ライフサイエンスコーパス: ASCVD

1 ASCVD prevalence in those with CTD was 29.7% for African

2 ASCVD risk management of patients with IBD is challengin

3 ASCVD risk was estimated using the pooled cohort equatio

4 ASCVD risk-reduction interventions including statin ther

5 ASCVD was defined as a first nonfatal myocardial infarct

6 ASCVD was defined as myocardial infarction, coronary hea

7 ASCVD was defined as myocardial infarction, coronary or

8 ASCVD was documented in 35.6% of patients, and statin in

9 Among 6,749 participants, 1,002 ASCVD events occurred during a median follow-up of 15 ye

10 tiple prior ASCVD events versus 10.7% with 1 ASCVD event and multiple high-risk conditions.

11 , 56% women, 23% black, 44% with FHx), 3,114 ASCVD events were observed during 21 years of follow-up.

12 curred in 84 participants with diabetes (135 ASCVD events), 115 with MetS (175 ASCVD events), and 157

13 betes (135 ASCVD events), 115 with MetS (175 ASCVD events), and 157 with neither (250 ASCVD events).

14 After 10 years of follow-up, 320 (6.2%) ASCVD events occurred.

15 175 ASCVD events), and 157 with neither (250 ASCVD events).

16 of 10.2 years of follow-up (2000-2012), 556 ASCVD events (8.2%) and 539 AFib events (7.9%) occurred.

17 risk was estimated by using the 2013 ACC/AHA ASCVD risk calculator.

18 vement among participants who experienced an ASCVD event (0.390; 95% CI, 0.312-0.467 vs 0.08; 95% CI

19 nificantly increased risk of experiencing an ASCVD event or death compared with individuals with neit

20 For example, among those with an ASCVD risk of <15% and who had an SBP of either 120 to 1

21 d the association between elevated Lp(a) and ASCVD events among family members.

22 part of inflammation in atherosclerosis and ASCVD is because of triglyceride-rich lipoprotein degrad

23 e was also a prognostic indicator of CHD and ASCVD after controlling for diabetes duration of 10 year

24 ndrome (MetS) or diabetes identifies CHD and ASCVD prognostic indicators during a long follow-up peri

25 ong-term prognostication of incident CHD and ASCVD using CAC scores among those with diabetes, MetS,

26 arge U.S. academic center identified CTD and ASCVD status for 287,467 African American and white adul

27 rotein significantly improved global CVD and ASCVD risk assessment.

28 , use of ezetimibe, coexistent diabetes, and ASCVD status can bear significantly on the likelihood of

29 t heart failure, or atrial fibrillation) and ASCVD (fatal or nonfatal myocardial infarction or stroke

30 rtiles of race/ethnicity-specific height and ASCVD/AFib events in our multivariable models.

31 es the epidemiological links between IBD and ASCVD and potential mechanisms underlying these associat

32 LDL-C polygenic score with LDL-C levels and ASCVD risk using linear regression and Cox-proportional

33 association between certain metabolites and ASCVD.

34 e heterogeneity in clinical presentation and ASCVD risk for individuals with FH.

35 btained from electronic medical records, and ASCVD events were ascertained by using validated algorit

36 iated with hematologic malignancy as well as ASCVD independently of age and other traditional risk fa

37 ege of Cardiology/American Heart Association ASCVD Pooled Cohort Risk Equations.

38 d 24-h BP for patients with varying baseline ASCVD risk scores, which was sustained to 3 years.

39 and had data on factors needed to calculate ASCVD risk.

40 or statin-treated participants with clinical ASCVD and comorbidities, and 20% to 29% (high risk) for

41 ar outcomes trials in patients with clinical ASCVD and in a smaller number of high-risk primary preve

42 ions are provided for patients with clinical ASCVD with or without comorbidities on statin therapy fo

43 d PCSK9 inhibitors in patients with clinical ASCVD with or without comorbidities.

44 Thus, we compared ASCVD risk reduction and T2D incidence increases across

45 For the composite ASCVD outcome there were 123 379 events, with 66.3 and 7

46 rlap between these groups, and corresponding ASCVD incidence rates.

47 e 10-year risk for hard atherosclerotic CVD (ASCVD) following the ACC/AHA guideline, 10-year risk of

48 nts: Women with 10-year atherosclerotic CVD (ASCVD) risk lower than 7.5% from 5 large population-base

49 a narrow focus on only atherosclerotic CVD (ASCVD).

50 k of atherosclerotic cardiovascular disease (ASCVD) and are prone to statin-related adverse events fr

51 with atherosclerotic cardiovascular disease (ASCVD) and CHD among asymptomatic subjects.

52 k of atherosclerotic cardiovascular disease (ASCVD) and to define high-risk and very high-risk patien

53 for atherosclerotic cardiovascular disease (ASCVD) associated with their CTD.

54 e of atherosclerosis cardiovascular disease (ASCVD) beyond well-established risk factors.

55 k of atherosclerotic cardiovascular disease (ASCVD) by implementing cardiovascular preventive strateg

56 ised Atherosclerotic Cardiovascular Disease (ASCVD) calculator.

57 ajor atherosclerotic cardiovascular disease (ASCVD) event or a single ASCVD event and multiple high-r

58 for atherosclerotic cardiovascular disease (ASCVD) events in contemporary and ethnically diverse pop

59 dent atherosclerotic cardiovascular disease (ASCVD) events, and atrial fibrillation (AFib) in a multi

60 icts atherosclerotic cardiovascular disease (ASCVD) events, inclusive of coronary heart disease (CHD)

61 for atherosclerotic cardiovascular disease (ASCVD) events.

62 for atherosclerotic cardiovascular disease (ASCVD) events.

63 duce atherosclerotic cardiovascular disease (ASCVD) events.

64 n of atherosclerotic cardiovascular disease (ASCVD) in adults 75 years and older.

65 for atherosclerotic cardiovascular disease (ASCVD) in familial hypercholesterolemia (FH) have been d

66 Atherosclerotic cardiovascular disease (ASCVD) is associated with significant morbidity and mort

67 s of atherosclerotic cardiovascular disease (ASCVD) risk are needed in older adults.

68 gher atherosclerotic cardiovascular disease (ASCVD) risk but not at high risk of bleeding.

69 year atherosclerotic cardiovascular disease (ASCVD) risk in diabetes mellitus patients is used to gui

70 the Atherosclerotic Cardiovascular Disease (ASCVD) risk score and the Framingham Heart Study Global

71 ACC) atherosclerosis cardiovascular disease (ASCVD) risk score.

72 e of atherosclerotic cardiovascular disease (ASCVD) risk to personalize systolic blood pressure (SBP)

73 cted atherosclerotic cardiovascular disease (ASCVD) risk, calculated using the pooled cohort risk equ

74 t of atherosclerotic cardiovascular disease (ASCVD) risk.

75 and atherosclerotic cardiovascular disease (ASCVD) risk.

76 ause atherosclerotic cardiovascular disease (ASCVD) to being innocent bystanders.

77 with atherosclerotic cardiovascular disease (ASCVD), a group who requires long-term therapy for secon

78 with atherosclerotic cardiovascular disease (ASCVD), guidelines recommend optimizing statin treatment

79 dent atherosclerotic cardiovascular disease (ASCVD), heart failure (HF), and chronic kidney disease (

80 ajor atherosclerotic cardiovascular disease (ASCVD)-related events; second, to evaluate the relative

81 e to atherosclerotic cardiovascular disease (ASCVD).

82 and atherosclerotic cardiovascular disease (ASCVD).

83 n of atherosclerotic cardiovascular disease (ASCVD).

84 for atherosclerotic cardiovascular disease (ASCVD).

85 ical atherosclerotic cardiovascular disease (ASCVD).

86 had atherosclerotic cardiovascular disease (ASCVD).

87 for atherosclerotic cardiovascular disease (ASCVD).

88 t of atherosclerotic cardiovascular disease (ASCVD).

89 n of atherosclerotic cardiovascular disease (ASCVD).

90 with atherosclerotic cardiovascular disease (ASCVD).

91 for atherosclerotic cardiovascular disease (ASCVD).

92 ture atherosclerotic cardiovascular disease (ASCVD).

93 ased atherosclerotic cardiovascular disease (ASCVD).

94 ture atherosclerotic cardiovascular disease (ASCVD).

95 n of atherosclerotic cardiovascular disease (ASCVD).

96 ture atherosclerotic cardiovascular disease (ASCVD).

97 and atherosclerotic cardiovascular disease (ASCVD).

98 To describe the prevalence of elevated ASCVD risk among nondiabetic adults younger than 50 year

99 es is evaluated, and strategies for enhanced ASCVD risk reduction in patients with IBD are outlined.

100 ral adult population, those with established ASCVD, and those at risk for ASCVD.

101 Among those with established ASCVD, statin use was 49.8% and 58.1% in 2002-2003 and 2

102 r, is underused in patients with established ASCVD.

103 ociation guidelines and using >20% estimated ASCVD risk to define higher risk.

104 han or similar to the NNH(5) among estimated ASCVD risk strata.

105 particularly among adults with an estimated ASCVD risk of 5% to 15% and prehypertension or mild hype

106 Existing ASCVD risk equations overestimate risk in veterans with

107 (discordance 38%) resulted in the following ASCVD event rates: hs-cTnT < LoD/CAC = 0: 2.8 per 1,000

108 were followed through December 31, 2017, for ASCVD events, including myocardial infarction, ischemic

109 1 (95% confidence interval, 0.640-0.723) for ASCVD risk and 0.703 (95% confidence interval, 0.663-0.7

110 cation of Diseases, Ninth Revision codes for ASCVD on 2 or more different dates in the prior 2 years.

111 l (LDL-C) are an independent risk factor for ASCVD, and clinical trial data have shown that lowering

112 t that IBD is an independent risk factor for ASCVD.

113 Patients were followed for ASCVD events comprising CHD, cerebrovascular disease, an

114 No sex- or race-based CAC interactions for ASCVD, CHD, and stroke events were observed.

115 The age- and sex-adjusted hazard ratios for ASCVD events among patients with very high risk, overall

116 ticipants (21.2%), who were at high risk for ASCVD (21.5 per 1000 person-years).

117 etectable hs-cTnT (32%) had similar risk for ASCVD as did those with a CAC of zero (50%) (5.2 vs. 5.0

118 tifies patients with a similar, low risk for ASCVD as those with a CAC score of zero.

119 n more accurate reclassification of risk for ASCVD events among these individuals.

120 al of this study was to compare the risk for ASCVD events and the use of statins among patients with

121 Very high risk for ASCVD events was defined as a history of >=2 major ASCVD

122 Despite having high risk for ASCVD events, patients with PAD were less likely to be t

123 in persons who have or are at high risk for ASCVD.

124 400 cells/muL and with/at increased risk for ASCVD.

125 ing in childhood to reduce lifetime risk for ASCVD.

126 ith established ASCVD, and those at risk for ASCVD.

127 ificant but opposite association with future ASCVD and AFib (hazard ratios were 0.72 (95% confidence

128 ombined CAC imaging and assessment of global ASCVD risk has the potential to guide personalized SBP g

129 -lowering therapy to adults with a very high ASCVD event rate.

130 Higher ASCVD risk was associated with an increased prevalence o

131 r stratification by sex (for every 1% higher ASCVD risk, year 4 NPZ-4 was lower by 0.84 [SD, 0.28] ov

132 or statins by USPSTF guidelines had a higher ASCVD event rate in the presence of CAC (2.8 per 1000 pe

133 ither elevated Lp(a) or FHx were at a higher ASCVD risk, while those with both had the highest risk (

134 apy, there was minimal evidence for improved ASCVD risk or adverse events with cholesterol-ester tran

135 ess whether CAC was associated with improved ASCVD risk predictions beyond the traditional risk facto

136 In ASCVD, adding PCSK9 inhibitors to statins was estimated

137 muscle (LTL/MTLA) was smaller (P=0.0001) in ASCVD than in controls.

138 e LTL-MTLA gap similarly widened with age in ASCVD patients and controls.

139 model shows more pronounced LTL attrition in ASCVD patients than controls.

140 ) and FHx resulted in greater improvement in ASCVD and CHD risk reclassification and discrimination i

141 be a major explanation of the shorter LTL in ASCVD patients.

142 for 32.0% of census tract-level variation in ASCVD event rates, compared with 10.0% accounted for by

143 account for neighborhood-level variation in ASCVD event rates.

144 Incident ASCVD events including coronary heart disease (CHD) and

145 nic, 49% CAC=0, 19% CAC >=100), 574 incident ASCVD events (333 CHD and 241 stroke) were observed over

146 abdominal aortic calcium score, and incident ASCVD (ie, myocardial infarction, ischemic stroke, or fa

147 iscriminate patients who experience incident ASCVD from those who did not over time.

148 tery calcium (CAC) score vs age for incident ASCVD and how risk prediction changes by adding CAC scor

149 at enrollment and were followed for incident ASCVD events.

150 (5.1%) suffered fatal and nonfatal incident ASCVD, respectively.

151 vels were independent predictors of incident ASCVD from which a risk equation with a Harrell C index

152 The risk of incident ASCVD may be estimated in patients with FH with simple c

153 ratios for the composite outcome of incident ASCVD or heart failure after further stratifying by CAC

154 en described, models for predicting incident ASCVD have not been reported.

155 ine key risk factors for predicting incident ASCVD in patients with FH.

156 Atherosclerosis) in relationship to incident ASCVD.

157 omes and Measures: Main outcome was incident ASCVD, including nonfatal myocardial infarction, coronar

158 s not significantly associated with incident ASCVD (n = 1386 events; median follow-up, 25.2 years; ha

159 Adults with HIV and increased ASCVD risk treated with LDMTX had more safety events tha

160 ; other inflammatory arthropathy), increased ASCVD rates were found in nearly all subsets, always wit

161 of risk factors, the prevalence of increased ASCVD risk is low among women younger than 50 and men yo

162 as associated with a trend towards increased ASCVD risk in all 3 cohorts individually.

163 sal risk factors for low-grade inflammation, ASCVD, and all-cause mortality.

164 aimed to evaluate risk equations for initial ASCVD events in US veterans with diabetes mellitus and i

165 lar calcification and at low to intermediate ASCVD risk.

166 with statins alone in individuals with known ASCVD or at high risk of ASCVD.

167 The main analyses excluded those with known ASCVD, diabetes mellitus, low-density lipoprotein choles

168 ded adults older than 60 years without known ASCVD at baseline.

169 Adults aged 30 to 49 years without known ASCVD or diabetes.

170 ended use of the Million Hearts Longitudinal ASCVD Risk Assessment Tool.

171 or ASCVD events and 7485 (62.7%) had 1 major ASCVD event and multiple high-risk conditions.

172 ASCVD events; hazard ratio=0.82 for 1 major ASCVD event and multiple high-risk conditions; P(interac

173 Among patients with >=2 major ASCVD events and with 1 event and >=2 high-risk conditio

174 with very high risk, overall, with >=2 major ASCVD events and with 1 event and >=2 high-risk conditio

175 events was defined as a history of >=2 major ASCVD events or 1 event and >=2 high-risk conditions.

176 baseline to the first occurrence of a major ASCVD event (myocardial infarction, stroke, or cardiovas

177 hout prevalent ASCVD underwent assessment of ASCVD risk.

178 overlooked as a contributor to the burden of ASCVD among young and middle-age adults, but meta-analys

179 -concordant practice to reduce the burden of ASCVD.

180 Secondary outcomes included a composite of ASCVD events (myocardial infarction, ischemic stroke, an

181 0.92 (95% CI, 0.91-0.94) for a composite of ASCVD events when comparing statin users with nonusers.

182 h person without an established diagnosis of ASCVD before enrollment in the registry by use of the SA

183 Discrimination of ASCVD events by the PCE was improved by deriving VA-spec

184 Although the discrimination of ASCVD risk for masked hypertension was not superior to c

185 vational studies were used for estimation of ASCVD risk.

186 SCVD beyond some well-established factors of ASCVD, and also suggest a potential utility of the ident

187 n (hsCRP) levels, and family history (FH) of ASCVD to the PCE in participants of MESA (Multi-Ethnic S

188 g US veterans 75 years and older and free of ASCVD at baseline, new statin use was significantly asso

189 ) data on adults 75 years and older, free of ASCVD, and with a clinical visit in 2002-2012.

190 the MarketScan database who had a history of ASCVD on January 1, 2016 (n = 27,775) were analyzed.

191 mendations among adults without a history of ASCVD or T2D who were eligible for statin treatment init

192 e event rates among adults with a history of ASCVD who met and did not meet the definition of very hi

193 iduals >=18 years with a reported history of ASCVD.

194 These individuals had low incidence of ASCVD (3.3 per 1000 person-years).

195 s associated with a 50% reduced incidence of ASCVD in those with CAC (5.4% vs. 10.5%; p = 0.003), FH

196 en SBP was 160 to 179 mm Hg, irrespective of ASCVD risk level.

197 or without (n=128) clinical manifestation of ASCVD.

198 Overall, the number of ASCVD events prevented was at least twice as large as th

199 f T2D cases incurred surpassed the number of ASCVD events prevented when higher statin-associated T2D

200 genetic variants that increase prediction of ASCVD beyond some well-established factors of ASCVD, and

201 es, are strong and independent predictors of ASCVD and all-cause mortality, and that their cholestero

202 , ABI, and FH were independent predictors of ASCVD events in the multivariable Cox models.

203 , ABI, and FH were independent predictors of ASCVD events.

204 holesterol likewise are strong predictors of ASCVD.

205 ing statin therapy for primary prevention of ASCVD (net 221 individuals appropriately downclassified

206 PCSK9) inhibitors in secondary prevention of ASCVD.

207 py in older adults for primary prevention of ASCVD.

208 h-risk comorbidities and across the range of ASCVD risk scores.

209 1.21 to 1.77; p < 0.001) had higher rates of ASCVD than those with undetectable results.

210 The prevalence ratio of ASCVD was particularly high in young African Americans.

211 disadvantage may be a powerful regulator of ASCVD event risk.

212 For patients at high risk of ASCVD already on background statin therapy, there was mi

213 dient-response fashion) with reduced risk of ASCVD events and increased risk of AFib.

214 lygenic score on levels of LDL-C and risk of ASCVD for individuals with monogenic FH.

215 tives with high Lp(a) and heightened risk of ASCVD, particularly when the proband has both FH and ele

216 ividuals with known ASCVD or at high risk of ASCVD.

217 dual variability in LDL-C levels and risk of ASCVD.

218 % CI, 2.40-3.47]), but the direct effects on ASCVD were poorly reported.

219 number needed to treat (NNT) to prevent one ASCVD event and the number needed to harm (NNH) to incur

220 itor use in patients with heterozygous FH or ASCVD did not meet generally acceptable incremental cost

221 nhibitors or ezetimibe in heterozygous FH or ASCVD.

222 h participants in the lowest (<5%) predicted ASCVD risk category, multivariable-adjusted prevalence r

223 both masked hypertension and high predicted ASCVD risk.

224 ks-to determine the association of predicted ASCVD risk with masked hypertension.

225 ially according to CAC levels when predicted ASCVD risk <15% and SBP <160mmHg (eg, 10-year number-nee

226 In each 5-year predicted ASCVD risk category, observed 5-year ASCVD risk was subs

227 Ten-year predicted ASCVD risk was calculated using the pooled cohort risk e

228 However, whether it predicts ASCVD beyond validated novel risk markers is unknown.

229 iduals aged 40 to 75 years without prevalent ASCVD underwent assessment of ASCVD risk.

230 Statins are being studied to prevent ASCVD in human immunodeficiency virus (HIV), but little

231 , ezetimibe use, and the absence of previous ASCVD were predictors of the attainment of LDL-C goals.

232 Age, male sex, history of previous ASCVD, high blood pressure, increased body mass index, a

233 population with FH with or without previous ASCVD.

234 BP-lowering therapy, and statins for primary ASCVD prevention and tobacco cessation drugs for smoking

235 fied as VHR: 4450 (37.3%) had multiple prior ASCVD events and 7485 (62.7%) had 1 major ASCVD event an

236 events occurred in 20.4% with multiple prior ASCVD events versus 10.7% with 1 ASCVD event and multipl

237 nd among patients at VHR with multiple prior ASCVD events versus a single prior ASCVD event (2.4% ver

238 group (hazard ratio=0.86 for multiple prior ASCVD events; hazard ratio=0.82 for 1 major ASCVD event

239 ple prior ASCVD events versus a single prior ASCVD event (2.4% versus 1.8%; P(interaction)=0.661).

240 lts with diabetes mellitus and without prior ASCVD who received care in the Veterans Affairs Healthca

241 ove adherence to essential therapy to reduce ASCVD morbidity and mortality.

242 pid-modifying therapies to statins to reduce ASCVD risk, we found evidence of benefit for ezetimibe a

243 Reduced ASCVD mortality rate was reported for 1 PCSK9 inhibitor.

244 There was evidence for reduced ASCVD morbidity with ezetimibe and 2 PSCK9 inhibitors.

245 ects on over 350 plasma proteins in relevant ASCVD pathways among HIV and non-HIV groups.

246 Similar ASCVD risk overestimation and poor calibration with mode

247 iovascular disease (ASCVD) event or a single ASCVD event and multiple high-risk conditions.

248 cluded in the analysis, the age-standardized ASCVD event rate per 1,000 person-years for those with a

249 In the general US population, the long-term ASCVD burden related to phenotypic FH, defined by low-de

250 The ASCVD event rate among patients with PAD only, CHD only,

251 th 1 event and >=2 high-risk conditions, the ASCVD event rate per 1,000 person-years was 89.8 (95% CI

252 nd with CHD and cerebrovascular disease, the ASCVD event rate was 72.8 (95% CI: 71.0 to 74.7), 63.9 (

253 ed only for cognitive function at entry, the ASCVD risk score significantly predicted year 4 NPZ-4 in

254 the Dallas Health Study were similar for the ASCVD outcome.

255 tins in the overall cohort (4.8%) and in the ASCVD cohort (4.3%) (P < .01 for slope for both).

256 cation) and 67.0% (after publication) in the ASCVD cohort, 50.6% (before publication) and 52.3% (afte

257 to high-intensity statins overall and in the ASCVD cohort, such a trend was already present before pu

258 ic height and sex was not significant in the ASCVD model (P = 0.78) but was significant in the AFib m

259 atients with and without very high risk, the ASCVD event rate per 1,000 person-years was 53.1 (95% co

260 uate baseline hs-cTnT and CAC in relation to ASCVD.

261 or nonfatal myocardial infarction) and total ASCVD (CHD or stroke).

262 lar patterns of results were found for total ASCVD risk, with hazard ratios up to 4.1 (95% confidence

263 The PCERM systematically underpredicted ASCVD event risk among patients from disadvantaged commu

264 strata when SBP was 160 to 179 mm Hg or when ASCVD risk was >/=15% at any SBP level.

265 Overall, 15,366 patients (55.3%) with ASCVD met the definition of very high risk.

266 sample included 509766 eligible adults with ASCVD at baseline (mean [SD] age, 68.5 [8.8] years; 4995

267 ted Lp(a) were independently associated with ASCVD (hazard ratio [HR]: 1.17; 95% confidence interval

268 ore >=100) was independently associated with ASCVD and CHD risk in all groups and with stroke risk in

269 High CAC burden comparably associated with ASCVD risk across sex and race groups.

270 Because the implication of CHIP with ASCVD, genetic loss-of-function studies of Tet2 and Dnmt

271 Of the 14 279 surveyed individuals with ASCVD, a weighted 12.6% (or 2.2 million [95% CI, 2.1-2.4

272 n about the temporal association of LTL with ASCVD.

273 However, few participants with ASCVD risk <5% had elevated CAC.

274 o identify a cohort of 105 269 patients with ASCVD enrolled from January 1, 2012, through December 31

275 One in 8 patients with ASCVD reports nonadherence to medications because of cos

276 MTLA (P=0.90), was shorter in patients with ASCVD than controls.

277 To estimate the percentage of patients with ASCVD who would require a PCSK9 inhibitor when oral lipi

278 tality in a national sample of patients with ASCVD.

279 Use of LLT among the population with ASCVD and distributions of LDL-C levels under various tr

280 ractice regarding LLT in the population with ASCVD.

281 2-2.16), and 1.91 (1.47-2.48) for those with ASCVD risk of 5% to <7.5%, 7.5% to <10%, and >/=10%, res

282 s, and 20% to 29% (high risk) for those with ASCVD without comorbidities or who have heterozygous fam

283 nducted of patients aged 21 to 84 years with ASCVD treated in the Veterans Affairs health care system

284 00, NNT(5)=140 versus NNH(5)=518) and within ASCVD risk strata.

285 ithout diabetes mellitus or patients without ASCVD and LDL-C >/=190 mg/dL not due to secondary causes

286 did not have a significantly higher 10-year ASCVD event rate in the presence of CAC, African America

287 eligible by ACC/AHA guidelines, the 10-year ASCVD incidence per 1000 person-years was 8.1 (95% CI, 5

288 gibility was determined by predicted 10-year ASCVD risk (5%, 7.5%, or 10%).

289 Hg, and 160-179 mm Hg) and estimated 10-year ASCVD risk (using the American College of Cardiology/Ame

290 Baseline 10-year ASCVD risk and FRS predicted future cognitive function i

291 In multivariable models, higher 10-year ASCVD risk and FRS predicted lower NPZ-4 in women.

292 ans to estimate baseline and updated 10-year ASCVD risk estimates for primary prevention patients adh

293 es of adults in each subgroup with a 10-year ASCVD risk greater than 5% and of those with an LDL-C le

294 The 10-year ASCVD risk is at least 30% (very high risk) for statin-t

295 ication) in the remaining group with 10-year ASCVD risk of 7.5% or higher.

296 mean age, 52 years; 20% women), mean 10-year ASCVD risk score at entry into the cohort was 6.8% (stan

297 10-year ASCVD risk was estimated by using the 2013 ACC/AHA ASCVD

298 vantage index (NDI) and the predicted 5-year ASCVD event rate from the Pooled Cohort Equations Risk M

299 edicted ASCVD risk category, observed 5-year ASCVD risk was substantially lower: 0.20% for predicted

300 We compared predicted versus observed 5-year ASCVD risk, overall and according to sex and race/ethnic