ライフサイエンスコーパス: ASCVD

1 ASCVD mortality rates in DP and in the GP were significa

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

3 ASCVD was defined as a first nonfatal myocardial infarct

4 ASCVD was defined as myocardial infarction, coronary hea

5 ASCVD was defined as myocardial infarction, coronary hea

6 We observed 2,061 ASCVD events during 1,515,142 person-years.

7 he number needed to treat (NNT) to prevent 1 ASCVD event over 5 years for each patient group and to a

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

9 A total of 165 ASCVD events occurred (64 nonfatal myocardial infarction

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

11 mmended statins, 41% had CAC = 0 and had 5.2 ASCVD events/1,000 person-years.

12 ,129,205 (96.1%) were statin-eligible (91.2% ASCVD, 6.6% diabetes, 0.3% off-treatment LDL-C >/=190 mg

13 A total of 247 (5.2%) ASCVD and 155 (3.3%) hard coronary heart disease 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 sease (ASCVD) with statins based on absolute ASCVD risk assessment.

18 The new AHA-ACC-ASCVD and 3 older Framingham-based risk scores overestim

19 Observed and expected events for the AHA-ACC-ASCVD score were compared with 4 commonly used risk scor

20 5 risk scores, 4, including the new AHA-ACC-ASCVD score, showed overestimation of risk (25% to 115%)

21 -specific activation of RCT protects against ASCVD in mice.

22 ne is a key target for new therapies against ASCVD.

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

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

25 ity statin, 338 (57%) had a CAC = 0, with an ASCVD event rate of 1.5 per 1,000 person-years.

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

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

28 ectional, multinational study, all-cause and ASCVD mortality rates were compared between GP and DP us

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

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

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

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

33 rotein significantly improved global CVD and ASCVD risk assessment.

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

35 trategy in the treatment of dyslipidemia and ASCVD.

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

37 es of effort, unhealthy lifestyle habits and ASCVD risk factor levels remain high and are increasing

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

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

40 the observed disproportionate CTD-associated ASCVD in African Americans, young adults, and those with

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

42 ttributable to the variability in background ASCVD mortality rates in the respective GP.

43 assessed among participants without baseline ASCVD who were enrolled in the Dallas Heart Study (DHS).

44 disease (ASCVD) and have potential for broad ASCVD prevention.

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

46 multiethnic cohort without baseline clinical ASCVD.

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

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

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

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

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

52 In the base-case scenario, the current ASCVD threshold of 7.5% or higher, which was estimated t

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

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

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

56 However, CIMT did not discriminate ASCVD (P=0.70).

57 Atherosclerotic cardiovascular disease (ASCVD) affects more than 1 in 3 American adults.

58 ) or atherosclerotic cardiovascular disease (ASCVD) and have potential for broad ASCVD prevention.

59 n of atherosclerotic cardiovascular disease (ASCVD) and probably in patients with diabetes without AS

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

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

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

63 Atherosclerotic cardiovascular disease (ASCVD) continues to increase annually in the United Stat

64 cing atherosclerotic cardiovascular disease (ASCVD) events by lowering blood cholesterol.

65 for atherosclerotic cardiovascular disease (ASCVD) events given its important etiologic role in athe

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

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

68 Atherosclerotic cardiovascular disease (ASCVD) events, including coronary heart disease and stro

69 d to atherosclerotic cardiovascular disease (ASCVD) in dialysis populations (DP) and in the backgroun

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

71 for atherosclerotic cardiovascular disease (ASCVD) in primary prevention.

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

73 t of atherosclerotic cardiovascular disease (ASCVD) is essential to effectively balance the risks and

74 Atherosclerotic cardiovascular disease (ASCVD) is the leading cause of death in developed and de

75 but atherosclerotic cardiovascular disease (ASCVD) outcomes of FH in the general US population have

76 year atherosclerotic cardiovascular disease (ASCVD) risk >/=7.5% based on traditional risk factors.

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

78 ical atherosclerotic cardiovascular disease (ASCVD) risk at enrollment.

79 the atherosclerotic cardiovascular disease (ASCVD) risk estimator (pooled cohort equation [PCE]) is

80 duce atherosclerotic cardiovascular disease (ASCVD) risk in adults.

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

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

83 and atherosclerotic cardiovascular disease (ASCVD) risk.

84 hard atherosclerotic cardiovascular disease (ASCVD) risk.

85 t of atherosclerotic cardiovascular disease (ASCVD) risk.

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

87 for atherosclerotic cardiovascular disease (ASCVD) with statins based on absolute ASCVD risk assessm

88 y of atherosclerotic cardiovascular disease (ASCVD) with statins.

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

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

91 n of atherosclerotic cardiovascular disease (ASCVD).

92 with atherosclerotic cardiovascular disease (ASCVD).

93 ical atherosclerotic cardiovascular disease (ASCVD).

94 for atherosclerotic cardiovascular disease (ASCVD).

95 ture atherosclerotic cardiovascular disease (ASCVD).

96 mary atherosclerotic cardiovascular disease (ASCVD).

97 had atherosclerotic cardiovascular disease (ASCVD).

98 with atherosclerotic cardiovascular disease (ASCVD).

99 nown atherosclerotic cardiovascular disease (ASCVD).

100 t of atherosclerotic cardiovascular disease (ASCVD).

101 for atherosclerotic cardiovascular disease (ASCVD).

102 t of atherosclerotic cardiovascular disease (ASCVD).

103 oup (atherosclerotic cardiovascular disease [ASCVD], diabetes, LDL-C >/=190 mg/dl, or an estimated 10

104 tal atherosclerotic cardiovascular diseases (ASCVD) is now inclusive of stroke in addition to hard co

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

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

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

108 r, is underused in patients with established ASCVD.

109 Estimated ASCVD events prevented and incremental costs per quality

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

111 was eligible because of a 10-year estimated ASCVD risk >/=7.5%.

112 years received statin treatment, experienced ASCVD events, and died from ASCVD-related or non-ASCVD-r

113 vided a cNRI of 0.20 (95% CI, 0.09-0.31) for ASCVD prediction.

114 1 (95% confidence interval, 0.640-0.723) for ASCVD risk and 0.703 (95% confidence interval, 0.663-0.7

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

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

117 rolemia is a major treatable risk factor for ASCVD, yet many individuals fail to reach target levels

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

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

120 .75; 95% CI, 0.70-0.81) reduced the risk for ASCVD.

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

122 ent, experienced ASCVD events, and died from ASCVD-related or non-ASCVD-related causes based on ASCVD

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

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

125 Hard ASCVD events were ascertained over a median follow-up of

126 Among these, 104 hard ASCVD events occurred.

127 Relative to CAC=0, adjusted hard ASCVD hazard ratios for each CAC category among persons

128 d 0.68 (95% CI, 0.64-0.73) in women for hard ASCVD (ACC/AHA), 0.67 (95% CI, 0.62-0.72) in men and 0.6

129 re was no increased adjusted hazard for hard ASCVD in high versus low CIMT categories.

130 dence rates (per 1000 person-years) for hard ASCVD were 4.4 for CAC, 0 (n=574; 46% of the sample); 8.

131 disease, CAC improved discrimination of hard ASCVD events (P<0.001).

132 isk vs observed cumulative incidence of hard ASCVD events was 21.5% (95% CI, 20.9%-22.1%) vs 12.7% (9

133 We calculated 10-year risks for "hard" ASCVD events (including fatal and nonfatal coronary hear

134 Higher ASCVD risk was associated with an increased prevalence o

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

136 Shifting from a 7.5% or higher ASCVD risk threshold to a 3.0% or higher ASCVD risk thre

137 her ASCVD risk threshold to a 3.0% or higher ASCVD risk threshold was estimated to be associated with

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

139 CEC improves ASCVD risk prediction beyond using CAC, FH, and hs-CRP a

140 In ASCVD, adding PCSK9 inhibitors to statins was estimated

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

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

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

144 is new paradigm will need to be evaluated in ASCVD outcomes trials.

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

146 g evidence that the benefits of reduction in ASCVD events from statin therapy exceed adverse events.

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

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

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

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

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

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

153 s, they ultimately account for most incident ASCVD.

154 (5.1%) suffered fatal and nonfatal incident ASCVD, respectively.

155 ntial 10-year and lifetime risks of incident ASCVD continue.

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

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

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

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

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

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

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

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

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

165 lar calcification and at low to intermediate ASCVD risk.

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

167 In 5,805 BioImage participants without known ASCVD at baseline, those with >/=7.5% 10-year ASCVD risk

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 More lenient ASCVD thresholds of 4.0% or higher (61% of adults treate

171 ofile (ICER, $37,000/QALY), but more lenient ASCVD thresholds would be optimal using cost-effectivene

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

173 onclusions and Relevance: Among women at low ASCVD risk, CAC was present in approximately one-third a

174 Results: Among 6739 women with low ASCVD risk from the 5 studies, mean age ranged from 44 t

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

176 itional cardiovascular risk factors had more ASCVD if they had CTD (prevalence ratio 2.9).

177 hat the ACC/AHA guidelines will prevent more ASCVD events than the trial-based and hybrid approaches,

178 D events, and died from ASCVD-related or non-ASCVD-related causes based on ASCVD natural history and

179 hs-CRP and warrants consideration as a novel ASCVD risk marker.

180 a 10-year cPCE risk <7.5% but with observed ASCVD event rates >7.5% who may warrant statin therapy c

181 hout prevalent ASCVD underwent assessment of ASCVD risk.

182 -concordant practice to reduce the burden of ASCVD.

183 duction program is an essential component of ASCVD prevention and management.

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

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

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

187 years recruited in 2003 to 2008, all free of ASCVD, diabetes, and statin use at baseline.

188 corresponding numbers for family history of ASCVD were 4.6%, 15.1%, 12%, 4.3 (95% CI, 3.0-6.4), and

189 tivity C-reactive protein, family history of ASCVD, and ankle-brachial index recommendations by the A

190 cholesterol >/=160 mg/dL; family history of ASCVD; high-sensitivity C-reactive protein >/=2 mg/dL; c

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

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

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

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

195 If validated, overestimation of ASCVD risk may have substantial implications for individ

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

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

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

199 holesterol likewise are strong predictors of ASCVD.

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

201 )-lowering therapy for primary prevention of ASCVD events.

202 isk-based approach for primary prevention of ASCVD with statins was superior to the trial-based and h

203 idence for CR in the secondary prevention of ASCVD, it remains vastly underutilized due to significan

204 statin, especially for primary prevention of ASCVD.

205 PCSK9) inhibitors in secondary prevention of ASCVD.

206 isk population sample, a large proportion of ASCVD events occurred among adults with a 10-year cPCE r

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

208 ite decades of research showing reduction of ASCVD risk with multiple approaches to lowering of LDL c

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

210 >0) was associated with an increased risk of ASCVD (incidence rates per 1000 person-years, 1.41 for C

211 and was associated with an increased risk of ASCVD and modest improvement in prognostic accuracy comp

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

213 hypercholesterolemia for patients at risk of ASCVD should start before they turn 80 years old.

214 k factors for calculation of 10-year risk of ASCVD, 633 (9%) >75 years of age, and 209 (3%) with low-

215 bust marker of absolute and relative risk of ASCVD, whereas CIMT is not.

216 related or non-ASCVD-related causes based on ASCVD natural history and statin treatment parameters.

217 erapy, statin, or tobacco cessation drugs on ASCVD events in individuals without prevalent ASCVD.

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

219 as a higher than 93% chance that the optimal ASCVD threshold was 5.0% or lower using a cost-effective

220 The optimal ASCVD threshold was sensitive to patient preferences for

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

222 nhibitors or ezetimibe in heterozygous FH or ASCVD.

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

224 both masked hypertension and high predicted ASCVD risk.

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

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

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

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

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

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

231 SCVD events in individuals without prevalent ASCVD.

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

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

234 population with FH with or without previous ASCVD.

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

236 h care professionals and patients in primary ASCVD prevention.

237 herapy of an appropriate intensity to reduce ASCVD risk and minimize adverse effects is recommended.

238 ove consistency in approaches to LDL-related ASCVD risk and to reduce gaps in implementation of evide

239 We compared the absolute and relative ASCVD risks among those with versus without elevated pos

240 e, patient-centered, comprehensive secondary ASCVD prevention.

241 Significant ASCVD risk heterogeneity exists among those eligible for

242 Similar ASCVD risk overestimation and poor calibration with mode

243 h the ultimate goal of preventing subsequent ASCVD events.

244 r exclusion of expert opinion, the suggested ASCVD risk assessment tool, the lipoproteins recommended

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

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

247 with CAC or CIMT added to variables from the ASCVD pooled cohort equation was also evaluated using re

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

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

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

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

252 During 10 years of follow-up, 57% of the ASCVD events (183 of 320) occurred among adults with a c

253 Among these statin-eligible subjects, the ASCVD event rate per 1,000 person-years was 9.8, 6.8, an

254 ns, 29 CHD deaths, and 72 strokes), with the ASCVD incidence rates ranging from 1.5 to 6.0 per 1000 p

255 A new approach to ASCVD prevention is needed.

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

257 -term coronary heart disease (CHD) and total ASCVD risks in US adults with an FH phenotype.

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

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

260 oups such as younger individuals with unique ASCVD risk factors.

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

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

263 ch lipoproteins are causally associated with ASCVD and all-cause mortality.

264 Association of CAC with ASCVD was examined using Cox proportional hazards models

265 n about the temporal association of LTL with ASCVD.

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

267 gh-intensity monotherapy among patients with ASCVD and diabetes mellitus, respectively.

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

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

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

271 tality in a national sample of patients with ASCVD.

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

273 ractice regarding LLT in the population with ASCVD.

274 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

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

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

277 d probably in patients with diabetes without ASCVD.

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

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

280 CAC = 0 at baseline and an observed 10-year ASCVD event rate of 4.2 per 1,000 person-years.

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

282 LDL-C >/=190 mg/dl, or an estimated 10-year ASCVD risk >/=7.5%) were described.

283 t LDL-C >/=190 mg/dl, 1.9% estimated 10-year ASCVD risk >/=7.5%).

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

285 f individuals who are likely to have 10-year ASCVD risk estimates >/=7.5%.

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

287 ntinues to be a major determinant of 10-year ASCVD risk for both men and women.

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

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

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

291 this group was 8.5 +/- 3.2%, and the 10-year ASCVD risk score was 28.0 +/- 19.5%.

292 to 75 years [corrected], the current 10-year ASCVD risk threshold (>/=7.5% risk threshold) used in th

293 We used the 10-year ASCVD risk threshold of >/=7.5% as a clinically relevant

294 was well calibrated around the 7.5% 10-year ASCVD risk treatment threshold and discriminated better

295 10-year ASCVD risk was estimated by using the 2013 ACC/AHA ASCVD

296 SCVD at baseline, those with >/=7.5% 10-year ASCVD risk were down-classified from statin eligible to

297 equation is presented for estimating 10-year ASCVD risk.

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