ライフサイエンスコーパス: cardiovascular mortality

1 nonfatal myocardial infarction, stroke, and cardiovascular mortality).

2 t risk factor for coronary heart disease and cardiovascular mortality.

3 arization and conduction, is associated with cardiovascular mortality.

4 lic fatty liver disease, cardiomyopathy, and cardiovascular mortality.

5 showed little or no benefit for all-cause or cardiovascular mortality.

6 longitudinal associations with all-cause and cardiovascular mortality.

7 arization, myocardial infarction, stroke, or cardiovascular mortality.

8 with increases in lagged non-accidental and cardiovascular mortality.

9 The primary outcome was cardiovascular mortality.

10 isease (CKD) is a well-known risk factor for cardiovascular mortality.

11 ors of calcification, a major determinant of cardiovascular mortality.

12 ction, stroke, congestive heart failure, and cardiovascular mortality.

13 e timing and burden of seasonal increases in cardiovascular mortality.

14 ndition associated with an increased risk of cardiovascular mortality.

15 e mortality, and the secondary end point was cardiovascular mortality.

16 n adjusted HR of 2.07 (95% CI 1.90-2.26) for cardiovascular mortality.

17 increased risk for cardiovascular events and cardiovascular mortality.

18 cified primary end points were all-cause and cardiovascular mortality.

19 egional differences in rates of all-cause or cardiovascular mortality.

20 ve impaired exercise tolerance and increased cardiovascular mortality.

21 ical composite end point or reduce long-term cardiovascular mortality.

22 ic bone disease, vascular calcification, and cardiovascular mortality.

23 8) for CAD and 0.97 (95% CI: 0.93, 1.00) for cardiovascular mortality.

24 st contributing risk factor to all-cause and cardiovascular mortality.

25 Atherosclerosis is the leading cause for cardiovascular mortality.

26 ed tissues, and leukocytosis correlates with cardiovascular mortality.

27 s is associated with a 50% increased risk in cardiovascular mortality.

28 HF) are obesity-related conditions with high cardiovascular mortality.

29 vents and significantly reduced bleeding and cardiovascular mortality.

30 e early referral for CA, was associated with cardiovascular mortality.

31 nt (>0) of 0.542 (95% CI: 0.205 to 0.840) in cardiovascular mortality.

32 tive heart failure, all-cause mortality, and cardiovascular mortality.

33 ction begins in early CKD and contributes to cardiovascular mortality.

34 increased FGF23 level with increased risk of cardiovascular mortality.

35 and independently associated with increased cardiovascular mortality.

36 ociated with increased arterial rigidity and cardiovascular mortality.

37 Secondary outcome was cardiovascular mortality.

38 y of growth hormone (GH) are associated with cardiovascular mortality.

39 These patients are at higher risk of cardiovascular mortality.

40 idence of stroke, myocardial infarction, and cardiovascular mortality.

41 d for presence of ER and total mortality and cardiovascular mortality.

42 e was a composite of nonfatal MI, stroke, or cardiovascular mortality.

43 ication and is associated with all-cause and cardiovascular mortality.

44 nal disease and is associated with increased cardiovascular mortality.

45 osite of time-to-first HF hospitalization or cardiovascular mortality.

46 The primary outcome was cardiovascular mortality.

47 ndition associated with an increased risk of cardiovascular mortality.

48 us thromboembolism (VTE), a leading cause of cardiovascular mortality.

49 disease, hypertension, and in some studies, cardiovascular mortality.

50 for positive pressure therapies for reducing cardiovascular mortality.

51 elderly men, although not significantly with cardiovascular mortality.

52 The risk of cardiovascular mortality (0.5% versus 1.2%; odds ratio,

53 3), stroke (0.92, 0.67-1.25; ptrend=0.7092), cardiovascular mortality (0.73, 0.53-1.02; ptrend=0.0568

54 tality (0.73, 0.53-1.02; ptrend=0.0568), non-cardiovascular mortality (0.84, 0.68-1.04; ptrend =0.003

55 90, 95% CI 0.82-0.99; p=0.033), a 13% RRR in cardiovascular mortality (0.87, 0.79-0.96; p=0.007), and

56 -1.11 and either LPA SNP 1.10, 0.92-1.31) or cardiovascular mortality (0.99, 0.81-1.2 and 1.13, 0.90-

57 iovascular (1.01, 0.93-1.12; p=0.81) and non-cardiovascular mortality (1.04, 0.90-1.26; p=0.66) were

58 e NT-proBNP thresholds reduced all-cause and cardiovascular mortality (2 of 4 studies) and the compos

59 y (7.92% vs. 10.07% vs. 16.81%; p < 0.0001), cardiovascular mortality (3.26% vs. 4.58% vs. 7.80%; p <

60 (8.0% versus 9.8%, respectively; P=0.54) or cardiovascular mortality (6.5% versus 9.1%; P=0.40).

61 ntions, and the effects of blood pressure on cardiovascular mortality, according to age, were calcula

62 Trends in cardiovascular mortality across Europe demonstrate signi

63 e group of <140 mm Hg (group 1), the risk of cardiovascular mortality (adjusted hazard ratio [HR]: 1.

64 Phosphorus density was associated with cardiovascular mortality [adjusted HR (95% CI): 3.39 (1.

65 0.37) and predicted all-cause mortality and cardiovascular mortality after adjustment for establishe

66 were found for aortic arch calcification and cardiovascular mortality (age- and sex-adjusted hazard r

67 olesterol efflux capacity is associated with cardiovascular mortality, all-cause mortality, and graft

68 valsartan was associated with a reduction in cardiovascular mortality, all-cause mortality, and hospi

69 IFG or IGT found no effects on all-cause or cardiovascular mortality, although lifestyle modificatio

70 Out-of-sample prediction of cardiovascular mortality among adults 65 years and older

71 ic embolic event, myocardial infarction, and cardiovascular mortality, analysed by intention to treat

72 actors associated with increased longer-term cardiovascular mortality and (2) incremental prognostic

73 ociated with a 0.27% (0.11-0.44) increase in cardiovascular mortality and a 0.56% (0.24-0.87) increas

74 with a 0.47% (95% CI 0.34-0.61) increase in cardiovascular mortality and a 0.57% (0.28-0.86) increas

75 re tested for association with all-cause and cardiovascular mortality and a composite end point of my

76 Secondary outcomes were cardiovascular mortality and all-cause mortality.

77 Statins substantially reduce cardiovascular mortality and appear to have beneficial e

78 ssociated with reduced risk of all-cause and cardiovascular mortality and coronary artery disease sev

79 ssociated with reduced risk of all-cause and cardiovascular mortality and CVD events, with greater ab

80 epression and anxiety also feature increased cardiovascular mortality and decreased heart-rate variab

81 ference and reclassification improvement for cardiovascular mortality and fatal and non-fatal cases o

82 already assessed for clinical purpose or if cardiovascular mortality and heart failure are outcomes

83 nsion, but remained significant with ACR for cardiovascular mortality and heart failure in those with

84 lic BP <140 mm Hg) decreased MACE, including cardiovascular mortality and heart failure.

85 ced or preserved ejection fraction, rates of cardiovascular mortality and HF hospitalization were hig

86 y, or supplemental calcium intake levels and cardiovascular mortality and highly inconsistent dose-re

87 e echocardiography and a composite endpoint (cardiovascular mortality and hospitalization) were evalu

88 formance for predicting all-cause mortality, cardiovascular mortality and major adverse cardiac event

89 ated with an 86% and a 38% increased risk of cardiovascular mortality and major cardiovascular events

90 ion, AKI associates with an elevated risk of cardiovascular mortality and major cardiovascular events

91 associated with an increase in all-cause and cardiovascular mortality and might both be therapeutic t

92 the positive association of neprilysin with cardiovascular mortality and morbidity further support t

93 from clinical practice, we aimed to compare cardiovascular mortality and morbidity in new users of S

94 sartan provides reasonable value in reducing cardiovascular mortality and morbidity in patients with

95 ate homeostasis, is strongly associated with cardiovascular mortality and morbidity.

96 We hypothesized that, as eGFR declines, cardiovascular mortality and mortality from infection ac

97 tudy confirms that exercise-based CR reduces cardiovascular mortality and provides important data sho

98 control did not reduce risk for all-cause or cardiovascular mortality and results for intensive blood

99 This analysis also suggests that risk of cardiovascular mortality and stent thrombosis might be l

100 ctrocardiogram significantly associates with cardiovascular mortality and sudden cardiac death indepe

101 Benefits appear to be maximum for both non-cardiovascular mortality and total mortality at three to

102 mic stroke, acute myocardial infarction, and cardiovascular mortality) and all-cause mortality up to

103 use mortality, 1.29 (95% CI: 0.83, 2.00) for cardiovascular mortality, and 1.10 (95% CI: 0.88, 1.37)

104 for ischemic cardiovascular events, 34% for cardiovascular mortality, and 23% for combined total mor

105 ates of major adverse cardiovascular events, cardiovascular mortality, and all-cause mortality accord

106 e-point major adverse cardiovascular events, cardiovascular mortality, and all-cause mortality risk,

107 -cause mortality) and secondary (separately, cardiovascular mortality, and combined all-cause mortali

108 entration, the risks of all-cause mortality, cardiovascular mortality, and fatal infection increased

109 with increased risk of all-cause mortality, cardiovascular mortality, and graft failure and, of all

110 e studied outcomes were all-cause mortality, cardiovascular mortality, and hospitalization for HF.

111 years, the incremental all-cause mortality, cardiovascular mortality, and major stroke rates were 12

112 The rates of all-cause mortality, cardiovascular mortality, and major stroke were 36.6%, 2

113 Observed rates of all-cause mortality, cardiovascular mortality, and myocardial infarction in 2

114 y disease (PAD) is associated with increased cardiovascular mortality, and PAD risk factors overlap w

115 al infarction, cardiovascular mortality, non-cardiovascular mortality, and total mortality in the mod

116 fatal strokes, cardiovascular mortality, non-cardiovascular mortality, and total mortality.

117 Additionally, cardiovascular and non-cardiovascular mortality are several times higher in pat

118 Geographic variations in cardiovascular mortality are substantial, but descriptio

119 The decreasing association with cardiovascular mortality as the time since last use of c

120 , multivariate models revealed all-cause and cardiovascular mortality associated with age, aortic PWV

121 The preventable fraction of cardiovascular mortality associated with complete elimin

122 Cardiovascular mortality at 30 days was 4.1% in the ball

123 Cardiovascular mortality at 90 days was 0% among T2MI201

124 e no significant differences in all-cause or cardiovascular mortality between groups.

125 There is a growing disparity in cardiovascular mortality between Western and Eastern Eur

126 Secondary end points included cardiovascular mortality, bleeding and vascular complica

127 pective estimation of influenza-attributable cardiovascular mortality burden combined with accurate a

128 hysical activity are associated with reduced cardiovascular mortality but its effect on age-related c

129 been postulated to delay arterial aging and cardiovascular mortality, but these intakes are beyond t

130 and rs3798220) with all-cause mortality and cardiovascular mortality by Cox regression analysis and

131 ith ACR than with eGFR, and more evident for cardiovascular mortality (C statistic difference 0.0139

132 ground: Sacubitril-valsartan therapy reduces cardiovascular mortality compared with enalapril therapy

133 h subsequent LVEF deterioration had a higher cardiovascular mortality compared with patients with sus

134 outcome of heart failure hospitalization or cardiovascular mortality compared with those without a h

135 ated with reduced cardiovascular disease and cardiovascular mortality compared with use of other gluc

136 icial effects on hemoglobin A1c, weight, and cardiovascular mortality (compared with sulfonylureas).

137 Multi-model ensembles indicated cardiovascular mortality could increase by an average pe

138 nted for 83.0% (73363 deaths) of nonpandemic cardiovascular mortality during influenza seasons, seaso

139 mechanism that could contribute to increased cardiovascular mortality during intensive glycemic thera

140 Adjusted cardiovascular mortality estimates at 10 years were 17%,

141 traditional predictors; the C statistic for cardiovascular mortality fell by 0.0227 (0.0158-0.0296)

142 Patients with CKD have an increased risk of cardiovascular mortality from arrhythmias and sudden car

143 Although cardiovascular mortality has declined, the devastating i

144 Cardiovascular mortality has decreased in recent decades

145 Cardiovascular mortality has decreased over the past 5 d

146 nts in diagnosis, prevention, and treatment, cardiovascular mortality has fallen in recent years.

147 Impressive decreases in cardiovascular mortality have been achieved through risk

148 that efflux capacity was not associated with cardiovascular mortality (hazard ratio [HR], 0.89; 95% c

149 1000 person-years, but did not have reduced cardiovascular mortality (hazard ratio, 0.88; 95% CI, 0.

150 1.85; P=0.006 per SD decrease) and increased cardiovascular mortality (hazard ratio, 1.55; 95% confid

151 confidence interval, 1.38-2.28; P<0.01) and cardiovascular mortality (hazard ratio, 1.59; confidence

152 nificantly associated with increased risk of cardiovascular mortality (hazard ratio, 2.99; 95% confid

153 y ST2 remained independently associated with cardiovascular mortality (hazard ratio: 1.27, 95% confid

154 mental temperature with all-cause mortality, cardiovascular mortality, heat-related mortality, and mo

155 all-cause mortality; secondary outcomes were cardiovascular mortality; HF hospitalization; and combin

156 social integration is associated with lower cardiovascular mortality; however, whether it is associa

157 bitors was associated with decreased risk of cardiovascular mortality (HR 0.53 [95% CI 0.40-0.71]), m

158 tment hsCRP concentrations less than 2 mg/L, cardiovascular mortality (HR(adj)=0.69, 95% CI 0.56-0.85

159 e 4 primary fatty acids were associated with cardiovascular mortality (HR, 0.92-1.05 for each standar

160 .16]; and HR,1.21 [95% CI,1.15 to 1.27]) and cardiovascular mortality (HR, 1.05 [95% CI,1.00 to 1.10]

161 dence interval [CI], 1.21-2.85; P=0.004) and cardiovascular mortality (HR, 1.70; 95% CI, 1.06-2.89; P

162 s were associated with an increased risk for cardiovascular mortality (HR, 12.0; 95% CI, 3.2-44.7).

163 ne significant trend for an association with cardiovascular mortality (HR, 2.86; 95% CI, 0.99-8.21; P

164 CI, 1.16-3.22; HR, 1.84; 95% CI, 1.02-3.31), cardiovascular mortality (HR, 4.36; 95% CI, 1.37-13.83;

165 mortality (HR: 1.17; 95% CI: 1.12-1.22), and cardiovascular mortality (HR: 1.17; 95% CI: 1.07-1.28).

166 % CI: 1.01 to 1.60), a 69% increased risk of cardiovascular mortality (HR: 1.69; 95% CI: 1.32 to 2.15

167 life-threatening arrhythmic events (LAE) and cardiovascular mortality; identify risk factors associat

168 ted with low adverse event rates but earlier cardiovascular mortality, illustrating the impact of gen

169 velop region-specific estimates of premature cardiovascular mortality in 2025 based on various scenar

170 or adverse cardiovascular events (MACEs) and cardiovascular mortality in a general population is not

171 sity were strongly associated with increased cardiovascular mortality in adulthood.

172 se cardiac remodeling in utero and increased cardiovascular mortality in adulthood.

173 of newborns and is associated with increased cardiovascular mortality in adulthood.

174 ight metalworking fluids have been linked to cardiovascular mortality in analyses using binary exposu

175 robust evidence of higher nonaccidental and cardiovascular mortality in association with short-term

176 in native chronic kidney disease as well as cardiovascular mortality in chronic kidney disease more

177 (Hcy) levels are positively correlated with cardiovascular mortality in diabetes.

178 to detect uremic cardiomyopathy and predict cardiovascular mortality in ESRD.

179 f offspring was not associated with total or cardiovascular mortality in fathers.

180 After 8+/-6 years, cardiovascular mortality in FG+ probands with HCM was si

181 ficacy of statin-based therapies in reducing cardiovascular mortality in individuals with CKD seems t

182 diac troponin is an independent predictor of cardiovascular mortality in individuals without symptoms

183 astric bypass (RYGB) reduces body weight and cardiovascular mortality in morbidly obese patients.

184 ndently associated with higher all-cause and cardiovascular mortality in multivariable analyses.

185 ntly associated with increased all-cause and cardiovascular mortality in patients treated with PCI.

186 c events have been associated with increased cardiovascular mortality in patients with diabetes, whic

187 endothelial injury and a potent predictor of cardiovascular mortality in patients with kidney failure

188 onference to further explore these trends in cardiovascular mortality in the context of what has come

189 h improved insulin sensitivity and decreased cardiovascular mortality in the general population, but

190 Considering the extraordinarily high rate of cardiovascular mortality in the hemodialysis population,

191 the association of HDL-C with all-cause and cardiovascular mortality in the Ludwigshafen Risk and Ca

192 Survival free of all-cause and cardiovascular mortality in the transfemoral patients fr

193 (lag 2 and 0-5 day) and Arizona (lag 3), for cardiovascular mortality in the United States (lag 2) an

194 with altered cardiac structure and increased cardiovascular mortality in the young.

195 erences in reductions of total mortality and cardiovascular mortality in those receiving active treat

196 Hypoglycemia is associated with increased cardiovascular mortality in trials of intensive therapy

197 The risk of cardiovascular mortality increased with increasing durat

198 PV distensibility also predicted cardiovascular mortality independent of peak VO2 in HF p

199 d socioeconomic factors were associated with cardiovascular mortality, independent of each other.

200 Studying cardiovascular mortality is challenging because symptoms

201 Cardiovascular mortality is high in ESRD, partly driven

202 the epidemiologic evidence that the risk of cardiovascular mortality is positively associated with c

203 Cardiovascular mortality is the leading cause of death i

204 In the United States, regional variation in cardiovascular mortality is well-known but county-level

205 boembolism (VTE), the third leading cause of cardiovascular mortality, is a complex thrombotic disord

206 r patterns of associations were observed for cardiovascular mortality.Lower grip strength and excess

207 Cardiovascular outcomes investigated were cardiovascular mortality, major adverse cardiovascular e

208 isk (RR) for the association between AKI and cardiovascular mortality, major cardiovascular events, a

209 The reduced cardiovascular mortality may be explained by reduced thr

210 The composite secondary end point of cardiovascular mortality, MI, and stroke was observed in

211 tality, major adverse cardiovascular events (cardiovascular mortality, myocardial infarction, and isc

212 The primary endpoints were cardiovascular mortality, myocardial infarction, and str

213 nd ARBs with respect to all-cause mortality, cardiovascular mortality, myocardial infarction, stroke,

214 ial infarction, fatal and non-fatal strokes, cardiovascular mortality, non-cardiovascular mortality,

215 rdiovascular disease, myocardial infarction, cardiovascular mortality, non-cardiovascular mortality,

216 imary outcome including, but not limited to, cardiovascular mortality, non-fatal myocardial infarctio

217 dverse cardiovascular event primary outcome (cardiovascular mortality, non-fatal myocardial infarctio

218 wed-up for cardiovascular events (defined as cardiovascular mortality, non-fatal stroke, or myocardia

219 this guideline included all-cause mortality, cardiovascular mortality, nonfatal cardiovascular diseas

220 ortality because of an increased risk of non-cardiovascular mortality not offset by a reduction in ca

221 Cardiovascular mortality occurred in 10 LGE-positive ver

222 terval, 0.29-0.77; P=0.003), a lower risk of cardiovascular mortality (odds ratio =0.41, 95% confiden

223 preserved CFR and maximal MBF had the lowest cardiovascular mortality of 0.4% (95 CI, 0.3-0.6) per ye

224 eserved CFR but impaired maximal MBF had low cardiovascular mortality of 0.9% (95% CI, 0.6-1.6) per y

225 ality that was consistent across approaches: cardiovascular mortality of 1.07 (95% CI: 1.03-1.11) per

226 reported 30-day all-cause mortality of 2.2%, cardiovascular mortality of 1.1%, stroke of 1.4%, major

227 ut preserved maximal MBF had an intermediate cardiovascular mortality of 1.7% (95% CI, 1.3-2.1) per y

228 t impairment of CFR and maximal MBF had high cardiovascular mortality of 3.3% (95% CI, 2.9-3.7) per y

229 The incidence of cardiovascular mortality or cardiovascular hospitalizati

230 istics and outcomes (all-cause mortality and cardiovascular mortality or HF hospitalization) of patie

231 benefit of the interventions on all-cause or cardiovascular mortality or morbidity (4 trials [n = 513

232 0.015; heterogeneity P = 0.63; I2 = 0%) and cardiovascular mortality (OR, 0.50 [CI, 0.23 to 1.10]; P

233 nfidence interval [CI], 0.79-1.5; P=0.53) or cardiovascular mortality (OR, 1.03; 95% CI, 0.72-1.46; P

234 ortality (odds ratio [OR]: 0.83; p = 0.285), cardiovascular mortality (OR: 0.66; p = 0.103), and hosp

235 imary composite outcome (HF hospitalization, cardiovascular mortality, or aborted cardiac arrest), it

236 o significant effect on all-cause mortality, cardiovascular mortality, or stroke; however, there is a

237 Great progress has been made in reducing cardiovascular mortality over the past 50 years.

238 ion, nonfatal stroke, and >30% reductions in cardiovascular mortality, overall mortality, and heart f

239 ian of 21 [IQR: 8 to 36] months) overall and cardiovascular mortality (p < 0.001 for all).

240 annose and glycocholate were associated with cardiovascular mortality (P < 1.23 x 10(-4)), but predic

241 n HDL-C and eGFR in predicting all-cause and cardiovascular mortality (P=0.04 and P=0.02, respectivel

242 ence was correlated year to year with excess cardiovascular mortality (Pearson correlation coefficien

243 terval, 0.76-1.15; P=0.53, respectively) and cardiovascular mortality plus HF hospitalization early p

244 increased all-cause mortality and short-term cardiovascular mortality plus HF hospitalization.

245 ed with a decrease in HF hospitalization and cardiovascular mortality (primary endpoint) in patients

246 The lowest cardiovascular mortality rates were found in the countie

247 iscounted price of $10311) and $483800 if no cardiovascular mortality reduction emerges.

248 to MED has a consistent beneficial effect on cardiovascular mortality regardless of age.

249 associated with higher risk of all-cause and cardiovascular mortality regardless of BMI levels, and t

250 Previous studies have demonstrated increased cardiovascular mortality related to azithromycin and lev

251 , 0.82; 95% confidence interval, 0.69-0.98), cardiovascular mortality (relative hazard, 0.66; 95% con

252 Overall, CR led to a reduction in cardiovascular mortality (relative risk: 0.74; 95% confi

253 azard ratio =2.49 and 2.94 for all-cause and cardiovascular mortality, respectively).

254 ith 29% and 50% lower risks of all-cause and cardiovascular mortality, respectively, compared with ne

255 nd 45% lower adjusted risks of all-cause and cardiovascular mortality, respectively, with a 3-year li

256 dence interval, 1.06-1.17) for all-cause and cardiovascular mortality, respectively.

257 d OR, 1.32; 95% CI, 1.06-1.63) all-cause and cardiovascular mortality, respectively.

258 I and waist-to-hip ratio (WHR) and total and cardiovascular mortality risk after adjustment for confo

259 In multivariable analysis, the cardiovascular mortality risk gradient across the 4 conc

260 e minor allele (T) associates with decreased cardiovascular mortality risk, independent of blood pres

261 r clot structure had increased all-cause and cardiovascular mortality risks (log rank P=0.004 and P=0

262 e associations of running with all-cause and cardiovascular mortality risks in 55,137 adults, 18 to 1

263 e [ARD], -0.40% [95% CI, -0.64% to -0.17%]), cardiovascular mortality (RR, 0.69 [95% CI, 0.54 to 0.88

264 use mortality (RR, 0.85; 95% CI, 0.70-1.03), cardiovascular mortality (RR, 0.84; 95% CI, 0.59-1.18),

265 e mortality (RR, 0.95 [CI, 0.89 to 1.01]) or cardiovascular mortality (RR, 0.97 [CI, 0.85 to 1.10]).

266 ACE (RR: 0.71; 95% CI: 0.60 to 0.84), 33% in cardiovascular mortality (RR: 0.67; 95% CI: 0.45 to 0.98

267 s good as coronary angiography at predicting cardiovascular mortality (RRR, MPS, 0.89; 95% CI, 0.38-2

268 ted case reports that reported all-cause and cardiovascular mortality, RRT, kidney function, BP, and

269 Successful device implantation free of cardiovascular mortality, stroke, and device malfunction

270 ot significantly increase overall mortality, cardiovascular mortality, stroke, myocardial infarction,

271 condary end points were all-cause mortality, cardiovascular mortality, stroke, myocardial infarction,

272 (major adverse cardiovascular events [MACE], cardiovascular mortality, stroke, myocardial infarction,

273 with increased risk of all-cause mortality, cardiovascular mortality, stroke, or myocardial infarcti

274 CFR was a stronger predictor of cardiovascular mortality than maximal MBF beyond traditi

275 CFR is a stronger predictor of cardiovascular mortality than maximal MBF.

276 long hypocoagulability, seem to have a lower cardiovascular mortality than the general population.

277 Mothers had increased risk of total and cardiovascular mortality that was consistent across appr

278 For cardiovascular mortality, the differences were similar f

279 In the pooled cohort for cardiovascular mortality, the HR was 1.00 (95% CI, 0.92-

280 isk of primary outcome, all-cause mortality, cardiovascular mortality, total MI, nonfatal MI, total s

281 Secondary outcomes were all-cause mortality, cardiovascular mortality, total MI, nonfatal MI, total s

282 These associations were similar for cardiovascular mortality (unadjusted HR: 0.83; 95% CI: 0

283 torial intervention on risk for all-cause or cardiovascular mortality versus standard control.

284 n causes of death were available, the HR for cardiovascular mortality was 1.51 (1.12-2.04, P = 0.0077

285 Cardiovascular mortality was 12% (n = 53) in the biomark

286 The 3-year all-cause mortality was 42.0% and cardiovascular mortality was 17.5%.

287 ction=0.062), whereas the benefit of CABG on cardiovascular mortality was consistent over all ages (P

288 Cardiovascular mortality was lower for metformin versus

289 In contrast, cardiovascular mortality was not statistically significa

290 use mortality, stroke-related mortality, and cardiovascular mortality was obtained between November 1

291 All-cause, cancer, and cardiovascular mortalities were assessed over 5 y of fol

292 s between time-varying PRAs and all-cause or cardiovascular mortality were assessed using Cox proport

293 antly central sleep apnea, but all-cause and cardiovascular mortality were both increased with this t

294 h risks of long-term all-cause mortality and cardiovascular mortality were evaluated with the use of

295 ereas the associations with incident CVD and cardiovascular mortality were no longer significant.

296 Adjusted hazard ratios (95% CIs) for cardiovascular mortality were significantly elevated amo

297 o kidney disease, adjusted hazard ratios for cardiovascular mortality were significantly higher among

298 All-cause mortality and cardiovascular mortality were significantly higher in th

299 Unexpectedly, lower odds of cardiovascular mortality were suggested with greater con

300 he prespecified primary efficacy outcome was cardiovascular mortality within 30 days, and the primary