ライフサイエンスコーパス: CVD

1 CVD (P = .02), history of ARCD (P = .001), and HAND (P =

2 CVD affects a significant proportion of the population g

3 CVD was also marginally associated with symptomatic HAND

4 During follow-up, 306 CVD events and 431 deaths occurred.

5 mean 10.1 years of follow-up, including 406 CVD and 283 cancer deaths.

6 biomarker measurements (9758 all-cause, 6492 CVD, and 1719 cancer deaths).

7 protein biomarkers for MPV and PLT among 71 CVD-related plasma proteins measured in FHS (Framingham

8 intake assessment (170,076 all-cause, 50,786 CVD, and 59,684 cancer deaths) and 65,411 participants w

9 ing median 15-year follow-up, there were 911 CVD events (including 609 incidents of coronary heart di

10 olitical events, perceived stress, and acute CVD events.

11 California, hospitalization rates for acute CVD were compared in the time period immediately prior t

12 -shaped relationship between DBP and adverse CVD outcomes; including MI.

13 gher (ie, worse) HMS in univariate analyses; CVD and ARCD persisted in multivariate analyses.

14 s (1994-2002) through 2014 for all-cause and CVD mortality by data linkage to national registries.

15 people with T2DM to reduce risks for CKD and CVD in alignment with the clinical trial entry criteria.

16 icial for preventing physical disability and CVD but not beneficial for prolonging disability-free su

17 In patients with CKD, the kidney and CVD benefits of canagliflozin were established by the CR

18 been shown to influence host metabolism and CVD, sometimes through specific identified host receptor

19 use is associated with reduced mortality and CVD risk but only among never smokers.

20 nding of the relationship between the MT and CVD risk.

21 Age, kidney function status, and CVD events were the key determinants of subsequent morbi

22 sex, educational level, marital status, and CVD risk factors.

23 on compliance and reduced risk of stroke and CVD.

24 posite of myocardial infarction, stroke, and CVD mortality; hazard ratio [HR], 0.92 [95% CI, 0.80-1.0

25 The secondary outcome was report of any CVD event.

26 rdiovascular Disease Policy Model-Argentina (CVD Policy Model-Argentina), a local adaptation of a wel

27 get for treating dyslipidemia and associated CVD.

28 ential therapeutic targets for MS-associated CVD within pathways that were previously unknown to core

29 summarizes the evidence for atherosclerotic CVD in patients with RA and provides a contemporary anal

30 Pooled Cohort equations for atherosclerotic CVD within five years in a contemporary cohort of indivi

31 n increased risk of incident atherosclerotic CVD in women.

32 n Heart Association (10-year atherosclerotic CVD event risk, 5% to < 20%), CAC scoring may also provi

33 IL6R p.Asp358Ala attenuated CVD event risk among participants with large CHIP clones

34 even after adjustment, stress' attributable CVD risk is similar to those risk factors, suggesting it

35 ence rates of MACE in those without baseline CVD were compared with reported large contemporary popul

36 nsight into compelling commonalities between CVD and cancer, including shared mechanisms for disease

37 or, identifying patients at low risk of both CVD and non-CVD mortality.

38 pathophysiological processes common to both CVD and cancer, such as inflammation, resistance to cell

39 on, 10) years) free of known cardiovascular (CVD) had ankle brachial index (ABI) assessment of their

40 lone-equivalent dose had increased all-cause CVD risk (HR = 1.74; 95% confidence interval [CI] 1.64-1

41 c kidney disease-cardiovascular disease (CKD-CVD) health outcomes model, a Markov state transition mo

42 ce intervals (CIs) were calculated comparing CVD rates in the 2 d following the 2016 election to rate

43 ng phylloquinone (vitamin K-1) and confirmed CVD events and mortality.

44 functionality not accessible by conventional CVD growth.

45 an the temperature required for conventional CVD.

46 that approximately 16%-46% of the decreased CVD-related death rate from 1999 to 2014 may be attribut

47 Chemical vapor deposition (CVD) has become a promising approach for the industrial

48 ene substrates by chemical vapor deposition (CVD) is limited by slow lateral growth rates, which resu

49 ch can increase a woman's risk of developing CVD postmenopausally.

50 Cardiovascular disease (CVD) affects individuals of all races and ethnicities; h

51 h is associated with cardiovascular disease (CVD) and all-cause mortality.

52 the pathogenesis of cardiovascular disease (CVD) and Alzheimer's disease (AD).

53 Cardiovascular disease (CVD) and associated comorbidities increase the risk of c

54 Cardiovascular disease (CVD) and cancer are leading causes of morbidity and mort

55 ondary outcomes were cardiovascular disease (CVD) and cancer mortality.

56 n (MI), stroke (ST), cardiovascular disease (CVD) and chronic kidney disease (CKD).

57 de information about cardiovascular disease (CVD) but are only extremes of the pressure waveform duri

58 an important role in cardiovascular disease (CVD) development.

59 risk of death due to cardiovascular disease (CVD) differently in men versus women.

60 ts ability to add to cardiovascular disease (CVD) event prediction.

61 omen with underlying cardiovascular disease (CVD) followed by a cardio-obstetrics team.

62 Cardiovascular disease (CVD) has become an increasingly common limitation to eff

63 ins may help prevent cardiovascular disease (CVD) in people with HIV (PWH) with chronic inflammation

64 Cardiovascular disease (CVD) is the leading cause of death among American Indian

65 Cardiovascular disease (CVD) is the leading cause of death among women in the Un

66 Cardiovascular disease (CVD) is the leading cause of death in women, who have a

67 Cardiovascular disease (CVD) is the major cause of morbidity, mortality, and hea

68 ing dyslipidemia and cardiovascular disease (CVD) may increase the risk of fatty liver disease and ot

69 Whereas cardiovascular disease (CVD) metrics define risk in individuals >40 years of age

70 individual incident cardiovascular disease (CVD) outcomes including myocardial infarction (MI), isch

71 Cardiovascular disease (CVD) remains the leading cause of morbidity and mortalit

72 physical activity on cardiovascular disease (CVD) risk and overall mortality.

73 k factor control and cardiovascular disease (CVD) risk in type 2 diabetes and to assess if the presen

74 ) intake to decrease cardiovascular disease (CVD) risk, but there is limited evidence on scalable and

75 ction have increased cardiovascular disease (CVD) risk.

76 riers would decrease cardiovascular disease (CVD) risk.

77 under-represented in cardiovascular disease (CVD) specialties.

78 tant risk factor for cardiovascular disease (CVD) through increased levels of stress hormones and vas

79 11.7 years) without cardiovascular disease (CVD) were recruited from the Cardiac Ageing Study.

80 ity from all causes, cardiovascular disease (CVD), and cancer.

81 positively linked to cardiovascular disease (CVD), diabetes, cancer, and increased mortality.

82 Cardiovascular disease (CVD), including coronary artery disease, atrial fibrilla

83 jor risk factors for cardiovascular disease (CVD), often occur together.

84 iabetes mellitus and cardiovascular disease (CVD), pharmacologic agents used to treat type 2 diabetes

85 k of atherosclerotic cardiovascular disease (CVD), resulting in acute cardiovascular events, such as

86 ement strategies for cardiovascular disease (CVD), the leading cause of death in the world.

87 th increased risk of cardiovascular disease (CVD).

88 k of atherosclerotic cardiovascular disease (CVD).

89 s the major cause of cardiovascular disease (CVD).

90 h increased risk for cardiovascular disease (CVD).

91 ibute chronically to cardiovascular disease (CVD).

92 y of atherosclerotic cardiovascular disease (CVD).

93 sequences, including cardiovascular disease (CVD).

94 rst manifestation of cardiovascular disease (CVD).

95 excluding HCC), and cardiovascular disease (CVD).

96 tion between DBP and cardiovascular disease (CVD).

97 are risk factors for cardiovascular disease (CVD).

98 etermine the risk of cardiovascular disease (CVD).

99 in those at risk for cardiovascular disease (CVD).

100 th increased risk of cardiovascular disease (CVD).

101 h risk of developing cardiovascular disease (CVD).

102 APOE) genotype with cerebrovascular disease (CVD) in a large neuropathological database maintained by

103 arction (MI), acute cerebrovascular disease (CVD), major bleeding, and all-cause hospitalization.

104 ne hazard ratios for coronary heart disease, CVD, and all-cause mortality according to categories of

105 f CAC and subsequent coronary heart disease, CVD, and all-cause mortality.

106 gy, as well as with cardiovascular diseases (CVD).

107 Cardiovascular diseases (CVDs) are among the leading causes of mortality and morb

108 Cardiovascular diseases (CVDs) cause significant mortality globally.

109 closely linked with cardiovascular diseases (CVDs), but recent studies suggest that it is also a risk

110 Cardiovascular diseases (CVDs), principally ischemic heart disease (IHD) and stro

111 e and type-specific cardiovascular diseases (CVDs).

112 subsequent risk of cardiovascular diseases (CVDs).

113 d the treatment for cardiovascular diseases (CVDs).

114 tes >=65 years of age and free of documented CVD, dementia, and disability.

115 vascular events in patients with established CVD.

116 We examined CVD mortality rates between 2007 and 2017 among all New

117 Cardiovascular risk factors, CVD, and associated deaths were identified in Danish reg

118 confidence interval (CI): 1.06, 1.75), fatal CVD (HR = 2.05, 95% CI: 1.42, 2.97), and nonfatal CVD ev

119 , major adverse cardiovascular events, fatal CVD, myocardial infarction, and stroke.

120 of PA level with all-cause mortality, fatal CVD, and nonfatal CVD events.

121 for CVD and 0.07 (95% CI: 0.03 to 0.19) for CVD mortality, and the population attributable fractions

122 confidence interval [CI]: 0.09 to 0.22) for CVD and 0.07 (95% CI: 0.03 to 0.19) for CVD mortality, a

123 24.7 for stroke events, and 62.8 vs 53.5 for CVD events.

124 ty, 0.87 (95% CI: 0.82, 0.92; I2 = 3.7%) for CVD mortality, and 0.89 (95% CI: 0.85, 0.93; I2 = 0%) fo

125 gh) CVH were 0.63 (95% CI: 0.47 to 0.74) for CVD and 0.81 (95% CI: 0.55 to 0.92) for CVD mortality.

126 y, 0.89 (95% CI: 0.85, 0.94; I2 = 28.9%) for CVD mortality, and 0.91 (95% CI: 0.84, 0.98; I2 = 26.3%)

127 for CVD and 0.81 (95% CI: 0.55 to 0.92) for CVD mortality.

128 ventive care, or be treated aggressively for CVD.

129 Obesity remains a risk factor for CVD independent of major metabolic factors.

130 Additional risk factors for CVD include low-density lipoprotein cholesterol levels,

131 ion and timing may be novel risk factors for CVD, independent of traditional CVD risk factors and sle

132 Hospitalization for CVD was defined as an inpatient or emergency department

133 The same pattern was observed for CVD.

134 The unadjusted hazard ratio for CVD events comparing Black to White participants was 1.4

135 D and SCI-Diabetes, pooled hazard ratios for CVD associated with 5 risk factors being elevated versus

136 further clarified about recommendations for CVD prevention in patients with RA compared with the gen

137 is per se, is the main predictor of risk for CVD events and death.

138 risk factors associated with future risk for CVD.

139 aged to develop new treatment strategies for CVD and may inform how periodontal disease influences CV

140 95% CI 1.34-1.43, p < 0.001) and dying from CVD (HR 1.45, 95% CI 1.29-1.62, p < 0.001), as well as b

141 e would be predicted to benefit greatly from CVD risk factor intervention.

142 ression in VSMCs protects T2DM patients from CVD.

143 is alarming given that BL women suffer from CVD at an equivalent rate to BL men and each has a great

144 d health scores had highest hazard of future CVD.

145 er these inflammatory markers predict future CVD events, and are possible therapeutic targets among P

146 low across sociodemographic subgroups (e.g., CVD rates per 1,000 person-years: age 18 to 24 years, 0.

147 equations, we updated the Framingham general CVD 1991 and 2008 equations and the Pooled Cohort equati

148 In individuals at high CVD risk, an er-MedDiet with increased PA did not result

149 ly managed people with T2D have a 21% higher CVD risk when compared with controls.

150 Thicker choroid and higher CVD were also correlated with poor treatment response af

151 involving both microbe and host) both impact CVD in animal models and show striking clinical associat

152 ients, and an unmet need exists for improved CVD preventive measures for patients with RA.

153 scuss the clinical value of Alphabeta1-40 in CVD prognosis and patient risk stratification, and prese

154 A total of 86% of PDs felt diversity in CVD as a field needs to increase, and 70% agreed that tr

155 ormed to evaluate associated risk factors in CVD.

156 ation of causality of abnormal blood flow in CVD.

157 earch, with a relatively modest footprint in CVD.

158 A causal contribution for gut microbiota in CVD has been further supported by a multitude of more di

159 failure, or death), along with reductions in CVD events, were observed.

160 of follow-up, we documented 15,837 incident CVD cases, including 9,794 coronary heart disease (CHD)

161 omen; 35% nonwhite), there were 858 incident CVD events and 1209 deaths over a median of 13.0 y.

162 re followed for total mortality and incident CVD events/mortality.

163 -up, CHIP associated with increased incident CVD event risk (hazard ratio, 1.27 [95% CI, 1.04-1.56],

164 reased the risk of diabetes but not incident CVD.

165 s associated with increased risk of incident CVD.

166 ined myocardial-vascular score with incident CVD), such that young adults with poorer metabolite-base

167 ammatory diets are associated with increased CVD risk.

168 ay inform how periodontal disease influences CVD.

169 c health in risk stratification to interrupt CVD at its earliest stage are warranted.

170 s for these measures may yield insights into CVD mechanisms.

171 orrelation coefficients (ICCs) of five major CVD risk factors (raised blood glucose, raised blood pre

172 For major CVD events, a treatment benefit was seen in those with d

173 he primary cardiovascular end point of major CVD events (composite of myocardial infarction, stroke,

174 tamin D supplementation did not reduce major CVD events (HR, 0.97 [95% CI, 0.85-1.12]) or other cardi

175 e found smoking to be a risk factor for many CVDs even after adjusting for alcohol.

176 rved no differences in the risk of acute MI, CVD, major bleeding, or all-cause hospitalization after

177 180-day event rates per 100 patients for MI, CVD, major bleeding, and all-cause hospitalization were

178 For HF, MI, CVD, and CKD, register-based models outperformed a refer

179 ferences were identified for the risk of MI, CVD, major bleeding, or all-cause hospitalization when c

180 A validated microsimulation model, CVD-PREDICT (Cardiovascular Disease Policy Model for Ris

181 ltiple dVSMC properties and decreases murine CVD.

182 out self-reported depressive symptoms and no CVD history at baseline.

183 l infarction (MI; cases) and 182 PWH with no CVD (controls), we measured soluble markers of interleuk

184 ing patients at low risk of both CVD and non-CVD mortality.

185 HR = 2.05, 95% CI: 1.42, 2.97), and nonfatal CVD events (HR = 1.67, 95% CI: 1.18, 2.37) in comparison

186 all-cause mortality, fatal CVD, and nonfatal CVD events.

187 FKBPL was a determinant of CVD in the non-diabetic group in addition to age, gender

188 Among the various risk factors of CVD, environmental and dietary exposures to mercury (Hg)

189 Follow-up Study (1986-2016) who were free of CVD and cancer at baseline.

190 ely in white and black men and women free of CVD at index ages of <40, 40 to 59, and >=60 years.

191 with complete information and no history of CVD and cancer, the mean age at baseline was 50.9 (SD 10

192 Hazard ratios (HRs) of CVD < 1 year after initiation of BEP treatment were as f

193 development of dementia and the incidence of CVD in several populations, suggesting the presence of o

194 be associated with a decreased incidence of CVD in the entire population, suggesting that plant-base

195 ls >40 years of age, the earliest lesions of CVD appear well before this age.

196 ed graphene (NPG) with a typical mobility of CVD-grown graphene (up to 3000 [Formula: see text]), ens

197 te the incidence, consistency, and nature of CVD event reporting in cancer drug trials.

198 ased risk of all-cause mortality, but not of CVD.

199 7 to 550 million) in 2019, and the number of CVD deaths steadily increased from 12.1 million (95% UI:

200 on has a pivotal role in the pathogenesis of CVD.

201 deep-learning systems for the prediction of CVD on the basis of the features of retinal vessels in r

202 Over the past 50 years, the prevalence of CVD has been rising among American Indians and Alaska Na

203 (3) (2000 IU/d) in the primary prevention of CVD and cancer among 25 871 US men aged >=50 and women a

204 control fuels hope for future prevention of CVD associated with diabetes.

205 ation guideline on the primary prevention of CVD introduced the concept of risk-enhancing factors tha

206 al of rosuvastatin for primary prevention of CVD, component GRSs discriminate genetic risk associated

207 k of death, to estimate the lifetime risk of CVD (composite of incident myocardial infarction, stroke

208 SFs were associated with a decreased risk of CVD [HR: 0.80 (0.66, 0.98); P-trend = 0.01] and colorect

209 C should be emphasized to reduce the risk of CVD among hypertension patients.

210 efits of PUFA intake in lowering the risk of CVD and premature death.

211 One year after BEP treatment, the risk of CVD decreased to normal levels, but after 10 years, incr

212 The risk of CVD did not significantly differ according to circulatin

213 isk factors controlled) had a higher risk of CVD events (adjusted hazard ratio, 1.21; 95% confidence

214 Black individuals had a higher risk of CVD events and mortality after MI than White individuals

215 standard glucose-lowering therapy on risk of CVD events in the ACCORD (Action to Control Cardiovascul

216 Although this high risk of CVD has been known for decades, patients with RA receive

217 We estimated the 10-year predicted risk of CVD using the American College of Cardiology/American He

218 ased dietary patterns may modify the risk of CVD, regardless of genetic susceptibility.

219 healthful-PDI was related to a lower risk of CVD, regardless of low/high GRS-stroke.

220 een plasma kallikrein levels and the risk of CVD.

221 such transition affects risks of subtypes of CVD in Chinese adults.

222 Initially, the global burden of CVDs and the standard of care for the primary CVD catego

223 k is of great significance for the future of CVDs diagnosis, as it has the potential to reduce the ri

224 this study, we observed an increased risk of CVDs associated with glucocorticoid dose intake even at

225 etween influenza vaccination and the risk of CVDs.

226 we aimed to investigate the impact of COC on CVD risk among newly-diagnosed hypertension patients.

227 n understanding the impact of Pb exposure on CVD mortality risk in adults.

228 verse effect of increasing DBP increments on CVD outcomes, including MI (MI hazard ratio, 1.07 per un

229 protective role of influenza vaccination on CVDs events.

230 In particular, an optimal CVD-derived Fe-N-C catalyst exclusively contains atomica

231 ardial infarction, stroke, heart failure, or CVD death) separately in white and black men and women f

232 Incidences of NADM or CVD were independent of HCV group, whereas those cured h

233 les had no effect on blood pressure or other CVD markers.

234 h aura to CVD incidence in relation to other CVD risk factors remains unclear.

235 MicroRNA significant in this analysis plus CVD-associated microRNAs from the literature were then q

236 ty was associated with 0.18% lower predicted CVD risk (P=3.2x10(-4)).

237 age and strain in adults without preexisting CVD.

238 associated with very low rates of premature CVD and mortality over 32 years, indicating the critical

239 ould be a worthwhile strategy for preventing CVD and mortality among older Mexican Americans with ins

240 21.8-22.3) years of life if without previous CVD and 18.6 (18.2-18.9) years if with CVD.

241 For the no-previous-CVD phenotype, the effect of OSA showed an adjusted haza

242 4; P value = 0.02), whereas for the previous-CVD phenotype, the effect of OSA showed an adjusted haza

243 VDs and the standard of care for the primary CVD categories, namely heart failure (HF) and acute coro

244 Community-based interventions have reduced CVD risk in American Indians and Alaska Natives.

245 and prevention programming aimed at reducing CVD in India.

246 inistration (FDA) drug reviews, all reported CVD events across latter-phase (II and III) trials suppo

247 emporary FDA-approved cancer drugs, reported CVD event rates trail expected population rates.

248 There was no association between reporting CVD events and drug efficacy (hazard ratio: 0.68 vs. 0.6

249 patients with diabetes have a high residual CVD risk.

250 with RA receive poorer primary and secondary CVD preventive care than other high-risk patients, and a

251 moking retained its association with several CVD outcomes including MI (OR = 1.84, 95% CI, 1.43, 2.37

252 HRs for type-specific CVDs and <5.0-mg daily dose use were: 1.69 (95% CI 1.54-

253 ase activity level and for all type-specific CVDs.

254 actor profile, the absolute age-standardized CVD mortality gap would decline by 33.3% (95% CI 25.1-40

255 The age-standardized CVD mortality rate was 2.7/1000 person-years among both

256 to doing so, applying it to the substantial CVD mortality gap between Russia and Norway using survey

257 er, in the conventional hot-wall CVD system, CVD-derived graphene films suffer from surface contamina

258 The CVD stagnation held back the increase of US life expecta

259 clinical trials designed to demonstrate the CVD safety of SGLT2 inhibitors in type 2 diabetes mellit

260 Our aim was to investigate the CVD events (CVDEs) and survival between the patients wit

261 t remains unknown how characteristics of the CVD learning environment affect diversity and how progra

262 aimed to investigate characteristics of the CVD learning environment that may affect diversity and s

263 ginal Framingham equations overestimated the CVD risk, whereas the original Pooled Cohort equations u

264 All persons, regardless of their CVD risk status, benefit from healthy eating behaviors a

265 of this composite and outcomes according to CVD history at baseline.

266 solute contribution of migraine with aura to CVD incidence in relation to other CVD risk factors rema

267 in which cytotoxic CD4 T cells contribute to CVD in HIV/CMV coinfection and in atherosclerosis via CX

268 erious effect of OSA and its contribution to CVD could depend on specific patient profiles.Objectives

269 Importantly, a causal link to CVD for these and other specific gut microbial metabolit

270 xisting data on the MT and how it relates to CVD.

271 athways of metabolic dysfunction relevant to CVD, associated with outcome in 2 independent cohorts.

272 onological and ovarian aging with respect to CVD risk.

273 Prevalent cases of total CVD nearly doubled from 271 million (95% uncertainty int

274 factors for CVD, independent of traditional CVD risk factors and sleep quantity and/or quality.

275 sed, and this was independent of traditional CVD risk factors.

276 anced seroconversion to oral cholera vaccine CVD 103-HgR among H. pylori seropositive African adults

277 nction and subsequent development of various CVDs.

278 Shown here is that the cold-wall CVD system is capable of suppressing the gas-phase react

279 However, in the conventional hot-wall CVD system, CVD-derived graphene films suffer from surfa

280 Yet, whether CVD events were consistently reported in pivotal trials

281 recommends offering or referring adults with CVD risk factors to behavioral counseling interventions

282 t mixtures if they are to be associated with CVD and all-cause mortality risk reduction.

283 iomarkers were independently associated with CVD events after adjustment for traditionally defined MH

284 or alcohol consumption to be associated with CVD risk factors, including high-density lipoprotein cho

285 remains common in HIV and is associated with CVD, ARCD, and to a lesser extent, HAND.

286 king, vigorous activity) in association with CVD risk and overall mortality.

287 ith an elevated risk of being diagnosed with CVD (HR 1.39, 95% CI 1.34-1.43, p < 0.001) and dying fro

288 vious CVD and 18.6 (18.2-18.9) years if with CVD.

289 age 29 years, 52.9% Hispanic or Latino) with CVD were seen.

290 ne versus 0.8% with placebo in patients with CVD and 2.2% with finerenone versus 1.0% with placebo in

291 e inverse associations of healthful-PDI with CVD were consistently observed in people with low GRS-MI

292 Persons with CVD represent an important target population for respira

293 selenium alone or antioxidants was seen with CVD and all-cause mortality.

294 e determined associations of HIV status with CVD mortality by sex and neighborhood poverty, defined a

295 dividuals without CVD; 64%-76% of those with CVD) was projected to increase their life expectancy by

296 icrovascular geometry, among Chinese without CVD.

297 ls (29%-44% of indicated individuals without CVD; 64%-76% of those with CVD) was projected to increas

298 versus 1.0% with placebo in patients without CVD).

299 s metabolic syndrome or an estimated 10-year CVD risk of 7.5% or greater.

300 r 3 years follow-up (SCI-Diabetes: 6 years), CVD events occurred among 27 900 (27%) CPRD-T2D, 101 362