ライフサイエンスコーパス: MI

1 MI was associated with higher risk of vascular dementia

2 MI-CHF rats exhibited a significantly enhanced hypoxic v

3 Pioglitazone also reduced the risk of type 1 MI (hazard ratio, 0.62; 95% confidence interval, 0.40-0.

4 Diagnosis of type 1 MI was adjudicated by study physicians.

5 imilar to those seen in patients with type 1 MI.

6 (8% [7%] vs 10% [8%]) than those with type 1 MIs or who underwent cardiac interventions.

7 Type 1 MIs result spontaneously from instability of atheroscler

8 nent effect in preventing spontaneous type 1 MIs.

9 cute coronary syndrome events, including 141 MIs and 84 episodes of unstable angina.

10 49, 95% confidence interval (CI) 1.02-2.17), MI (OR 1.58, 95% CI 1.06-2.35), LDL-cholesterol (0.21 st

11 erson-years), older participants (7.5 vs 2.2 MI per 1000 person-years for adults 40 years and older v

12 0.40-0.96; log-rank P=0.03), but not type 2 MI (hazard ratio, 1.05; 95% confidence interval, 0.58-1.

13 type 2 and identifying the causes of type 2 MI.

14 Type 2 MIs are uncommon in the general population, but their fr

15 k factors among those with type 1 and type 2 MIs differed, suggesting the need to specifically consid

16 ty of atherosclerotic plaque, whereas type 2 MIs occur in the setting of a mismatch between oxygen de

17 A higher proportion of patients with type 2 MIs were younger than 40 years (47 of 288 [16.3%] vs 32

18 cteristics among those with type 1 vs type 2 MIs, and the causes of type 2 MIs.

19 he number and proportion of type 1 vs type 2 MIs, demographic and clinical characteristics among thos

20 pe 1 vs type 2 MIs, and the causes of type 2 MIs.

21 3.5%]) were the most common causes of type 2 MIs.

22 V-infected individuals with type 1 vs type 2 MIs.

23 s, including type; identify causes of type 2 MIs; and compare demographic and clinical characteristic

24 41 women) with definite or probable MIs, 288 MIs (50.4%) were type 2 and 283 (49.6%) were type 1.

25 A total of 11 595 MI patients survived to 1 year postdischarge; there were

26 nt-induced control of the magnetization in a MI has so far remained elusive.

27 l CHD included deaths </=28 days of an acute MI and acute CHD deaths.

28 be a promising therapeutic target for acute MI.

29 n bone marrow cells from patients with acute MI and discovered a poorly characterized secreted protei

30 ular tissue samples from patients with acute MI.

31 f an alcohol abuse diagnosis on incident AF, MI, and CHF.

32 ce with an IFNAR-neutralizing antibody after MI ablated the interferon response and improved left ven

33 accumulation of unengulfed dead cells after MI, resulting in exacerbated inflammatory responses and

34 In mice given CMCs 2 days after MI, LV ejection fraction 28 days later was significantly

35 fibrotic genes and collagen deposition after MI compared to WT counterparts.

36 PGE2/Ep3 axis promotes cardiac healing after MI by activating reparative Ly6C(low) Mos/Mps, indicatin

37 in Mos/Mps markedly attenuates healing after MI by reducing neovascularization in peri-infarct zones.

38 sults indicate that T2DM aggravates HF after MI through defective mitophagy, associated exaggerated i

39 erlying accelerated heart failure (HF) after MI in T2DM remain unclear.

40 d in the circulation of wild-type mice after MI.

41 n in parallel with increased mortality after MI in T2DM mice compared with control mice.

42 ctivation, granulopoiesis, and outcome after MI.

43 idative stress and cytokine production after MI.

44 ted against adverse cardiac remodeling after MI, maintaining ventricular wall thickness and contracti

45 eir involvement in fibrotic remodeling after MI.

46 clusters during inflammatory responses after MI, we surgically removed the pericardial AT and perform

47 nt in IRF3 or IFNAR, improved survival after MI as compared to controls.

48 visits before MI and 3.8 (2.4) visits after MI.

49 Event rates at 1 year after MI were lower for MI, stroke, and bleeding when medical

50 ilarly effective during the first year after MI.

51 AURKB is the sole CPC kinase, does not alter MI completion timing, and no change in localization of t

52 cut-off by CMR during the acute phase of an MI to predict viability was </=75% TEI and this would ha

53 e healthy group was compared with the CP and MI groups but not when the CP group was compared with th

54 healthy and CP groups and between the CP and MI groups.

55 ence of the composite of all-cause death and MI (hazard ratio [HR]: 0.65; 95% confidence interval [CI

56 een adherence to MI performance measures and MI-ERR (adjusted odds ratio, 0.94; 95% CI, 0.81-1.08, pe

57 Siewert I), were randomized between open and MI esophagectomy with curative intent.

58 ree and overall 3-year survival for open and MI esophagectomy.

59 icant difference between MI size3-slices and MI sizefull LV (P = 0.93) with an excellent correlation

60 Furthermore, using AAR3-slices and MI sizefull LV resulted in 'negative' MSI in 7/48 patien

61 affect outcome measurements in large animal MI models.

62 RQoL/QoL, myocardial infarction/heart attack/MI and predict*/factor.

63 yone with a prior history of any MACE before MI were censored and adjusted for follow-up times.

64 there was a mean of 3.8 (2.5) visits before MI and 3.8 (2.4) visits after MI.

65 e was also no significant difference between MI size3-slices and MI sizefull LV (P = 0.93) with an ex

66 Health System (Detroit and West Bloomfield, MI), between February 2014 and May 2015, with a modified

67 ea incidence was similarly increased in both MI-CHF and AV-CHF rats compared to control.

68 To characterize MIs, including type; identify causes of type 2 MIs; and

69 ws for the diagnosis of subacute and chronic MI with high accuracy.

70 Compared with the general population cohort, MI was not associated with all-cause dementia (aHR, 1.01

71 of myocardial infarction (MI) due to common MI risk factors and HIV-specific factors.

72 une 2014 to November 2015 in Genesee County, MI (where Flint is located) was directly linked to the s

73 th or myocardial infarction (MI); (3) death, MI, or repeat revascularization (RR); and (4) hospitaliz

74 combined endpoint was cardiovascular death, MI, or stroke at 1 year.

75 The risk of CV death, MI, or stroke in the placebo arm remained roughly consta

76 The rates of cardiovascular (CV) death, MI, and stroke as well as TIMI major bleeding were analy

77 ere independent risk indicators for CV death/MI/iCVA (p < 0.001).

78 to 9.7%) absolute risk reduction in CV death/MI/iCVA at 7 years with ezetimibe/simvastatin, thus tran

79 y was assessed by baseline risk for CV death/MI/iCVA, the IMPROVE-IT composite endpoints (CE), and in

80 The adjusted risk of death/MI was higher among women (odds ratio, 1.6; 95% CI, 1.1-

81 Comparisons between the Discovery MI and SIGNA showed a similar spatial resolution and ove

82 ns were also performed between the Discovery MI, Discovery 690 PET/CT, and SIGNA PET/MR systems.

83 monstrated the high quality of the Discovery MI.

84 ere conducted independently on two Discovery MI scanners installed at Stanford University and Uppsala

85 The Pooled Cohort Equations discriminated MI risk and were moderately calibrated in this multicent

86 sembly checkpoint (SAC) kinase, Mps1, during MI exit in young oocytes replicates this phenotype.

87 ting kinase Cak1 phosphorylaytes T207 during MI, and 2) Smk1 autophosphorylates Y209 as MII draws to

88 Despite these elevated MI rates, optimal methods to predict MI risks for HIV-in

89 n rates and outcomes of ST-segment elevation MI (STEMI) in renal transplant recipients vs the stage 5

90 I (0.8% annually), with ST-segment elevation MI constituting one-third of all cases.

91 presented more often as ST-segment elevation MI versus MI not related to a stented site (59% vs. 26%,

92 nted with MI; 25.7% had ST-segment elevation MI, 74.3% had non-ST-segment elevation MI, and 8.9% had

93 ation MI, 74.3% had non-ST-segment elevation MI, and 8.9% had ventricular tachycardia/ventricular fib

94 Dynamic changes in post-ST-segment-elevation MI edema highlight the need for standardization of CMR t

95 patients with anterior ST-segment-elevation MI successfully treated by primary angioplasty and 16 ma

96 s, including arterial thromboembolic events, MI, stroke or transient ischemic attack, vascular deaths

97 mote HRQoL among patients after experiencing MI.

98 are LA structural remodeling in experimental MI swine models recapitulating the effects of left ventr

99 Infarction (FAST-MI) 2005 (n=3670) and FAST-MI 2010 (n=4169).

100 7 individual QIs could be assessed from FAST-MI 2010.

101 Four QIs were not recorded in FAST-MI 2010 and 4 in 2005, either because of treatment nonav

102 In FAST-MI 2010, 12 individual and 2 composite QIs could be asse

103 Non-ST-Elevation Myocardial Infarction (FAST-MI) 2005 (n=3670) and FAST-MI 2010 (n=4169).

104 Major end points subsequent to first MI were assessed using landmark analyses to compare the

105 ammation, hypertrophy and fibrosis following MI, accompanied by exaggerated HSPC activity and impaire

106 ast stretch, and matrix stiffening following MI may separately regulate different profibrotic traits

107 ts identified by medical claims was 4.3% for MI, 0.9% for stroke, and 5.0% for bleeding.

108 To evaluate the association between ERR for MI with in-hospital process of care measures and 1-year

109 ensity statins following hospitalization for MI increased progressively from 2011 through 2014.

110 ed those residents who were hospitalized for MI or stroke.

111 vent rates at 1 year after MI were lower for MI, stroke, and bleeding when medical claims were used t

112 l importance of these cells in recovery from MI.

113 nts with MI during the study period, 43% had MI-ERR greater than 1.

114 pants had ischemic stroke and 395 (6.7%) had MI with 1 or more disability assessment after the event.

115 bleeding complications increased with higher MI-ERR.

116 are not caused by alterations in meiosis I (MI or meiosis II (MII) chromosome dynamics, but instead

117 ad a similar risk of CV ischemic events (ie, MI or IS; hazard ratio, 1.16; 95% CI, 0.97 to 1.38) duri

118 n-computer interface-assisted motor imagery (MI-BCI) or transcranial direct current stimulation (tDCS

119 ysis, we found no significant differences in MI risk between patients who started PPIs vs H2RAs for t

120 nths is associated with an early increase in MI risk, mainly unrelated to stent thrombosis; the magni

121 95% CI, 0.81-1.08, per 0.1-unit increase in MI-ERR for overall defect-free care).

122 In vivo, we assessed the effects of Meto in MI wild-type and beta3AR knockout mice.

123 upply to the CB region was decreased only in MI-CHF rats compared to Sham and AV-CHF rats.

124 4 times higher in patients with VLST than in MI not related to a stented site.

125 We identified a linear risk of incident MI (0.8% annually), with ST-segment elevation MI constit

126 In stable CAD outpatients, incident MI occurs at a stable rate of 0.8% annually, is related

127 used as a time-dependent variable, incident MI was associated with an increased risk of death (hazar

128 rapy, discontinuation at 12 months increases MI hazard regardless of DAPT score group.

129 ong patients with EF </=35% during the index MI admission, 66.8% (95% confidence interval [CI], 65.9-

130 by revascularization status during the index MI admission.

131 e control outcomes of myocardial infarction (MI) and herpes zoster were also studied.

132 an increased risk for myocardial infarction (MI) and stroke.

133 artery disease (CAD), myocardial infarction (MI) and their risk factors.

134 Mortality rates after myocardial infarction (MI) are significantly increased in T2DM patients because

135 f all-cause death and myocardial infarction (MI) at 3 years.

136 ospital discharge for myocardial infarction (MI) between 2011 and 2014.

137 in beta4 (Tbeta4) and myocardial infarction (MI) by reactivating a fetal gene programme to promote ne

138 for future stroke or myocardial infarction (MI) derive more benefit from the insulin-sensitizing dru

139 e an elevated risk of myocardial infarction (MI) due to common MI risk factors and HIV-specific facto

140 urrence of stroke and myocardial infarction (MI) during follow-up.

141 Myocardial infarction (MI) elicits inflammation, but the dominant molecular dri

142 Myocardial infarction (MI) elicits massive inflammatory leukocyte recruitment t

143 f patients with acute myocardial infarction (MI) have been described, but little is known about race

144 therapies after acute myocardial infarction (MI) have produced mostly neutral results.

145 perfusion alters post-myocardial infarction (MI) healing; however, very few systematic studies report

146 ction in the risk for myocardial infarction (MI) in patients with chronic kidney disease requiring lo

147 ective treatments for myocardial infarction (MI) induced cardiac fibrosis are lacking.

148 s play a role in post-myocardial infarction (MI) inflammatory responses and cardiac outcome.

149 Myocardial infarction (MI) is a leading cause of heart failure and death worldw

150 Phagocytosis after myocardial infarction (MI) is a prerequisite to cardiac repair.

151 gional function after myocardial infarction (MI) is currently incomplete.

152 isease resulting from myocardial infarction (MI) is the most prevalent form of heart disease in the U

153 ar of the index acute myocardial infarction (MI) of 12365 patients enrolled in the Treatment With Ade

154 DAPT Study, combined myocardial infarction (MI) or stent thrombosis and moderate/severe bleeding wer

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

156 nary stenting reduces myocardial infarction (MI) risk and increases bleeding risk in comparison with

157 eto) may improve post-myocardial infarction (MI) structural and functional outcomes via restored S1PR

158 njury without ensuing myocardial infarction (MI) to elaborate a spatial- and chronologic model of car

159 0 patients with acute myocardial infarction (MI) treated with primary percutaneous coronary intervent

160 early mortality after myocardial infarction (MI) vary by age.

161 r follow-up of death, myocardial infarction (MI), and revascularization through the Dutch population

162 ified for early onset myocardial infarction (MI), modified the association of LC n-3 PUFAs with nonfa

163 edural death, stroke, myocardial infarction (MI), or nonperiprocedural ipsilateral stroke was not sig

164 ardiovascular events, myocardial infarction (MI), or target vessel revascularization in SVG intervent

165 In chronic myocardial infarction (MI), segments with a transmural extent of infarct (TEI)

166 In response to myocardial infarction (MI), time-dependent leukocyte infiltration is critical t

167 ects, but its role in myocardial infarction (MI)-induced cardiac remodeling remains unclear.

168 vels in patients with myocardial infarction (MI)-to test whether ANGPTL3 deficiency is associated wit

169 dontitis (CP); and 3) myocardial infarction (MI).

170 remodeling following myocardial infarction (MI).

171 y and over time after myocardial infarction (MI).

172 including stroke and myocardial infarction (MI).

173 ery process following myocardial infarction (MI).

174 ) death; (2) death or myocardial infarction (MI); (3) death, MI, or repeat revascularization (RR); an

175 cause death, nonfatal myocardial infarction [MI], heart failure, stroke, transient ischemic attack, p

176 CHD events included myocardial infarctions (MIs; nonfatal and fatal) and acute CHD deaths.

177 istration via optimizing mutual information (MI) is based on the assumption that intensity distributi

178 In the case of magnetic insulators (MIs), although charge currents cannot flow, spin current

179 The theory of multiple intelligences (MI) seeks to describe and encompass the range of human c

180 measures and measures of the most invasive (MI) EOL care (eg, mechanical ventilation < 14 days from

181 from somatic alterations in muscle-invasive (MI) primary tumors, highlighting a major mechanism(s) co

182 s, target vessel revascularization, and late MI.

183 iovascular, and noncardiovascular mortality, MI, and heart failure at different levels of troponins.

184 rom 1932 case subjects with a first nonfatal MI and 2055 population-based control subjects who were l

185 The OR of nonfatal MI was 0.84 (95% CI: 0.72, 0.98) per 0.1% increase in to

186 he association of LC n-3 PUFAs with nonfatal MI risk in Costa Rican Hispanics.We analyzed cross-secti

187 We observed MI rates over the course of follow-up that were scaled t

188 tent implantation, VLST was causal in 20% of MI cases and presented more often as ST-segment elevatio

189 We therefore studied the activity of MI-2 against CLL and ibrutinib-resistant CLL.

190 The primary outcome was a composite of MI and stroke events based on primary discharge diagnost

191 al design to resemble the clinical course of MI.

192 electing features, enabling the diagnosis of MI on nonenhanced cine MR images by using LGE imaging as

193 ation, but the dominant molecular drivers of MI-associated inflammation remain unclear.

194 For patients with a history of MI >1 year previously, long-term treatment with ticagrel

195 The incidence of MI did not significantly decrease in the past decade and

196 Cumulative incidence of MI was assessed over 3 months after randomization (month

197 mpared with the highest, had reduced odds of MI (adjusted odds ratio: 0.65; 95% confidence interval:

198 oth a key contributor to the pathogenesis of MI and a potential therapeutic target, bolstering the id

199 ule attachments during early prometaphase of MI.

200 progress in primary prevention, the rate of MI has not declined in young adults.

201 e who were event-free at 12 months, rates of MI or stent thrombosis between 12 and 30 months were sim

202 PT scores <2 or >/=2 both had lower rates of MI with continued thienopyridine (MI monthly incidence 0

203 Reduction of MI or stent thrombosis with continued thienopyridine bey

204 rapy was not associated with a lower risk of MI but was associated with increased bleeding risk.

205 ental plans (2001-2014), we compared risk of MI in patients who started a new prescription for PPIs v

206 ared with white men and the adjusted risk of MI was higher in minorities (odds ratio, 2.6; 95% CI, 1.

207 The 12-month weighted risk of MI was low overall (approximately 2 cases per 1000 among

208 The majority of MIs in both time periods (74% and 76%) were not related

209 onditions that may have affected hs-cTnT, or MI associated with the visit, or insufficient informatio

210 tcomes, except for a higher rate of death or MI in the early invasive group compared with the rates f

211 ttack, patients at higher risk for stroke or MI derive a greater absolute benefit from pioglitazone c

212 ssociated with lower rates of periprocedural MI and cranial nerve palsy than CEA.

213 Post-MI cardiac remodeling is a multifaceted process that inc

214 Post-MI leukocyte density, residence time in the infarcted ar

215 ting S1P levels, nor does it ameliorate post-MI dysfunction, as in wild-type mice.

216 os and improved ejection fraction at d5 post-MI.

217 ear relationship between T (req) 2 days post-MI and global longitudinal strain 6 months later (r = 0.

218 ew therapeutic targets to improve early post-MI remodeling.

219 ng cells and histamine in heart failure post-MI using HDC-EGFP transgenic mice and HDC-knockout (HDC(

220 lity by increasing cardiac fibrogenesis post-MI.

221 e as a potential therapeutic target for post-MI cardioprotection.

222 (1 microg/kg/day) was injected 3 hours post-MI for (d)1 or continued daily till d5.

223 es were obtained on admission, 24 hours post-MI, and 4 months post-MI.

224 formin, a drug associated with improved post-MI LV function in experimental studies.

225 However, the role of 15-epi LXA4 in post-MI acute inflammatory response and resolving phase is un

226 known about race and sex differences in post-MI angina and long-term risk of unplanned rehospitalizat

227 A4 will expedite the resolving phase in post-MI inflammation.

228 ciation with 1-year ICD implantation in post-MI patients with low EF.

229 phase early to discontinue inflammation post-MI, thereby reducing LV dysfunction.

230 At 3 months post-MI, cardiac structure and function were evaluated by ser

231 mission, 24 hours post-MI, and 4 months post-MI.

232 LVEF and ISZ were assessed 4 months post-MI.

233 Better treatment of post-MI angina may improve patient quality of life and qualit

234 atients, given their high prevalence of post-MI angina.

235 Higher risk of post-MI death among women in comparison to men was restricted

236 The higher risk of post-MI death among women with MI-CAD was most pronounced at

237 lammation and wound healing proteins on post-MI day 7.

238 and obstructive CAD status and outcomes post-MI has not been established.

239 determinant in heart failure pathology post-MI.

240 o pathway effectors, developed profound post-MI pericardial inflammation and myocardial fibrosis, res

241 ofiles related to factors that regulate post-MI LV remodeling and repair.

242 scriminatory power to differentiate the post-MI patients (at 1 year) from the controls.

243 n adaptive immune regulation during the post-MI recovery phase.

244 To determine whether post-MI transendocardial injection of allogeneic CBSCs reduce

245 This longitudinal study identified potential MIs among patients with HIV receiving clinical care at 6

246 levated MI rates, optimal methods to predict MI risks for HIV-infected persons remain unclear.

247 tment, treatment arm independently predicted MI at months 12 to 15 (P<0.001) and 30 to 33 (P=0.011).

248 able ICERs, including patients with >1 prior MI, multivessel disease, diabetes, renal dysfunction (al

249 D and IHD mortality in patients with a prior MI.

250 coronary artery bypass graft surgery, prior MI, and smoking.

251 grelor + low-dose ASA in patients with prior MI within the prior 3 years.

252 vent, categorizing each definite or probable MI as type 1 or type 2 and identifying the causes of typ

253 men and 141 women) with definite or probable MIs, 288 MIs (50.4%) were type 2 and 283 (49.6%) were ty

254 ventricular (LV) function following a recent MI.

255 Recurrent MI, CHD events (recurrent MI or a coronary revasculariza

256 rate was 19.9% (death rate: 1.2%; recurrent MI: 16.8%; stroke/transient ischemic attack: 1.2%; revas

257 Recurrent MI, CHD events (recurrent MI or a coronary revascularization procedure), and morta

258 e interval [CI]: 1.30 to 1.73) for recurrent MI, 1.51 (95% CI: 1.34 to 1.70) for CHD events, and 0.96

259 sociated with a 36% higher rate of recurrent MI (41.1 vs. 30.1 per 1,000 person-years, respectively),

260 ars of follow-up, there were 4,450 recurrent MIs, 6,250 CHD events, and 14,311 deaths.

261 As expected, both IPC and CsA reduced MI size.

262 driven by a higher rate of procedure-related MI in the early invasive group (6.5% vs. 2.4%; HR: 2.82;

263 events primarily because of nonstent-related MIs.

264 ne model of myocardial ischemia-reperfusion (MI/R) injury with a bell shape therapeutic profile.

265 hest accuracy for diagnosing large and small MI on cine MR images, with an area under the curve of 0.

266 he 10-year composite of death or spontaneous MI.

267 atments were compared by sex and CAD status (MI-CAD or MINOCA).

268 the development of heart failure in a swine MI model.

269 n with placebo, on acute coronary syndromes (MI and unstable angina) among IRIS participants.

270 scale; 95% CI, 0.57 to 1.20; P < .001) than MI (0.20 points on the disability scale; 95% CI, 0.06 to

271 ative incidence of all-cause dementia in the MI cohort was 9% (2.8% for Alzheimer disease, 1.6% for v

272 The median ages of patients in the MI-ERR greater than 1 and tertiles 1, 2, and 3 of the MI

273 CBSC administration into the MI border zone reduces pathological cardiac structural a

274 Of concern, rates of the MI-EOL care have increased over time despite increased p

275 eater than 1 and tertiles 1, 2, and 3 of the MI-ERR greater than 1 groups were 64, 63, 64, and 63 yea

276 not when the CP group was compared with the MI group.

277 The MIs included 28 (19%) with ST-segment elevation.

278 r rates of MI with continued thienopyridine (MI monthly incidence 0.16% versus 0.51%, P<0.001, for sc

279 s associated with a lower risk of first-time MI and stroke than ASA monotherapy.

280 significant association between adherence to MI performance measures and MI-ERR (adjusted odds ratio,

281 210 (12.5%) were on statin therapy prior to MI and were excluded.

282 phages in the heart fuel a fatal response to MI by activating IRF3 and type I IFN production.

283 d invading injured myocardium in response to MI.

284 or therapeutic efficacy in mice subjected to MI.

285 One highly tumorigenic MI line harbored membrane-bound, constitutively active,

286 V-infected individuals to further understand MI outcomes and to guide prevention and treatment.

287 mooth muscle, and restores Wt1 activity upon MI.

288 more often as ST-segment elevation MI versus MI not related to a stented site (59% vs. 26%, p = 0.001

289 ed risk factors are strongly associated with MI.

290 No association was found with MI (adjusted HR 1.04; 95% confidence interval 1.00-1.08)

291 that treated a total of 176644 patients with MI during the study period, 43% had MI-ERR greater than

292 ional analysis of hospitalized patients with MI from National Cardiovascular Data Registry/Acute Coro

293 s are commonly performed among patients with MI with an initially reduced EF.

294 Among patients with MI-CAD, women had higher mortality than men (3.9% versus

295 rison to men was restricted to patients with MI-CAD.

296 ival and quality of life among patients with MI.

297 dentify correlates of HRQoL in patients with MI.

298 All presented with MI; 25.7% had ST-segment elevation MI, 74.3% had non-ST-

299 The control group was treated with MI and given oral hygiene instructions.

300 igher risk of post-MI death among women with MI-CAD was most pronounced at younger ages.