ライフサイエンスコーパス: lipoprotein(a

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

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

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

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

5 42 (95% CI, 0.86 to 2.32, P trend =0.19) for lipoprotein(a).

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

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

8 oximately 22% of the 25% overall variance in lipoprotein(a).

9 and PAI-1, and a lesser effect on HDL2-C and lipoprotein(a).

10 sity, low density, and high density, but not lipoprotein(a).

11 unction that circulates in plasma as part of lipoprotein(a).

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

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

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

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

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

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

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

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

20 sterol; apolipoprotein A-I (91.7 mg/dL); and lipoprotein(a) (4.1 nmol/L), but normal levels of trigly

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

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

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

24 ] is the distinguishing protein component of lipoprotein(a), a major inherited risk factor for athero

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

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

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

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

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 significant factors included height and high lipoprotein(a) and low density lipoprotein cholesterol l

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

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

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

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

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

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

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

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

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

41 ar risk by decreasing LDL-C, fibrinogen, and lipoprotein(a), and by increasing HDL2-C without raising

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

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

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

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

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

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

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

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

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

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

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

53 ctivator, plasminogen activator inhibitor 1, lipoprotein(a), and plasminogen or global fibrinolytic a

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

55 otein (VLDL) cholesterol, VLDL3 cholesterol, lipoprotein(a), and systolic and diastolic blood pressur

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

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

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

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

60 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

61 lycerides, HDL cholesterol, LDL cholesterol, lipoprotein(a), apolipoprotein (apo)A-I, and apoB], and

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

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

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

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

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

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

68 dosages of raloxifene significantly lowered lipoprotein(a) by 7% to 8% (P < .001), less than the 19%

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

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

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

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

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

74 7 (1.07-1.50; p=0.007) per 1-SD increment in lipoprotein(a) concentration due to rs3777392, which was

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

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

77 ion of 105 mg/dL (1.19 mmol/L), and the mean lipoprotein(a) concentration of 25 mg/dL (0.25 g/L) were

78 (1.05-1.14; p<0.0001) per 1-SD increment in lipoprotein(a) concentration, after adjustment for LPA K

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

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

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

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

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

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

85 any of the sites had any direct effect upon lipoprotein(a) concentration.

86 nary apo(a) rose in proportion to the plasma lipoprotein(a) concentration.

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

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

89 poprotein cholesterol, apolipoprotein B, and lipoprotein(a) concentrations and lower high density lip

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

91 ze, there were clear differences between the lipoprotein(a) concentrations associated with alleles of

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 ir relationship with isoform size and plasma lipoprotein(a) concentrations investigated.

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

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

98 n a restricted range of sizes and associated lipoprotein(a) concentrations.

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

100 Lipoprotein(a) contributes to the development of atheros

101 ntia with stroke for the highest quartile of lipoprotein(a)-corrected LDL cholesterol was 4.1 (95% CI

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

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

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

105 The ratio of LDL to HDL cholesterol and lipoprotein(a) decreased on therapies including CE but i

106 ), the distinguishing protein of atherogenic lipoprotein(a), directs accumulation of the lipoprotein(

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

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

109 The role of lipoprotein(a) excess in vascular disease is controversi

110 ntricular hypertrophy, hyperhomocysteinemia, lipoprotein(a) excess, hypertriglyceridemia, oxidative s

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

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

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

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

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

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

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

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

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

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

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

122 ome, and work activity, and higher levels of lipoprotein(a), IMT, hemostasis factor VIII, and von Wil

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

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

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

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

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

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

129 Lipoprotein(a) induces monocyte chemoattraction and smoo

130 Lipoprotein(a) is a plasma particle which is considered

131 Lipoprotein(a) is an atherogenic and thrombogenic lipopr

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

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

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

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

136 Lipoprotein(a) is ubiquitous in human coronary atheroma.

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

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

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

140 5 study participants, who simultaneously had lipoprotein(a) level measurements, and in a replication

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

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

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

150 10455872 and rs3798220, which correlate with lipoprotein(a) levels and coronary artery disease (CAD),

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

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

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

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

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

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

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

158 levels decreased by 25% overall (P < 0.001); lipoprotein(a) levels did not change significantly.

159 VLDL, and HDL cholesterol, triglyceride, and lipoprotein(a) levels did not differ between the groups.

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

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

162 triglyceride levels, low HDL levels and high lipoprotein(a) levels have been documented.

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

164 Lipoprotein(a) levels increased (difference between grou

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

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

167 10-year MI and CHD risk, addition of extreme lipoprotein(a) levels or corresponding LPA risk genotype

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

169 Lipoprotein(a) levels were found to correlate inversely

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

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

172 Lipoprotein(a) levels were reduced by canakinumab compar

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

174 872 variant, which is associated with higher lipoprotein(a) levels, is also associated with increased

175 for a paradoxical 3.3-fold increase in serum lipoprotein(a) levels, nor was there any evidence of ren

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

177 Lipoprotein(a)-lowering interventions could be preferent

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

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

180 t for its covalent linkage to apo(a) to form lipoprotein(a) (Lp(a)) are incompletely understood.

181 Plasma concentrations of the atherogenic lipoprotein(a) (Lp(a)) are predominantly determined by i

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

183 Although it is known that lipoprotein(a) (Lp(a)) binds to proteoglycans, the mecha

184 Elevated plasma levels of lipoprotein(a) (Lp(a)) can be a risk factor for atherosc

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

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

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

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

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

190 ted from human peripheral blood, with either lipoprotein(a) (Lp(a)) or free apolipoprotein(a) (apo(a)

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

192 Plasma levels of lipoprotein(a) (Lp(a)) vary over 1000-fold between indiv

193 protein (apo) A-I and higher levels of apoB, lipoprotein(a) (Lp(a)), and the ratio of apoB to apoA-I

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

195 ch circulates in human plasma in the form of lipoprotein(a) (Lp(a)).

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

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

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

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

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

201 ein A1 (ApoA1), apolipoprotein B (ApoB), and lipoprotein(a) (Lp[a]) were measured in a group of 160 m

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

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

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

205 was the investigation of the in vivo role of lipoprotein(a) [Lp(a)] and inflammatory infiltrates in t

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

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

208 Elevated levels of lipoprotein(a) [Lp(a)] are associated with premature ath

209 gle modules of apolipoprotein(a) [apo(a)] of lipoprotein(a) [Lp(a)] are highly homologous with kringl

210 Lipoprotein(a) [Lp(a)] consists of low-density lipoprote

211 Although the mechanism by which lipoprotein(a) [Lp(a)] contributes to vascular disease r

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

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

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

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

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

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

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

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

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

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

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

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

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

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

226 Considering that lipoprotein(a) [Lp(a)] is structurally similar to LDL, d

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

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

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

230 Elevated lipoprotein(a) [Lp(a)] levels have been associated with

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

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

233 AD), apolipoprotein E (apo E) phenotype, and lipoprotein(a) [Lp(a)] on the response of plasma lipids

234 Lipoprotein(a) [Lp(a)] represents an important independe

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

236 p72, plays a dominant role in the binding of lipoprotein(a) [Lp(a)] to lysine.

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 the development of atherosclerotic lesions, lipoprotein(a) [Lp(a)], a highly atherogenic lipoprotein

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 kringle 4 repeats and circulates as part of lipoprotein(a) [Lp(a)].

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

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

251 hey expressed apo(a) [18.5 +/- 2.5%, without lipoprotein(a), Lp(a), vs. 16.0 +/- 1.7%, with Lp(a)].

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

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

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

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

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

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

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

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

262 The distributions of plasma lipoprotein(a), or Lp(a), levels differ significantly am

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

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

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

266 lipoprotein(a), directs accumulation of the lipoprotein(a) particle to sites in the arterial wall wh

267 is the distinguishing protein portion of the lipoprotein(a) particle, elevated plasma levels of which

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

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

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

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

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

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

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

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

276 2; r = 0.52]; apolipoprotein A-I (r = 0.49); lipoprotein(a) (r = 0.49); electrophoresis measurements

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

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

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

280 Lipoprotein(a) showed no association with educational at

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

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

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

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

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

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

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

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

289 Lipoprotein(a) undergoes a dramatic, reversible conforma

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

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

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

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