ライフサイエンスコーパス: Lp(a)

1 Lp(a) concentrations (median [25th-75th percentile], in

2 Lp(a) concentrations were measured in plasma using an im

3 Lp(a) internalization was also dependent on clathrin-coa

4 Lp(a) internalization was reduced 0.35-fold in HAP1 and

5 Lp(a) is an independent predictor of CVD in men and wome

6 Lp(a) is composed of apolipoprotein(a) (apo(a)) covalent

7 Lp(a) levels were elevated among carriers of rs10455872

8 Lp(a) molar concentration fully explained the Lp(a) asso

9 Lp(a) molar concentration was associated dose-dependentl

10 Lp(a) reduction may be an important mediator of this eff

11 Lp(a) transports oxidized phospholipids with a high cont

12 Lp(a) was maximally internalized by 2 hours and was dete

13 Lp(a) was measured in 25 096 patients in the FOURIER tri

14 Lp(a) was measured using a standardized isoform-independ

15 Lp(a), a low-density lipoprotein (LDL) particle linked t

16 Lp(a)-bound PCSK9 may be pursued as a biomarker for card

17 In 1995, Lp(a) was measured in 826 men and women (age range, 45 t

18 R-B1 is also a receptor for lipoprotein (a) (Lp(a)), mediating cellular uptake of Lp(a) in vitro and

19 sed plasma concentrations of lipoprotein(a) (Lp(a)) are associated with an increased risk for cardiov

20 Elevated levels of lipoprotein(a) (Lp(a)) have been identified as an independent risk facto

21 oB, ApoAI, ApoAII, ApoE and lipoprotein (a) (Lpa) levels were measured in serum samples obtained prio

22 r, the relationship between Lipoprotein (a) [Lp(a)] and healthy cognitive aging has not yet been suff

23 made in agreeing a role for lipoprotein (a) [Lp(a)] in clinical practice and developing therapies wit

24 Lipoprotein (a) [Lp(a)] is an independent risk factor for atherosclerosis

25 ine the relationship between lipoprotein(a) [Lp(a)] and cardiovascular disease (CVD) in a large cohor

26 ociated with highly elevated lipoprotein(a) [Lp(a)] and pathways related to the metabolism of procalc

27 ents with elevated levels of lipoprotein(a) [Lp(a)] are hallmarked by increased metabolic activity in

28 sterolemia (FH) and elevated lipoprotein(a) [Lp(a)] are inherited disorders associated with premature

29 Recent studies showed that lipoprotein(a) [Lp(a)] is a causal risk factor for cardiovascular diseas

30 Lipoprotein(a) [Lp(a)] is a causal risk factor for cardiovascular diseas

31 Lipoprotein(a) [Lp(a)] is a highly atherogenic low-density lipoprotein-l

32 Lipoprotein(a) [Lp(a)] is a low-density lipoprotein-like lipoprotein and

33 RATIONALE: Lipoprotein(a) [Lp(a)] is a low-density lipoprotein-like lipoprotein and

34 Lipoprotein(a) [Lp(a)] is a low-density lipoprotein-like particle largel

35 Elevated lipoprotein(a) [Lp(a)] is a prevalent, independent cardiovascular risk f

36 Lipoprotein(a) [Lp(a)] is a risk factor for cardiovascular disease (CVD)

37 Lipoprotein(a) [Lp(a)] is an atherogenic lipoprotein.

38 Lipoprotein(a) [Lp(a)] is an independent risk factor for cardiovascular

39 d causal association between lipoprotein(a) [Lp(a)] levels and coronary risk, but the nature of the a

40 Lipoprotein(a) [Lp(a)] may play a causal role in atherosclerosis.

41 tudies have highlighted that lipoprotein(a) [Lp(a)] was associated with calcific aortic valve disease

42 Lipoprotein(a) [Lp(a)], a major carrier of oxidized phospholipids (OxPL)

43 s in HDL level, no SCARB1 variants affecting Lp(a) have been reported.

44 k of CVD is higher in those patients with an Lp(a) level >50 mg/dl and carrying a receptor-negative m

45 On multivariate analysis, Lp(a) was an independent predictor of cardiovascular dis

46 cant for OxPL/apoB (OR: 1.99; p = 0.004) and Lp(a) (OR: 1.96; p < 0.001) in the IL-1(+) group versus

47 body-mass index less than 32.0 kg/m(2), and Lp(a) concentration of 25 nmol/L (100 mg/L) or more.

48 .62; 95% confidence interval, 0.43-0.90) and Lp(a) less than the median (hazard ratio, 0.46; 95% conf

49 flects the biological activity of Lp(a), and Lp(a) levels were measured in 220 patients with mild-to-

50 xPL on apolipoprotein B-100 (OxPL/apoB), and Lp(a) levels were measured in 499 patients undergoing co

51 Interaction between ATX and Lp(a) was confirmed by in situ proximity ligation assay.

52 DL (low-density lipoprotein) cholesterol and Lp(a) (lipoprotein [a])were comparable to published repo

53 re screened for combined HDL cholesterol and Lp(a) elevations.

54 ject with high levels of HDL cholesterol and Lp(a), SCARB1 was sequenced and demonstrated a missense

55 d by high levels of both HDL cholesterol and Lp(a).

56 ith the extreme phenotype (HDL >80 mg/dL and Lp(a) >100 nmol/L in GeneSTAR, n=8, and >100 mg/dL in CC

57 minogen-independent cytokine inhibition, and Lp(a)/apo(a) inhibits plasminogen activation and regulat

58 pective clinical trials of PCSK9i on LDL and Lp(a) reduction and on tolerability are applicable to a

59 Characterize the association of PCSK9 and Lp(a) in 39 subjects with high Lp(a) levels (range 39-32

60 also dependent on clathrin-coated pits, and Lp(a) was targeted for lysosomal and not proteasomal deg

61 ed with Lp(a) purified from human plasma and Lp(a) uptake studied using Western blot analysis and int

62 ed with Lp(a) purified from human plasma and Lp(a) uptake studied using Western blot analysis and int

63 lly associated with cardiovascular risk, and Lp(a) is commonly measured in those with FHx.

64 in the plasminogen-deficient background and Lp(a)tg mice were resistant to inhibition of macrophage

65 ivation was markedly reduced in apo(a)tg and Lp(a)tg mice in both peritonitis and vascular injury inf

66 ApoAI, ApoAII, ApoE and Lpa were not associated with T2 lesions.

67 In patients with AS, Lp(a) and OxPL drive valve calcification and disease pro

68 into account the limited number of available Lp(a)-targeted drugs, L-carnitine might be an effective

69 % CI, 0.67-0.88) in patients with a baseline Lp(a) >median, and by 7% (hazard ratio, 0.93; 95% CI, 0.

70 s a significant interaction between baseline Lp(a) concentration and magnitude of VTE risk reduction

71 umab for coronary risk reduction by baseline Lp(a) concentration.

72 a) levels, and patients with higher baseline Lp(a) levels experienced greater absolute reductions in

73 7), whereas, in patients with lower baseline Lp(a) levels, evolocumab reduced Lp(a) by only 7 nmol/L

74 The median (interquartile range) baseline Lp(a) concentration was 37 (13-165) nmol/L.

75 lar disease among participants with baseline Lp(a) greater than or equal to the median (hazard ratio,

76 In the placebo arm, patients with baseline Lp(a) in the highest quartile had a higher risk of coron

77 ntly greater in those patients with baseline Lp(a) of </=125 nmol/l, the absolute reduction was subst

78 Because Lp(a) is the prominent carrier of proinflammatory oxidiz

79 re applied to assess the association between Lp(a) and performance in specific cognitive domains.

80 k, but the nature of the association between Lp(a) levels and risk of type 2 diabetes (T2D) is unclea

81 es, there was an inverse association between Lp(a) levels and T2D: hazard ratio was 0.63 (95% CI 0.49

82 tion to disentangle the relationship between Lp(a) and cardiovascular risk.

83 ] size, and whether the relationship between Lp(a) and T2D risk is causal.

84 evaluated to assess the relationship between Lp(a) and T2D.

85 However, the relationship between Lp(a) levels, PCSK9 inhibition, and cardiovascular risk

86 Oxidized phospholipids can be carried by Lp(a) into valve leaflets but can also be formed in situ

87 ication in valvular cells and are carried by Lp(a).

88 whether cardiovascular risk is conferred by Lp(a) molar concentration or apolipoprotein(a) [apo(a)]

89 ATX is transported in the aortic valve by Lp(a) and is also secreted by valve interstitial cells.

90 amilial hypercholesterolemia; in both cases, Lp(a) internalization was not affected by PCSK9.

91 Conversely, Lp(a) internalization was enhanced 2-fold in HAP1 and 1.

92 f ISIS-APO(a)Rx (50-400 mg) did not decrease Lp(a) concentrations at day 30, six doses of ISIS-APO(a)

93 Elevated Lp(a) and OxPL-apoB levels are associated with faster AS

94 Elevated Lp(a) levels and corresponding genotypes were associated

95 Elevated Lp(a) levels were associated with multivariable adjusted

96 Elevated Lp(a) predicts 15-year CVD outcomes and improves CVD ris

97 Elevated Lp(a) was defined as levels >=50 mg/dl.

98 Elevated Lp(a) was defined as the highest race-specific quintile.

99 After multivariable adjustment, elevated Lp(a) or OxPL-apoB levels remained independent predictor

100 rd ratio [HR]: 2.47; p = 0.036) and elevated Lp(a) (HR: 3.17; p = 0.024) alone were associated with a

101 erved in relatives with both FH and elevated Lp(a) (HR: 4.40; p < 0.001), independent of conventional

102 g from index cases with both FH and elevated Lp(a) identified 1 new case of elevated Lp(a) for every

103 udy) were tested for genetic FH and elevated Lp(a) via an established screening program.

104 FHx and elevated Lp(a) were independently associated with ASCVD (hazard r

105 ly when the proband has both FH and elevated Lp(a).

106 nvestigated the association between elevated Lp(a) and ASCVD events among family members.

107 Presence of both elevated Lp(a) and FHx resulted in greater improvement in ASCVD a

108 onelevated Lp(a), those with either elevated Lp(a) or FHx were at a higher ASCVD risk, while those wi

109 Testing for elevated Lp(a) during cascade screening for FH is effective in id

110 are no similar recommendations for elevated Lp(a).

111 shed CVD whose major risk factor is elevated Lp(a) levels and propose clinical studies and trials to

112 ated Lp(a) identified 1 new case of elevated Lp(a) for every 2.4 screened.

113 d with risk of T2D, suggesting that elevated Lp(a) levels are not causally associated with a lower ri

114 However, a genetic variant that elevated Lp(a) levels was not associated with risk of T2D, sugges

115 However, it remains unclear whether elevated Lp(a) and OxPL drive disease progression and are therefo

116 We show that subjects with elevated Lp(a) (108 mg/dL [50-195 mg/dL]; n=30) have increased ar

117 tic valve stenosis in patients with elevated Lp(a) concentration.

118 Participants with elevated Lp(a) concentrations (125-437 nmol/L in cohort A; >/=438

119 s being developed for patients with elevated Lp(a) concentrations with existing cardiovascular diseas

120 nocytes isolated from subjects with elevated Lp(a) remain in a long-lasting primed state, as evidence

121 om index cases with FH, but without elevated Lp(a), identified 1 individual for 5.8 screened.

122 Emerging Lp(a)-lowering therapies with specific and potent loweri

123 athophysiological insights, have established Lp(a) as an independent, genetic, and likely causal risk

124 Finally, Lp(a)-associated PCSK9 levels directly correlated with p

125 VS of 1.6 (95% CI: 1.2 to 2.1) for a 10-fold Lp(a) increase, comparable to the observational hazard r

126 ultiple independent genetic determinants for Lp(a)-cholesterol.

127 ne the intracellular trafficking pathway for Lp(a) and the receptor responsible for its uptake in liv

128 This study investigated whether testing for Lp(a) was effective in detecting and risk stratifying in

129 known locus on chromosome 6q25-26 and found Lp(a) levels also to be significantly associated with a

130 he prevalence and yield of new cases of high Lp(a) in relatives of FH probands both with and without

131 effective in identifying relatives with high Lp(a) and heightened risk of ASCVD, particularly when th

132 old increase) was seen in subjects with high Lp(a) and normal low-density lipoprotein.

133 of PCSK9 and Lp(a) in 39 subjects with high Lp(a) levels (range 39-320 mg/dL) and in transgenic mice

134 ion with Lp(a) particles in humans with high Lp(a) levels and in mice carrying human Lp(a).

135 es of FH probands both with and without high Lp(a), and prospectively investigated the association be

136 th FH, especially those with CVD, had higher Lp(a) plasma levels compared with their unaffected relat

137 R) for incident CVD was 1.37 per 1-SD higher Lp(a) level (SD = 32 mg/dl) and 2.37 when comparing the

138 high Lp(a) levels and in mice carrying human Lp(a).

139 expressing either human apo(a) only or human Lp(a) (via coexpression of human apo(a) and human apolip

140 study used measured and genetically imputed Lp(a) molar concentration, kringle IV type 2 (KIV-2) rep

141 t was the percentage change from baseline in Lp(a) concentration at 30 days in the single-dose cohort

142 The percent change in Lp(a) and low-density lipoprotein cholesterol at 48 week

143 5% CI: 1.2 to 1.7) for a 10-fold increase in Lp(a) plasma levels.

144 e role of a specific plasminogen receptor in Lp(a) uptake.

145 s experienced greater absolute reductions in Lp(a) and tended to derive greater coronary benefit from

146 fidence interval) dose-related reductions in Lp(a) compared to control: 29.5% (23.3% to 35.7%) and 24

147 IS-APO(a)-LRx resulted in mean reductions in Lp(a) of 66% (SD 21.8) in the 10 mg group, 80% (SD 13.7%

148 ed in significant dose-related reductions in Lp(a).

149 trong evidence that the LDLR plays a role in Lp(a) catabolism and that this process can be modulated

150 Statins tend to increase Lp(a) levels, possibly contributing to the "residual ris

151 These data indicate that, in inflammation, Lp(a)/apo(a) suppresses neutrophil recruitment by plasmi

152 , the apo(a) component from the internalized Lp(a) was resecreted back into the cellular media, where

153 These findings provide new insights into Lp(a) regulation.

154 Low Lp(a) concentration (bottom 10%) increases T2D risk.

155 nts point towards an association between low Lp(a) concentrations and better cognitive performance.

156 in LPA associated with small apo(a) but low Lp(a) molar concentration to disentangle the relationshi

157 r subjects genetically predicted to have low Lp(a) levels were evaluated to assess the relationship b

158 similar among participants with high or low Lp(a).

159 kexin-type 9 inhibitors and mipomersen lower Lp(a) 20% to 30%, and emerging RNA-targeted therapies lo

160 ecific therapy exists to substantially lower Lp(a) concentrations.

161 %, and emerging RNA-targeted therapies lower Lp(a) >80%.

162 antisense oligonucleotides designed to lower Lp(a) concentrations.

163 c potential of PCSK9 in effectively lowering Lp(a) levels.

164 These findings suggest lowering Lp(a) or inactivating OxPL may slow AS progression and p

165 dies and trials to demonstrate that lowering Lp(a) levels will effectively reduce the risk of calcifi

166 a tool to test the hypothesis that lowering Lp(a) plasma levels will lead to clinical benefit.

167 designs to test the hypothesis that lowering Lp(a) will reduce progression aortic stenosis and the ne

168 Men within the lowest Lp(a)-quintile showed better cognitive performance in th

169 icipants assigned to IONIS-APO(a)Rx had mean Lp(a) reductions of 66.8% (SD 20.6) in cohort A and 71.6

170 ignificant dose-dependent reductions in mean Lp(a) concentrations were noted in all single-dose IONIS

171 combined 2 prospective cohorts and measured Lp(a) and OxPL-apoB levels in patients with AS (V(max) >

172 IONIS-APO(a)-LRx might mitigate Lp(a)-mediated cardiovascular risk and is being develope

173 validation of biological pathways modulating Lp(a) metabolism are lacking.

174 95% CI: 1.12 to 1.40, respectively), and no Lp(a)-by-FHx interaction was noted (p = 0.75).

175 loss-of-function mutations had little or no Lp(a) and increased the risk of T2D.

176 ed with subjects without FHx and nonelevated Lp(a), those with either elevated Lp(a) or FHx were at a

177 rial wall compared with subjects with normal Lp(a) (7 mg/dL [2-28 mg/dL]; n=30).

178 ), which reflects the biological activity of Lp(a), and Lp(a) levels were measured in 220 patients wi

179 The addition of Lp(a) to the RRS increased the C-index by 0.016.

180 sing 3 different approaches: (1) analysis of Lp(a) fractions isolated by ultracentrifugation; (2) imm

181 Transcriptome analysis of Lp(a)-stimulated human arterial endothelial cells reveal

182 otein [apo(a)], the unique apolipoprotein of Lp(a), and a mimic of plasminogen.

183 These assays revealed the assembly of Lp(a) from apo(a) and LDL, as well as potential pathophy

184 n this study, we assessed the association of Lp(a) levels with risk of incident T2D and tested whethe

185 demonstrate a strong inverse association of Lp(a) levels with risk of T2D.

186 ermine independent and joint associations of Lp(a) and FHx with atherosclerotic cardiovascular diseas

187 Independent and joint associations of Lp(a) and FHx with cardiovascular risk were determined u

188 On 6q locus, we detected associations of Lp(a)-cholesterol with 118 common variants (P = 5 x 10(-

189 The attribute of Lp(a) that affects cardiovascular risk is not establishe

190 Molar concentration is the attribute of Lp(a) that affects risk of cardiovascular diseases.

191 data implicating the potential causality of Lp(a)/oxidized phospholipids, describe emerging therapeu

192 of Lp(a) in vitro and promoting clearance of Lp(a) in vivo.

193 he role of LDL receptors in the clearance of Lp(a), is poorly defined, and no mechanistic studies of

194 ther than the apolipoprotein(a) component of Lp(a).

195 In vitro studies investigated the effects of Lp(a) and OxPL on valvular interstitial cells.

196 can combat the pathophysiological effects of Lp(a).

197 lications for the catabolism and function of Lp(a).

198 We evaluated the impact of Lp(a) on the endothelium and describe that Lp(a), throug

199 Internalization of Lp(a) was markedly reduced following treatment of HepG2

200 ramatically increased the internalization of Lp(a).

201 s review summarizes the current landscape of Lp(a), discusses controversies, and reviews emerging the

202 Higher levels of Lp(a) are associated with an increased risk of cardiovas

203 Low levels of Lp(a) have been associated with type 2 diabetes (T2D).

204 plaques of patients with elevated levels of Lp(a).

205 t analysis and intracellular localization of Lp(a) by confocal microscopy.

206 t analysis and intracellular localization of Lp(a) by confocal microscopy.

207 erapies with specific and potent lowering of Lp(a) are in phase II clinical trials and provide a tool

208 However, the mechanism of Lp(a) catabolism in vivo and the role of PCSK9 in this p

209 s potential pathophysiological mechanisms of Lp(a), including (i) binding to fibrin, (ii) stimulation

210 In vitro studies of the pathophysiology of Lp(a) on monocytes were performed with an in vitro model

211 ction of apo(a); (3) ELISA quantification of Lp(a)-associated PCSK9.

212 comparing the top versus bottom quintile of Lp(a).

213 Pharmacologic reduction of Lp(a) concentration in the 20% of individuals with the g

214 and specific treatments for the reduction of Lp(a) levels and the associated risk of cardiovascular d

215 a-analysis showed a significant reduction of Lp(a) levels following L-carnitine supplementation (WMD:

216 The pathogenic risk of Lp(a) is associated with elevated plasma concentration,

217 Nevertheless, the role of Lp(a) as a predictor of CVD in patients with FH has been

218 AS severity, patients in the top tertile of Lp(a) or OxPL-apoB had increased risk of aortic valve re

219 as faster in patients in the top tertiles of Lp(a) (peak aortic jet velocity: +0.26 +/- 0.26 vs. +0.1

220 a reduced binding/intracellular transport of Lp(a).

221 provide a rationale for randomized trials of Lp(a)-lowering and OxPL-apoB-lowering therapies in AS.

222 Progress in the understanding of Lp(a) metabolism has the potential to lead to the develo

223 in (a) (Lp(a)), mediating cellular uptake of Lp(a) in vitro and promoting clearance of Lp(a) in vivo.

224 rationale for the potential clinical use of Lp(a)-lowering therapies in high-risk patients or patien

225 o assess the independent prognostic value of Lp(a) and the efficacy of evolocumab for coronary risk r

226 OxPLs are pro-inflammatory, circulate on Lp(a), and mediate CAD.

227 markedly attenuated by inactivating OxPL on Lp(a) or removing OxPL on apolipoprotein(a).

228 Optimal Lp(a) internalization in both hepatic and primary human

229 at least partially due to disagreement over Lp(a) measurement methodologies, its physiological role

230 y IL-1 genotype, oxidation of phospholipids, Lp(a), and genetic predisposition to CAD and cardiovascu

231 Plasma Lp(a) levels are reduced by monoclonal antibodies target

232 Plasma Lp(a) was measured and FHx was ascertained in 2 cohorts.

233 DL-C by 55.1%, LDL-apoB by 56.3%, and plasma Lp(a) by 18.7%.

234 Elevated plasma Lp(a) and FHx have independent and additive joint associ

235 ere mean percentage change in fasting plasma Lp(a) concentration at day 85 or 99 in the per-protocol

236 ere mean percentage change in fasting plasma Lp(a) concentration, safety, and tolerability at day 30

237 pendent, mean percentage decreases in plasma Lp(a) concentration of 39.6% from baseline in the 100 mg

238 istration, a significant reduction in plasma Lp(a) concentration was observed with oral (WMD: -9.00 m

239 No effective therapies to lower plasma Lp(a) concentrations exist.

240 The regulation of plasma Lp(a) levels, including the role of LDL receptors in the

241 se-dependent, selective reductions of plasma Lp(a).

242 also play a role in the reduction of plasma Lp(a).

243 o assess the impact of L-carnitine on plasma Lp(a) concentrations through systematic review and meta-

244 ve been shown to significantly reduce plasma Lp(a) concentration.

245 reviews emerging therapies to reduce plasma Lp(a) levels to decrease risk of CVD and CAVS.

246 PCSK9 levels directly correlated with plasma Lp(a) levels but not with total plasma PCSK9 levels.

247 rest given the ongoing development of potent Lp(a) inhibitors.

248 effective alternative to effectively reduce Lp(a).

249 Current therapeutic options to reduce Lp(a) are limited.

250 a novel, tolerable, potent therapy to reduce Lp(a) concentrations.

251 rotein(a) (Lp[a]) levels, evolocumab reduced Lp(a) by 33 nmol/L and risk of VTE by 48% (HR, 0.52 [95%

252 er baseline Lp(a) levels, evolocumab reduced Lp(a) by only 7 nmol/L and had no effect on VTE risk (P(

253 t 48 weeks, evolocumab significantly reduced Lp(a) by a median (interquartile range) of 26.9% (6.2%-4

254 Evolocumab significantly reduced Lp(a) levels, and patients with higher baseline Lp(a) le

255 Selective Lp(a) apheresis has offered some evidence that Lp(a)-low

256 on, the meta-analysis suggests a significant Lp(a) lowering by oral L-carnitine supplementation.

257 Allele-specific Lp(a) levels did not add to the predictive ability of th

258 ctice and developing therapies with specific Lp(a)-lowering activity.

259 Similarly, on-statin Lp(a) concentrations were associated with residual risk

260 IONIS-APO(a)-L(Rx) targets Lp(a).

261 These findings demonstrate that Lp(a) induces monocyte trafficking to the arterial wall

262 f Lp(a) on the endothelium and describe that Lp(a), through its oxidized phospholipid content, activa

263 (a) apheresis has offered some evidence that Lp(a)-lowering can improve cardiovascular end-points.

264 The novel findings that Lp(a) is internalized by the plasminogen receptor, plasm

265 These findings support the hypothesis that Lp(a) mediates AS progression through its associated OxP

266 We hypothesized that Lp(a) induces endothelial cell inflammation by rewiring

267 We report that Lp(a) internalization by hepatic HepG2 cells and primary

268 Collectively, our findings show that Lp(a) activates the endothelium by enhancing PFKFB3-medi

269 In vitro studies show that Lp(a) contains OxPL and augments the proinflammatory res

270 These findings suggest that Lp(a) levels may be used in risk assessment of subjects

271 p(a) molar concentration fully explained the Lp(a) association with CAD, and there was no residual as

272 detected a high level of ATX activity in the Lp(a) fraction in circulation.

273 y defined, and no mechanistic studies of the Lp(a) lowering by alirocumab in humans have been publish

274 These approaches will allow testing of the "Lp(a) hypothesis" in clinical trials.

275 icipants treated with potent statin therapy, Lp(a) was a significant determinant of residual risk.

276 e predictive ability of the FRS or RRS or to Lp(a).

277 During follow-up, patients in the top Lp(a) tertile had increased progression of valvular comp

278 ron emission tomography, patients in the top Lp(a) tertile had increased valve calcification activity

279 Baseline and on-treatment Lp(a) concentrations were assessed in 9612 multiethnic p

280 In vitro, Lp(a) induced osteogenic differentiation of valvular int

281 This study sought to determine whether Lp(a) and OxPL are associated with hemodynamic progressi

282 his study was conducted to determine whether Lp(a) improves CVD risk prediction.

283 However, whether Lp(a) modifies clinical risk assessment was not establis

284 This study investigated whether Lp(a) and OxPL on apolipoprotein B-100 (OxPL-apoB) level

285 with risk of incident T2D and tested whether Lp(a) levels are causally linked to T2D.

286 findings provide a novel mechanism by which Lp(a) mediates cardiovascular disease.

287 mpany new classes of therapeutic agents with Lp(a)-lowering effects.

288 thesized that it can also be associated with Lp(a) in plasma.

289 how that PCSK9 is physically associated with Lp(a) in vivo using 3 different approaches: (1) analysis

290 enetic variant (rs10455872), associated with Lp(a) levels, in calcific AVS.

291 2 numbers were significantly associated with Lp(a)-cholesterol (P = 2.28 x 10(-9)).

292 to identify genetic variants associated with Lp(a)-cholesterol levels in the Old Order Amish.

293 s3798220 and rs10455872 were associated with Lp(a)-cholesterol levels independent of each other and K

294 d two variants most strongly associated with Lp(a)-cholesterol, rs3798220 (P = 1.07 x 10(-14)) and rs

295 at plasma PCSK9 is found in association with Lp(a) particles in humans with high Lp(a) levels and in

296 Plasma PCSK9 levels correlated with Lp(a) levels, but not with the number of kringle IV-2 re

297 Preferential association of PCSK9 with Lp(a) versus low-density lipoprotein (1.7-fold increase)

298 o(a) only, and the association of PCSK9 with Lp(a) was not affected by the loss of the apo(a) region

299 S AND Human hepatoma cells were treated with Lp(a) purified from human plasma and Lp(a) uptake studie

300 Human hepatoma cells were treated with Lp(a) purified from human plasma and Lp(a) uptake studie