ライフサイエンスコーパス: MACE

1 MACE included hospitalization for acute myocardial infar

2 MACE occurred in 131 (6.7%) patients in the Yoga-CaRe gr

3 MACE occurred in 35.4% and 40.0% of patients with total

4 MACE rates within 1 year after PCI were progressively lo

5 MACE risk progressively increased with EAT volume >=113

6 MACE that occurred after discharge were independently as

7 MACE was defined as myocardial infarction, late (>180 da

8 MACE within 5 years of imaging was adjudicated.

9 1.2 years for sulfonylurea), there were 1048 MACE outcomes (23.0 per 1000 person-years) among metform

10 There were 42 (4.0%) deaths and 188 MACE in 174 (16.6%) patients.

11 A total of 450 MACE occurred during follow-up.

12 otes (36% of participants) experienced a 51% MACE reduction in response to fenofibrate (hazard ratio

13 ing follow-up, 328 deaths and/or MIs and 528 MACE occurred.

14 ge], 5.6 [3.6-7.3] years); 117 experienced a MACE (12.3%).

15 -48) months, 46 patients (10%) experienced a MACE event.

16 f 3 years, 34 subjects (21.3%) experienced a MACE.

17 idinium and 76 (4.2%) placebo patients had a MACE (HR, 0.89; 1-sided 97.5% CI, 0-1.23); the expanded

18 tients treated by low-volume operators had a MACE compared with 16.9% of patients treated by high-vol

19 iation was associated with a lower risk of a MACE (HR, 0.40; 95% CI, 0.24-0.66).

20 The relationship of LA performance to a MACE within 12 months after AMI was evaluated by using C

21 ypotheses that NBResilience protects against MACE, and that it does so through decreased bone marrow

22 ammation (0.203 [0.055-0.351], P=0.007), and MACE risk (standardized hazard ratio [95% CI]: 1.927 [1.

23 : 1.12; 95% CI: 1.01 to 1.24; p = 0.038) and MACE (HR: 1.11; 95% CI: 1.03 to 1.20; p = 0.006) after a

24 01; RMI: HR: 1.54; 95% CI: 1.14 to 2.09) and MACE.

25 01; RMI: HR: 2.45; 95% CI: 1.89 to 3.18) and MACE.

26 stressors known to associate with AmygA and MACE (ie, transportation noise exposure, neighborhood me

27 Primary bleeding and MACE outcomes were the prespecified definitions in each

28 evel associates with the risk of any CVD and MACE in T1D individuals.

29 Death and MACE at 30 and 720 days were the prognostic endpoints.

30 BF, the adjusted hazard ratios for death and MACE were 1.93 (95% CI, 1.08-3.48, P=0.028) and 2.14 (95

31 PR, the adjusted hazard ratios for death and MACE were 2.45 (95% CI, 1.42-4.24, P=0.001) and 1.74 (95

32 ined independently associated with death and MACE, with stress MBF remaining associated with MACE onl

33 independently associated with both death and MACE.

34 The association between GLS and MACE remained significant (P<0.001) after adjustment for

35 igher risk of both myocardial infarction and MACE in anemic patients.

36 ve decreased risk of all-cause mortality and MACE (composite of all-cause mortality, coronary artery

37 omega-3 intake) with all-cause mortality and MACE.

38 The relation between NAFLD and MACE was assessed by using multivariable Cox regression

39 During follow-up, NFAT and MACE do not show clinically relevant changes in size or

40 y was 11.2% and was similar between NFAT and MACE.

41 ry), PCI was performed in 1,621 patients and MACE occurred in 18.0% of patients, of which 8.3% were c

42 he relationship between rmPFC reactivity and MACE, respectively.

43 predictor for coronary revascularization and MACE and showed better agreement with additional diagnos

44 predictor for coronary revascularization and MACE than stenosis of 50% and greater at triple-rule-out

45 hen considering cardiovascular mortality and MACEs at 90 days (adjHR: 2.42; 95% CI: 1.36 to 4.28; p =

46 risk score for both all-cause mortality and MACEs.

47 sed to calculate hazard ratios (HRs) for any MACE, MALE, and MALE including lower extremity revascula

48 Our analysis showed a decreased risk of both MACE (odds ratio, 0.41; CI, 0.25-0.70) and mortality (od

49 Si micropillars produced by MACE often show a porous Si/SiO(x) shell on crystalline

50 isk ratios for all-cause mortality, combined MACE events.

51 Secondary end points included 3-component MACE (myocardial infarction, ischemic stroke, and mortal

52 lacebo on the rates of the primary composite MACE end point (cardiovascular death, myocardial infarct

53 ts were randomly assigned to a third course, MACE (amsacrine, Ara-C, and etoposide), plus a fourth co

54 preferred option for the rule-out of 30-day MACE + UA.

55 time to ED discharge, and low rate of 30-day MACE associated with the routine clinical use of the ESC

56 p < 0.001), while maintaining similar 30-day MACE rates (0.6%; 95% CI: 0.3% to 1.1% vs. 0.4%; 95% CI:

57 Proportion of patients with 30-day MACE were 0.2% (95% confidence interval: 03% to 0.5%) in

58 We defined MACE as a composite of cardiovascular death, myocardial

59 The primary endpoint (MACE) comprised death of CAD, nonfatal myocardial infarc

60 achieved in metal-assisted chemical etching (MACE) has enabled the production of high-quality micropi

61 ex ACS, time to major adverse cardiac event (MACE) was investigated using Cox regression models.

62 primary major adverse cardiovascular event (MACE) outcome of cardiovascular death, myocardial infarc

63 clusion to first major cardiovascular event (MACE) were analyzed by Cox regression.

64 etween sex and major adverse cardiac events (MACE) (cardiac death, myocardial infarction [MI], or isc

65 0-day rates of major adverse cardiac events (MACE) (the composite of cardiovascular death and MI).

66 a predictor of major adverse cardiac events (MACE) and all-cause mortality (ACM).

67 ry outcome was major adverse cardiac events (MACE) defined by death, myocardial infarction, unstable

68 mortality and major adverse cardiac events (MACE) have not been definitively investigated.

69 of short-term major adverse cardiac events (MACE) in patients with suspected acute myocardial infarc

70 Major adverse cardiac events (MACE) included cardiac death, myocardial infarction, def

71 ction predicts major adverse cardiac events (MACE) independently of NAFLD.

72 36 (12%) first major adverse cardiac events (MACE) occurred (47 cardiovascular deaths and 89 readmiss

73 larization and major adverse cardiac events (MACE) was assessed over a 1-year follow-up period.

74 Major adverse cardiac events (MACE) were defined as a composite of cardiogenic shock,

75 events (CVEs), major adverse cardiac events (MACE), and cardiovascular mortality.

76 ified risks of major adverse cardiac events (MACE).

77 nd/or MI), and major adverse cardiac events (MACE).

78 tality, major adverse cardiovascular events (MACE) (cardiovascular death, myocardial infarction, stro

79 ence of major adverse cardiovascular events (MACE) (composite of all-cause mortality, myocardial infa

80 -FT and major adverse cardiovascular events (MACE) after AMI.

81 related major adverse cardiovascular events (MACE) after percutaneous coronary intervention (PCI) are

82 fenofibrate on major cardiovascular events (MACE) among 3,065 self-reported white subjects treated w

83 (PCI) for major acute cardiovascular events (MACE) and angina reduction.

84 reduced major adverse cardiovascular events (MACE) and death in the ODYSSEY OUTCOMES trial (Evaluatio

85 risk of major adverse cardiovascular events (MACE) and myocardial infarction in fully adjusted multiv

86 risk of major adverse cardiovascular events (MACE) compared with aspirin alone after percutaneous cor

87 risk of major adverse cardiovascular events (MACE) compared with those without PAD.

88 oint of major adverse cardiovascular events (MACE) comprised coronary heart disease death, nonfatal m

89 tor for major adverse cardiovascular events (MACE) in individuals with coronary artery disease.

90 educing major adverse cardiovascular events (MACE) in patients with CKD and an estimated glomerular f

91 risk of major adverse cardiovascular events (MACE) in patients with type 2 diabetes mellitus and a hi

92 well as major adverse cardiovascular events (MACE) in the Diabetes Control and Complications Trial (D

93 ast 122 major adverse cardiovascular events (MACE) occurred.

94 ts were major adverse cardiovascular events (MACE) within 12 months.

95 2-year major adverse cardiovascular events (MACE), a composite of cardiac death, myocardial infarcti

96 ence of major adverse cardiovascular events (MACE), all-cause mortality, and readmission for cardiova

97 use on major adverse cardiovascular events (MACE), defined as cardiovascular death, nonfatal myocard

98 port of major adverse cardiovascular events (MACE), defined as incident myocardial infarction, stroke

99 ence of major adverse cardiovascular events (MACE), defined by cardiovascular death or nonfatal myoca

100 ath and major adverse cardiovascular events (MACE), including myocardial infarction, stroke, heart fa

101 Major adverse cardiovascular events (MACE), which included death, stroke, myocardial infarcti

102 tion in major adverse cardiovascular events (MACE).

103 predict major adverse cardiovascular events (MACE).

104 risk of major adverse cardiovascular events (MACE).

105 edicted major adverse cardiovascular events (MACE).

106 ath and major adverse cardiovascular events (MACE).

107 ence of major adverse cardiovascular events (MACE, adjusted HR 0.80, 95% CI 0.70-0.93) and all-cause

108 5-year major adverse cardiovascular events (MACE; a composite of cardiac death, myocardial infarctio

109 porting major adverse cardiovascular events (MACE; ie, cardiovascular death, stroke, or myocardial in

110 e mortality and major cardiovascular events (MACEs) (cardiovascular mortality, reinfarction, or ische

111 risk of major adverse cardiovascular events (MACEs) and death.

112 P) with major adverse cardiovascular events (MACEs) and major adverse limb events (MALEs).

113 hed for major adverse cardiovascular events (MACEs) in the high-risk primary prevention PREDIMED (Pre

114 Major adverse cardiovascular events (MACEs) were analyzed.

115 mposite major adverse cardiovascular events (MACEs), all-cause mortality, and hypoglycemia.

116 of death and major adverse coronary events (MACEs; defined as death, readmission for myocardial infa

117 heart failure (major adverse cardiac events [MACE]).

118 We also examined MACE in several subgroups based on patient characteristi

119 mas causing mild autonomous cortisol excess (MACE), but their natural history is unclear.

120 .89; 1-sided 97.5% CI, 0-1.23); the expanded MACE definition included 168 (9.4%) aclidinium vs 160 (8

121 g stress-exposed individuals, 12 experienced MACE over a median follow-up of 3.75 years.

122 eriod of 4 years, 8% (21 of 259) experienced MACE.

123 follow-up of 162 days, 51 (51%) experienced MACE.

124 primary bleeding outcome and 937 experienced MACE.

125 rimary outcome was the incidence of extended MACE (composite of 6 outcomes), defined as first occurre

126 e primary safety end point was time to first MACE over up to 3 years (hazard ratio [HR] 1-sided 97.5%

127 For MACE, higher plasma kallikrein levels were associated wi

128 There seemed to be a greater benefit for MACE within 2 years after the last acute event ( P for i

129 tervals) differed across CABG categories for MACE (no CABG 1.3% [0.5% to 2.2%], index CABG 0.9% [-2.3

130 Population risk differences for MACE were estimated.

131 sure is a modifiable cardiac risk factor for MACE and ACM, supporting the need for early recognition

132 on was not associated with higher hazard for MACE or MALE in patients with peripheral artery disease.

133 EXSCEL-observed HRs for MACE and ACM remained robust after right censoring or ap

134 to estimate overall hazard ratios (HRs) for MACE, its components, death from any cause, hospital adm

135 hazard ratios (95% confidence intervals) for MACE (no CABG 0.86 [0.78 to 0.95], index CABG 0.85 [0.54

136 were able to capture important knowledge for MACE risk assessment.

137 or to CABG, and CABG was superior to PCI for MACE in 54.5% of patients and in 100% of patients with h

138 hypertension, the adjusted hazard ratio for MACE was 0.94, 95% CI, 0.82-1.08; P=0.39, and the adjust

139 k factors improved risk reclassification for MACE prediction, and C-statistic improved from 0.71 to 0

140 lthough women with PAD are at lower risk for MACE and all-cause mortality, risk for limb events was s

141 ivity) may be informative of future risk for MACE.

142 rom 9.78% to 10.18%, with relative risks for MACE ranging from 0.99 to 1.02.

143 erotic cardiovascular disease risk score for MACE prediction.

144 During follow-up, 211 patients had MACE, 108 died, and 130 were readmitted for CV causes.

145 (16.4%) patients died, and 1,048 (20.7%) had MACEs.

146 However, MACE rates between 1 and 5 years increased from BMS to D

147 graphy-LVEF, CMR-LVEF significantly improved MACE prediction in the group of patients with echocardio

148 k reductions showed no meaningful changes in MACE or ACM HRs or P values, although simulations of sub

149 MAR was not associated with a difference in MACE [HR 1.04 (0.87-1.26)], and a lower rate of long-ter

150 SAR does not correlate with a difference in MACE amongst patients with GFR between 30 and 60 and bet

151 There was no significant difference in MACE at 1 year between intervention and usual care group

152 ed statistical power to show a difference in MACE.

153 was to evaluate sex-specific differences in MACE and limb events in the EUCLID (Examining Use of Tic

154 There were no differences in MACE or LEA rates with exenatide versus placebo.

155 S was associated with a 1.5-fold increase in MACE among patients with a reduced EF (hazard ratio: 1.5

156 cardiovascular events were more prevalent in MACE (15.5%) than NFAT (6.4%).

157 he mean) associates with a >50% reduction in MACE risk, potentially via reduced arterial inflammation

158 us aspirin produced consistent reductions in MACE (PCI: 4.0% versus 5.5%; hazard ratio [HR], 0.74 [95

159 associated with large absolute reductions in MACE and death in those with CABG preceding the ACS even

160 th aspirin produced consistent reductions in MACE and mortality but with increased major bleeding wit

161 n produced consistent (robust) reductions in MACE irrespective of time since previous PCI (as early a

162 was inversely associated with both incident MACE and CV readmission (hazard ratio [HR]: 0.76; 95% co

163 with a significantly lower risk of incident MACE.

164 tress reactivity is associated with incident MACE.

165 nuous or categorical variables) and incident MACEs (N = 6,901; n cases = 263).

166 ry flow reserve was a predictor of increased MACE rate (hazard ratio [HR]: 1.06; 95% confidence inter

167 r worsened HTN was associated with increased MACEs (hazard ratio [HR], 2.17; 95% confidence interval

168 Very-late MACE (a composite of cardiac death, myocardial infarctio

169 Between years 1 and 5, very-late MACE occurred in 9.4% of patients (including 2.9% cardia

170 Very-late MACE occurred in 9.7%, 11.0%, and 8.3% of patients treat

171 021) were independently associated with less MACE.

172 phy-LVEF>=50% (629, 56%), and they had a low MACE rate (57/629, 9%).

173 Very low MACE rates were confirmed in multiple subgroups, includi

174 lower AmygA despite stress exposure) lowers MACE risk.

175 s improve cardiovascular outcomes (mortality/MACE) in patients with refractory angina.

176 abetes (10.2% vs. 5.8%, P < 0.01), with most MACE occurring in patients with LVEF >=35%.

177 vel, the unadjusted hazard ratio (HR) for NC-MACE was 1.21 (95% CI 1.09-1.35; p=0.0004) for each 100-

178 4mm) more than 400, the unadjusted HR for NC-MACE was 2.18 (1.48-3.22; p<0.0001) and adjusted HR was

179 The 2-year cumulative incidence of NC-MACE was 9% (n=103).

180 nd segments at higher risk for subsequent NC-MACE.

181 Analysis of MACE risk was performed in placebo-treated patients, whe

182 The 2 primary end points were composite of MACE (cardiovascular death, MI, or ischemic stroke) and

183 The frequency of MACE was 37.1%; mortality 18.9%; stroke 13.3%; and major

184 ith a significantly lower rate and hazard of MACE at 5 years compared with no PCI (31.5% vs 39.1%; ha

185 th a significantly higher rate and hazard of MACE at 5 years compared with no PCI (33.3% vs 24.4%; HR

186 ting to compare the cause-specific hazard of MACE between treatments and estimate cumulative risk acc

187 In contrast, there was a higher hazard of MACE in patients with out-of-target low and high SBP.

188 was associated with the lowest incidence of MACE (adjusted HR 0.70, 95% CI 0.57-0.86), all-cause mor

189 dependent predictor of a higher incidence of MACE (hazard ratio, 2.26 [95% CI, 1.52-3.35]; P<0.001).

190 The incidence of MACE in the placebo group was related to PRS for CAD: 17

191 n follow-up of 30 months, 1,148 incidents of MACE (375 heart failure, 253 myocardial infarction, 180

192 nificantly associated with the occurrence of MACE (hazard ratio, 2.46 [95% CI, 1.69-3.60]; and hazard

193 rognostic value to predict the occurrence of MACE in patients with HFrEF.

194 benefit over infarct size for prediction of MACE (hazard ratio, 1.3; P < .01).

195 ced efficacy and safety in the prediction of MACE, whereas the extended algorithm is the preferred op

196 , female sex was an independent predictor of MACE (hazard ratio [HR:]: 1.14; 95% confidence interval

197 n (P = 0.024) were independent predictors of MACE in patients without diabetes, GLS was in patients w

198 ent experienced a lower annual event rate of MACE (1.8%) than those with both ischemia and late gadol

199 years, women had a higher unadjusted rate of MACE (18.9% vs. 17.7%; p = 0.003), all-cause death (10.4

200 rsus SAR was associated with a lower rate of MACE [hazard ratio (HR) 0.87 (0.80-0.94)], and a lower r

201 ignificantly associated with a lower rate of MACE for ischemic lesions and a higher rate of MACE for

202 CE for ischemic lesions and a higher rate of MACE for nonischemic lesions.

203 l shows that the significantly lower rate of MACE in the complete revascularization group, previously

204 had higher unadjusted and adjusted rates of MACE compared with patients without PAD (13.6% versus 11

205 ooled reported annualized incidence rates of MACE in those without baseline CVD were compared with re

206 The 5-year rates of MACE progressively declined with evolution in stent tech

207 The cause-specific adjusted hazard ratio of MACE for metformin was 0.80 (95% CI, 0.75-0.86) compared

208 Both the absolute and relative reduction of MACE by alirocumab compared with placebo was greater in

209 ) and did not appear to increase the risk of MACE (2.51% versus 2.98%; HR, 0.85 [95% CI, 0.70-1.03]).

210 ]), with no increase observed in the risk of MACE (2.73% versus 3.11%; HR, 0.88 [95% CI, 0.77-1.02]),

211 w-up of 30 months, women had a lower risk of MACE (9.5% vs. 11.2%; adjusted hazard ratio: 0.77; 95% c

212 iated with a significantly increased risk of MACE (adjusted hazard ratio [HR]: 1.05/Gy; 95% CI: 1.02

213 olume were associated with increased risk of MACE (hazard ratio [95%CI]: 1.03 [1.01-1.04]; 1.25 [1.19

214 33.7 to 67.2 mg/dl), and reduced the risk of MACE (hazard ratio [HR]: 0.85; 95% confidence interval [

215 s was associated with a 21% increase risk of MACE (hazard ratio, 1.21 [95% CI, 1.08-1.37]).

216 mHg was associated with an increased risk of MACE (HR, 1.10 [95% CI, 1.06-1.14]; P<0.001), a marginal

217 mHg was associated with an increased risk of MACE (HR, 1.19 [95% CI, 1.09-1.31]; P<0.001) but not MAL

218 ductions by alirocumab predicted the risk of MACE after recent ACS.

219 ght loss thresholds for reduction in risk of MACE and all-cause mortality in patients with obesity an

220 ctors contributing to a reduction in risk of MACE and all-cause mortality in the surgical cohort.

221 mellitus and previous MI are at high risk of MACE and cardiovascular death/hospitalization for heart

222 orary PCI trials, women had a higher risk of MACE and ID-TLR compared with men at 5 years following P

223 LVT was associated with a very high risk of MACE and mortality.

224 New approaches to reduce the ongoing risk of MACE beyond 1 year after stent implantation are necessar

225 , dapagliflozin reduced the relative risk of MACE by 16% and the absolute risk by 2.6% (15.2% versus

226 t confounders, women were at similar risk of MACE compared with men (hazard ratio [HR]: 1.04; 95% con

227 es from a diverse set of models, the risk of MACE decreases after approximately 10% of weight is lost

228 ruption was associated with a higher risk of MACE outcomes.

229 inium was noninferior to placebo for risk of MACE over 3 years.

230 The absolute risk of MACE ranged from 9.78% to 10.18%, with relative risks fo

231 They were at higher risk of MACE than patients without diabetes (10.2% vs. 5.8%, P <

232 The risk of MACE was also significantly higher in the high NLR group

233 The risk of MACE was higher with a lower GLS among patients with eit

234 An increased risk of MACE was not observed after discontinuation of aspirin,

235 LDL-C independently predicted lower risk of MACE, after adjustment for baseline concentrations of bo

236 nylurea, was associated with a lower risk of MACE.

237 djustment for baseline differences, risks of MACE (HR: 0.93; 95% CI: 0.88 to 0.98; p < 0.01) and all-

238 y high surface potential on the sidewalls of MACE-synthesized pillars (+ 0.5 V), which is restored to

239 With placebo, the incidence of MACEs by respective vascular categories was 10.0%, 22.2%

240 simvastatin 20 mg daily reduced the odds of MACEs in this patient population.

241 differentiated subjects at a higher risk of MACEs compared with those at lower concentrations, regar

242 lar disease is associated with high risks of MACEs and death.

243 s were both associated with similar risks of MACEs and hypoglycemia but a lower risk of all-cause mor

244 evious PCI 1 year and beyond, the effects on MACE and mortality were consistent irrespective of time

245 The rs6008845-by-fenofibrate interaction on MACE was replicated in African Americans from ACCORD (N

246 The effect of NBResilience on MACE risk was significantly mediated by lower arterial i

247 t beneficial effects of metabolic surgery on MACE and survival.

248 for the primary safety endpoints of death or MACE, with no between-catheter differences observed.

249 dictors of very-late stent-related events or MACE by stent type.

250 orted outcomes of 4121 patients with NFAT or MACE, 61.5% of whom were women; the mean age was 60.2 ye

251 to develop (<0.1%) in patients with NFAT or MACE.

252 reductions, but the exenatide versus placebo MACE effect size and statistical significance were incre

253 vascular death, all-cause mortality, 3-point MACE and hospitalization for heart failure with empaglif

254 In the placebo group, 3-point MACE occurred during the trial in 7.3%, 9.4%, 12.6%, and

255 major adverse cardiovascular events (3-point MACE), cardiovascular and all-cause death, and hospitali

256 mortality and no difference in postdischarge MACEs.

257 esterol content in lipoprotein(a)] predicted MACE.

258 hocardiography-LVEF) independently predicted MACE occurrence.

259 interaction of NAFLD and male sex predicted MACE (hazard ratio, 1.45; 95% confidence interval: 1.08,

260 res, a similar behavior observed in previous MACE studies.

261 The primary MACE outcome was coronary heart disease death, nonfatal

262 associated with elevated risk for recurrent MACE after acute coronary syndrome and a larger absolute

263 ted with the risk of mortality and recurrent MACEs.

264 ll, GLP-1 receptor agonist treatment reduced MACE by 12% (HR 0.88, 95% CI 0.82-0.94; p<0.0001).

265 found for the CONUT score and PNI regarding MACEs.

266 nd the 2-year rate of culprit lesion-related MACE was not significantly associated with maxLCBI(4mm)

267 Very-late (>1-year) stent-related MACE have not been well described.

268 However, GLS emerged as the strongest MACE prognosticator among strain parameters (area under

269 At 14+/-3 years, 223 subjects suffered MACE.

270 ase remain at substantial risk for long-term MACE after revascularization with percutaneous coronary

271 ntly predicted the occurrence of medium-term MACE in contemporary revascularized ST-elevation myocard

272 The MACE effect size was not altered meaningfully by right c

273 The MACE model included 8 variables and treatment interactio

274 The MACE rate significantly increased only in patients with

275 echocardiography-LVEF<50% (n=490, 44%), the MACE rate was also low in those with CMR-LVEF>=40% (24/2

276 IPTW decreased the MACE HR from 0.91 (P=0.061) to 0.85 (P=0.008) and the AC

277 alirocumab is an independent contributor to MACE reduction, which suggests that lipoprotein(a) shoul

278 from reduced kidney function threshold until MACE, treatment change, loss to follow-up, death, or stu

279 The secondary endpoint was MACE + unstable angina (UA) receiving early (<=24 h) rev

280 The primary endpoint was MACE, including all-cause death, cardiac arrest, AMI, ca

281 The primary outcome was MACE, defined as the composite of stroke, myocardial inf

282 Key efficacy outcomes were MACE (cardiovascular [CV] death, myocardial infarction,

283 ascular dysfunction remained associated with MACE (adjusted hazard ratio, 1.46; 95% confidence interv

284 ctors, GRS was significantly associated with MACE (hazard ratio [HR] 1.81, P = .006) when comparing g

285 ial parameters were strongly associated with MACE (hazard ratio [HR], epsilon(s) = 0.9, epsilon(e) =

286 AT attenuation was inversely associated with MACE (hazard ratio, 0.83 [95% CI, 0.72-0.96]; P=0.01), w

287 sion were also independently associated with MACE and cardiovascular mortality during short-time (3 m

288 Lower GLS was strongly associated with MACE in ICI myocarditis presenting with either a preserv

289 E, with stress MBF remaining associated with MACE only.

290 tion were both independently associated with MACE.

291 etermination of future risks associated with MACE.

292 ow median were significantly associated with MACE.

293 Results Study participants with MACE had worse LA performance parameters compared with s

294 train indices were impaired in patients with MACE (all P<0.001).

295 9 mmol/l] in women) was also associated with MACEs (HR: 1.44; 95% CI: 1.04 to 2.00; p = 0.030).

296 terol (LDL-C) or HDL-C, were associated with MACEs.

297 ers compared with study participants without MACE (epsilon(s) = 21.2% vs 16.2%, epsilon(e) = 8.8% vs

298 itors and no significant reduction in 1-year MACE outcomes.

299 e authors developed models to predict 5-year MACE (all-cause mortality, nonfatal myocardial infarctio

300 The 5-year MACE occurred in 346 (18.2%) patients, and 310 (16.3%) h