ライフサイエンスコーパス: LDL-C

1 LDL-C levels <1.8 mmol/l were achieved at week 8 by 95.7

2 LDL-C lowering and relative clinical efficacy and safety

3 LDL-C reduction with evolocumab compared with placebo at

4 LDL-C was corrected (LDL-C(corrected)) for cholesterol c

5 riglycerides (38.8 vs 28.1 mg/dl, p < 0.05), LDL-C (39.2 vs 23.7 mg/dl, p < 0.001).

6 s: OR, 1.014 [95% CI, 0.965-1.065], P = .19; LDL-C: OR, 1.010 [95% CI, 0.967-1.055], P = .19; ApoB: O

7 2 randomized treatment arms and by achieved LDL-C at 4 weeks.

8 aseline LDL-C is >=100 mg/dL, or if achieved LDL-C is low.

9 A potential association of very low achieved LDL-C with alirocumab treatment at month 4 and subsequen

10 rent adverse relation between lower achieved LDL-C and incidence of hemorrhagic stroke in the alirocu

11 emorrhagic stroke did not depend on achieved LDL-C levels within the alirocumab group.

12 median follow-up of 3.1 years, the achieved LDL-C concentrations were 64 mg/dL (1.64 mmol/L) in the

13 treatment, even among patients who achieved LDL-C <20 mg/dl.

14 roup, all-cause death declined with achieved LDL-C at 4 months of treatment, to a level of approximat

15 infarction (AMI) patients, higher admission LDL-C and TG levels have been shown to be associated wit

16 Label Study of Long Term Evaluation Against LDL-C Trial [OSLER-1]; NCT01439880).

17 Label Study of Long Term Evaluation Against LDL-C Trial) evaluated longer-term effects of evolocumab

18 Aggressive LDL-C lowering with fully human PCSK9 monoclonal antibod

19 low levels, suggesting that more aggressive LDL-C targets should be adopted.

20 An LDL-C level of <70 mg/dl was achieved in 73.3% of patien

21 CCE reductions only in those who achieved an LDL-C <70 mg/dl.

22 with ischemic stroke and atherosclerosis, an LDL-C target of <70 mg/dL (1.8 mmol/L) did not reduce th

23 We assessed the influence of an LDL-C polygenic score on levels of LDL-C and risk of ASC

24 egression of carotid atherosclerosis than an LDL-C target of 90 to 110 mg/dL.

25 Study) included 201 patients assigned to an LDL-C concentration of <70 mg/dL and 212 patients assign

26 th TC (beta = 0.244, 95% CI 0.034-0.454) and LDL-C (beta = 0.193, 95% CI 0.028-0.357) concentrations.

27 ocumab-induced changes in lipoprotein(a) and LDL-C independently predicted major adverse cardiovascul

28 At baseline, median lipoprotein(a) and LDL-C(corrected) were 21 and 75 mg/dL, respectively; wit

29 which were confirmed by genetic analyses and LDL-C-lowering trials.

30 statin dosing lowered total cholesterol and LDL-C levels.

31 3.1% for LDL-C between 70 and <100 mg/dl and LDL-C <70 mg/dl, respectively; p = 0.016).

32 quartile range [IQR]: 6.7 to 59.6 mg/dl) and LDL-C [corrected for cholesterol content in lipoprotein(

33 ceride-lowering variants in the LPL gene and LDL-C-lowering variants in the LDLR gene, respectively,

34 y was to assess the feasibility, safety, and LDL-C-lowering efficacy of evolocumab initiated during t

35 e relationship of maternal folate and TC and LDL-C concentrations may indicate the importance of fola

36 LDLR expression, leading to increased TC and LDL-C.

37 ciated (P <= 2 x 10-9) with increased TC and LDL-C.

38 A 1 SD higher TG and LDL-C level caused a 0.062 (95% CI 0.040, 0.083) and a 0

39 inite FH, use of lipid-lowering therapy, and LDL-C achieved 1-year post MI.

40 linical benefit of lowering triglyceride and LDL-C levels may be proportional to the absolute change

41 s, the associations between triglyceride and LDL-C levels with the risk of CHD became null after adju

42 Triglyceride-lowering LPL variants and LDL-C-lowering LDLR variants were associated with simila

43 ApoB, LDL-C, and non-HDL-C were highly correlated (r>0.90), wh

44 hose with genetic predisposition for average LDL-C.

45 %), and 5629 (29.7%) patients had a baseline LDL-C of <80, 80 to 100, and >100 mg/dL, respectively.

46 stroke was evaluated, stratified by baseline LDL-C concentration and history of cerebrovascular disea

47 s from the trial, was stratified by baseline LDL-C levels >=100 mg/dl and <100 mg/dl.

48 S relationship was not explained by baseline LDL-C or other established risk factors.

49 ly greater for patients with higher baseline LDL-C, but there was no formal evidence of heterogeneity

50 ent is maintained for >=3 years, if baseline LDL-C is >=100 mg/dL, or if achieved LDL-C is low.

51 CI, 1.03-1.20] per 10 years), lower baseline LDL-C (OR, 1.19 [95% CI, 1.17-1.22] per 10 mg/dL), high-

52 x, high-intensity statin use, lower baseline LDL-C, and North American location predicted 1-year LDL-

53 Mean baseline LDL-C decreased from 140 to 61 mg/dl on treatment.

54 the risk of stroke, irrespective of baseline LDL-C and history of cerebrovascular disease, over a med

55 hemorrhagic stroke, irrespective of baseline LDL-C and of history of cerebrovascular disease.

56 er-risk individuals, independent of baseline LDL-C and other known risk factors, who might derive gre

57 The overall mean (SD) baseline LDL-C was 91.6 mg/dL (24.0) and geometric mean (95% CI)

58 nts with lower LDL-C, patients with baseline LDL-C >=100 mg/dL (2.59 mmol/L) had a greater absolute r

59 e, with good value in patients with baseline LDL-C >=100 mg/dl but less economic value with LDL-C <10

60 US$41,800 per QALY in patients with baseline LDL-C >=100 mg/dl, whereas in those with LDL-C <100 mg/d

61 6 in a single tertiary center, with baseline LDL-C <=70 mg/dl and serial high-sensitivity C-reactive

62 Among patients undergoing PCI with baseline LDL-C <=70 mg/dl, persistent high RIR is frequent and is

63 high RIR after PCI in patients with baseline LDL-C <=70 mg/dl.

64 PCIs, and to assess the association between LDL-C and longer-term cardiovascular events after PCIs.

65 We assessed the association between LDL-C polygenic score with LDL-C levels and ASCVD risk u

66 egression model that included terms for both LDL-C and triglyceride (surrogates for low-density lipop

67 with coronary heart disease (CHD)(6,7), but LDL-C-lowering trials demonstrated similar risk reductio

68 estimates for regional variants weighted by LDL-C on AD risk from 2 large samples (total n = 24,718

69 endpoint was percentage change in calculated LDL-C from baseline to 8 weeks.

70 ion of apolipoproteins, direct or calculated LDL-C.

71 h low circulating levels of LDL cholesterol (LDL-C) and a reduced risk of coronary artery disease.

72 tions suggesting that lower LDL cholesterol (LDL-C) increases T2D risk.

73 igher triglyceride (TG) and LDL cholesterol (LDL-C) levels caused elevated ACR.

74 ) low-density lipoprotein (LDL) cholesterol (LDL-C) on CVD events.

75 s a key regulator of plasma LDL-cholesterol (LDL-C) and a clinically validated target for the treatme

76 ng drug that reduces plasma LDL-cholesterol (LDL-C), total cholesterol (TC) and TG in hyperlipidemic

77 sis and low-density lipoprotein cholesterol (LDL-C) >=70 mg/dl or non-high-density lipoprotein choles

78 aseline low-density lipoprotein cholesterol (LDL-C) <=70 mg/dl are scarce.

79 ion and low-density lipoprotein cholesterol (LDL-C) achieved 1-year post MI.

80 and the low-density lipoprotein cholesterol (LDL-C) and blood urea nitrogen (BUN) levels were decreas

81 vels of low-density lipoprotein cholesterol (LDL-C) and increased risk of premature atherosclerotic c

82 o lower low-density lipoprotein cholesterol (LDL-C) and lower systolic blood pressure (SBP) with the

83 fasting low-density lipoprotein cholesterol (LDL-C) and non-high-density lipoprotein cholesterol (non

84 ulating low-density lipoprotein cholesterol (LDL-C) and triglycerides (TG) levels.

85 TC) and low-density lipoprotein cholesterol (LDL-C) are heritable risk factors for cardiovascular dis

86 rol and low-density lipoprotein cholesterol (LDL-C) at 6 months or more of follow-up.

87 chieved low-density lipoprotein cholesterol (LDL-C) between 25 and 50 mg/dL.

88 +/- SE low-density lipoprotein cholesterol (LDL-C) by 56% +/- 0.6% (n = 1,071), 57% +/- 0.8% (n = 1,

89 reasing low-density lipoprotein cholesterol (LDL-C) concentration and exposure duration.

90 eting a low-density lipoprotein cholesterol (LDL-C) concentration of <70 mg/dL in terms of reducing t

91 er mean low-density lipoprotein cholesterol (LDL-C) concentration.

92 o reach low-density lipoprotein cholesterol (LDL-C) goals.

93 Low-density lipoprotein cholesterol (LDL-C) has been associated with the occurrence of abdomi

94 levated low-density lipoprotein cholesterol (LDL-C) is associated with increased cardiovascular event

95 Low-density lipoprotein cholesterol (LDL-C) is causally associated with a high risk of corona

96 aseline low-density lipoprotein cholesterol (LDL-C) level >=70 mg/dl, non-high-density lipoprotein ch

97 tion in low-density lipoprotein cholesterol (LDL-C) level with available lipid-lowering therapies.

98 ulating low-density lipoprotein cholesterol (LDL-C) level.

99 ase and low-density lipoprotein cholesterol (LDL-C) levels >=70 mg/dl or non-high-density cholesterol

100 owering low-density lipoprotein cholesterol (LDL-C) levels.

101 (a) and low-density lipoprotein cholesterol (LDL-C) levels.

102 rolling low-density lipoprotein cholesterol (LDL-C) may improve outcomes after PCI, practice guidelin

103 but not low-density lipoprotein cholesterol (LDL-C) or HDL-C, were associated with MACEs.

104 levated low-density lipoprotein cholesterol (LDL-C) polygenic risk score further increased CVD risk i

105 vels of low-density lipoprotein cholesterol (LDL-C) predicted greater benefit from alirocumab treatme

106 (ACS), low-density lipoprotein cholesterol (LDL-C) target levels are frequently not attained.

107 ns with low-density lipoprotein cholesterol (LDL-C) using data from lipid genetics consortia (n up to

108 C), and low-density lipoprotein cholesterol (LDL-C) were measured by using MOL-300 automatic biochemi

109 CRP and low-density lipoprotein cholesterol (LDL-C) were measured in baseline plasma samples from all

110 HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglycerides, for cholesterol and triglycer

111 reduces low-density lipoprotein cholesterol (LDL-C), for the treatment of ALD using a rat model of ch

112 sterol, low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), an

113 cluding low-density lipoprotein cholesterol (LDL-C), reduces the risk of ischemic stroke.

114 en, for low-density lipoprotein cholesterol (LDL-C), uric acid (UA) and diabetes-related traits such

115 (a) and low-density lipoprotein cholesterol (LDL-C).

116 they do low-density lipoprotein cholesterol (LDL-C): fibrates, niacin, and marine-derived omega-3 fat

117 24) in low-density lipoprotein cholesterol (LDL-C); secondary endpoints included achievement of LDL-

118 f LDL (low-density lipoprotein) cholesterol (LDL-C) or triglyceride (TG)-increasing variants associat

119 creased low-density lipoprotein-cholesterol (LDL-C) and cholesterol blood levels, and elevated SREBP-

120 rt hypobetalipoproteinemia (LDL cholesterol [LDL-C] and apolipoprotein B below the fifth percentile)

121 4 studies; 121,282 people], LDL-Cholesterol [LDL-C; 61 studies; 86,854 people], and triglycerides [TG

122 culated low-density lipoprotein cholesterol [LDL-C], and apolipoproteins [Apo] A1 and B) with CVD wer

123 risk among individuals with low circulating LDL-C and of the underlying mechanisms, including those

124 ltaneously associated with lower circulating LDL-C and increased T2D risk, using data on LDL-C from t

125 ed 31 loci associated with lower circulating LDL-C and increased T2D, capturing several potential mec

126 Biobank, we found that levels of circulating LDL-C were negatively associated with T2D prevalence (od

127 despite positive associations of circulating LDL-C with HbA(1c) and BMI.

128 protein (VLDL), the precursor of circulating LDL-C.

129 g/dl or switched to placebo if 2 consecutive LDL-C levels were <15 mg/dl.

130 d reductions of lipoprotein(a) and corrected LDL-C independently predicted lower risk of MACE, after

131 Baseline lipoprotein(a) and corrected LDL-C levels and their reductions by alirocumab predicte

132 5.0 mg/dl (IQR: 0 to 13.5 mg/dl), corrected LDL-C by 51.1 mg/dl (IQR: 33.7 to 67.2 mg/dl), and reduc

133 LDL-C was corrected (LDL-C(corrected)) for cholesterol content in lipoprotein

134 risk factors, 1 SD increase in ApoB, direct LDL-C, and non-HDL-C had similar associations with compo

135 Additionally, an elevated LDL-C polygenic score (>=80th percentile) was associated

136 therapy, and the vast majority had elevated LDL-C at 1 year.

137 In this study, elevated LDL-C levels increased the risk of developing aneurysms

138 with monogenic FH and superimposed elevated LDL-C polygenic risk scores have the greatest risk of pr

139 patients hospitalized for ACS with elevated LDL-C levels (>=1.8 mmol/l on high-intensity statin for

140 To date, decades of research has established LDL-C (low-density lipoprotein cholesterol) as a causal

141 The purpose of this study was to evaluate LDL-C testing and levels after PCIs, and to assess the a

142 -1 trial demonstrated consistently excellent LDL-C-lowering efficacy, tolerance, and safety of evoloc

143 For LDL-C and UA, the evidence of G$\times$S is especially n

144 risk of MACCE (17.2% vs. 13.3% vs. 13.1% for LDL-C between 70 and <100 mg/dl and LDL-C <70 mg/dl, res

145 ooled means (mg/dl) were 193 for TC, 120 for LDL-C, 47 for HDL-C, and 139 for TG; no strong trends.

146 (95% confidence interval: 1.09 to 1.26) for LDL-C of 70 to <100 mg/dl, and 1.78 (95% confidence inte

147 RS (odds ratio, 1.26 [95% CI, 1.16-1.38] for LDL-C and 1.24 [95% CI, 1.13-1.36] for TG PRS).

148 ar, the percent at goal increased to 52% for LDL-C and 75% for SBP.

149 (95% confidence interval: 1.64 to 1.94) for LDL-C >=100 mg/dl when compared with LDL-C <70 mg/dl.

150 utcome, which persisted after adjustment for LDL-C and other risk factors, with adjusted ORs (95% CI)

151 r vascular events, even after adjustment for LDL-C lowering, although the effect is less than that fo

152 zation remained stable after adjustments for LDL-C and triglycerides.

153 d) with available data, 35% were at goal for LDL-C, and 65% were at goal for SBP at baseline.

154 ermine predictors of meeting trial goals for LDL-C (low-density lipoprotein cholesterol, goal <70 mg/

155 the notion that there is no lower limit for LDL-C.

156 In contrast, the paradox for LDL-C persisted for all primary outcomes after adjustmen

157 ores (PRSs) with ~6M variants separately for LDL-C and TG with weights from a UK Biobank-based genome

158 g, although the effect is less than that for LDL-C and attenuated when REDUCE-IT is excluded.

159 ic risk from triglycerides and HDL-C as from LDL-C.

160 d 2010 and followed up through 2018, genetic LDL-C and SBP scores were used as instruments to divide

161 Among 47,884 included patients, 52% had LDL-C measured within 6 months of PCI and 57% had LDL-C

162 within 6 months after PCI, and only 57% had LDL-C <70 mg/dl.

163 measured within 6 months of PCI and 57% had LDL-C <70 mg/dl.

164 One in 2 patients had LDL-C measured within 6 months after PCI, and only 57% h

165 Patients who had LDL-C measurement within 6 months after PCI were categor

166 High LDL-C was not causally associated with risk of retinopat

167 estimates were 21% for high TC, 20% for high LDL-C, 48% for low HDL-C, and 21% for high TG; no strong

168 of retinopathy and neuropathy; however, high LDL-C was observationally and genetically associated wit

169 Observationally, high LDL-C did not associate with high risk of retinopathy or

170 of this study was to determine whether high LDL-C causally relates to risk of retinopathy, neuropath

171 0.7-mg/dL (95% CI, 0.03-1.4; P = .04) higher LDL-C levels; while the LDLR score was associated with 1

172 duals with genetic predisposition for higher LDL-C had a lesser decrease in LDL-C on average than tho

173 risk ratio of disease for a 1 mmol/l higher LDL-C was 1.06 (95% CI: 0.24 to 4.58) for retinopathy, 1

174 increases in risk of CKD and PAD with higher LDL-C (both p for trend <0.001), with hazard ratios of 1

175 Alirocumab was blindly titrated to 150 mg if LDL-C remained >=50 mg/dl or switched to placebo if 2 co

176 nd point was percent change from baseline in LDL-C level at week 12.

177 Mean change in LDL-C from baseline to week 12 was -21.2% (-59.8 mg/dl)

178 th HoFH who were up-titrated, mean change in LDL-C improved from -19.6% at week 12 to -29.7% after 12

179 uropsychiatric events and minimal changes in LDL-C and non-HDL-C compared with EFV/FTC/TDF.

180 events; secondary endpoints were changes in LDL-C and other lipids.

181 HDL-C and 14% (+/-20%; p < 0.05) decline in LDL-C.

182 on for higher LDL-C had a lesser decrease in LDL-C on average than those with genetic predisposition

183 es associated with equivalent differences in LDL-C in Mendelian randomization analyses.

184 CI]=0.13 [0.072-0.19] per a 20% increase in LDL-C polygenic score percentile, P<0.0001).

185 TG concentration, had an 18% in reduction in LDL-C (+/-12%; p < 0.05) and a 23% (+/-23%; p < 0.05) in

186 er 1-mmol/L (0.79 per 40 mg/dL) reduction in LDL-C and 0.84 (95% CI, 0.75-0.94; P=0.0026) per 1-mmol/

187 er 1-mmol/L (0.78 per 40 mg/dL) reduction in LDL-C and 0.91 (95% CI, 0.81-1.006; P=0.06) per 1-mmol/L

188 ted and resulted in substantial reduction in LDL-C levels, rendering >95% of patients within currentl

189 at Gcgr signaling plays an essential role in LDL-C (low-density lipoprotein cholesterol) homeostasis

190 s substantial interindividual variability in LDL-C levels and risk of ASCVD.

191 h met randomization criteria, which included LDL-C level 70 mg/dL (1.8 mmol/L) or greater while recei

192 Lowering low-density lipoprotein (LDL-C) and triglyceride (TG) levels form the cornerstone

193 sed first-trimester low-density lipoprotein (LDL-C) concentration has been associated with adverse pr

194 ong the 2,338 patients who achieved very low LDL-C levels (<20 mg/dl) compared to the 3,613 patients

195 er, concerns have been raised about very low LDL-C levels and a potential increased risk of hemorrhag

196 (95% CI, 13.6-14.8; P = 1.4 x 10-465) lower LDL-C and 1.9-mg/dL (95% CI, 0.1-3.9; P = .04) lower tri

197 In NSTEMI, a lower LDL-C was paradoxically associated with worse outcomes f

198 to increasing genetic risk scores and lower LDL-C levels and SBP was associated with dose-dependent

199 ined odds ratio per standard deviation lower LDL-C inducible by the drug target = 1.45, 95% confidenc

200 ysis, combined exposure to 38.67-mg/dL lower LDL-C and 10-mm Hg lower SBP was associated with an OR o

201 higher than the median had 14.7-mg/dL lower LDL-C levels and an OR of 0.73 for major coronary events

202 higher than the median had 13.9-mg/dL lower LDL-C, 3.1-mm Hg lower SBP, and an OR of 0.61 for major

203 For CKD, a 1-mmol/l lower LDL-C conferred a higher eGFR of 1.95 ml/min/1.73 m(2) (

204 with coronary heart disease with T2DM, lower LDL-C at 1 year is associated with improved long-term MA

205 into groups with lifetime exposure to lower LDL-C, lower SBP, or both.

206 r than the median were associated with lower LDL-C and lower SBP.

207 found that, compared to patients with lower LDL-C, patients with baseline LDL-C >=100 mg/dL (2.59 mm

208 Bempedoic acid lowered LDL-C levels significantly more than placebo at week 12

209 of wild-type (WT) mice with glucagon lowered LDL-C levels, whereas this response was abrogated in Pcs

210 Lowering LDL-C is still likely to have net benefit for the preven

211 the efficacy and safety of markedly lowering LDL-C (low-density lipoprotein cholesterol).

212 excess risks of ICH associated with lowering LDL-C(14,15) may have prevented the more widespread use

213 Mean LDL-C levels decreased from 3.61 to 0.79 mmol/l at week

214 At baseline, mean LDL-C level was 120.4 (SD, 37.9) mg/dL.

215 Among Chinese adults, who have low mean LDL-C, CRP, but not fibrinogen, was independently associ

216 In FINRISK, median LDL-C was 3.39 (95% CI, 3.38-3.40) mmol/L, and it ranged

217 e of lipoprotein(a) (P(trend)=0.03), but not LDL-C(corrected) (P(trend)=0.50).

218 e of lipoprotein(a) (P(trend)=0.06), but not LDL-C(corrected) (P(trend)=0.85).

219 seline to Month 4 in lipoprotein(a), but not LDL-C(corrected), was associated with the risk of VTE an

220 vels of triglycerides and remnant-C, but not LDL-C, were associated with cardiovascular outcomes inde

221 secondary endpoints included achievement of LDL-C <70 mg/dl and percent change in other plasma lipid

222 esults demonstrated positive associations of LDL-C with IS and equally strong inverse associations wi

223 ies reported weaker positive associations of LDL-C with IS than with coronary heart disease (CHD)(6,7

224 e responsible for the diabetogenic effect of LDL-C-lowering medications.

225 rognostic information that is independent of LDL-C levels.

226 is study sought to evaluate the influence of LDL-C on the incidence of cardiovascular events either f

227 nce of an LDL-C polygenic score on levels of LDL-C and risk of ASCVD for individuals with monogenic F

228 were categorized according to the levels of LDL-C at 1 year following randomization.

229 Higher levels of LDL-C were associated with an increased incidence of lat

230 Levels of LDL-C were significantly associated with LDL-C polygenic

231 lacebo resulted in a significant lowering of LDL-C level over 12 weeks.

232 4; 95% CI, 0.0000, 0.0008) or any measure of LDL-C.

233 ended to associate with baseline quartile of LDL-C(corrected) (P(trend)=0.06); VTE tended to associat

234 he phenotypic and genotypic relationships of LDL-C with T2D.

235 d time course of area accumulation (slope of LDL-C curve) were significantly associated with CVD even

236 Mendelian randomization studies of LDL-C and IS have reported conflicting results(11-13), a

237 0.41 [95% CI 0.39, 0.43] per mmol/L unit of LDL-C), despite positive associations of circulating LDL

238 LDL-C and increased T2D risk, using data on LDL-C from the UK Biobank (n = 431,167) and the Global L

239 BEIJERINCK (EvolocumaB Effect on LDL-C Lowering in SubJEcts with Human Immunodeficiency V

240 (Safety, Tolerability & Efficacy on LDL-C of Evolocumab in Subjects With HIV & Hyperlipidemi

241 ines do not have specific recommendations on LDL-C management for this subgroup.

242 rease, emphasizing the importance of optimal LDL-C control starting early in life.

243 sidual inflammation in patients with optimal LDL-C control may further improve outcomes after PCI.

244 s are related to levels of lipoprotein(a) or LDL-C.

245 However, adding ApoB or LDL-C to a model already containing non-HDL-C did not fu

246 Differences in plasma LDL-C and SBP compared with participants with both genet

247 Differences in plasma LDL-C, SBP, and cardiovascular event rates between the g

248 These PCSK9 inhibitors lowered plasma LDL-C levels by approximately 60%, even in patients alre

249 ell tolerated and effectively reduced plasma LDL-C levels in patients with HoFH and severe HeFH over

250 monstrated that BBR treatment reduced plasma LDL-C, TC and TG in LDLR wildtype (WT) mice fed a high f

251 Evolocumab, a rapidly acting, potent LDL-C-lowering drug, has not been studied in the acute p

252 The potent LDL-C lowering efficacy of PCSK9 inhibitors provides the

253 esent a novel therapeutic strategy to reduce LDL-C and cardiovascular disease.

254 Evolocumab reduced LDL-C by 56.9% (95% confidence interval: 61.6% to 52.3%)

255 G (mean age, 9 years), together with reduced LDL-C and apolipoprotein B in clinically unaffected hete

256 monstrated its superior efficacy in reducing LDL-C and subsequent cardiovascular risk.

257 e trials occurred in the setting of reducing LDL-C levels to unprecedentedly low levels, suggesting t

258 A serum LDL-C cutoff of 100 mg/dL was unable to identify individ

259 Elevated serum LDL-C levels increased the risk of aneurysm by 5.8-fold

260 543), and the cutoff value of level of serum LDL-C was 3.08 mmol/l.

261 els of 25 to 50 mg/dL and avoiding sustained LDL-C <15 mg/dL.

262 despite intensive statin therapy, targeting LDL-C levels of 25 to 50 mg/dL and avoiding sustained LD

263 sitively associated with serum levels of TC, LDL-C, and TG, but inversely associated with serum level

264 osphate (PLP), and total B-12 with serum TC, LDL-C, HDL-C, and TG concentrations across trimesters.

265 ify the lipoprotein profile (e.g., serum TG, LDL-C, and HDL-C concentrations).

266 Given that LDL-C was also reduced in a group of clinically unaffect

267 h high risks of PAD and CKD, suggesting that LDL-C is causally involved in the pathogenesis of these

268 The LDL-C levels was higher in the aneurysm group than in th

269 events were 55.2/1,000 person-years for the LDL-C <70 mg/dl group, 60.3/1,000 person-years for 70 to

270 s ratio was 1.36 (95% CI, 1.24-1.49) for the LDL-C PRS and 1.31 (95% CI, 1.19-1.43) for the TG PRS.

271 l/L between the lowest and highest 5% of the LDL-C PRS distribution.

272 Area under the LDL-C versus age curve is a possible risk parameter.

273 Polygenic contributions to LDL-C explain some of the heterogeneity in clinical pres

274 risk depends on cumulative prior exposure to LDL-C and, independently, time course of area accumulati

275 nd traditional risk factors, both area under LDL-C versus age curve and time course of area accumulat

276 , we assessed the relationship of area under LDL-C versus age curve to incident CVD event risk and mo

277 We constructed a weighted LDL-C polygenic score, composed of 28 single-nucleotide

278 C independently predicted CVD events whereas LDL-C did not.

279 However, whether LDL-C elevation associated with aneurysms in large vesse

280 lower concentrations, regardless of whether LDL-C levels were on target at <=100 mg/dl (2.59 mmol/l)

281 Ss discriminate genetic risk associated with LDL-C from risk associated with reciprocal genetic effec

282 of LDL-C were significantly associated with LDL-C polygenic score in the Nutrition, Metabolism and A

283 94) for LDL-C >=100 mg/dl when compared with LDL-C <70 mg/dl.

284 I: 1.23 to 1.62) for PAD in individuals with LDL-C above the 95th percentile versus below the 50th pe

285 with the reference group, participants with LDL-C genetic scores higher than the median had 14.7-mg/

286 0 mg/dl) compared to the 3,613 patients with LDL-C >=100 mg/dl (3.8% vs. 4.5%, p = 0.57).

287 Among patients with LDL-C >=100 mg/dl, incremental cost-effectiveness ratios

288 The proportion of patients with LDL-C >=70 mg/dl was higher among FH patients (82.2%) co

289 iovascular events in high-risk patients with LDL-C levels >=70 mg/dL on maximally tolerated oral ther

290 sociation between LDL-C polygenic score with LDL-C levels and ASCVD risk using linear regression and

291 ine LDL-C >=100 mg/dl, whereas in those with LDL-C <100 mg/dl the cost per QALY was US$299,400.

292 L-C >=100 mg/dl but less economic value with LDL-C <100 mg/dl.

293 In patients with 1-year LDL-C >=70 mg/dl, patients undergoing CABG had significa

294 the ISCHEMIA trial with baseline and 1-year LDL-C and SBP values by January 28, 2019.

295 were less likely than men to achieve 1-year LDL-C goal (OR, 0.68 [95% CI, 0.58-0.80]).

296 Adjusted odds of 1-year LDL-C goal attainment were greater with older age (odds

297 and North American location predicted 1-year LDL-C goal attainment, whereas lower baseline SBP and No

298 Patients whose 1-year LDL-C remained >=100 mg/dl experienced higher 4-year cum

299 ted with improved outcomes across all 1-year LDL-C strata.

300 experienced a MACCE reduction only if 1-year LDL-C was <70 mg/dl (hazard ratio: 0.61; 95% confidence