ライフサイエンスコーパス: MI

1 MI and cardiovascular death were categorized as: 1) proc

2 MI was induced in animals and borax, a sodium salt of bo

3 MI-MAAP has a user-friendly interface which provides res

4 MIs were centrally adjudicated and categorized by type u

5 %), followed by type 2 MI (34.2%) and type 1 MI (12%) (p < 0.001).

6 In ISCHEMIA, type 1 MI events using the primary and secondary definitions du

7 ian age 44 years; 30% women); 55% had type 1 MI, 32% had type 2 MI, and 13% had myocardial injury.

8 erm mortality among young adults with type 1 MI, type 2 MI, or myocardial injury.

9 1.4 to 5.1; p = 0.003) compared with type 1 MI.

10 yocardial injury (45.6%), followed by type 2 MI (34.2%) and type 1 MI (12%) (p < 0.001).

11 In an adjusted model, type 2 MI was associated with higher all-cause (hazard ratio: 1

12 0% women); 55% had type 1 MI, 32% had type 2 MI, and 13% had myocardial injury.

13 ty among young adults with type 1 MI, type 2 MI, or myocardial injury.

14 In total, 3,300 MI case days were matched to 10,441 control days.

15 Overall, 366 MIs occurred during follow-up.

16 1; 95% confidence interval [CI], 1.18-1.46), MI (HR, 1.30; 95% CI, 1.15-1.46), CHF (HR, 1.29; 95% CI,

17 tinopathy (CVA: HR, 2.53; 95% CI, 1.84-3.48; MI: HR, 1.89; 95% CI, 1.26-2.83; CHF: HR, 1.96; 95% CI,

18 h outcome (CVA: HR, 1.56; 95% CI, 1.29-1.89; MI: HR, 1.92; 95% CI, 1.57-2.34; CHF: HR, 1.90; 95% CI,

19 ng sites and hourly nonfatal MI cases from a MI registry in Augsburg, Germany, during 2005-2015.

20 lth insurance in the United States who had a MI hospitalization in 2015 or 2016.

21 Patients with a MI were frequency matched by age and calendar year to 68

22 umors and depletion of these cells abrogated MI-induced tumor growth.

23 The pGold chip assay achieved MI diagnostic sensitivity of 100% and specificity of 95.

24 Acute MI block was more frequently achieved in the VOM-Et grou

25 and improved functional recovery after acute MI relative to wild-type (WT).

26 hanol infusion (VOM-Et) can facilitate acute MI block.

27 observed no differences in the risk of acute MI, CVD, major bleeding, or all-cause hospitalization af

28 measured at admission in patients with acute MI was independently associated with the risk of mortali

29 s studied in a cohort of patients with acute MI.

30 adverse remodeling parameters 28 days after MI.

31 tality (Medicare only) in the 365 days after MI.

32 t ventricular dilation and dysfunction after MI.

33 cardiac injury and cardiac dysfunction after MI.

34 ht enable the direct imaging of EpiSCs after MI to better understand their biology, but also may perm

35 roportion of reduced ejection fraction after MI (7% versus 12%), previous heart failure (10% versus 1

36 ion on cardiac remodeling and function after MI by echocardiography, quantitative immunohistochemistr

37 cidence, and improved cardiac function after MI.

38 levels were increased in mouse hearts after MI and in isolated cardiomyocytes in response to hypertr

39 o locally regulate cardiac homeostasis after MI.

40 ration through IDO is markedly induced after MI in mice.

41 ely map macrophage-driven inflammation after MI.

42 igher risk of CVD events and mortality after MI than White individuals.

43 extent of endogenous revascularization after MI is insufficient, and MI can often result in ventricul

44 When applied as a single agent, MI-3454 induced complete remission or regression of leuk

45 Procedural MIs accounted for 20.1% of all MI events with the primary definition and 40.6% of all M

46 with the primary definition and 40.6% of all MI events with the secondary definition.

47 The tool guided an MI-based conversation between coach and patient to ident

48 ults in a decline of detyrosinated MTs in an MI model.

49 .001), and the mortality of patients with an MI was 10.4% (HR, 5.06 [95% CI, 3.72-6.90]; P<0.001), wh

50 ons (MIs) and for the first time proposed an MIs-triggered ratiometric persistent luminescence (R-Per

51 (RR, 0.69 [95% CI, 0.53-0.90]; P=0.007) and MI (RR, 0.74 [95% CI, 0.62-0.90]; P=0.002).

52 gest that the association between 9p21.3 and MI is modified by glucose homeostasis and lifestyle.

53 The fatal impact of bleeding and MI persisted beyond one year.

54 eeding, repetitive MI, and both bleeding and MI were 16.1%, 19.2%, and 19.0%, and their HRs for 2-yea

55 er ablation (RFCA) alone is challenging, and MI reconnection is common.

56 PCI prevents death, cardiac death, and MI in patients with unstable CAD.

57 rtality among patient with heart failure and MI.

58 ascularization after MI is insufficient, and MI can often result in ventricular remodelling, progress

59 ociation between hourly particle metrics and MI cases, adjusted for air temperature and relative humi

60 findings that the association between PM and MI incidence is robust to adjustment for road traffic no

61 d exposures to 2% sevoflurane) groups before MI/R.

62 ds ratio [95% CI], 3.25 [2.63-4.02]) in both MI and heart failure cohorts.

63 prognosis by treatment assignment using both MI definitions.

64 After index T2MI, the most common MI during follow-up was a recurrent T2MI, whereas the oc

65 We compared MI type, frequency, and prognosis by treatment assignmen

66 re used to adjust for potential confounders (MI risk factors and HIV-related parameters) and for cumu

67 revealed sensitivity to linguistic content: MI was highest for sentences at the phrasal (0.8-1.1 Hz)

68 ficantly associated with future risk of CVA, MI, CHF, and death, with higher degrees of retinopathy a

69 k associations were evaluated for total CVD (MI, IS, PAD, and CVD death), coronary and cerebrovascula

70 major adverse cardiac events (cardiac death, MI, unstable angina, or progressive angina) at latest fo

71 reducing the combined 1-year risk of death, MI, and stroke without increasing the risk of bleeding.

72 e primary endpoint was a composite of death, MI, or stroke during 1-year follow-up, and the safety en

73 SF-PreCon decreased MI/R injury in AMPK-DN mice.

74 resulting from the magnetic field-dependent MI transition.

75 Our DLA successfully detected MI using a 12-lead ECG or a 6-lead ECG.

76 on methods has low reliability for detecting MI and is difficulty to apply to limb 6-lead ECG based l

77 l intelligence algorithm (DLA) for detecting MI using 6-lead ECG.

78 ck inpatients at an urban center in Detroit, MI.

79 Of the 22,882 women, 641 developed MI during a mean follow-up of 18.6 y, 121 (18.9%) of whi

80 uivalent prognostic impact as post-discharge MI.

81 risk for mortality following post-discharge MI.

82 eath), coronary and cerebrovascular disease (MI, IS, CVD death), and individual outcomes (MI, IS, and

83 venous administration of atorvastatin during MI limits cardiac damage, improves cardiac function, and

84 an intravenous bolus of atorvastatin during MI; A2 received an intravenous bolus of vehicle during M

85 We conclude that delivering TMS during MI is capable of inducing plastic changes in the motor s

86 eived an intravenous bolus of vehicle during MI; and A3 received oral atorvastatin within 2 h post-MI

87 s to be investigated in ST-segment elevation MI patients.

88 in 1,398 patients with ST-segment elevation MI who enrolled in a prospective cohort.

89 ely to have experienced ST-segment elevation MI, have higher troponin values, and have more severe an

90 r symptomatic CAD including non-ST elevation MI, along with healthy age-matched subjects, were collec

91 posite of all serious cardiovascular events (MI, stroke, coronary revascularization, and cardiovascul

92 Previous work suggests that an experimental MI can accelerate atherosclerosis via monocytosis.

93 All mice subjected to experimental MI had significantly reduced left ventricular function.

94 In Model 1 for incident fatal MI, we observed a strong association with a 3-y running

95 e associations for PM2.5 and PM10 with fatal MI.

96 A first MI-induced bone marrow "memory" via a circulating signal

97 after recurrent MI compared with their first MI.

98 tudy identified adults presenting with first MI at Duke University Medical Center in Durham, North Ca

99 ted in events leading to mortality following MI.

100 -9.4 years) undergoing adjunctive VOM-Et for MI block.

101 ion 180-day event rates per 100 patients for MI, CVD, major bleeding, and all-cause hospitalization w

102 ays that had no snowfall, odds of death from MI increased 34% (95% confidence interval: 0%, 80%) on d

103 emission bands of CSD-PLNPs, resulting from MI-triggered R-PersL signal transductions.

104 9, 0.97) in model 2] and those with high GRS-MI [HR 0.91 (0.82, 0.99) in model 1; HR 0.94 (0.86, 1.04

105 consistently observed in people with low GRS-MI [HR 0.85 (95% CI: 0.76, 0.94) in model 1; HR 0.88 (0.

106 For HF, MI, CVD, and CKD, register-based models outperformed a r

107 Motor imagery (MI) is capable of activating the motor system and affect

108 The emergence of molecular imaging (MI), championed by radiolabeled (18)F-FDG PET, has expan

109 ng, in particular, has leveraged advances in MI agents and technology to improve the accuracy of tumo

110 Boron might be beneficial as a supplement in MI and may be a good candidate substance for anti-fibros

111 nd NOx, with both overall and fatal incident MI.

112 in Stroke) study participants with incident MI between 2003 and 2016.

113 ociation with several CVD outcomes including MI (OR = 1.84, 95% CI, 1.43, 2.37, P value = 2.0 x 10-6)

114 ng DBP increments on CVD outcomes, including MI (MI hazard ratio, 1.07 per unit mm Hg increase in DBP

115 ween DBP and adverse CVD outcomes; including MI.

116 Here we show that myocardial infarction (MI) accelerates breast cancer outgrowth and cancer-speci

117 atients with previous myocardial infarction (MI) and elevated high-sensitivity C-reactive protein (hs

118 ary analysis included myocardial infarction (MI) and fatal CHD.

119 ST-segment elevation myocardial infarction (MI) and multivessel coronary artery disease.

120 n patients with prior myocardial infarction (MI) and residual inflammatory risk (high-sensitivity C-r

121 isk scores (GRSs) for myocardial infarction (MI) and stroke were calculated to assess interactions be

122 etween post-discharge myocardial infarction (MI) and subsequent mortality.

123 drome (ACS) including myocardial infarction (MI) are discussed.

124 ) concentrations, and myocardial infarction (MI) at an hourly timescale.

125 diac remodeling after myocardial infarction (MI) causes structural and functional changes in the hear

126 gh Medicare who had a myocardial infarction (MI) hospitalization between 2008 and 2017.

127 dministration on post myocardial infarction (MI) immune responses in vivo and paracrine-mediated immu

128 e aortic constriction/myocardial infarction (MI) in mice and post-MI remodeling in rats.

129 evidence on PM2.5 and myocardial infarction (MI) incidence is mixed.

130 w blood vessels after myocardial infarction (MI) is essential for the survival of existing and regene

131 rt regeneration after myocardial infarction (MI) on postnatal day 1 (P1), but this ability is lost by

132 lly, and particularly myocardial infarction (MI) results in 7.4 million deaths per year.

133 n mice one week after myocardial infarction (MI) surgery.

134 Acute myocardial infarction (MI) triggers a local and systemic inflammatory response.

135 Rapid diagnosis of myocardial infarction (MI) using electrocardiography (ECG) is the cornerstone o

136 administration during myocardial infarction (MI) with oral administration immediately post-MI.

137 t disease (especially myocardial infarction (MI)) and cancer are major causes of death.

138 mortality after acute myocardial infarction (MI), a large number of patients with MI develop chronic

139 y outcomes were acute myocardial infarction (MI), acute cerebrovascular disease (CVD), major bleeding

140 ccurrences of stroke, myocardial infarction (MI), and hospitalisation for heart failure; annual kidne

141 ons of HCV, including myocardial infarction (MI), are a topic of active research.

142 s, particularly acute myocardial infarction (MI), is one of the leading causes of mortality worldwide

143 ary disease, previous myocardial infarction (MI), ischemic heart disease (IHD), heart failure (HF), a

144 D) outcomes including myocardial infarction (MI), ischemic stroke (IS), and peripheral artery disease

145 n prognosis following myocardial infarction (MI), racial disparities persist.

146 e composite of death, myocardial infarction (MI), recurrent ischemia, or thrombotic bailout at 96 h (

147 increase the risk of myocardial infarction (MI), reflecting a J- or U-shaped relationship.

148 f heart failure (HF), myocardial infarction (MI), stroke (ST), cardiovascular disease (CVD) and chron

149 erosclerotic cause of myocardial infarction (MI), typically in young women.

150 In a mouse model of myocardial infarction (MI), wild-type EPC-derived exosome treatment significant

151 ic constriction-, and myocardial infarction (MI)-induced heart failure mouse models.

152 e and mortality after myocardial infarction (MI).

153 g-term outcomes after myocardial infarction (MI).

154 complication of acute myocardial infarction (MI).

155 heart dilation after myocardial infarction (MI).

156 complication of acute myocardial infarction (MI).

157 ients presenting with myocardial infarction (MI).

158 tients with suspected myocardial infarction (MI).

159 g, and function after myocardial infarction (MI).

160 ment elevation (NSTE) myocardial infarction (MI).

161 and remodeling after myocardial infarction (MI); however, how these factors crosstalk with other cel

162 5 PWH with first-time myocardial infarction (MI; cases) and 182 PWH with no CVD (controls), we measur

163 meeting criteria for myocardial infarction [MI]) using the universal definition.

164 curs in 6% to 15% of myocardial infarctions (MIs) and disproportionately affects women.

165 accounts for 20% of myocardial infarctions (MIs) in several populations.

166 Mutual information (MI) analysis revealed sensitivity to linguistic content:

167 A first-order metal-insulator (MI) transition of transition temperature T (MI) ~ 28 K i

168 Interestingly, MIs revealed the different regulating efficiencies for t

169 o had training in motivational interviewing (MI), and (3) 5 phone calls with the same coach for betwe

170 nce nanoparticles (D-PLNPs) with metal ions (MIs) and for the first time proposed an MIs-triggered ra

171 Achieving bidirectional mitral isthmus (MI) block using radiofrequency catheter ablation (RFCA)

172 BP increments on CVD outcomes, including MI (MI hazard ratio, 1.07 per unit mm Hg increase in DBP; P<

173 Disruptive systems (with negative MI) were activated by social cognition and autobiographi

174 e second co-primary outcome of CV death, new MI, or ischemia-driven revascularization was determined.

175 e first coprimary outcome of CV death or new MI and the second co-primary outcome of CV death, new MI

176 44; 2 SDH, 2.05; >=3 SDH, 2.86) and nonfatal MI (0 SDH, 3.91; 1 SDH, 4.33; >=2 SDH, 5.44).

177 adjudicated fatal incident CHD and nonfatal MI.

178 7), respectively; hazard ratios for nonfatal MI among those with >=2 SDH were 1.57 (95% CI, 1.30 to 1

179 kground monitoring sites and hourly nonfatal MI cases from a MI registry in Augsburg, Germany, during

180 ssociated with a lower risk of nonprocedural MI and unstable angina with greater freedom from angina

181 Neither diabetes nor MI led to increased atherosclerotic lesion size, but dia

182 In summary, diabetes, but not MI, accelerates lesion progression, suggesting that the

183 the Tuscaloosa HRR to 3.7 in the Royal Oak, MI HRR.

184 he SYNTAX and Fourth Universal Definition of MI were more strongly associated with mortality than EXC

185 ) trials; the Fourth Universal Definition of MI; and the Society for Cardiovascular Angiography and I

186 in-MLL1 inhibitors, we report development of MI-3454, a highly potent and orally bioavailable inhibit

187 and fibrosis along the temporal evolution of MI in mice.

188 with MI in the absence of medical history of MI.

189 re are also reservations about the impact of MI and its added value over conventional, often less exp

190 3 to 4.4 years), the cumulative incidence of MI or stroke was 9.8% and that of major amputation or pe

191 sk-allele carriers (CC+GC), the incidence of MI was reduced in the surgery group compared with the co

192 and PSC were associated with an increase of MI 6 h later by 3.27% [95% confidence interval (CI): 0.2

193 alidated its effects in an in vitro model of MI/IRI in mammalian cardiac cells.

194 (FMN2) orchestrates the initial movement of MI spindle.

195 ion were severely affected from the onset of MI.

196 differences were identified for the risk of MI, CVD, major bleeding, or all-cause hospitalization wh

197 an approximately 1.5-fold increased risk of MI, supporting the rationale to target IL-1 activation t

198 re not significantly associated with risk of MI.

199 gency department with symptoms suggestive of MI.

200 EF at the time of MI and within 180 days post-MI were determined from all

201 ular death were similar after either type of MI (hazard ratio, 0.8 [95% CI, 0.7-1.0], P=0.11).

202 There has been an evolution in the type of MI occurring in the community over a decade, with the in

203 ery regarding sex, age (+/-3 years), year of MI (+/-3 years), and body mass index (+/-3).

204 he preventive effect of bariatric surgery on MI incidence.

205 h (RR, 0.89 [95% CI, 0.71-1.12]; P=0.33), or MI (RR, 0.96 [95% CI, 0.86-1.08]; P=0.54).

206 I were strongly associated with death and/or MI (UMI: hazard ratio [HR]: 2.15; 95% confidence interva

207 = 0.79; p(interaction) = 0.36 ) or death or MI at 30 days (adjusted OR: 1.07; 95% CI: 0.77 to 1.48;

208 ere was a trend for higher rates of death or MI at 30 days (adjusted OR: 1.29; 95% CI: 0.98 to 1.70;

209 -way endpoint) and the composite of death or MI at 30 days.

210 RNA [modRNA]) of AC function post hypoxia or MI.

211 Additional bleeding or MIs resulted in a poorer prognosis.

212 MI, IS, CVD death), and individual outcomes (MI, IS, and PAD).

213 sure to PM2.5, PM10, NO2, or NOx and overall MI incidence, but we observed positive associations for

214 While LV tissue modulus for P1 MI and sham mice were similar (341.9 kPa vs 363.4 kPa, p

215 s 363.4 kPa, p = 0.6140), the modulus for P7 MI mice was significantly greater than that for P7 shams

216 In parallel, MI increased circulating Ly6C(hi) monocyte levels and re

217 Post-MI MAC-Mmp14 KO hearts contained fewer cells undergoing

218 /myocardial infarction (MI) in mice and post-MI remodeling in rats.

219 F at the time of MI and within 180 days post-MI were determined from all available medical records.

220 ler scar size than control mice 28 days post-MI.

221 rrelations among patients who developed post-MI HF in comparison with event-free controls (data set 1

222 rdiac recovery and reduce heart failure post-MI in humans.

223 KE-2 did not influence cardiac fibrosis post-MI.

224 buted the improvement in heart function post-MI after AC modRNA delivery to decreased ceramide levels

225 3 received oral atorvastatin within 2 h post-MI.

226 I) with oral administration immediately post-MI.

227 cardioprotective role of eosinophils in post-MI hearts.

228 ied proteins potentially coregulated in post-MI HF using weighted gene co-expression network analysis

229 ies are needed to reduce disparities in post-MI outcomes.

230 ejection fraction measured at 4 months post-MI and identified proteins potentially coregulated in po

231 ejection fraction measured at 4 months post-MI.

232 farct region as source and substrate of post-MI arrhythmias.

233 included well-established biomarkers of post-MI HF: N-terminal B-type natriuretic peptide and troponi

234 Other properties of post-MI remodelling are present in both peri-infarct and remo

235 f Cardiac Remodelling]) of 223 patients post-MI, of which 33 patients were hospitalized for HF (media

236 sis, reduced MI scar size, and promoted post-MI neovascularization, whereas IL-10 knockout EPC-derive

237 ro-inflammatory or reparative responses post-MI.

238 e sphingolipid metabolism and signaling post-MI.

239 ivery of small molecules to improve the post-MI healing process.

240 studied the mechanisms triggering these post-MI arrhythmias in vivo and their relation to regional my

241 effects on mortality: unrevascularized post-MI relative risk (RR) 0.68 (95% CI, 0.45-1.03); P=0.07;

242 At 1 week post-MI, lack of Gal-3 markedly attenuated F4/80+ macrophage

243 fied 36 plasma proteins associated with post-MI HF (data set 2), whereas single-cell transcriptomes i

244 ts undergoing the first attempt of posterior MI ablation were grouped according to their MI block ind

245 Pre-MI, fewer younger adults met guideline indications for 3

246 , 1.14-1.73]), but further adjusting for pre-MI health status (1.25 [95% CI, 1.00-1.56]) and characte

247 of the underlying pathology from a previous MI.

248 Of 566 patients with previous MI registered in the SWEDEHEART registry (Swedish Web-Sy

249 , diabetes, hypertension, sleep apnea, prior MI and IHD (all P<0.001) as well as AF, stroke and HF (a

250 cardiovascular events in patients with prior MI and evidence of residual inflammatory risk.

251 Procedural MI rates were greater in the invasive strategy and with

252 at the expense of higher rates of procedural MI.

253 Procedural MIs accounted for 20.1% of all MI events with the primar

254 Recurrent MI was induced by ligating the left circumflex artery fo

255 unt in 28 patients was lower after recurrent MI compared with their first MI.

256 Women and men were followed up for recurrent MI, recurrent CHD events (ie, recurrent MI or coronary r

257 rent MI, recurrent CHD events (ie, recurrent MI or coronary revascularization), heart failure hospita

258 study assessed sex differences in recurrent MI, recurrent CHD events, and mortality among patients w

259 gesting that the increased risk of recurrent MI in diabetes is due to a higher lesional burden and/or

260 This study examined the effect of recurrent MI on bone marrow response and cardiac inflammation.

261 rom 2008 to 2017, age-standardized recurrent MI rates per 1000 person-years decreased from 89.2 to 72

262 function, inhibited cell apoptosis, reduced MI scar size, and promoted post-MI neovascularization, w

263 SF-PreCon markedly reduced MI/R injury in DM mice, as evidenced by improved cardiac

264 in ND mice, SF-PreCon significantly reduced MI/R-induced activation of p38, a pro-death MAPK, withou

265 y increases myocardial ischemia/reperfusion (MI/R) injury.

266 atients with repetitive bleeding, repetitive MI, and both bleeding and MI were 16.1%, 19.2%, and 19.0

267 at 4 different time points before the case's MI.

268 e strategy and with the use of the secondary MI definition.

269 s MI included periprocedural and spontaneous MIs according to the Third Universal Definition.

270 s associated with greater risk of subsequent MI or stroke (hazard ratio: 1.34; 95% confidence interva

271 a surgical mouse model in which 2 subsequent MIs affected different left ventricular regions in the s

272 (MI) transition of transition temperature T (MI) ~ 28 K is observed at zero magnetic fields (B).

273 Short-term MI experiments along with complementary murine studies r

274 inical and clinical results demonstrate that MI induces alterations in systemic homeostasis, triggeri

275 and Chil1, markers of M2 macrophages at the MI zone.

276 of Ran in mouse oocytes while examining the MI spindle dynamics.

277 iscusses seminal research directions for the MI field that have the potential to result in added valu

278 % CI, 1.00-1.56]) and characteristics of the MI (1.01 [95% CI, 0.80-1.27]) resulted in substantial at

279 ible for statin therapy at the time of their MI than the 2013 guideline (46.4% vs. 56.7%; p < 0.01).

280 MI ablation were grouped according to their MI block index strategy: adjunctive VOM-Et and RFCA alon

281 lized with a primary diagnosis of first-time MI (54.9% NSTEMI and 45.1% STEMI).

282 at all time points leading up to first-time MI, and higher levels of IL-1Ra were associated with an

283 nical outcomes of patients with a first-time MI.

284 lerotic plaques and their rupture leading to MI.

285 oral azithromycin (AZM), initiated prior to MI, reduces inflammation and its negative sequelae on th

286 ation between chronic HCV (RNA+) and time to MI while adjusting for demographic characteristics, card

287 f 110 patients (60.9+/-9.2 years) undergoing MI ablation using RFCA alone.

288 Hypercholesterolemic pigs underwent MI induction (90 min of ischemia) and were kept for 42 d

289 s were individuals who had a first validated MI between 2006 and 2012.

290 search Consortium (BARC) 2, 3, or 5, whereas MI included periprocedural and spontaneous MIs according

291 DL-C, HDL-P was consistently associated with MI and ischemic stroke in the overall population.

292 late gadolinium enhancement consistent with MI in the absence of medical history of MI.

293 n=44) could be matched 1:1 to a control with MI from SWEDEHEART, but no subsequent metabolic surgery

294 tor 4 (Par4) expression in mouse hearts with MI and investigated the effects of Par4 deletion on card

295 HD events, and mortality among patients with MI and compared these associations with sex differences

296 rge population-based cohort of patients with MI between April 1, 2002, and March 31, 2016, we examine

297 Of the 220 patients with MI block achieved during the index procedure, 81 underwe

298 rction (MI), a large number of patients with MI develop chronic heart failure over time.

299 dynamic biomarker of treatment response with MI-3454 in leukemia, and demonstrated that this compound

300 0.54) and 84.5 versus 99.3 among those with MI (HR: 0.87; 95% CI: 0.85 to 0.89).