ライフサイエンスコーパス: HDL-C

1 HDL-C and TGs were not causally associated with CIMT.

2 HDL-C level is unlikely to represent a CV-specific risk

3 13.2] vs 7.8% [95% CI, 5.7-10.4]; P = .006), HDL-C (17.9% [95% CI, 15.0-21.0] vs 12.8% [95% CI, 9.8-1

4 ensive lipid-lowering treatment (n = 2,046), HDL-C was not associated with recurrent vascular events

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

6 nuclear magnetic resonance spectroscopy, and HDL-C and apolipoprotein A-I (apoA-I) were chemically as

7 TG and HDL-C concentrations were not associated with risk of in

8 n APOC3 (rs138326449) with triglycerides and HDL-C.

9 ryl esters followed a similar time course as HDL-C.

10 The study showed little correlation between HDL-C levels and asymptomatic ICAS.

11 Complex associations exist between HDL-C levels and sociodemographic, lifestyle, comorbidit

12 ession analyses revealed interaction between HDL-C and eGFR in predicting all-cause and cardiovascula

13 No association was noted between HDL-C and PWV.

14 ing the epidemiological relationship between HDL-C and CVD risk and the correlations between some HDL

15 te, ABCA1 up-regulation should increase both HDL-C and RCT rate.

16 x-, and region-specific z-scores for WC, BP, HDL-C, and TGs.

17 dent associations among the levels of LDL-C, HDL-C, and PIB index.

18 Increased LDL-C, HDL-C, and possibly TG levels are associated with a lowe

19 ALS patients had increasing levels of LDL-C, HDL-C, apoB, and apoA-I, whereas gradually decreasing le

20 .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 high

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

22 ing miR-148a to ameliorate an elevated LDL-C/HDL-C ratio, a prominent risk factor for cardiovascular

23 0.9-mg/kg dose did not significantly change HDL-C; however, 6 hours after doses of 3.0, 9.0, and 13.

24 macological manipulation of HDL cholesterol (HDL-C) and examine whether medication-induced changes we

25 In the general population, HDL cholesterol (HDL-C) is associated with reduced cardiovascular events.

26 re strongly associated with HDL cholesterol (HDL-C) levels, metabolic syndrome, and coronary heart di

27 terol concentration of HDL (HDL cholesterol (HDL-C)) without apoC-III was inversely associated with r

28 resistance, triglycerides, HDL cholesterol (HDL-C), and C-reactive protein].

29 iations between circulating HDL cholesterol (HDL-C), LDL cholesterol (LDL-C), and triglycerides and T

30 high-density lipoprotein (HDL) cholesterol (HDL-C).

31 are associated with reduced HDL-cholesterol (HDL-C) levels.

32 The recent failures of HDL-cholesterol (HDL-C) raising therapies have initiated a re-examination

33 ict coronary ED better than HDL-cholesterol (HDL-C).

34 l, non-high-density lipoprotein cholesterol (HDL-C) <100 mg/dl, and apolipoprotein B (ApoB) <80 mg/dl

35 g/dL), high-density lipoprotein cholesterol (HDL-C) (<40 mg/dL), and non-HDL-C (>/= 145 mg/dL) (to co

36 )) and high-density lipoprotein cholesterol (HDL-C) (p = 1.35 x 10(-32)) with each copy of the minor

37 crease high-density lipoprotein cholesterol (HDL-C) and apolipoprotein A-I levels as monotherapy and

38 etween high-density lipoprotein cholesterol (HDL-C) and risk of cardiovascular disease (CVD) has been

39 nce of high-density lipoprotein cholesterol (HDL-C) and triglycerides (TGs) is uncertain.

40 High-density lipoprotein cholesterol (HDL-C) and triglycerides are cardiovascular risk factors

41 els of high-density lipoprotein cholesterol (HDL-C) are common in individuals with human immunodefici

42 nce of high-density lipoprotein cholesterol (HDL-C) as a specific risk factor for cardiovascular (CV)

43 reased high-density lipoprotein cholesterol (HDL-C) compared with those of rats fed a cholesterol-ric

44 plasma high-density lipoprotein cholesterol (HDL-C) has been associated with increased risk of intrac

45 Gs) or high-density lipoprotein cholesterol (HDL-C) have produced inconsistent effects on CIMT and co

46 vel of high-density lipoprotein cholesterol (HDL-C) is also considered to be a predictor for stroke.

47 High-density lipoprotein cholesterol (HDL-C) is an independent risk factor for CVD and is supe

48 reased high-density lipoprotein cholesterol (HDL-C) level by 0.05 mmol/L (2.0 mg/dL) (95% CI, 0.04 to

49 lating high-density lipoprotein cholesterol (HDL-C) levels in vivo.

50 ole in high-density lipoprotein cholesterol (HDL-C) metabolism in selective cholesteryl ester uptake

51 er low high-density lipoprotein cholesterol (HDL-C) or high non-HDL-C This warrants additional evalua

52 C) and high-density lipoprotein cholesterol (HDL-C) were either directly measured or calculated from

53 LDL-C, high-density lipoprotein cholesterol (HDL-C), and triglycerides.

54 DL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides.

55 n mean high-density lipoprotein cholesterol (HDL-C), LDL-C, and apolipoprotein B (apoB) levels in par

56 High density lipoprotein cholesterol (HDL-C), low density lipoprotein cholesterol (LDL-C) and

57 terol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and

58 High-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and

59 (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and

60 terol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and

61 terol, high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), non

62 (TC), high-density-lipoprotein cholesterol (HDL-C), low-density-lipoprotein cholesterol (LDL-C), and

63 d with high-density lipoprotein cholesterol (HDL-C).

64 nd low high-density lipoprotein cholesterol (HDL-C).

65 ise in high-density lipoprotein cholesterol (HDL-C).

66 d with high-density lipoprotein cholesterol (HDL-C; beta = 8.36; 95% CI: -0.15, 16.9 and beta = 5.98;

67 es and high-density lipoprotein cholesterol (HDL-C; cg27243685; P=8.1E-26 and 9.3E-19) was associated

68 robust high density lipoprotein-cholesterol (HDL-C) elevation and low density lipoprotein-cholesterol

69 n that high-density lipoprotein-cholesterol (HDL-C) levels are inversely correlated with cardiovascul

70 sterol/high-density lipoprotein-cholesterol (HDL-C) ratio, HDL-C, and non HDL-C with incident HF.

71 gulate high-density lipoprotein-cholesterol (HDL-C) uptake, through direct targeting and repression o

72 ansport (among other molecules) cholesterol (HDL-C).

73 DL-C], high-density lipoprotein cholesterol [HDL-C], and triglycerides), APOE genotype, and cognitive

74 [TGs], high-density lipoprotein cholesterol [HDL-C], low-density lipoprotein cholesterol [LDL-C], tot

75 fic for low-density lipoprotein cholesterol, HDL-C, and TGs were derived based on single nucleotide p

76 = 0.05) and decreased the total cholesterol-HDL-C ratio by 0.27 (CI, -0.52 to -0.01; P = 0.039).

77 ceride, low HDL-C, or high total cholesterol/HDL-C ratio (3.59 [2.03-6.33], 3.62 [2.06-6.36], and 3.5

78 non-HDL-C levels, and the total cholesterol/HDL-C ratio were positively associated with CV events in

79 on in mice resulted in decreased circulating HDL-C levels.

80 In contrast, HDL-C and other traditional lipid risk factors did not d

81 lesterol, triglycerides (TGs), high-density (HDL-C), and low-density lipoprotein cholesterol (LDL-C)

82 igh-density lipoprotein (HDL), HDL-diameter, HDL-C, HDL2-C, and HDL3-C (all P < 0.003).

83 31.1 mg/dl; non-HDL-C: 124.0 +/- 33.5 mg/dl; HDL-C: 53 +/- 12.8 mg/dl; and apoB: 90.7 +/- 24 mg/dl; m

84 ion in cholesterol efflux capacity than does HDL-C.

85 (SR-BI knockout mice) have markedly elevated HDL-C levels but, paradoxically, increased atheroscleros

86 A number of clinical trials have evaluated HDL-C modification from use of a CETP inhibitor.

87 ies of SCARB1 in 95 individuals with extreme HDL-C levels selected from a population-based sample of

88 ipidemia identified individuals with extreme HDL-C levels.

89 er adjustment for conventional risk factors, HDL-C levels still showed no significant association wit

90 ant loci was 10 for TC, 12 for LDL-C, 10 for HDL-C, and 6 for TG levels.

91 05, 95% CI: 0.50, 2.21; P-trend = 0.44) (for HDL-C with apoC-III vs. HDL-C without apoC-III, P-hetero

92 ) for LDL-C and 0.83 (95% CI, 0.76-0.90) for HDL-C per 1-SD elevation.

93 97, P=0.03) after additionally adjusting for HDL-C.

94 one remained significant after adjusting for HDL-C: hazard ratios for insulin, 1.06 (CI, 0.98-1.16);

95 After correction for HDL-C, both efflux capacity and HDL-PIMA remained signif

96 The corresponding OR for HDL-C (equivalent to a 16-mg/dL increase) was 0.95 (95%

97 sease risk, and this initiated the quest for HDL-C-increasing therapies.

98 plaining 7.9% of its variance), 140 SNPs for HDL-C (6.6% of variance), and 140 SNPs for TGs (5.9% of

99 of major cardiovascular events, whereas for HDL-C this was not the case.

100 More RPV- than EFV-treated patients had HDL-C values below these cutoffs (P = .02).

101 ciated with changes in BMI, FAT%, TC, HbA1c, HDL-C and ADI at post-treatment, whereas basal ADI level

102 rast, compared with isolated low HDL-C, high HDL-C was associated with 20% to 40% lower CVD risk exce

103 L-C (130 mg/dL) and compared low versus high HDL-C phenotypes using logistic regression analysis to a

104 ction (eGFR<60 ml/min per 1.73 m(2)), higher HDL-C did not associate with lower risk for mortality (e

105 ction (eGFR>90 ml/min per 1.73 m(2)), higher HDL-C was associated with reduced risk of all-cause and

106 nfirmed a lack of association between higher HDL-C and lower mortality in an independent cohort of pa

107 060 mmol/l lower TAG and 0.041 mmol/l higher HDL-C.

108 In summary, higher HDL-C levels did not associate with reduced mortality ri

109 cognitive decline (P < .01), whereas higher HDL-C attenuated decline (P = .02) in HIV(+) men.

110 DNA sequence variants associated with higher HDL-C also increase risk for ICH.

111 ate of death/MI was 33% lower in the highest HDL-C quartile as compared with the lowest quartile, wit

112 d studies had as primary goal the changes in HDL-C after gastric bypass.

113 rplasia (BPH) and liver-mediated decrease in HDL-C.

114 A significant (P < 0.0001) increase in HDL-C concentrations was observed only in the surgical a

115 s have demonstrated significant increases in HDL-C.

116 otein cholesterol), rather than increases in HDL-C.

117 It is also unknown whether a rise in HDL-C or apoA-I after initiation of statin therapy is as

118 evels in addition to its established role in HDL-C metabolism.

119 tic score of CETP variants found to increase HDL-C by approximately 2.85mg/dl in the Global Lipids Ge

120 ion of miR-223 in mice resulted in increased HDL-C levels and particle size, as well as increased hep

121 T mice, treatment with perhexiline increased HDL-C levels and cholesterol efflux capacity via KLF14-m

122 irmed that alleles associated with increased HDL-C are associated with a modest increase in GALNT2 ex

123 c variants in CETP associated with increased HDL-C raise the risk of ICH.

124 The effect of increasing HDL-C serum levels was assessed using Cox proportional h

125 urs after doses of 3.0, 9.0, and 13.5 mg/kg, HDL-C was elevated by 6%, 36%, and 42%, respectively, an

126 ose, triglycerides (TG), cholesterol levels (HDL-C and LDL-C), and plasma von Willebrand factor (vWF)

127 Low HDL-C (<40 mg/dL in men and <50 mg/dL in women) was defi

128 Although low HDL-C level is a powerful and independent predictor of c

129 tal muscle IR, hypertriglyceridemia, and low HDL-C become fully established.

130 Four cohorts with stable CHD and low HDL-C were dosed (0.9, 3.0, 9.0, and 13.5 mg/kg, single

131 s with well-controlled HIV infection and low HDL-C.

132 The residual risk conferred by low HDL-C in patients with a satisfactory LDL-C was recently

133 Isolated low HDL-C subjects also demonstrated an increase in beta-cel

134 , we studied nine subjects with isolated low HDL-C with no ABCA1 mutations (age 26 +/- 6 years) and n

135 Compared with isolated low HDL-C, CVD risks were higher when low HDL-C was accompan

136 In contrast, compared with isolated low HDL-C, high HDL-C was associated with 20% to 40% lower C

137 To account for any effect of low HDL-C on insulin secretion, we studied nine subjects wit

138 lial LCAT deficiency, a rare disorder of low HDL-C.

139 nsity lipoprotein cholesterol (LDL-C) or low HDL-C levels who were enrolled in a phase 2 trial of eva

140 diabetes who also had high triglyceride, low HDL-C, or high total cholesterol/HDL-C ratio (3.59 [2.03

141 ed low HDL-C, CVD risks were higher when low HDL-C was accompanied by LDL-C >/=100 mg/dL and TG <100

142 When low HDL-C was analyzed with higher thresholds for TG (>/=150

143 established, it remains unclear whether low HDL-C remains a CVD risk factor when levels of low-densi

144 ticipants without CVD on stable ART with low HDL-C (men <40 mg/dL, women <50 mg/dL) and triglycerides

145 , and triglycerides to HDL-C ratio and lower HDL-C and systolic blood pressure (all P</=.01).

146 Higher LDL-C and lower HDL-C levels were both associated with a higher PIB inde

147 eline total cholesterol and LDL-C, but lower HDL-C and higher triglycerides than controls (P < .001).

148 g those between genetically determined lower HDL-C (beta = -0.12, P = 0.03) and T2D and genetically d

149 allele T of BsmI were associated with lower HDL-C levels [OR 0.60 (0.37, 0.96), p=0.03] and obesity

150 Individuals with lower HDL-C levels were independently associated with higher r

151 Individuals with lower HDL-C levels were more likely to have low incomes, unhea

152 hest triglyceride (>/= 198 mg/dl) and lowest HDL-C (<33 mg/dl) tertiles, ER niacin showed a trend tow

153 Plasma concentration of ApoA4, a major HDL-C protein fraction, significantly increased 1 year a

154 all, p < 0.0001) in a dose-dependent manner; HDL-C and triglyceride levels were relatively unchanged.

155 t was 57.2 years, 55.4% were women, and mean HDL-C level was 55.2 mg/dl.

156 Median HDL-C was 32 mg/dL for men and 38 mg/dL for women, low-d

157 s using intensive lipid-lowering medication, HDL-C levels are not related to vascular risk.

158 In men, HDL-C increased a median of 3 mg/dL with niacin and 6.5

159 in-cholesterol (HDL-C) ratio, HDL-C, and non HDL-C with incident HF.

160 s with LDL-C levels <70 mg/dl, 15% had a non-HDL-C level >/= 100 mg/dl (guideline-based cutpoint) and

161 (guideline-based cutpoint) and 25% had a non-HDL-C level >/= 93 mg/dl (percentile-based cutpoint); if

162 ein cholesterol (HDL-C) (<40 mg/dL), and non-HDL-C (>/= 145 mg/dL) (to convert TC, HDL-C, and non-HDL

163 12.8% [95% CI, 9.8-16.2]; P = .003), and non-HDL-C (13.6% [95% CI, 11.3-16.2] vs 8.4% [95% CI, 5.9-11

164 ity lipoprotein cholesterol (LDL-C), and non-HDL-C are routinely available from the standard lipid pr

165 C/HDL-C, Friedewald-estimated LDL-C, and non-HDL-C in 1 310 432 US adults from the Very Large Databas

166 mpares the predictive power of LDL-C and non-HDL-C to apolipoprotein B and LDL particle numbers in pa

167 /= 145 mg/dL) (to convert TC, HDL-C, and non-HDL-C to millimoles per liter, multiply by 0.0259) and h

168 on with response of LDL subfractions and non-HDL-C to rosuvastatin or placebo for 1 year among 7046 p

169 l discordance of TC/HDL-C with LDL-C and non-HDL-C, because discordance suggests the possibility of a

170 -induced changes in LDL subfractions and non-HDL-C.

171 rdance between TC/HDL-C versus LDL-C and non-HDL-C.

172 e units discordance between TC/HDL-C and non-HDL-C.

173 tial additional information to LDL-C and non-HDL-C.

174 ion in LDL (low-density lipoprotein) and non-HDL-C.

175 re in the same population percentiles as non-HDL-C values of 93, 125, 157, 190, and 223 mg/dl, respec

176 fication for the present guideline-based non-HDL-C cutpoints of 30 mg/dl higher than the LDL-C cutpoi

177 ficant patient-level discordance between non-HDL-C and LDL-C percentiles at lower LDL-C and higher tr

178 density lipoprotein cholesterol (LDL-C), non-HDL-C, and triglyceride levels measured during pregnancy

179 variability in the reductions of LDL-C, non-HDL-C, and apoB achieved with a fixed statin dose.

180 The reductions of LDL-C, non-HDL-C, and apoB levels achieved with statin therapy disp

181 on-high-density lipoprotein cholesterol (non-HDL-C) presented similar inverted U-shaped quadratic tra

182 on-high-density lipoprotein cholesterol (non-HDL-C), apolipoprotein B, and LDL particle number (all,

183 on-high-density lipoprotein cholesterol (non-HDL-C), apolipoprotein B, total number of LDL particles,

184 on-high-density lipoprotein cholesterol (non-HDL-C), or apolipoprotein B (apoB) levels achieved with

185 on-high-density lipoprotein cholesterol (non-HDL-C).

186 ociated with elevated total cholesterol, non-HDL-C, and triglyceride levels, regardless of gestationa

187 ve elevated levels of total cholesterol, non-HDL-C, and triglycerides during all trimesters of pregna

188 TC (>/=200 mg/dl), LDL-C (>/=130 mg/dl), non-HDL-C (>/=160 mg/dl), and triglycerides/HDL-C ratio (>/=

189 33.1 mg/dl; LDL-C: 109.9 +/- 31.1 mg/dl; non-HDL-C: 124.0 +/- 33.5 mg/dl; HDL-C: 53 +/- 12.8 mg/dl; a

190 Similar associations were observed for non-HDL-C and apoB.

191 On a smaller scale, TC/HDL-C > non-HDL-C discordance by >/=25 percentile units increased fr

192 lipoprotein cholesterol (HDL-C) or high non-HDL-C This warrants additional evaluation as per the NHB

193 ion correlated significantly with higher non-HDL-C, triglycerides, and triglycerides to HDL-C ratio a

194 In-trial LDL-C levels, non-HDL-C levels, and the total cholesterol/HDL-C ratio were

195 s to be largely explained by lowering of non-HDL-C (high-density lipoprotein cholesterol), rather tha

196 ercentile levels of LDL-C (<70 mg/dL) or non-HDL-C (<93 mg/dL), a respective 58% and 46% were above t

197 n adverse concentration of TC, HDL-C, or non-HDL-C and 11.0% (95% CI, 8.8-13.4) had either high or bo

198 rse lipid concentration of TC, HDL-C, or non-HDL-C and slightly more than 1 in 10 had either borderli

199 High apoB and low LDL-C or non-HDL-C discordance was also associated with Y25 CAC in ad

200 he discordance between apoB and LDL-C or non-HDL-C in young adults and measured coronary artery calci

201 nse for >/= 1 of the LDL subfractions or non-HDL-C, 20 single-nucleotide polymorphisms could be clust

202 oprotein B but not on LDL cholesterol or non-HDL-C.

203 ces of cardiovascular risk than LDL-C or non-HDL-C.

204 roups, based on median apoB and LDL-C or non-HDL-C.

205 We assigned population percentiles to non-HDL-C and Friedewald-estimated LDL-C values of 1,310,440

206 The LDL-C GRS, but not HDL-C or TG GRS, was significantly associated with prese

207 Plasma LDL-C, but not HDL-C or TG, was significantly associated with incident

208 In humans, high amounts of HDL-C in plasma are associated with a lower risk of coro

209 tudy sought to reappraise the association of HDL-C level with CV and non-CV mortality using a "big da

210 We examined the association of HDL-C with all-cause and cardiovascular mortality in the

211 CVD risk as a function of HDL-C phenotypes is modulated by other components of the

212 ariation contributes more to heritability of HDL-C levels than rare variation, and screening for mend

213 wed no gradual decrease with the increase of HDL-C levels.

214 subjects with coronary ED, independently of HDL-C.

215 Normal levels of HDL-C are not an independent risk factor for asymptomati

216 ers of pregnancy, as well as lower levels of HDL-C during the third trimester.

217 of blood sampling, and with lower levels of HDL-C in the third trimester.

218 ntroversy regarding whether plasma levels of HDL-C reflect HDL function, or that HDL is even as prote

219 demonstrate that increased plasma levels of HDL-C resulted in decreased cardiovascular disease risk,

220 With emtricitabine/tenofovir, levels of HDL-C were increased, TC and LDL-C were unchanged, and t

221 P score was associated with higher levels of HDL-C, lower LDL-C, concordantly lower apoB, and a corre

222 on between HDL function and plasma levels of HDL-C.

223 Pharmacological manipulation of HDL-C has not improved the cardiovascular outcomes.

224 n or whether CIMT is an inadequate marker of HDL-C or TG-mediated effects.

225 We used the average between the negative of HDL-C z-score and TGs z-score to give similar weight to

226 d with the lowest quartile, with quartile of HDL-C being a significant, independent predictor of deat

227 with individuals in the reference ranges of HDL-C levels.

228 sight into the KLF14-dependent regulation of HDL-C and subsequent atherosclerosis and indicate that i

229 rds models were used to evaluate the risk of HDL-C on vascular events in patients using no, usual dos

230 ally diverse fine-mapping genetic studies of HDL-C, LDL-C, and triglycerides to-date using SNPs on th

231 Compound 6 had minimal effect on HDL-C levels in cynomolgus monkeys and showed human cada

232 1511G>A; p.Arg504His]) with large effects on HDL-C and/or triglycerides.

233 inical trials have evaluated drug therapy on HDL-C and cardiovascular outcomes.

234 ociated with apolipoprotein B (apoB; n=4) or HDL-C (n=3; P<0.05).

235 significantly associated with either apoB or HDL-C.

236 obilization of cholesterol on HDL particles (HDL-C) from extravascular tissues to plasma, ultimately

237 ot a predictable relationship between plasma HDL-C and risk for age-related macular degeneration; (ii

238 n 328 individuals with extremely high plasma HDL-C levels, we identified a homozygote for a loss-of-f

239 protein (CETP) gene activity increase plasma HDL-C; as such, medicines that inhibit CETP and raise HD

240 a specific NAMPT knockdown increased plasma HDL-C levels, reduced the plaque area of the total aorta

241 l dose lipid-lowering medication, low plasma HDL-C levels are related to increased vascular risk, whe

242 ave significantly increased levels of plasma HDL-C.

243 n and determined that KLF14 regulates plasma HDL-C levels and cholesterol efflux capacity by modulati

244 In epidemiological studies, plasma HDL-C levels have an inverse relationship to the risk of

245 raises HDL-C are more important than plasma HDL-C levels.

246 ncluding fasting plasma glucose and possibly HDL-C.

247 such, medicines that inhibit CETP and raise HDL-C are in clinical development.

248 ter transfer protein (CETP) inhibitors raise HDL-C in animals and humans and may be antiatherosclerot

249 Nevertheless, drugs that raise HDL-C concentrations, cholesteryl ester transfer protein

250 on whether all target modulations that raise HDL-C would be atheroprotective.

251 ity lipoprotein cholesterol (49%) and raised HDL-C (6.1%), apoA-I (2.1%), HDL-P (3.8%), and HDL size

252 echanism by which a therapeutic agent raises HDL-C are more important than plasma HDL-C levels.

253 nsity lipoprotein-cholesterol (HDL-C) ratio, HDL-C, and non HDL-C with incident HF.

254 trials of cardiovascular therapies targeting HDL-C and TGs is questionable and requires further study

255 nd non-HDL-C (>/= 145 mg/dL) (to convert TC, HDL-C, and non-HDL-C to millimoles per liter, multiply b

256 f youths had an adverse concentration of TC, HDL-C, or non-HDL-C and 11.0% (95% CI, 8.8-13.4) had eit

257 rs had an adverse lipid concentration of TC, HDL-C, or non-HDL-C and slightly more than 1 in 10 had e

258 /=25 percentile units discordance between TC/HDL-C and LDL-C, whereas 1 in 4 had >/=25 percentile uni

259 /=25 percentile units discordance between TC/HDL-C and non-HDL-C.

260 ariance in percentile discordance between TC/HDL-C versus LDL-C and non-HDL-C.

261 to high-density lipoprotein cholesterol (TC/HDL-C) ratio, estimated low-density lipoprotein choleste

262 46% were above the percentile-equivalent TC/HDL-C of 2.6.

263 he extent of patient-level discordance of TC/HDL-C with LDL-C and non-HDL-C, because discordance sugg

264 We compared population percentiles of TC/HDL-C, Friedewald-estimated LDL-C, and non-HDL-C in 1 31

265 On a smaller scale, TC/HDL-C > non-HDL-C discordance by >/=25 percentile units

266 f patient-level discordance suggests that TC/HDL-C may offer potential additional information to LDL-

267 Decreases in the TC/HDL-C ratio were similar with RPV and EFV.

268 The proportion of patients with TC/HDL-C > LDL-C by >/=25 percentile units increased from 3

269 Although insulin, HOMA-IR, and TG/HDL-C remained associated with increased CVD risk after

270 ); for HOMA-IR, 1.06 (CI, 0.98-1.15); for TG/HDL-C, 1.11 (CI, 0.99-1.25); and for glucose, 1.20 (CI,

271 ), in HOMA-IR of 1.19 (CI, 1.11-1.28), in TG/HDL-C of 1.35 (CI, 1.26-1.45), and for impaired fasting

272 igh-density lipoprotein-cholesterol ratio TG/HDL-C, or impaired fasting glucose (serum glucose >/=110

273 sma glucose (p = 0.008), TG (p = 0.003), TG: HDL-C ratio (p = 0.010), and vWF levels (p = 0.004).

274 sterol efflux capacity more effectively than HDL-C (r=0.54 and 0.36, respectively).

275 nalyzing the composition of HDL, rather than HDL-C, may be useful in assessing cardiovascular risk in

276 Our study shows that HDL-C and ApoA4 significantly increase after gastric byp

277 However, the association between the HDL-C level and asymptomatic ICAS is uncertain.

278 implemented to assess the connection of the HDL-C levels and the prevalence of asymptomatic ICAS.

279 Among patients treated with statin therapy, HDL-C and apoA-I levels were strongly associated with a

280 les in influencing GALNT2 expression at this HDL-C locus.

281 d with significantly higher triglycerides to HDL-C ratio (all P</=.02).

282 etabolic parameters (except triglycerides to HDL-C ratio [P=.04]).

283 n-HDL-C, triglycerides, and triglycerides to HDL-C ratio and lower HDL-C and systolic blood pressure

284 , 0.85; P-trend = 0.002), more so than total HDL-C (HR = 0.60, 95% CI: 0.35, 1.03; P-trend = 0.04), w

285 placebo-allocated individuals, on-treatment HDL-C, apoA-I, and HDL-P had similar inverse association

286 non-HDL-C (>/=160 mg/dl), and triglycerides/HDL-C ratio (>/=3.0).

287 ular, the model has been used to explore two HDL-C raising target modulations, Cholesteryl Ester Tran

288 roughly uniform-sized factions with varying HDL-C levels.

289 P-trend = 0.44) (for HDL-C with apoC-III vs. HDL-C without apoC-III, P-heterogeneity = 0.002).

290 95% CI: 0.35, 1.03; P-trend = 0.04), whereas HDL-C with apoC-III was not associated (HR = 1.05, 95% C

291 DM patients decreased significantly, whereas HDL-C was significantly increased.

292 cause recent studies have questioned whether HDL-C is truly an independent predictor of CVD.

293 entified three novel signals associated with HDL-C (LPL, APOA5, LCAT) and two associated with LDL-C (

294 < 5 x 10-8) three novel loci associated with HDL-C near CD163-APOBEC1 (P = 7.4 x 10-9), NCOA2 (P = 1.

295 es excluding variants weakly associated with HDL-C or TG, the LDL-C GRS remained associated with aort

296 -wide association studies as associated with HDL-C or triglyceride levels modify 1-year treatment res

297 ~100 common genetic variants associated with HDL-C, LDL-C, and/or TG levels, mostly in populations of

298 057844 showed the strongest association with HDL-C (P=0.0035).

299 s and tested this score for association with HDL-C as well as ICH risk.

300 ipoprotein cholesterol and CIMT but not with HDL-C and TGs.

301 In women, HDL-C increased a median of 16 mg/dL with niacin and 8 m