RD, 0.001 [CI, -0.011 to 0.013]), myocardial infarction (RD, 0.003 [CI, -0.010 to 0.017]),

244 The Universal Definition of Myocardial Infarction recommends high-sensitivity cardia

245 d, particularly for non-ST-segment-elevation myocardial infarction, reflecting a more conservative ap

246 it of aspirin in the immediate phase after a myocardial infarction remains incontrovertible, a number

247 osite of all-cause mortality, non-procedural myocardial infarction, repeat revascularisation, and str

248 All-cause mortality and the composite of myocardial infarction, repeat revascularization, stroke,

249 asure for patients with ST-segment-elevation myocardial infarction requiring inter-hospital transfers

250 te-targeted strategy, after acute or chronic myocardial infarction, resulted in increased cardiomyocy

251 l and triglycerides each explain part of the myocardial infarction risk from apoB-containing lipoprot

252 7 patients (14.8%) and clinically recognized myocardial infarction (RMI) in 358 patients (15.2%).

253 essel disease following ST-segment-elevation myocardial infarction (RR, 0.84 [95% CI, 0.69-1.04]; P=0

254 atients presenting with ST-segment-elevation myocardial infarction scheduled for pPCI.

255 m cardiovascular causes, ischemic stroke, or myocardial infarction (secondary composite 2), both test

256 crophages in the heart and lung of mice with myocardial infarction, sepsis, or pneumonia.

257 t strategy for treating ST-segment-elevation myocardial infarction (STEMI) in context of the coronavi

258 se in general and acute ST-segment-elevation myocardial infarction (STEMI) in particular is increasin

259 Circulating EPA in ST-segment elevation myocardial infarction (STEMI) relates to smaller infarct

260 ial damage due to acute ST-segment elevation myocardial infarction (STEMI) remains a significant glob

261 Admissions were classified as ST-elevation myocardial infarction (STEMI), non-STEMI (NSTEMI), myoca

262 ated cytokines in patients with ST-elevation myocardial infarction (STEMI).

263 tcomes were MACE (cardiovascular [CV] death, myocardial infarction, stroke), CV death/HHF, and progre

264 end point of major CVD events (composite of myocardial infarction, stroke, and CVD mortality; hazard

265 zations, a composite of HF hospitalizations, myocardial infarction, stroke, and heart disease death,

266 ase events (defined as cardiovascular death, myocardial infarction, stroke, and heart failure) and mo

267 Post-ACS death, myocardial infarction, stroke, and overall major adverse

268 quiring admission to an intensive care unit, myocardial infarction, stroke, aortic dissection, valve

269 Secondary outcomes included myocardial infarction, stroke, composite of death/myocar

270 tiology of many serious conditions including myocardial infarction, stroke, deep vein thrombosis, and

271 HR) for the composite outcome of AIDS, acute myocardial infarction, stroke, end-stage renal diseases,

272 major adverse cardiovascular events (death, myocardial infarction, stroke, heart failure) and COVID-

273 lifetime risk of CVD (composite of incident myocardial infarction, stroke, heart failure, or CVD dea

274 ts (MACE) (composite of all-cause mortality, myocardial infarction, stroke, or emergency cardiovascul

275 major vascular events (cardiovascular death, myocardial infarction, stroke, or major adverse limb eve

276 ardia (requiring treatment) and hypotension, myocardial infarction, stroke, surgical site infection,

277 rdial infarction, stroke, composite of death/myocardial infarction/stroke, any amputation, fasciotomy

278 t failure, unstable angina, non-ST-elevation myocardial infarction, syncope).

279 were retrospectively classified into type 1 myocardial infarction (T1MI, atherothombotic event), T2M

280 Type 2 myocardial infarction (T2MI) occurs because of an acute

281 findings were sensitive to the definition of myocardial infarction that was used.

282 For myocardial infarction, the greatest risk reductions were

283 a 57-year-old man with a history of anterior myocardial infarction three years earlier.

284 re cohort (IMMACULATE [Improving Outcomes in Myocardial Infarction through Reversal of Cardiac Remode

285 neumonia, pneumothorax, respiratory failure, myocardial infarction, thyrotoxicosis, alcohol, pericard

286 ts with subclinical hypothyroidism and acute myocardial infarction, treatment with levothyroxine, com

287 Elderly patients with acute myocardial infarction undergoing percutaneous coronary i

288 arison in patients with ST-segment-elevation myocardial infarction undergoing primary percutaneous co

289 MACE as a composite of cardiovascular death, myocardial infarction, unstable angina with revasculariz

290 We investigated 2 individual manifestations (myocardial infarction, unstable angina) as secondary out

291 [95% CI 0.74-1.59]; p=0.68); non-procedural myocardial infarction was estimated in 8% after PCI vers

292 Using a preclinical mouse model of myocardial infarction, we demonstrate that a single intr

293 our nanotracer in atherosclerotic mice with myocardial infarction, we observed rapid myeloid cell eg

294 e hundred patients with ST-segment-elevation myocardial infarction were randomized to therapy (50 pat

295 % CI, 0.37-0.93) were particularly linked to myocardial infarction, whereas high HDL oxidative-inflam

296 ociated with an increased short term risk of myocardial infarction which is associated with subsequen

297 tion into treatments for patients with acute myocardial infarction, who typically are of advanced age

298 Myocardial infarction with nonobstructive coronary arter

299 nselected patients with ST-segment-elevation myocardial infarction with paired acute and 6-month card

300 by qualifying event type (range: 7.1% [acute myocardial infarction without procedure] to 55.3% [coron