ライフサイエンスコーパス: MACE

1 MACE associated with presence of a CMR diagnosis, extent

2 MACE during follow-up included death (16%), valve surger

3 MACE occurred in 103 (25%) patients.

4 MACE occurred in 272 (26.5%) of 1,029 lesions.

5 MACE occurred in 31% of subjects during a median follow-

6 MACE rates increased simultaneously with higher levels o

7 MACE risks were at least as high for low-risk (OR, 9.96;

8 MACE was associated with plaque burden >/=70% (hazard ra

9 MACE was seen in 15 patients: 10 of 45 (22%) MPC-treated

10 MACE were observed in 6 patients (3.1%) in the metformin

11 -ray angiography, 104 (16.6%) had at least 1 MACE.

12 During follow-up, there were 22 MACE and 29 6-mo revascularizations.

13 o 75th percentile, 581-1377), a total of 278 MACEs were observed.

14 rozygous FH was estimated to prevent 316,300 MACE at a cost of $503,000 per QALY gained compared with

15 rd ratio [HR], 0.63 [95% CI, 0.55 to 0.72]), MACEs (HR, 0.68 [CI, 0.55 to 0.83]), ischemic stroke (HR

16 A MACE was reported at a minimum of 12 months in 1.7% of p

17 atelets/mul were more likely to experience a MACE (hazard ratio: 4.65; 95% confidence interval: 1.78

18 ged after an initial admission experienced a MACE when evaluated with an hsTnT (7.2% vs. 3.4%; OR: 2.

19 r directly discharged patients experienced a MACE when evaluated with an hsTnT compared with a conven

20 2.3 to 7.3 years), 98 patients experienced a MACE.

21 1 SPRINT patients, 755 patients (8.1%) had a MACE or death event and 338 patients (3.6%) had a treatm

22 an m-HS</=3, with 1 (0.2%) patient having a MACE, and 248 (37.5%) patients had an m-HS>/=4, with 5 (

23 an m-HS</=3, with 1 (0.2%) patient having a MACE, and 262 (33.7%) patients had an m-HS>/=4, with 6 (

24 omization to first confirmed occurrence of a MACE.

25 -up of 9 years, 265 participants underwent a MACE, and these participants had higher levels of sVAP-1

26 dictive accuracy for MACE) of <0.84 for ACS (MACE 21% vs. 36%; p = 0.007) and <0.81 for SIHD (MACE 17

27 For the 25% interim analysis, MACE occurred in 59 placebo-treated patients (1.3%) and

28 ently predicted incident MACE (P=0.0046) and MACE mortality (P=0.026).

29 rtality (HR: 2.30; 95% CI: 1.72 to 3.07) and MACE (HR: 1.75; 95% CI: 1.44 to 2.12) for long versus sh

30 SE, 1.09; 95% CI, 0.12-10.05; P = 0.93), and MACE (RRR: MPS, 1.09; 95% CI, 0.64-1.86; P = 0.74; DSE,

31 iated with higher rates of recurrent ACS and MACE compared with masculine characteristics.

32 Outcomes included recurrent ACS and MACE over 12 months.

33 CVD and MACE were associated with seven other conventional facto

34 Abeta40 independently predicted CV death and MACE in patients with CHD (p < 0.05 for all).

35 1 associated with increased risk of MACE and MACE mortality in people aged >50 years without prior MA

36 significantly increased 30-day mortality and MACE compared with a 3- to 4-day LOS.

37 erol, and apolipoprotein B100 reductions and MACE among patients within the ODYSSEY trials that compa

38 Safety and MACE were evaluated for up to 3 years.

39 The associations between baseline WBC and MACE (composite of cardiac death, stent thrombosis, spon

40 The association between WBC and MACE was consistent in acute coronary syndrome and non-a

41 normal CMR study corresponded to low annual MACE and death rates of 0.8% and 0.3%, respectively.

42 the surviving patients, the long-term annual MACE rate and the stent thrombosis rate appeared constan

43 Annualized MACE rates were 4.8% and 2.1% corresponding to LGE prese

44 y where everyone with a prior history of any MACE before MI were censored and adjusted for follow-up

45 low-up is independently associated with both MACE and death.

46 t, (2) induce cardiomyocyte death, (3) cause MACE, and (4) induce cardiac scar formation after antibi

47 In contrast, MACE rates with bare metal stent placement increased fro

48 dial infarction [MI] or stroke) and any-CVD (MACE plus confirmed angina, silent MI, revascularization

49 nd our own mouse ONECUT1/HNF6 ChIP-exo data, MACE is able to define TFBSs with high sensitivity, spec

50 compared regarding the occurrence of 30-day MACE and CV risk profile based on information from natio

51 tcome was an adjudicated diagnosis of 30-day MACE defined as acute myocardial infarction, unstable an

52 allowed fast rule-out and rule-in of 30-day MACE in a majority of ED patients with chest pain and pe

53 Sensitivity for 30-day MACEs ranged from 87.9% to 100%; pooled sensitivity was

54 ciated with lower risks for all-cause death, MACEs, ischemic stroke, and hypoglycemia when used as ad

55 P control (systolic BP <140 mm Hg) decreased MACE, including cardiovascular mortality and heart failu

56 nts employing massive analysis of cDNA ends (MACE) and RT-qPCR.

57 rols without a family history for estimating MACE-free survival.

58 bricated by metal-assisted chemical etching (MACE) procedure.

59 occurrence of a major adverse cardiac event (MACE) assessed as the composite of cardiac death, myocar

60 y outcome) or a major adverse cardiac event (MACE) or death within 30 days (secondary outcomes), by r

61 n to placebo on major adverse cardiac event (MACE) rates in patients with type 2 diabetes and recent

62 e composite of major adverse cardiac events (MACE) (cardiovascular death, myocardial infarction, and

63 re adjudicated major adverse cardiac events (MACE) (death, myocardial infarction, unplanned revascula

64 74 to 1.34) or major adverse cardiac events (MACE) (death, readmission for myocardial infarction, unp

65 urrent ACS and major adverse cardiac events (MACE) (e.g., ACS, cardiac mortality, revascularization)

66 dicting 30-day major adverse cardiac events (MACE) and to compare it with the algorithm using hs-cTnT

67 ome was 2-year major adverse cardiac events (MACE) comprising death, readmission for MI, or stroke; t

68 ollowed up for major adverse cardiac events (MACE) defined as a composite end point of long runs of n

69 nia experience major adverse cardiac events (MACE) during or after pneumonia.

70 prediction of major adverse cardiac events (MACE) in ST-segment-elevation myocardial infarction.

71 probability of major adverse cardiac events (MACE) of cardiac death or myocardial infarction and the

72 e incidence of major adverse cardiac events (MACE) up to 30 days.

73 Major adverse cardiac events (MACE) were assessed in the 2 prospective cohorts (n = 87

74 Major adverse cardiac events (MACE), comprising significant nonfatal ventricular arrhy

75 a composite of major adverse cardiac events (MACE), including cardiac death, myocardial infarction (M

76 int was 1-year major adverse cardiac events (MACE), which included death/myocardial infarction (MI)/t

77 ) for reducing major adverse cardiac events (MACE).

78 postoperative major adverse cardiac events (MACE).

79 mortality and major adverse cardiac events (MACE).

80 oints included major adverse cardiac events (MACE; cardiac death, myocardial infarction, or revascula

81 e incidence of major adverse cardiac events (MACE; the combined end point of death, reinfarction, or

82 int was major adverse cardiovascular events (MACE) (cardiovascular death, MI, stroke) and the primary

83 nces of major adverse cardiovascular events (MACE) (defined as CV death, MI, or stroke) and major adv

84 major atherosclerotic cardiovascular events (MACE) (fatal or nonfatal myocardial infarction [MI] or s

85 MI) or major adverse cardiovascular events (MACE) (hard events and other cardiovascular events defin

86 reduce major adverse cardiovascular events (MACE) after PCI, principally by resulting in a larger po

87 d fewer major adverse cardiovascular events (MACE) and deaths but higher rates of treatment-related s

88 del for major adverse cardiovascular events (MACE) and determined the continuous net reclassification

89 tion in major adverse cardiovascular events (MACE) and mortality in this population.

90 studied major adverse cardiovascular events (MACE) at 2 years in 607 patients in whom all stenoses we

91 ath and major adverse cardiovascular events (MACE) at follow-up.

92 tion of major adverse cardiovascular events (MACE) defined as the occurrence of cardiac death, heart

93 -C) and major adverse cardiovascular events (MACE) has been observed in statin and ezetimibe outcomes

94 reduce major adverse cardiovascular events (MACE) in patients after myocardial infarction (MI) or th

95 creased major adverse cardiovascular events (MACE) in the setting of acute coronary syndrome.

96 PA has higher major cardiovascular events (MACE) than essential hypertension (23.3% vs 19.3%, p = 0

97 Major adverse cardiovascular events (MACE) were defined as the primary endpoint for each tria

98 oint of major adverse cardiovascular events (MACE), defined as a composite of all-cause mortality, my

99 ity and major adverse cardiovascular events (MACE), defined as myocardial infarction, stroke, heart f

100 1-year major adverse cardiovascular events (MACE), which included death, myocardial infarction (MI),

101 future major adverse cardiovascular events (MACE).

102 AF with major adverse cardiovascular events (MACE).

103 MI, and major adverse cardiovascular events (MACE, a composite of all-cause death, nonfatal myocardia

104 ifetime major adverse cardiovascular events (MACE: cardiovascular death, nonfatal myocardial infarcti

105 Risk of major adverse cardiovascular events (MACE; including ischemic stroke, acute myocardial infarc

106 atient-oriented major acute coronary events (MACE) (death, myocardial infarction [MI], and any revasc

107 d incidence of major adverse cardiac events (MACEs) and cardiovascular (CV) risk profile in patients

108 Evaluation for major adverse cardiac events (MACEs) occurred at 30 days (death or AMI).

109 Major adverse cardiac events (MACEs) were defined as late revascularization (>90 days

110 -term risk for major adverse cardiac events (MACEs), but its effect on daily practice is unknown.

111 tality, major adverse cardiovascular events (MACEs) (including ischemic stroke and myocardial infarct

112 ospital major adverse cardiovascular events (MACEs) and all-cause mortality at 1 year.

113 ncident major adverse cardiovascular events (MACEs) and cardiovascular mortality in a general populat

114 graphy, major adverse cardiovascular events (MACEs), and procedural complications.

115 predict major adverse cardiovascular events (MACEs).

116 V-associated death, major adverse CV events (MACEs), and all-cause mortality.

117 /stroke (i.e., major adverse cardiac events [MACE]) and secondary endpoints of death/MI/revasculariza

118 ailure (major adverse cardiovascular events [MACE]).

119 scular (major adverse cardiovascular events [MACE], cardiovascular mortality, stroke, myocardial infa

120 After 50% of planned events, MACE occurred in 102 patients (2.3%) in the placebo grou

121 In total, 104 patients experienced MACE (median time to event, 36 weeks).

122 sts, similar numbers of patients experienced MACE after an abnormal test result compared with a norma

123 ocardiography, 37 (53%) patients experienced MACE during a median follow-up period of 5.3 (interquart

124 nsthoracic echocardiography and experiencing MACE was significantly shorter for patients with FAC <23

125 Patients experiencing MACE showed higher left ventricle end-diastolic volume,

126 The prespecified exploratory extended MACE endpoint was all-cause mortality, non-fatal myocard

127 The exploratory extended MACE endpoint was seen in 433 (16.0%) patients assigned

128 ith unspecified chest pain experienced fewer MACEs and had a better risk profile when evaluated with

129 he 1-year number needed to treat was 200 for MACE and 239 for all-cause mortality.

130 Hazards ratios were 0.80 for MACE and 0.81 for overall mortality.

131 ed FFR cutoffs (best predictive accuracy for MACE) of <0.84 for ACS (MACE 21% vs. 36%; p = 0.007) and

132 On Cox proportional hazards analysis for MACE, ACS had a hazard ratio of 2.8 (95% confidence inte

133 in mean HbA1c, the risk for any-CVD and for MACE increased by 31 and 42%, respectively.

134 d HbA1c, taken together with any-CVD and for MACE, were 0.70 and 0.77, respectively, and for the fina

135 IPC is a novel biomarker for MACE risk stratification in patients with CAD.

136 t differences between the 2 stent groups for MACE rates (HR: 0.89, 95% CI: 0.73 to 1.08; p = 0.23), t

137 the upper limit of the 95% CI of the HR for MACE for naltrexone-bupropion treatment, compared with p

138 nce was added to the multivariable model for MACE.

139 mpared with patients without stroke, ORs for MACE were 14.23 (95% CI, 11.61-17.45) for stroke less th

140 dividuals without any cPB, hazard ratios for MACE were 0.78 (95% confidence interval [CI]: 0.31 to 1.

141 imated in nonculprit lesions responsible for MACE (n=22) versus matched control lesions (n=22).

142 PSS is increased in plaques responsible for MACE and improves the ability of intracoronary imaging t

143 Plaques responsible for MACE had larger superficial calcium inclusions, which ac

144 those with AP remained at increased risk for MACE (hazard ratio [HR]: 1.30, 95% confidence interval [

145 rs are associated with an increased risk for MACE in patients with ARVC/D with advanced disease and a

146 INT, we developed models to predict risk for MACE or death and treatment-related SAE to allow for ind

147 l was 70.7% sensitive and 82.1% specific for MACE.

148 was a nonstatistically significant trend for MACE (hazard ratio: 1.54; 95% confidence interval: 0.90

149 ere identified as the best cutoff values for MACE prediction.

150 or CV-associated death, 1.08 (0.90-1.29) for MACEs, and 1.09 (0.94-1.28) for all-cause mortality.

151 or CV-associated death, 1.53 (1.27-1.86) for MACEs, and 1.35 (1.15-1.59) for all-cause mortality.

152 overall absolute risk reduction of 0.9% for MACEs (odds ratio = 0.74; 95% CI, 0.62-0.89).

153 ECT, CMR is a stronger predictor of risk for MACEs, independent of cardiovascular risk factors, angio

154 disease) study for a minimum of 5 years for MACEs (cardiovascular death, acute coronary syndrome, un

155 re assessed whether PSS could predict future MACE in high-risk nonculprit lesions identified on virtu

156 dence interval, 0.20-1.43; P=0.21) or global MACE (SVG-DES: 36.7%, SVG-MT: 44.6%; hazard ratio, 0.73;

157 pensity score matching (200 patients/group), MACE remained significantly higher (ACS 25% vs. SIHD 12%

158 of 4.7 years, 334 (44%) patients died or had MACE (incidence rate: 82 events/1,000 person-years).

159 One in 3 subjects had MACE; risk doubled in those with a CMR diagnosis and som

160 d an m-HS>/=4, with 6 (2.3%) patients having MACEs (P=0.007).

161 d an m-HS>/=4, with 5 (2.0%) patients having MACEs (P=0.03).

162 /=2 points) resulted in significantly higher MACE rates in high-risk patients (9.0% versus 2.2%; P=0.

163 Mitral PVL was associated with higher MACE (hazard ratio [HR], 1.83; P=0.011).

164 CVI was associated with reduced in-hospital MACE (4.6% versus 7.2%; P=0.010) and mortality at 1 year

165 ndependent predictor for reduced in-hospital MACE (odds ratio, 0.38; 95% CI, 0.15-0.96; P=0.040) and

166 ndependent predictor for reduced in-hospital MACE (odds ratio, 0.49; 95% confidence interval [CI], 0.

167 ts in propensity-matched cohort (in-hospital MACE: odds ratio, 0.49; 95% CI, 0.32-0.76; P=0.002; and

168 An average decrease in MACE per 0.05-unit increase in FFR was statistically sig

169 no statistically significant differences in MACE rates.

170 no significant differences between groups in MACE related to the target SVG lesion (SVG-DES: 10.0%, S

171 The strongest increase in MACE occurred for FFR values between 0.80 and 0.60.

172 r lesions but was significantly increased in MACE lesions at high-risk regions, including plaque burd

173 ering was associated with a 29% reduction in MACE (RR: 0.71; 95% CI: 0.60 to 0.84), 33% in cardiovasc

174 n therapy was associated with a reduction in MACE and all-cause mortality among participants without

175 The relative risk reduction in MACE with ticagrelor was consistent for the pooled doses

176 Whereas the relative risk reduction in MACE with ticagrelor was consistent, regardless of PAD,

177 iority margin of a 3.0% absolute increase in MACEs within 6 weeks was set.

178 With a 26% reduction in MACEs following the guidelines, it would appear that the

179 net reclassification improvement of incident MACE.

180 nt), sVAP-1 independently predicted incident MACE (P=0.0046) and MACE mortality (P=0.026).

181 Secondary efficacy outcomes included MACE related to the target SVG lesion and overall MACE.

182 adjusted analysis, AP patients had increased MACE and death/MI/revascularization (both p < 0.001), lo

183 d is independently associated with increased MACE due to revascularization with similar risk of death

184 n whom all lesions were deferred had a lower MACE rate (5.3%) than those with at least 1 lesion revas

185 statins was estimated to prevent 4.3 million MACE compared with adding ezetimibe at $414,000 per QALY

186 Primary end point was the 12-month MACE rate consisting of death, reinfarction, and new con

187 ee relative affected by AF did not have more MACE.

188 antly lower in the MACE group versus the non-MACE group (0.68 [interquartile range: 0.54 to 0.77] vs.

189 ion, we show that the fundamental advance of MACE is the identification of two boundaries of a TFBS w

190 d to compare the groups for the incidence of MACE (myocardial infarction, cardiac revascularization,

191 The cumulative incidence of MACE significantly increased with increasing FFR quartil

192 Incidence of MACE was 19.7 and 24.7 events per 1,000 person-years in

193 Overall incidence of MACE was 2.3% per year.

194 -C were associated with a lower incidence of MACE, including very low levels of LDL-C (<50 mg/dL).

195 A stepwise increase of MACE was present with increasing CAC scores, both in pat

196 efficacy outcome was the first occurrence of MACE defined as the composite of cardiac death, myocardi

197 The adjusted odds of MACE for the unstable angina group were similar to those

198 eous coronary intervention, adjusted odds of MACE were significantly higher in the MI group compared

199 ohort, the score showed a good prediction of MACE (area under the curve: 0.76).

200 ed a higher performance in the prediction of MACE as compared to TTE-LVEF resulting in net reclassifi

201 d FAC constituted the strongest predictor of MACE (hazard ratio, 1.08 per 1% decrease; 95% confidence

202 Increased WBC is an independent predictor of MACE after percutaneous coronary intervention in a conte

203 ion fraction was an independent predictor of MACE.

204 and CAC score were independent predictors of MACE (CAC score >/=1000: hazard ratio, 7.7; P<0.001 and

205 core and SPECT are independent predictors of MACE in patients suspected for coronary artery disease.

206 ersity cohort, the independent predictors of MACE were cardiogenic shock, renal disease, history of p

207 re both strong and independent predictors of MACE.

208 herapies was associated with a lower rate of MACE and cost savings, with a threshold effect at >80% a

209 rent group had a significantly lower rate of MACE than the nonadherent (18.9% vs. 26.3%; hazard ratio

210 rent group had a significantly lower rate of MACE than the nonadherent (8.42% vs. 17.17%; HR: 0.56; p

211 Crude incidence rates of MACE among patients with (n = 7137) and without (n = 474

212 those with PAD (n = 404) had higher rates of MACE at 3 years than those without (n = 6,663; 19.3% vs.

213 tertile was associated with higher rates of MACE compared with the intermediate and low tertiles (60

214 ents on triple therapy had a similar risk of MACE (adjusted hazard ratio [HR]: 0.99 [95% confidence i

215 associated with a more than doubling risk of MACE (hazard ratio [HR]: 2.22; 95% confidence interval [

216 e) corresponded to a 79% increase in risk of MACE (HR: 1.79; 95% CI: 1.25 to 2.57; p = 0.002).

217 sVAP-1 associated with increased risk of MACE and MACE mortality in people aged >50 years without

218 y 39 mg/dL lower achieved LDL-C, the risk of MACE appeared to be 24% lower (adjusted hazard ratio, 0.

219 alone was not associated with higher risk of MACE at 1 year of follow-up (hazard ratio, 0.89; 95% con

220 inhibitors significantly reduced the risk of MACE by 14% in women (hazard ratio [HR]: 0.86; 95% confi

221 alculate the average decrease in the risk of MACE per 0.05-U increase in FFR.

222 -1 in predicting the 9-year absolute risk of MACE was analyzed using integrated discrimination improv

223 atients with diabetes were at higher risk of MACE, the absolute risk reduction tended to be greater i

224 ociated with a mean 2.2+/-2.6% lower risk of MACE/death compared with standard treatment (range, 20.7

225 For internal verification of MACE data, candidate genes were tested via RT-qPCR and a

226 Six-week incidence of MACEs during HEART care was 1.3% lower than during usual

227 In low-risk patients, incidence of MACEs was 2.0% (95% CI, 1.2% to 3.3%).

228 ble adjustment, the HR (95% CI) for death or MACE in patients with HbA1c levels of 7.1% to 8.0%, 8.1%

229 ed with increased long-term risk of death or MACE.

230 and any revascularization), device-oriented MACE (cardiac death, MI, and target lesion revasculariza

231 BES group (p = 0.83) and the device-oriented MACE rate was 12% in BVS and 9% in the EES/BES group (p

232 re similar at 9 months: the patient-oriented MACE rate was 27% in BVS and 26% in the EES/BES group (p

233 related to the target SVG lesion and overall MACE.

234 During the follow-up period, MACE occurred in 346 (32.5%) in the group receiving a si

235 Postoperative MACE rates were significantly higher in the MI group (7.

236 In addition, postoperative MACE rates decreased from 4.2% to 3.3% (P = .002).

237 n the indication for stent and postoperative MACE rates was examined using logistic regression to con

238 Composite 30-day postoperative MACE rates including all-cause mortality, MI, or revascu

239 was associated with increased postoperative MACE rates compared with other stent indications.

240 usted associations with 2-year postoperative MACEs.

241 istology intravascular ultrasound to predict MACE in plaques with plaque burden >/=70% (adjusted log-

242 ratios, defined by the annualized predicted MACE-to-LAR ratio and the predicted 6-mo-revascularizati

243 0.08% vs. 0.06%, P < 0.001), lower predicted MACE-to-LAR ratio (median, 1.5 vs. 4.3, P < 0.001), and

244 8% vs. 0.07%, P < 0.001) and lower predicted MACE-to-LAR ratio (median, 1.9 vs. 3.3, P < 0.001) and 6

245 nd women in LAR (P = 0.94) and the predicted MACE-to-LAR ratio (P = 0.97).

246 (OR, 1.43; 95% CI, 1.19-1.73) all predicted MACEs [major adverse cardiac events]." These ORs and 95%

247 ality in people aged >50 years without prior MACE, and inclusion of sVAP-1 in the risk prediction mod

248 nd control patients in survival probability, MACE-free probability, and all-cause mortality.

249 We noted procedural MACE in four (3%) of 158 patients in the OCT group, one

250 The primary safety endpoint was procedural MACE.

251 In these patients, ticagrelor reduced MACE, with a large absolute risk reduction, and MALE.

252 conducted a post hoc analysis of HF-related MACE (HF hospitalization, successfully resuscitated card

253 infarction, or unplanned revascularization (MACE) at 1 year was recorded.

254 A broader secondary MACE endpoint also included all-cause death, unstable an

255 21% vs. 36%; p = 0.007) and <0.81 for SIHD (MACE 17% vs. 9%; p = 0.01).

256 n affected first-degree relative had similar MACE-free survival.

257 T2MI strongly predicted risk for subsequent MACE (adjusted hazard ratio, 1.90; 95% confidence interv

258 nts identified for early discharge suffering MACE at 30 days.

259 en medication adherence levels and long-term MACE in these patients.

260 describe a novel analysis framework, termed MACE (model-based analysis of ChIP-exo) dedicated to ChI

261 The MACE rate did not differ significantly within the first

262 The MACE workflow consists of four steps: (i) sequencing dat

263 The MACE/death and the SAE model had C statistics of 0.72 an

264 The MACE/death model had 10 variables including treatment in

265 ; p = 0.79), but from years 1 through 5, the MACE rate was lower with EES (HR: 0.71, 95% CI: 0.55 to

266 enosis >/=70% were more often present in the MACE group (p < 0.01).

267 Median FFR was significantly lower in the MACE group versus the non-MACE group (0.68 [interquartil

268 .4 (interquartile range: 2.8-3.9) years, the MACE rate related to the target SVG was not significantl

269 n further examination of trends across time, MACE rates with DES placement began to decrease prior to

270 rtended to a near 3-fold increased hazard to MACE (HR: 2.93; 95% CI: 1.79 to 4.80; p < 0.001).

271 Measurements: Prediction of time to MACE was assessed by using univariable (log-rank test) a

272 At 5-year follow-up, MACE rate was significantly lower with EES- than with SE

273 Also measured was MACE-free survival after AF was diagnosed.

274 re strongly associated with any-CVD and with MACE.

275 ucible perfusion defects was associated with MACE (adjusted HRs: 1.76 to 3.21).

276 , WBC remained independently associated with MACE (hazard ratio [HR] per 10(3) cells/muL increase, 1.

277 1.4-3.6]) were independently associated with MACE (P<0.01).

278 e nonculprit lesion features associated with MACE during long-term follow-up (median: 1115 days) were

279 t type was not significantly associated with MACE regardless of indication.

280 lysis, FFR was significantly associated with MACE up to 2 years (hazard ratio: 0.87; 95% confidence i

281 he only factor independently associated with MACE was the degree of persisting leak at follow-up (HR,

282 decrease) was independently associated with MACE.

283 ence maintained significant association with MACE (HR: 1.72; 95% CI: 1.08 to 2.76; p = 0.023).

284 dwall LGE showed strongest associations with MACE (HR: 2.55; 95% CI: 1.77 to 3.83 and HR: 2.39; 95% C

285 in lipids from baseline were correlated with MACE (coronary heart disease death, nonfatal myocardial

286 from baseline were inversely correlated with MACE rates (hazard ratio, 0.71; 95% confidence interval,

287 t prevalence as compared to patients without MACE.

288 d higher levels of sVAP-1 than those without MACE (868 ng/mL and 824 ng/mL, respectively, P<0.001).

289 d and insurance status, contribute to 1-year MACE among women and minorities.

290 norities experience a similar risk of 1-year MACE but a higher adjusted risk of recurrent ischemic ev

291 regimen, resulted in a lower risk of 1-year MACE in uncertain candidates for DES implantation.

292 Unadjusted 1-year MACE rates (white men, 7.6%; women, 8.6%; minorities, 9.

293 The relationship between FFR and 2-year MACE was assessed as a continuous function.

294 One-year MACE was 6.9%; patients in whom all lesions were deferre

295 At 1 year, MACE events were infrequent, with 2 in each arm of the p

296 re cohort, the long-term (3.4 +/- 1.6 years) MACE rate was higher in the ACS group than in the SIHD g

297 sociated deaths, 169 (42 463.5 person-years) MACEs, and 231 (42 941.7 person-years) all-cause deaths

298 At 5-years, MACE occurred in 14.0% and 17.4% in the EES and SES grou

299 Over a median follow-up of 2.7 years, MACE occurred in 216 patients (4.2%), of which 82 (1.5%)

300 an those without T2MI (per 100 person-years: MACE, 53.7 versus 21.1, P<0.001; all-cause death, 23.3 v