ライフサイエンスコーパス: LDL-C

1 LDL-C level at week 24 with ezetimibe was 181.5 mg/dL; m

2 LDL-C levels <25 or <15 mg/dl on alirocumab were not ass

3 LDL-C variability was defined as the intraindividual sta

4 LDL-C was lower in both PAH (2.6 +/- 0.8 mmol/l) and CTE

5 LDL-C, even at levels currently considered normal, is in

6 For the mean of weeks 22 and 24, LDL-C level with ezetimibe was 183.0 mg/dL; mean percent

7 Factors associated with a >/=50% LDL-C reduction from untreated levels included high-inte

8 n LDL-C <100 mg/dL and 41% achieved a >/=50% LDL-C reduction.

9 The achieved absolute LDL-C level was significantly associated with the absolu

10 ared with 76.6% in those who did not achieve LDL-C <25 mg/dl.

11 outcomes in patients stratified by achieved LDL-C level at 1 month in the Improved Reduction of Outc

12 For every 39 mg/dL lower achieved LDL-C, the risk of MACE appeared to be 24% lower (adjust

13 significant association between the achieved LDL-C level and any of the 9 prespecified safety events.

14 ut an event in the first month, the achieved LDL-C values at 1 month were less than 30 mg/dL, 30 to 4

15 ry atherosclerosis in proportion to achieved LDL-C levels.

16 ronary death or MI) associated with achieved LDL-C level.

17 eared to be increased in the group achieving LDL-C levels <25 mg/dl.

18 dverse events occurred in patients achieving LDL-C <25 and <15 mg/dl (72.7% and 71.7%, respectively),

19 nge from baseline or % of patients achieving LDL-C goals at Week 24 for alirocumab versus control (in

20 Novel adaptable LDL-C estimation performs better in nonfasting samples t

21 assessed the relationship between additional LDL-C, non-high-density lipoprotein cholesterol, and apo

22 te in life and often do not achieve adequate LDL-C lowering, despite a high prevalence of coronary he

23 LDL-C levels (P = .005) and had an adjusted LDL-C level of 18 mg/dL (95% CI, 9-27 mg/dL) higher than

24 -Label Study of Long-term Evaluation Against LDL-C (OSLER-1) evaluated the durability of long-term ef

25 Together with male sex and age, LDL-C was independently associated with atherosclerosis

26 intensification of oral LLT could achieve an LDL-C level of less than 70 mg/dL in most patients, with

27 ment intensification, 99.3% could achieve an LDL-C level of less than 70 mg/dL, including 67.3% with

28 LDL-lowering medication(s), 25% achieved an LDL-C <100 mg/dL and 41% achieved a >/=50% LDL-C reducti

29 Only 25.2% achieved an LDL-C level of less than 70 mg/dL.

30 significantly lower in patients achieving an LDL-C level less than 30 mg/dL at 1 month (adjusted haza

31 Patients achieving an LDL-C level less than 30 mg/dL at 1 month had a similar

32 Overall, 2.9% (CI, 2.3% to 3.5%) had an LDL-C level of 4.92 mmol/L (190 mg/dL) or greater.

33 ery high-risk and high-risk patients with an LDL-C >/=130 mg/dl.

34 VD risk greater than 5% and of those with an LDL-C level of 4.92 mmol/L (190 mg/dL) or greater were e

35 /discordant groups, based on median apoB and LDL-C or non-HDL-C.

36 betes mellitus or patients without ASCVD and LDL-C >/=190 mg/dL not due to secondary causes.

37 ycerides (TG), cholesterol levels (HDL-C and LDL-C), and plasma von Willebrand factor (vWF).

38 density lipoprotein cholesterol (VLDL-C) and LDL-C.

39 n had similar baseline total cholesterol and LDL-C, but lower HDL-C and higher triglycerides than con

40 s ratio 1.3 [1.0, 1.6]), TG >/=100 mg/dL and LDL-C <100 mg/dL (odds ratio 1.3 [1.1, 1.5]), or TG and

41 higher thresholds for TG (>/=150 mg/dL) and LDL-C (>/=130 mg/dL), results were essentially the same.

42 s were observed between statin type/dose and LDL-C % change from baseline or % of patients achieving

43 was no correlation between PCSK9 levels and LDL-C levels (rho = 0.03 [95% CI, -0.04 to 0.10] for non

44 sed to stratify patients into quartiles, and LDL-C level was measured at baseline and weeks 10 and 12

45 mg/dL (odds ratio 1.3 [1.1, 1.5]), or TG and LDL-C >/=100 mg/dL (odds ratio 1.6, [1.2, 2.2]), after a

46 in women) was defined as isolated if TG and LDL-C were both low (<100 mg/dL).

47 20% to 40% lower CVD risk except when TG and LDL-C were elevated.

48 103 patients with ACS, age </=65 years, and LDL-C levels >/=160 mg/dl.

49 significantly on the likelihood of attaining LDL-C treatment goals.

50 33.1% of the pooled cohort achieved average LDL-C <50 mg/dL (44.7%-52.6% allocated to alirocumab, 6.

51 Baseline LDL-C levels were similar across pools, regardless of st

52 Baseline LDL-C was lower (mean 100.3 vs. 134.3 mg/dl) in patients

53 erotic cardiovascular disease and a baseline LDL-C of less than 70 mg/dL and in those receiving backg

54 Of 2034 patients (7.4%) who had a baseline LDL-C of less than 70 mg/dL, evolocumab reduced the risk

55 Patients were classified by a baseline LDL-C of less than 70 or at least 70 mg/dL and by statin

56 ee as in the 25529 patients who had baseline LDL-C of at least 70 mg/dL (HR 0.86; 95% CI, 0.79-0.92;

57 < .001) and had significantly lower baseline LDL-C level (123 mg/dL, 124 mg/dL, 128 mg/dL, and 137 mg

58 timibe/simvastatin (85%), had lower baseline LDL-C values, and were more likely older, male, nonwhite

59 mean age, 62 years; 24% women; mean baseline LDL-C level of 3.16 mmol/L [122.3 mg/dL]) from 49 trials

60 interaction; 1 patient was missing baseline LDL-C data).

61 r disease regardless of whether the baseline LDL-C was less than 70 or at least 70 mg/dL and whether

62 e between apoB and apoA-I as well as between LDL-C and HDL-C may be an etiological mechanism for ALS

63 were used to assess the association between LDL-C and mortality.

64 o evidence was found for interaction between LDL-C variability and pravastatin treatment for both cog

65 ighlighting the complex relationship between LDL-C and diabetes.

66 The relationship between LDL-C response and genetic mutations was assessed by add

67 use leads to extensive lipid changes beyond LDL-C and appears efficacious for lowering remnant chole

68 ere higher when low HDL-C was accompanied by LDL-C >/=100 mg/dL and TG <100 mg/dL (odds ratio 1.3 [1.

69 d LDL-C (LDL-CN or LDL-CF) was stratified by LDL-C and triglyceride categories.

70 ascular disease were included, stratified by LDL-C levels into those with LDL-C <190 mg/dL (n=2969; m

71 igh-density lipoprotein cholesterol (HDL-C), LDL-C, and apolipoprotein B (apoB) levels in participant

72 verse fine-mapping genetic studies of HDL-C, LDL-C, and triglycerides to-date using SNPs on the Metab

73 ar sensor characteristic to LDL cholesterol (LDL-C) from 4 to 400 mg/dL or 0.10-10.34 mmol/L in 100 m

74 ciated with lower levels of LDL cholesterol (LDL-C) have recently been associated with an increased r

75 ase (CHD), independently of LDL cholesterol (LDL-C) levels.

76 ions of low-density lipoprotein cholesterol (LDL-C) >/=190 mg/dL are at a higher risk of atherosclero

77 mg/dl, low-density lipoprotein cholesterol (LDL-C) <160 mg/dl, and high-density lipoprotein choleste

78 C), and low-density lipoprotein cholesterol (LDL-C) (n=627).

79 vels of low-density lipoprotein cholesterol (LDL-C) alter this association is unknown.

80 vels of low-density lipoprotein cholesterol (LDL-C) and accelerated atherosclerotic cardiovascular di

81 l (TC), low-density lipoprotein cholesterol (LDL-C) and apolipoprotein B (apo B) compared with E2 car

82 reduce low-density lipoprotein cholesterol (LDL-C) and associated atherosclerotic cardiovascular ris

83 vels of low-density lipoprotein cholesterol (LDL-C) and extremely high risk of premature atherosclero

84 Serum low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C)

85 ions in low-density lipoprotein cholesterol (LDL-C) and major adverse cardiovascular events (MACE) ha

86 vels of low-density lipoprotein cholesterol (LDL-C) are an independent risk factor for ASCVD, and cli

87 affect low-density lipoprotein cholesterol (LDL-C) estimation.

88 vels of low-density lipoprotein cholesterol (LDL-C) have shown modest results in identifying individu

89 %) or a low-density lipoprotein cholesterol (LDL-C) level of 4.92 mmol/L (190 mg/dL) or greater.

90 reshold low-density lipoprotein cholesterol (LDL-C) level of less than 70 mg/dL for the highest-risk

91 trolled low-density lipoprotein cholesterol (LDL-C) levels and history of intolerance to 2 or more st

92 reduces low-density lipoprotein cholesterol (LDL-C) levels by 55% to 75%.

93 levated low-density lipoprotein cholesterol (LDL-C) levels despite use of statins.

94 levated low-density lipoprotein cholesterol (LDL-C) levels in young adults may help to inform populat

95 s lower low-density lipoprotein cholesterol (LDL-C) levels without reducing cardiovascular events, su

96 was the low-density lipoprotein cholesterol (LDL-C) levels.

97 reduced low-density lipoprotein cholesterol (LDL-C) on cardiovascular events.

98 vels of low-density lipoprotein cholesterol (LDL-C) or non-high-density lipoprotein cholesterol (non-

99 tion in low-density lipoprotein cholesterol (LDL-C) predicts both cerebrovascular and cardiovascular

100 Low-density lipoprotein cholesterol (LDL-C) reductions with the PCSK9 monoclonal antibody ali

101 reduce low-density lipoprotein cholesterol (LDL-C) remains uncertain.

102 reduce low-density lipoprotein cholesterol (LDL-C) to very low levels when added to background lipid

103 ment of low-density lipoprotein cholesterol (LDL-C) treatment goals in FH patients enrolled in a larg

104 treated low-density lipoprotein cholesterol (LDL-C) was 239 mg/dL.

105 vels of low-density lipoprotein cholesterol (LDL-C) with intensive statin therapy reduces progression

106 HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglycerides (TG).

107 HDL-C), low-density lipoprotein cholesterol (LDL-C), and triglycerides were obtained, in addition to

108 HDL-C), low-density-lipoprotein cholesterol (LDL-C), and/or triglycerides (TG).

109 cularly low-density lipoprotein cholesterol (LDL-C), is frequently seen in obese women.

110 rtance: Low-density lipoprotein cholesterol (LDL-C)-lowering alleles in or near NPC1L1 or HMGCR, enco

111 tensive low-density lipoprotein cholesterol (LDL-C)-reducing therapy with ezetimibe/simvastatin compa

112 educing low-density lipoprotein cholesterol (LDL-C).

113 plasma low-density lipoprotein cholesterol (LDL-C).

114 vels of low-density lipoprotein cholesterol (LDL-C).

115 gulates low-density lipoprotein cholesterol (LDL-C).

116 tion in low density lipoprotein-cholesterol (LDL-C), an increase in CEC and beneficial changes in pla

117 HDL-C], low-density lipoprotein cholesterol [LDL-C], total cholesterol [TC]) were studied as continuo

118 Low-density lipoprotein cholesterol(LDL-C) is a well established metabolic marker of cardiov

119 ncers in the setting of elevated circulating LDL-C, which may be important contributing factors to th

120 larger tumors in mice with high circulating LDL-C concentrations than in mice with lower LDL-C.

121 er with the novel method across all clinical LDL-C categories (range, 87%-94%) compared with the Frie

122 aternal prepregnancy and parental concurrent LDL-C levels in association with adult offspring LDL-C l

123 patients, 839 (25.1%) achieved 2 consecutive LDL-C values <25 mg/dl, and 314 (9.4%) achieved <15 mg/d

124 ated in patients with at least 2 consecutive LDL-C values <25 or <15 mg/dl in the ODYSSEY program, wi

125 In summary, alirocumab provided consistent LDL-C reductions and was generally well tolerated indepe

126 Alirocumab decreased LDL-C and LDL-apoB by increasing IDL- and LDL-apoB FCRs

127 eads to LDL receptor upregulation, decreased LDL-C and attenuation of atherosclerosis, independently

128 Adding ezetimibe to reduce low-density LDL-C by 20% would provide a 5-year NNT </=50 for very h

129 ws: total cholesterol: 177.3 +/- 33.1 mg/dl; LDL-C: 109.9 +/- 31.1 mg/dl; non-HDL-C: 124.0 +/- 33.5 m

130 statin trial demonstrated safe and effective LDL-C reduction with rosuvastatin 20 mg alone or added t

131 These findings support more effective LDL-C lowering for primordial prevention, even in indivi

132 riants and classic risk factors for elevated LDL-C levels.

133 .5-9.8) times higher odds of having elevated LDL-C levels (P = .005) and had an adjusted LDL-C level

134 t of long-term exposure to markedly elevated LDL-C levels.

135 e were used to study the effects of elevated LDL-C in human triple-negative (MDA-MB-231) and mouse He

136 entage of LDL-CD falling within an estimated LDL-C (LDL-CN or LDL-CF) category by clinical cut points

137 ent differences between LDL-CD and estimated LDL-C (LDL-CN or LDL-CF) was stratified by LDL-C and tri

138 For low estimated LDL-C (<70 mg/dL), we evaluated accuracy by triglyceride

139 on materially similar to those described for LDL-C were observed with achieved non-high-density lipop

140 ucleotide polymorphisms (SNPs) were used for LDL-C (explaining 7.9% of its variance), 140 SNPs for HD

141 etimibe with simvastatin resulted in greater LDL-C reductions compared with simvastatin alone at 33 w

142 In the CTEPH group, LDL-C increased (from 2.6[2.1-3.2] to 4.0[2.8-4.9]mmol/l

143 dvocated in young patients with ACS and high LDL-C levels to allow prompt identification of patients

144 HR = 0.62; 95% CI = 0.42-0.93), whereas high LDL-C/HDL-C (>/=3.50; HR = 1.50; 95% CI = 1.15-1.96) and

145 Higher LDL-C and TC concentrations at baseline were associated

146 Higher LDL-C variability was associated with lower cognitive fu

147 riod compared with patients achieving higher LDL-C concentrations.

148 Furthermore, higher LDL-C variability was associated with lower cerebral blo

149 o 13 y of follow-up, we observed that higher LDL-C and TC concentrations were associated with an incr

150 benefit of lowering LDL-C may depend on how LDL-C is lowered.

151 ly attenuated risk of CHD per unit change in LDL-C level (OR, 0.916 [95% CI, 0.890-0.943] vs 0.831 [9

152 y end points were the mean percent change in LDL-C level from baseline to the mean of weeks 22 and 24

153 Placebo-controlled percentage change in LDL-C level with evolocumab, 140 mg every 2 weeks and 42

154 cantly less than expected per unit change in LDL-C.

155 r RRs of major vascular events per change in LDL-C.

156 For week 24, between-group difference in LDL-C was -36.1%; absolute difference, -71.7 mg/dL.

157 weeks 22 and 24, between-group difference in LDL-C was -37.8%; absolute difference, -75.8 mg/dL.

158 was associated with a 74.9 mg/dL increase in LDL-C.

159 s associated with a significant reduction in LDL-C level by 61% (95% CI, -63% to -60%) vs 2% (95% CI,

160 vents per 1-mmol/L (38.7-mg/dL) reduction in LDL-C level was 0.77 (95% CI, 0.71-0.84; P < .001) for s

161 or vascular events per 1-mmol/L reduction in LDL-C level.

162 e) associated with the absolute reduction in LDL-C level; 5-year rate of major coronary events (coron

163 lted in a significantly greater reduction in LDL-C levels after 24 weeks.

164 re was associated with the same reduction in LDL-C levels but an attenuated reduction in apoB levels

165 predicted 1-mmol/L [38.7-mg/dL] reduction in LDL-C of 0.61 [95% CI, 0.42-0.88]; P = .008) and directl

166 genetically predicted 1-mmol/L reduction in LDL-C of 2.42 [95% CI, 1.70-3.43]; P < .001).

167 1-mmol/L genetically predicted reduction in LDL-C was 1.19 (95% CI, 1.02-1.38; P = .03).

168 For a given reduction in LDL-C, genetic variants were associated with a similar r

169 was associated with discordant reductions in LDL-C and apoB levels and a corresponding risk of cardio

170 SEY trials, greater percentage reductions in LDL-C and lower on-treatment LDL-C were associated with

171 Percent reductions in LDL-C from baseline were inversely correlated with MACE

172 re associated with significant reductions in LDL-C levels between 64% and 71% (P < .001), regardless

173 evolocumab produced sustained reductions in LDL-C levels.

174 nd that higher visit-to-visit variability in LDL-C, independently of mean LDL-C levels and statin tre

175 Increased LDL-C, HDL-C, and possibly TG levels are associated with

176 Reversal of PH increases LDL-C levels.

177 ype 9 (PCSK9) inhibitors produce incremental LDL-C lowering in statin-treated patients; however, the

178 ary hypertension (PH) reversal can influence LDL-C levels.

179 irocumab reduced ultracentrifugally isolated LDL-C by 55.1%, LDL-apoB by 56.3%, and plasma Lp(a) by 1

180 High apoB and low LDL-C or non-HDL-C discordance was also associated with

181 icular accuracy advantage in settings of low LDL-C and high triglycerides.

182 The safety of very low LDL-C levels over the long-term is unknown.

183 y higher-risk patients resulting in very low LDL-C levels.

184 in blacks and 13 mg/dL (95% CI, 11-16) lower LDL-C in whites.

185 (95% confidence interval [CI], 32-39) lower LDL-C in blacks and 13 mg/dL (95% CI, 11-16) lower LDL-C

186 ssociated with higher levels of HDL-C, lower LDL-C, concordantly lower apoB, and a corresponding lowe

187 [95% CI, 2.9%-6.4%] per each 1-mmol/L lower LDL-C level; P < .001).

188 [95% CI, 0.5%-2.6%] per each 1-mmol/L lower LDL-C level; P = .008) and secondary prevention trials (

189 In PAH patients lower LDL-C significantly predicted death (HR:0.44/1 mmol/l, 9

190 Adding a PCSK9 monoclonal antibody to lower LDL-C by at least 50% would provide an NNT </=50 for ver

191 -1002) is a small molecule intended to lower LDL-C in hypercholesterolemic patients, and has been pre

192 orated genetic risk information led to lower LDL-C levels than disclosure of CHD risk based on conven

193 CSK9 LOF variants were associated with lower LDL-C and coronary heart disease incidence.

194 LDL-C concentrations than in mice with lower LDL-C.

195 ins) have been the main therapy for lowering LDL-C.

196 tion; (iii) only some mechanisms of lowering LDL-C appeared to increase risk for type 2 diabetes (T2D

197 he short- and long-term benefits of lowering LDL-C for the primary prevention of cardiovascular disea

198 The clinical benefit of lowering LDL-C levels may therefore depend on the corresponding r

199 esting that the clinical benefit of lowering LDL-C may depend on how LDL-C is lowered.

200 clinical trial data have shown that lowering LDL-C generally reduces cardiovascular risk.

201 Mean LDL-C was 481 mg/dl (range: 229 to 742 mg/dl) on placebo

202 those with LDL-C >/=190 mg/dL (n=2560; mean LDL-C 206+/-12 mg/dL).

203 to those with LDL-C <190 mg/dL (n=2969; mean LDL-C 178+/-6 mg/dL) and those with LDL-C >/=190 mg/dL (

204 h coronary heart disease [34.6%]; entry mean LDL-C level, 212.3 [SD, 67.9] mg/dL), muscle symptoms oc

205 ezetimibe and 145 to evolocumab; entry mean LDL-C level, 219.9 [SD, 72] mg/dL).

206 nts, and all analyses were adjusted for mean LDL-C levels and cardiovascular risk factors.

207 = 1.05, 95% CI: 0.92, 1.20) and who had mean LDL-C concentrations less than 130 mg/dL.

208 s 2 negative LDL receptor mutations had mean LDL-C reductions of 23.5% (p = 0.0044) and 14% (p = 0.03

209 variability in LDL-C, independently of mean LDL-C levels and statin treatment, is associated with lo

210 ezetimibe monotherapy (n = 138) showed mean LDL-C decreases of 28% (95% CI, -31% to -25%) from basel

211 9.8 years [SD, 9.2]; 269 [27.8%] women; mean LDL-C level, 92.5 mg/dL [SD, 27.2]), 846 had evaluable i

212 acentrifugation was used to directly measure LDL-C content (LDL-CD).

213 At enrollment, median LDL-C was 141 mg/dL; 42% of patients were taking high-in

214 anged from baseline, at week 208, the median LDL-C level reduction was 58%.

215 The median LDL-C level was 133 mg/dL (to convert to millimoles per

216 , and 4 years of study follow-up, the median LDL-C level was reduced by 59% (95% CI, -60% to -57%), 5

217 t time the impact of fasting status on novel LDL-C accuracy.

218 Accuracy of LDL-C <70 mg/dL further decreased as triglycerides incre

219 s ASCVD were predictors of the attainment of LDL-C goals.

220 We aimed to assess the benefits of LDL-C lowering on cardiovascular outcomes among individu

221 s vs the expected RRs based on the degree of LDL-C reduction in the trials were 0.94 (95% CI, 0.89-0.

222 pe 2 diabetes and coronary artery disease of LDL-C-lowering genetic variants were investigated in met

223 e population with ASCVD and distributions of LDL-C levels under various treatment intensification sce

224 lished data on the cardiovascular effects of LDL-C lowering among a primary prevention population wit

225 among individuals with primary elevations of LDL-C >/=190 mg/dL without preexisting vascular disease

226 among individuals with primary elevations of LDL-C >/=190 mg/dL.

227 One-unit increase of LDL-C (hazard ratio [HR] = 1.14; 95% confidence interval

228 of achieving a very low (<30 mg/dL) level of LDL-C at 1 month using data from the Improved Reduction

229 idence of MACE, including very low levels of LDL-C (<50 mg/dL).

230 vascular events per unit change in levels of LDL-C (and apoB).

231 the association between changes in levels of LDL-C (and other lipoproteins) and the risk of cardiovas

232 ally occurring discordance between levels of LDL-C and apoB was associated with a similar risk of CHD

233 ociated with concordant changes in levels of LDL-C and apoB.

234 nosis, ALS patients had increasing levels of LDL-C, HDL-C, apoB, and apoA-I, whereas gradually decrea

235 oA-I, whereas gradually decreasing levels of LDL-C/HDL-C and apoB/apoA-I ratios.

236 Lowering of LDL-C levels by statin therapy modestly increases the ri

237 ovascular risk due to inadequate lowering of LDL-C levels or non-LDL-related dyslipidemia.

238 The novel method of LDL-C estimation (LDL-CN) uses a flexible approach to de

239 We compared the primary end point of LDL-C levels at 6 months and assessed whether any differ

240 Whether further reduction of LDL-C beyond these boundaries would be beneficial is unk

241 specific associations with metabolic risk of LDL-C-lowering alleles.

242 Studies of 9 different types of LDL-C reduction approaches were included.

243 ined 13% of the variation in adult offspring LDL-C levels beyond common genetic variants and classic

244 Adult offspring LDL-C levels were associated with maternal prepregnancy

245 Adult offspring LDL-C levels were examined as both a continuous and dich

246 C levels in association with adult offspring LDL-C levels.

247 The effect of PH reversal on LDL-C levels was assessed in 34 patients with chronic th

248 mes included dyslipidemia (TC>/=200 mg/dL or LDL-C>/=130 mg/dL) and atherosclerosis in childhood; myo

249 ded 538 parent-offspring pairs with parental LDL-C levels measured in the study prior to the offsprin

250 with ezetimibe was 183.0 mg/dL; mean percent LDL-C change, -16.7% (95% CI, -20.5% to -12.9%), absolut

251 e attainment of guideline-recommended plasma LDL-C goals at entry and follow-up was investigated in r

252 idual standard deviation over 4 postbaseline LDL-C measurements, and all analyses were adjusted for m

253 s were associated with maternal prepregnancy LDL-C levels after adjustment for family relatedness and

254 Maternal prepregnancy LDL-C levels compared with paternal prepregnancy and par

255 Maternal prepregnancy LDL-C levels explained 13% of the variation in adult off

256 en exposed to elevated maternal prepregnancy LDL-C levels were at a 3.8 (95% CI, 1.5-9.8) times highe

257 ls and consistently and substantially reduce LDL-C levels.

258 evolocumab as part of the Program to Reduce LDL-C and Cardiovascular Outcomes Following Inhibition o

259 ulation of LDL receptor expression to reduce LDL-C were associated with similar RRs of major vascular

260 s than 70 mg/dL either had a final screening LDL-C of at least 70 mg/dL or a final screening non-high

261 can potentially be repurposed to lower serum LDL-C.

262 tients with cardiac glycosides reduced serum LDL-C levels.

263 estering agents (n = 332, 8-52 weeks) showed LDL-C reductions of 10% to 20%.

264 isk, many patients do not achieve sufficient LDL-C lowering due to muscle-related side effects, indic

265 B) compared with E2 carriers; and higher TC, LDL-C and apo B compared with E3/E3.

266 We concluded that LDL-C level is low in patients with PAH and is associate

267 The LDL-C response in children and adults was related to und

268 The authors sought to assess the LDL-C efficacy of rosuvastatin versus placebo in HoFH ch

269 he gene/variant-dependent specificity of the LDL-C-T2D association.

270 glycemia and highlight the asymmetry of the LDL-C-T2D relationship and/or the gene/variant-dependent

271 ty in PCSK9 levels and determine whether the LDL-C level reduction achieved with evolocumab differs b

272 In this LDL-C range, 19% of fasting and 30% of nonfasting patien

273 timize cardiovascular risk reduction through LDL-C lowering need to be applied in patients experienci

274 elevance: In this meta-analysis, exposure to LDL-C-lowering genetic variants in or near NPC1L1 and ot

275 e reductions in LDL-C and lower on-treatment LDL-C were associated with a lower incidence of MACE, in

276 mab group achieved lower mean, time-weighted LDL-C levels (93.0 vs 36.6 mg/dL; difference, -56.5 mg/d

277 Therefore we assessed whether LDL-C levels are altered in PAH patients, if they are as

278 To determine whether LDL-C level reductions with evolocumab persist across di

279 Objective: To investigate whether LDL-C-lowering alleles in or near NPC1L1 and other genes

280 his observation begs the question of whether LDL-C-raising alleles are associated with a decreased ri

281 With LDL-C <70 mg/dL, nonfasting LDL-CN accuracy (92%) was su

282 n patients with ACS age </=65 years and with LDL-C levels >/=160 mg/dl is high (approximately 9%).

283 C (LPL, APOA5, LCAT) and two associated with LDL-C (ABCG8, DHODH).

284 Among individuals with LDL-C >/=190 mg/dL, pravastatin reduced the risk of coro

285 iated with incident CHD in participants with LDL-C concentrations of 130 mg/dL or higher (hazard rati

286 r NNT </=50 for very high-risk patients with LDL-C >/=130 mg/dl or for high-risk patients with LDL-C

287 n NNT </=30 for very high-risk patients with LDL-C >/=160 mg/dl.

288 >/=130 mg/dl or for high-risk patients with LDL-C >/=190 mg/dl, and an NNT </=30 for very high-risk

289 r very high-risk and high-risk patients with LDL-C >/=70 mg/dl, and an NNT </=30 for very high-risk a

290 hibitors in primary prevention patients with LDL-C <190 mg/dL with or without diabetes mellitus or pa

291 ate of cataracts was higher in patients with LDL-C <25 mg/dl (2.6%) versus >/=25 mg/dl (0.8%; hazard

292 mean 100.3 vs. 134.3 mg/dl) in patients with LDL-C <25 versus >/=25 mg/dl.

293 Patients with LDL-C values less than 30 mg/dL (median, 25 mg/dL; inter

294 g among a primary prevention population with LDL-C >/=190 mg/dL.

295 69; mean LDL-C 178+/-6 mg/dL) and those with LDL-C >/=190 mg/dL (n=2560; mean LDL-C 206+/-12 mg/dL).

296 , stratified by LDL-C levels into those with LDL-C <190 mg/dL (n=2969; mean LDL-C 178+/-6 mg/dL) and

297 rval (CI): 1.05, 1.60) but not in those with LDL-C concentrations less than 130 mg/dL (HR = 0.88, 95%

298 ent intensification algorithms in those with LDL-C levels of at least 70 mg/dL.

299 d the association of PCSK9 LOF variants with LDL-C and incident coronary heart disease and stroke thr

300 4) consistently among those with and without LDL-C >/=190 mg/dL (P-interaction >0.9).