ライフサイエンスコーパス: lipoprotein(a)

1 ery-low-density lipoprotein cholesterol, and lipoprotein(a).

2 poprotein cholesterol, apolipoprotein B, and lipoprotein(a).

3 -beam computed tomography, homocysteine, and lipoprotein(a).

4 its except the factor V variant and elevated lipoprotein(a).

5 nd treating elevated levels of OxPL/apoB and lipoprotein(a).

6 oncentrations of LDL-IIIA (24.7-25.5 nm) and lipoprotein(a).

7 42 (95% CI, 0.86 to 2.32, P trend =0.19) for lipoprotein(a).

8 d, such as LDL cholesterol, homocysteine and lipoprotein(a).

9 ave higher serum levels of triglycerides and lipoprotein(a).

10 irocumab, particularly among those with high lipoprotein(a).

11 LDL-C(corrected)) for cholesterol content in lipoprotein(a).

12 poprotein through a disulfide bridge to form lipoprotein(a).

13 ol, apolipoprotein AI, apolipoprotein B, and lipoprotein(a) (2-6% change; P < 0.05), whereas iTFA did

14 B (-26.3%), total cholesterol (-19.4%), and lipoprotein(a) (-21.1%) compared with placebo (all P<0.0

15 ficantly reduced apolipoprotein B (-38%) and lipoprotein(a) (-24%) (p < 0.001).

16 l (44%-65%), apolipoprotein B (48%-59%), and lipoprotein(a) (27%-50%) without major adverse effects i

17 s placebo and 24% [16-31] vs ezetimibe), and lipoprotein(a) (31% [25-37] vs placebo and 26% [16-35] v

18 lipoprotein B and A-I would reclassify 1.1%; lipoprotein(a), 4.1%; and lipoprotein-associated phospho

19 ic blood pressure,.21; immunoglobulin E,.63; lipoprotein(a),.77; and body-mass index,.54.

20 Controversy exists as to whether lipoprotein(a), a lipoprotein with homology to plasminog

21 poprotein cholesterol, apolipoprotein B, and lipoprotein(a) (all p < 0.0001).

22 en activator (t-PA), leukocyte elastase, and lipoprotein(a) (all P<0.01), as well as von Willebrand f

23 Plasma levels of lipoprotein(a) and 25(OH)D did not associate.

24 sity lipoprotein cholesterol), novel lipids [lipoprotein(a) and apolipoprotein A1 and B-100], creatin

25 This study compared the levels of lipoprotein(a) and associated genetic factors between in

26 the apolipoprotein(a) [apo(a)] component of lipoprotein(a) and COOH-terminal Lys residues generated

27 Alirocumab-induced reductions of lipoprotein(a) and corrected LDL-C independently predict

28 Baseline lipoprotein(a) and corrected LDL-C levels and their redu

29 rotein cholesterol, glycosylated hemoglobin, lipoprotein(a) and fibrinogen levels, and lower triglyce

30 arkers, decreases central fat, and increases lipoprotein(a) and glucose levels without affecting lipi

31 rmined whether alirocumab-induced changes in lipoprotein(a) and LDL-C independently predicted major a

32 At baseline, median lipoprotein(a) and LDL-C(corrected) were 21 and 75 mg/dL

33 se subtilisin/kexin type 9 inhibitor, lowers lipoprotein(a) and low-density lipoprotein cholesterol (

34 e subtilisin/kexin type 9) inhibitors reduce lipoprotein(a) and low-density lipoprotein cholesterol (

35 After extraction of both lipoprotein(a) and low-density lipoprotein with glycerol

36 ew emerging data on the relationship between lipoprotein(a) and oxidized phospholipids.

37 ous studies have examined the association of lipoprotein(a) and risk of stroke; however, the results

38 rrelation was found between plasma levels of lipoprotein(a) and the content of oxidized phospholipids

39 The unusual species distribution of lipoprotein(a) and the extreme polymorphic nature of its

40 The structure of lipoprotein(a) and the interactions between low-density

41 singly, human genetic evidence suggests that lipoprotein(a) and triglyceride-rich lipoproteins causal

42 domisation studies support a causal role for lipoprotein(a) and triglycerides in ischaemic heart dise

43 erol (TC), LDL cholesterol, triacylglycerol, lipoprotein(a), and apolipoprotein B were higher after V

44 in(a), high-density lipoprotein cholesterol, lipoprotein(a), and apolipoprotein E genotype.

45 y affect changes in LDL, apolipoprotein A-I, lipoprotein(a), and body weight when dietary fats are re

46 served on VLDL-cholesterol, triacylglycerol, lipoprotein(a), and C-reactive protein concentrations or

47 oy compared with control; P = 0.016), plasma lipoprotein(a), and dietary iron.

48 including total cholesterol, triglycerides, lipoprotein(a), and fibrinogen.

49 nsferase; and, in women, C-reactive protein, lipoprotein(a), and glycated hemoglobin levels.

50 olesterol, total cholesterol, triglycerides, lipoprotein(a), and HDL cholesterol at 12 weeks for evol

51 lglycerol) and lipoprotein [LDL cholesterol, lipoprotein(a), and HDL cholesterol] concentrations in I

52 smoking, ratio of total to HDL cholesterol, lipoprotein(a), and high-sensitivity C-reactive protein

53 itivity C-reactive protein, serum amyloid-A, lipoprotein(a), and homocysteine were assessed.

54 , including low HDL, and high triglycerides, lipoprotein(a), and homocysteine, where prospective stud

55 Apolipoprotein A-I, apolipoprotein B, lipoprotein(a), and LDL peak particle diameter were eval

56 nd 2 and decreased high-density lipoprotein, lipoprotein(a), and leptin (P<0.02).

57 ein subclass profile (NMR-LSP), apoA1, apoB, lipoprotein(a), and susceptibility of LDL to oxidation.

58 ylglycerol, apolipoprotein (apo) A-I, apo B, lipoprotein(a), and total, LDL, and HDL cholesterol and

59 HDL-cholesterol, apo A-I, lipoprotein(a), and triacylglycerol concentrations were

60 articles, including low-density lipoprotein, lipoprotein(a), and triglyceride-rich particles such as

61 ging therapies for lowering LDL cholesterol, lipoprotein(a), and triglycerides for prevention of isch

62 B, non-high-density lipoprotein cholesterol, lipoprotein(a), and triglycerides.

63 and A-I; 0.0016 (95% CI, 0.0009-0.0023) for lipoprotein(a); and 0.0018 (95% CI, 0.0010-0.0026) for l

64 or non-high-density lipoprotein cholesterol; lipoprotein(a), apolipoprotein B, and high-density lipop

65 Plasma levels of lipoprotein(a) are affected by different types of dietar

66 onfirmed that plasma-derived and recombinant lipoprotein(a) as well as purified recombinant apo(a) va

67 Lipoprotein(a) at baseline was measured among 27,736 ini

68 duction (median -7.7% [IQR -21.6 to 6.8]) in lipoprotein(a) at week 12 (p=0.0015), with some addition

69 essure, low-density lipoprotein cholesterol, lipoprotein(a), body mass index (BMI), and fibrinogen le

70 umab, the change from baseline to Month 4 in lipoprotein(a), but not LDL-C(corrected), was associated

71 ults suggest that FH does not cause elevated lipoprotein(a), but that elevated lipoprotein(a) increas

72 Alirocumab reduced lipoprotein(a) by 5.0 mg/dl (IQR: 0 to 13.5 mg/dl), corr

73 the switch to measure serum lipid fractions, lipoprotein(a), C-reactive protein, and homocysteine.

74 Subclass pattern of LDL, lipoprotein(a) cholesterol, intermediate-density lipopro

75 ent in LPA KIV2 repeats after adjustment for lipoprotein(a) concentration and conventional lipid conc

76 s mendelian randomisation study, we measured lipoprotein(a) concentration and determined apolipoprote

77 apolipoprotein(a) isoform size and increased lipoprotein(a) concentration are independent and causal

78 7 (1.07-1.50; p=0.007) per 1-SD increment in lipoprotein(a) concentration due to rs3777392, which was

79 with all-cause mortality (highest tertile of lipoprotein(a) concentration in plasma 0.95, 0.81-1.11 a

80 We tested associations of tertiles of lipoprotein(a) concentration in plasma and two LPA singl

81 Lipoprotein(a) concentration is associated with cardiova

82 (1.05-1.14; p<0.0001) per 1-SD increment in lipoprotein(a) concentration, after adjustment for LPA K

83 ller apolipoprotein(a) isoform size, but not lipoprotein(a) concentration, and rs3777392 as a variant

84 , and rs3777392 as a variant associated with lipoprotein(a) concentration, but not apolipoprotein(a)

85 mate whether apolipoprotein(a) isoform size, lipoprotein(a) concentration, or both were causally asso

86 olipoprotein(a) isoform size and circulating lipoprotein(a) concentration, to coronary heart disease.

87 -SD difference in either LPA KIV2 repeats or lipoprotein(a) concentration.

88 r apolipoprotein(a) isoform size in serum or lipoprotein(a) concentration.

89 ith either apolipoprotein(a) isoform size or lipoprotein(a) concentration.

90 ients with prevalent coronary heart disease, lipoprotein(a) concentrations and genetic variants showe

91 l, apolipoprotein A-I, apolipoprotein B, and lipoprotein(a) concentrations and on LDL peak particle d

92 Lipoprotein(a) concentrations in plasma are associated w

93 f coronary heart disease was associated with lipoprotein(a) concentrations in plasma in the highest t

94 Lipoprotein(a) concentrations increased with both the CH

95 Whether lipoprotein(a) concentrations or LPA genetic variants pr

96 Results for plasma lipoprotein(a) concentrations were validated in five ind

97 oprotein, triglyceride-rich lipoproteins, or lipoprotein(a)] consistently increase risk for CHD.

98 correlation coefficient 0.13, p = 0.001) and lipoprotein(a) (correlation coefficient -0.11, p < 0.001

99 protein, fibrinogen, sICAM-1, homocysteine, lipoprotein(a), creatinine clearance, high-density lipop

100 In participants for whom KIV2 repeat and lipoprotein(a) data were available, the OR for myocardia

101 f hormone therapy during the first year, and lipoprotein(a) emerged as a possible modifier during the

102 documented in transgenic mice overexpressing lipoprotein(a), even in mice not fed atherogenic diets o

103 des, homocysteine, C-reactive protein (CRP), lipoprotein(a), fibrinogen, and apolipoproteins (apo) A-

104 A1 are decreased and levels of homocysteine, lipoprotein(a), fibrinogen, and C-reactive protein are i

105 served do not support routine measurement of lipoprotein(a) for cardiovascular stratification in wome

106 mbin activatable fibrinolysis inhibitor, and lipoprotein(a) for major adverse cardiac events is highl

107 teins, apolipoprotein A-I, apolipoprotein B, lipoprotein(a), glucose, insulin, HDL subfractions, and

108 ent groups, women in the highest quintile of lipoprotein(a) (> or =44.0 mg/dL) were 1.47 times more l

109 ally healthy women, extremely high levels of lipoprotein(a) (> or =90th percentile), measured with an

110 bfractionation, apolipoproteins B and A, and lipoprotein(a) have not yet met current standards for bi

111 adhesion molecule-1 (sICAM-1), homocysteine, lipoprotein(a), hemoglobin A1c, creatinine, and conventi

112 (LDL) cholesterol, LDL levels corrected for lipoprotein(a), high-density lipoprotein cholesterol, li

113 ntithrombin, factors VIII/IX/XI, fibrinogen, lipoprotein(a), homocysteine, lupus anticoagulant, antic

114 lial hypercholesterolemia (FH) have elevated lipoprotein(a); however, it remains unclear why.

115 In 2 of 4 studies, high-STA diets increased lipoprotein(a) in comparison with diets high in saturate

116 essure, and the strong causal association of lipoprotein(a) in coronary artery disease development (b

117 into the role of oxidized phospholipids and lipoprotein(a) in human atherogenesis and cardiovascular

118 d phospholipids detected by E06 are bound to lipoprotein(a) in human plasma.

119 We investigated causes of elevated lipoprotein(a) in individuals with clinically diagnosed

120 duced LDL cholesterol, apolipoprotein B, and lipoprotein(a) in patients with hypercholesterolemia wit

121 ent may contribute to selective retention of lipoprotein(a) in the vasculature.

122 B-containing lipoproteins, including LDL and lipoprotein(a), in HeFH patients with coronary artery di

123 e elevated lipoprotein(a), but that elevated lipoprotein(a) increases the likelihood that an individu

124 Lipoprotein(a) is an atherogenic low-density lipoprotein

125 Lipoprotein(a) is an atherogenic, cholesterol ester-rich

126 he purpose of this study was to test if high lipoprotein(a) is associated with high risk of ischemic

127 ,202 phenotypes to demonstrate that elevated lipoprotein(a) is associated with increased low-density

128 High lipoprotein(a) is associated with increased risk of myoc

129 Lipoprotein(a) is composed of low-density lipoprotein li

130 Lipoprotein(a) is considered a risk factor for coronary

131 In addition, it has been shown that lipoprotein(a) is the primary carrier of oxidized phosph

132 The correlation of OxPL/apoB to lipoprotein(a) is very strong in individuals with small

133 ng carbamazepine also had a 31.2% decline in lipoprotein(a) level (p = 0.0004), whereas those taken o

134 hile increasing age (P<0.001) and increasing lipoprotein(a) level (P=0.005) were associated with incr

135 y syndrome, risk of PAD events is related to lipoprotein(a) level and is reduced by alirocumab, parti

136 to confirm whether risk of VTE is related to lipoprotein(a) level and its reduction with alirocumab.

137 primary end point was the percent change in lipoprotein(a) level from baseline to month 6 of exposur

138 5 study participants, who simultaneously had lipoprotein(a) level measurements, and in a replication

139 otein A1 level of less than 1.2 g/L, a serum lipoprotein(a) level of at least 1.61 micromol/L (> or =

140 analyses for a 50 mg/dl (105 nmol/l) higher lipoprotein(a) level the age- and sex-adjusted hazard ra

141 Lipoprotein(a) level was measured in blood samples obtai

142 The lipoprotein(a) level was measured with an isoform-indepe

143 high-density lipoprotein cholesterol level, lipoprotein(a) level, and creatinine clearance).

144 asured by electron-beam computed tomography, lipoprotein(a) level, homocysteine level, leukocyte coun

145 sex, increased creatinine clearance, higher lipoprotein(a) level, proteinuria, azathioprine treatmen

146 sion, diabetes, obesity (in women), elevated lipoprotein(a) level, smoking (in men), and low socioeco

147 For individuals with lipoprotein(a) levels >/=80th percentile (>/=47 mg/dl),

148 viduals with no events occurred, addition of lipoprotein(a) levels >/=80th percentile overall yielded

149 duals >70 years of age with hypertension and lipoprotein(a) levels >93 mg/dl (>199 nmol/l: 96th to 10

150 rval [CI]:1.24 to 2.05) for individuals with lipoprotein(a) levels >93mg/dl (>199 nmol/L: 96th to 100

151 Compared with individuals with lipoprotein(a) levels <10 mg/dl (<18 nmol/l: first to 50

152 Baseline lipoprotein(a) levels (median: 21.2 mg/dl; interquartile

153 Our objective was to determine whether lipoprotein(a) levels and a common genetic variant that

154 10455872 and rs3798220, which correlate with lipoprotein(a) levels and coronary artery disease (CAD),

155 this study was to determine whether elevated lipoprotein(a) levels and corresponding LPA risk genotyp

156 ependent manner in patients who had elevated lipoprotein(a) levels and established cardiovascular dis

157 For two traits, lipoprotein(a) levels and neutrophil count, aggregate te

158 The study tested whether extreme lipoprotein(a) levels and/or corresponding LPA risk geno

159 Using predefined cutpoints for extreme lipoprotein(a) levels and/or corresponding LPA risk geno

160 tic variant that is strongly associated with lipoprotein(a) levels are associated with an increased r

161 Patients with high lipoprotein(a) levels are at increased risk for AVS.

162 Lipoprotein(a) levels are genetically determined and, wh

163 Elevated lipoprotein(a) levels cause MI and CHD.

164 However, within the FH cohort, lipoprotein(a) levels did not differ based on the presen

165 riables listed above, the HR associated with lipoprotein(a) levels exceeding the 90th percentile (> o

166 is subgroup, the adjusted HR associated with lipoprotein(a) levels exceeding the 90th percentile was

167 APO(a)-L(Rx) reduced lipoprotein(a) levels in a dose-dependent manner in pati

168 o prospective study has suggested a role for lipoprotein(a) levels in the pathophysiology of AVS.

169 The median baseline lipoprotein(a) levels in the six groups ranged from 204.

170 Lipoprotein(a) levels increased (difference between grou

171 There is also poor agreement among lipoprotein(a) levels obtained by different assays.

172 blished cardiovascular disease and screening lipoprotein(a) levels of at least 60 mg per deciliter (1

173 Extreme lipoprotein(a) levels or corresponding LPA KIV-2/rs10455

174 10-year MI and CHD risk, addition of extreme lipoprotein(a) levels or corresponding LPA risk genotype

175 s in the FH cohort had significantly greater lipoprotein(a) levels than either the general population

176 Lipoprotein(a) levels were also not statistically differ

177 rum amyloid polypeptide A, inteleukin-6, and lipoprotein(a) levels were determined at baseline and 6

178 Lipoprotein(a) levels were found to correlate inversely

179 and low-density lipoprotein cholesterol and lipoprotein(a) levels were independent predictors of inc

180 Serum lipoprotein(a) levels were measured in 17 553 participan

181 Lipoprotein(a) levels were reduced by canakinumab compar

182 ell as sections on the genetic regulation of lipoprotein(a) levels, genes regulating the inverse rela

183 872 variant, which is associated with higher lipoprotein(a) levels, is also associated with increased

184 (Rx) resulted in dose-dependent decreases in lipoprotein(a) levels, with mean percent decreases of 35

185 no approved pharmacologic therapies to lower lipoprotein(a) levels.

186 hreshold effect among those with the highest lipoprotein(a) levels.

187 Lipoprotein(a) lowering by alirocumab is an independent

188 Lipoprotein(a)-lowering interventions could be preferent

189 nditioned medium from incubation mixtures of lipoprotein(a) (Lp(a)) and HUVECs (LCM) contained CCL1 a

190 tudy sought to determine the relationship of lipoprotein(a) (Lp(a)) and other cardiac risk factors to

191 Increased plasma concentrations of lipoprotein(a) (Lp(a)) are associated with an increased

192 sminogen was discovered in 1987, the role of lipoprotein(a) (Lp(a)) as an inhibitor of the normal fib

193 Elevated levels of lipoprotein(a) (Lp(a)) have been identified as an indepe

194 Lipoprotein(a) (Lp(a)) hyperlipoproteinemia is a major r

195 Accumulation of lipoprotein(a) (Lp(a)) in atherosclerotic plaques is med

196 Lipoprotein(a) (Lp(a)) is an LDL variant that has been s

197 Lipoprotein(a) (Lp(a)) is associated with cardiovascular

198 B100 of low density lipoprotein, to form the lipoprotein(a) (Lp(a)) particle, or as proteolytic fragm

199 r mates, all of the same strain, with either lipoprotein(a) (Lp(a)), full-length free apo(a), or its

200 Elevated lipoprotein(a) (Lp[a]) and family history (FHx) of coron

201 Elevated lipoprotein(a) (Lp[a]) is a highly prevalent (around 20%

202 Lipoprotein(a) (Lp[a]) is a risk factor for cardiovascul

203 Elevated lipoprotein(a) (Lp[a]) is associated with aortic stenosi

204 Although circulating lipoprotein(a) (Lp[a]) is likely to be a causal risk fac

205 Evidence that elevated lipoprotein(a) (Lp[a]) levels contribute to cardiovascul

206 n contrast, in patients with higher baseline lipoprotein(a) (Lp[a]) levels, evolocumab reduced Lp(a)

207 otein (CRP) level correlated positively with lipoprotein(a) (Lp[a]), intercellular adhesion molecule

208 dy was to determine the relationship between lipoprotein(a) [Lp(a)] and cardiovascular disease (CVD)

209 ociation between the plasma concentration of lipoprotein(a) [Lp(a)] and coronary heart disease (CHD)

210 n shown to increase plasma concentrations of lipoprotein(a) [Lp(a)] and of triacylglycerol- rich lipo

211 is cases are associated with highly elevated lipoprotein(a) [Lp(a)] and pathways related to the metab

212 Elevated plasma levels of lipoprotein(a) [Lp(a)] are an independent risk factor fo

213 Patients with elevated levels of lipoprotein(a) [Lp(a)] are hallmarked by increased metab

214 ilial hypercholesterolemia (FH) and elevated lipoprotein(a) [Lp(a)] are inherited disorders associate

215 Lipoprotein(a) [Lp(a)] exhibits many of the same propert

216 Lipoprotein(a) [Lp(a)] has been identified as an indepen

217 Recent studies showed that lipoprotein(a) [Lp(a)] is a causal risk factor for cardi

218 Lipoprotein(a) [Lp(a)] is a causal risk factor for cardi

219 Lipoprotein(a) [Lp(a)] is a highly atherogenic low-densi

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

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

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

223 Elevated lipoprotein(a) [Lp(a)] is a prevalent, independent cardi

224 Lipoprotein(a) [Lp(a)] is a risk factor for atherosclero

225 Lipoprotein(a) [Lp(a)] is a risk factor for cardiovascul

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

227 Lipoprotein(a) [Lp(a)] is an emerging risk factor for ca

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

229 s of studies with limited statistical power, lipoprotein(a) [Lp(a)] is not considered a risk factor f

230 orts a direct and causal association between lipoprotein(a) [Lp(a)] levels and coronary risk, but the

231 on-study apolipoproteins (apo) A-1 and B and lipoprotein(a) [Lp(a)] levels and the development of sub

232 Lipoprotein(a) [Lp(a)] levels are increased in dialysis

233 in end-stage renal disease, such as elevated lipoprotein(a) [Lp(a)] levels.

234 udies have provided increasing evidence that lipoprotein(a) [Lp(a)] may be a potential causal, geneti

235 Lipoprotein(a) [Lp(a)] may play a causal role in atheros

236 nship of a panel of oxidative biomarkers and lipoprotein(a) [Lp(a)] to CAD risk is not fully determin

237 sclerotic lesions and promote the binding of lipoprotein(a) [Lp(a)] to vascular cells without a conco

238 randomization studies have highlighted that lipoprotein(a) [Lp(a)] was associated with calcific aort

239 Although lipoprotein(a) [Lp(a)] was first described more than 35

240 s study assesses whether the relationship of lipoprotein(a) [Lp(a)] with cardiovascular risk may be m

241 Lipoprotein(a) [Lp(a)], a major carrier of oxidized phos

242 LDL-C, HDL-C, lipoprotein(a) [Lp(a)], and in women but not men, trigly

243 Serum levels of apo(AII), apo(CIII), lipoprotein(a) [Lp(a)], and triglyceride were significan

244 olipoprotein B-100 detected by antibody E06, lipoprotein(a) [Lp(a)], autoantibodies to malondialdehyd

245 Lipoprotein(a) [Lp(a)], consisting of LDL and the unique

246 n-HDL, total cholesterol, triglycerides, and lipoprotein(a) [Lp(a)].

247 in(a) [apo(a)] is a component of atherogenic lipoprotein(a) [Lp(a)].

248 Lipoprotein(a), Lp(a), an athero-thrombotic risk factor,

249 fic multikringle glycoprotein constituent of lipoprotein(a), Lp(a), occurs in the plasma mostly bound

250 of the analytical challenges in the study of lipoprotein(a), (Lp(a)).

251 One SNP in the lipoprotein(a) (LPA) locus (rs10455872) reached genomewi

252 City Heart Study with measurements of plasma lipoprotein(a), LPA kringle-IV type 2 number of repeats,

253 he lipoprotein lipase pathway or circulating lipoprotein(a) may be efficacious for multiple atheroscl

254 ggesting additional mechanisms through which lipoprotein(a) may be pro-atherogenic.

255 proposed that a unique physiological role of lipoprotein(a) may be to bind and transport proinflammat

256 ctin-3, high-sensitivity C-reactive protein, lipoprotein(a), N-terminal pro-B-type natriuretic peptid

257 otropic consequences of genetically elevated lipoprotein(a) on diverse morbidities via electronic hea

258 zation uncover wide-spread causal effects of lipoprotein(a) on overall lipoprotein metabolism and we

259 and if such effects are related to levels of lipoprotein(a) or LDL-C.

260 esterol, triacylglycerol, apo A-I, apo B, or lipoprotein(a) or the LDL peak particle diameter.

261 the combination of apolipoprotein B and A-I, lipoprotein(a), or lipoprotein-associated phospholipase

262 levels strongly paralleled the acute rise in lipoprotein(a), or Lp(a), in the MI group, suggesting th

263 This study sought to determine the effect of lipoprotein(a), or Lp(a), levels and apolipoprotein(a),

264 Apolipoprotein E, lipoprotein(a), oxidized LDL (low density lipoprotein)'s

265 Nonsignificant baseline elevations of lipoprotein(a) (P =.40) and homocysteine (P =.90) were o

266 poprotein cholesterol, apolipoprotein B, and lipoprotein(a) (P<0.001 for all comparisons).

267 D events was related to baseline quartile of lipoprotein(a) (P(trend)=0.0021), and tended to associat

268 mab was associated with baseline quartile of lipoprotein(a) (P(trend)=0.03), but not LDL-C(corrected)

269 ended to associate with baseline quartile of lipoprotein(a) (P(trend)=0.06), but not LDL-C(corrected)

270 imvastatin produced a modest increase in log[lipoprotein(a)] (P=0.03) at days 7 and 14.

271 ed preparations without glycerol extraction, lipoprotein(a) particles had an irregular mass of densit

272 In contrast, lipoprotein(a) particles treated with 6-aminohexanoic ac

273 Lipoprotein(a) particles with smaller, rather than large

274 The lipoprotein(a) pathway is a causal factor in coronary he

275 lipoprotein cholesterol, triglycerides, and lipoprotein(a) peaked during late peri- and early postme

276 ctors (plasminogen activator inhibitor 1 and lipoprotein(a)); platelet surface receptors; and vascula

277 LDL-C [corrected for cholesterol content in lipoprotein(a)] predicted MACE.

278 otary-shadowed and unidirectionally shadowed lipoprotein(a) prepared without glycerol revealed that i

279 t-PA, intercellular adhesion molecule 1, and lipoprotein(a)] provided some added discrimination.

280 2; r = 0.52]; apolipoprotein A-I (r = 0.49); lipoprotein(a) (r = 0.49); electrophoresis measurements

281 (for triglyceride reduction) and apo(a) (for lipoprotein(a) reduction) are showing a promising trajec

282 ors include elevated serum concentrations of lipoprotein(a), remnant lipoproteins, and homocysteine.

283 The atherogenic potential of lipoprotein(a) seems to be neutralized by effective redu

284 butor to MACE reduction, which suggests that lipoprotein(a) should be an independent treatment target

285 tom lipoprotein(a) tertile, those in the top lipoprotein(a) tertile had a higher risk of AVS (hazard

286 lk, compared with participants in the bottom lipoprotein(a) tertile, those in the top lipoprotein(a)

287 olesterol, triacylglycerol, LDL cholesterol, lipoprotein(a), the ratio of total to HDL cholesterol, a

288 HDL, and LDL cholesterol; triacylglycerols; lipoprotein(a); the percentage of small dense LDL; gluco

289 mvastatin raised HDL cholesterol and lowered lipoprotein(a) to a greater extent than simvastatin alon

290 better understanding of the ability of human lipoprotein(a) to bind oxidized phospholipids may allow

291 ve promising markers of cardiovascular risk: lipoprotein(a), total plasma homocysteine, fibrinolytic

292 terol, high-density lipoprotein cholesterol, lipoprotein(a), triglycerides, hypertension, diabetes me

293 Lipoprotein(a) was measured at randomization and 4 and 1

294 However, when lipoprotein(a) was treated with a lysine analogue, 6-ami

295 Levels of LDL corrected for lipoprotein(a) were an even stronger predictor of dement

296 eral population study, high plasma levels of lipoprotein(a) were associated with increased risk of is

297 art Study, risk estimates for high levels of lipoprotein(a) were in the same direction but did not re

298 owering of triglyceride-rich lipoproteins or lipoprotein(a) will reduce risk for CHD, but this remain

299 A 1-mg/dl reduction in lipoprotein(a) with alirocumab was associated with a HR

300 Interaction of lipoprotein(a) with fibrin associated with atherosclerot