ライフサイエンスコーパス: HDL-C

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

2 HDL-C raising genetic variants in the gene locus of the

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 ference (WC) (OR 0.98, 95% CI 0.96-0.99) and HDL-C (OR 0.99, 95% CI 0.98-0.99) was associated with si

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

6 oprotein profile (e.g., serum TG, LDL-C, and HDL-C concentrations).

7 Measurement of total cholesterol and HDL-C in the nonfasted state is sufficient to capture th

8 Adding either total cholesterol and HDL-C, or ApoB and ApoA, to a CVD risk prediction model

9 ion was largely attenuated for SBP, DBP, and HDL-C.

10 (triglycerides >150 mg/dl [1.69 mmol/l] and HDL-C <40 mg/dl [1.03 mmol/l] in men or <50 mg/dl [1.29

11 ontrol subject after adjustments for sex and HDL-C levels, 12 proteins some of which participate in a

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

13 Once total and HDL-C were in the model, no further substantive improvem

14 lated to genetic risk from triglycerides and HDL-C as from LDL-C.

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

16 iprocal genetic effects on triglycerides and HDL-C.

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

18 or HDL-P attenuated all associations between HDL-C and events.

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

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

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

22 Differential associations of both HDL-C and HDL-P for MI by Black ethnicity suggest that a

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

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

25 (PLP), and total B-12 with serum TC, LDL-C, HDL-C, and TG concentrations across trimesters.

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

27 .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

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

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

30 0.9-mg/kg dose did not significantly change HDL-C; however, 6 hours after doses of 3.0, 9.0, and 13.

31 0.036) and positively with HDL cholesterol (HDL-C) (beta = 0.442, 95% CI (0.011,0.873), p = 0.045).

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

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

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

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

36 High-density lipoprotein (HDL) cholesterol (HDL-C) levels decline during sepsis, and lower levels ar

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

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

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

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

41 luding high-density lipoprotein cholesterol (HDL-C) (beta 0.40, 95% confidence interval (CI), 0.04-0.

42 ), non-high-density lipoprotein cholesterol (HDL-C) (HR: 1.05; 95% CI: 1.01 to 1.10, per 10 mg/dl [0.

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

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

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

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

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

48 els of high-density lipoprotein cholesterol (HDL-C) decline drastically during sepsis, and this pheno

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

50 plasma high-density lipoprotein cholesterol (HDL-C) increase and, potentially, a reduced cardiovascul

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

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

53 nd non-high-density lipoprotein cholesterol (HDL-C) level on the expected rates of atherosclerotic ca

54 plasma high density lipoprotein cholesterol (HDL-C) levels by inhibition of cholesteryl ester transfe

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

56 ol and high-density lipoprotein cholesterol (HDL-C) measurements are central to cardiovascular diseas

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

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

59 (DBP), high-density-lipoprotein cholesterol (HDL-C), and glycated haemoglobin (HbA1c).

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

61 DL-C), high-density lipoprotein cholesterol (HDL-C), and triglycerides (TG) were evaluated preconcept

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

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

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

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

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

67 els of high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), and

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

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

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

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

72 els of high-density lipoprotein cholesterol (HDL-C).

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

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

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

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

77 6 studies; 168,553 people], HDL-Cholesterol [HDL-C; 84 studies; 121,282 people], LDL-Cholesterol [LDL

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

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

80 sting lipid measurements (total cholesterol, HDL-C, non-HDL-C, direct and calculated low-density lipo

81 = 0.05) and decreased the total cholesterol-HDL-C ratio by 0.27 (CI, -0.52 to -0.01; P = 0.039).

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

83 TEI) intakes as regards waist circumference, HDL-C, blood pressure, glucose, insulin and HOMA2-IR as

84 lipoprotein (HDL) cholesterol concentration (HDL-C) is an established atheroprotective marker, in par

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

86 ated cholesterol efflux by 53% demonstrating HDL-C functionality.

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

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

89 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

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

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

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

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

94 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

95 g/dl) were 193 for TC, 120 for LDL-C, 47 for HDL-C, and 139 for TG; no strong trends.

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

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

98 Adjustment for HDL-C did not attenuate the inverse relationship between

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

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

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

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

103 For this endpoint, the interaction term for HDL-C and type of MI was significant even after adjustme

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

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

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

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

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

109 Genetic predisposition to higher HDL-C levels was associated with lower risk of small ves

110 Genetic predisposition to higher HDL-C, specifically to cholesterol in medium-sized high-

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

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

113 the genetic mechanisms underlying changes in HDL-C during sepsis, and whether the relationship with s

114 DL metabolism would contribute to changes in HDL-C levels and clinical outcomes during sepsis.

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

116 ration, a 28% (+/-21%; p < 0.05) increase in HDL-C and 14% (+/-20%; p < 0.05) decline in LDL-C.

117 Associations for 1 SD increase in HDL-C and ApoA1 were also similar (hazard ratios, 0.81 [

118 A 10 mg/dL increase in HDL-C change from preconception to 28 weeks was associat

119 For >=25 BMI only, 10 mg/dL increase in HDL-C change was associated with decreased SGA odds (OR

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

121 cose (p = 0.019) and significant increase in HDL-C levels (p < 0.01) with saroglitazar compared to pl

122 [95% CI, 0.59-1.00] per 1 mmol/L increase in HDL-C) and iSPAAR cohorts (hazard ratio, 0.60 [95% CI, 0

123 [95% CI, 0.37-0.98] per 1 mmol/L increase in HDL-C).

124 05) and a 23% (+/-23%; p < 0.05) increase in HDL-C.

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

126 as associated with significant reductions in HDL-C levels during sepsis.

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

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

129 r, alcohol was associated with and increased HDL-C, decreased TRG, and increased BP, which may indica

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

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

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

133 In conclusion, increasing HDL-C levels by inhibiting CETP activity is associated w

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

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

136 tion, and a higher high-density lipoprotein (HDL-C) is thought to be protective.

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

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

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

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

141 ed with an elevated risk of experiencing low HDL-C and high TG (all p < 0.05).

142 for high TC, 20% for high LDL-C, 48% for low HDL-C, and 21% for high TG; no strong trends.

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

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

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

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

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

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

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

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

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

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

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

154 For NSTEMI patients, a lower HDL-C was associated with a higher risk of death during

155 ospitalization but in STEMI patients a lower HDL-C was paradoxically associated with a lower risk of

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

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

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

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

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

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

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

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

164 edian triglycerides level, 240 mg/dL; median HDL-C level, 36 mg/dL; and median high-sensitivity C-rea

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

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

167 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

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

169 events and minimal changes in LDL-C and non-HDL-C compared with EFV/FTC/TDF.

170 1 SD increase in ApoB, direct LDL-C, and non-HDL-C had similar associations with composite fatal/nonf

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

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

173 /= 145 mg/dL) (to convert TC, HDL-C, and non-HDL-C to millimoles per liter, multiply by 0.0259) and h

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

175 ApoB, LDL-C, and non-HDL-C were highly correlated (r>0.90), while HDL-C was s

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

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

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

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

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

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

182 ctors (C-index, 0.7118) were improved by non-HDL-C (C-index change, 0.0030; 95% CI, 0.0012, 0.0048) o

183 measurements (total cholesterol, HDL-C, non-HDL-C, direct and calculated low-density lipoprotein cho

184 on-high-density lipoprotein cholesterol (non-HDL-C) across a lifespan are associated with increased r

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

186 on-high-density lipoprotein cholesterol (non-HDL-C) were significantly different between DOR/3TC/TDF

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

188 on-high-density lipoprotein cholesterol (non-HDL-C), diabetes mellitus, and smoking.

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

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

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

192 B or LDL-C to a model already containing non-HDL-C did not further improve discrimination.

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

194 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

195 Most adults with elevated non-HDL-C early in life continue to have high non-HDL-C over

196 ns of 28% for SBP>=130 mm Hg and 17% for non-HDL-C>=130 mg/dL.

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

198 Those with high non-HDL-C in young adulthood had a 22.6% risk of CVD in the

199 DL-C early in life continue to have high non-HDL-C over their life course, leading to significantly i

200 as also higher with older age and higher non-HDL-C level.

201 k were greater with older age and higher non-HDL-C level.

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

203 uld be reliably assigned to high and low non-HDL-C groups based on 2 measurements collected between 2

204 pared with a 6.4% risk in those with low non-HDL-C.

205 aplan-Meier analyses for those with mean non-HDL-C >=160 mg/dl ("high") and <130 mg/dl ("low") at the

206 table over the 30-year life course; mean non-HDL-C measured in young adulthood were highly predictive

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

208 Levels of non-HDL-C for participants on lipid treatment were adjusted

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

210 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

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

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

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

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

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

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

217 : 1.1%, 2.3%, 5.4%, 10.3%, respectively; non-HDL-C: 1.1%, 2.0%, 3.7%, 5.9%, respectively).

218 In contrast, adding either SBP, non-HDL-C, diabetes mellitus, or smoking to a model with oth

219 f age free of CVD and diabetes had their non-HDL-C progression modeled over 8 study examinations (mea

220 Overall, 80% of those with non-HDL-C >=160 mg/dl at the first 2 exams remained in the h

221 ars) in 40- to 49-year-old patients with non-HDL-C >=160 mg/dL would be expected to reduce their aver

222 in individuals in their 40s and 50s with non-HDL-C >=160 mg/dL.

223 -year testing, whereas 88% of those with non-HDL-C <130 mg/dl remained below 160 mg/dl.

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

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

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

227 The associations of HDL-C and HDL-P with ischemic stroke and myocardial infa

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

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

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

231 ut inversely associated with serum levels of HDL-C after the adjustment for age, sex, and race.

232 ted with anacetrapib had preserved levels of HDL-C and apolipoprotein-AI and increased survival relat

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

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

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

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

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

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

239 The abnormal rates of HDL-C and TG increased as the students maturated through

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

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

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

243 w-density lipoprotein cholesterol (LDL-C) or HDL-C, were associated with MACEs.

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

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

246 el and demonstrated a 56% increase in plasma HDL-C.

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

248 A-I levels by 24 +/- 5.5%, increased plasma HDL-C levels by 93 +/- 26% and reduced intimal hyperplas

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

250 ivity of CETP, a major determinant of plasma HDL-C levels.

251 ave significantly increased levels of plasma HDL-C.

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

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

254 ncluding fasting plasma glucose and possibly HDL-C.

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

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

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

258 Similarly, HDL-C was inversely associated with MI among White parti

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

260 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

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

262 /=25 percentile units discordance between TC/HDL-C and LDL-C, whereas 1 in 4 had >/=25 percentile uni

263 /=25 percentile units discordance between TC/HDL-C and non-HDL-C.

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

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

266 46% were above the percentile-equivalent TC/HDL-C of 2.6.

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

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

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

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

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

272 g despite adjusting for baseline weight, TG, HDL-C and HbA1c (p = 0.002).

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

274 ); 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,

275 ), 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

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

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

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

279 These analyses indicate that HDL-C raising strategies could be considered for the pre

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

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

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

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

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

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

288 le 1 [Q1], 0.64 [95% CI, 0.52-0.78]), as was HDL-C (HR for Q4 versus Q1, 0.76 [95% CI, 0.61-0.94]).

289 95% CI: 0.35, 1.03; P-trend = 0.04), whereas HDL-C with apoC-III was not associated (HR = 1.05, 95% C

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

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

292 HDL-C were highly correlated (r>0.90), while HDL-C was strongly correlated with ApoA1 (r=0.92).

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

296 Compared with HDL-C, HDL-P was consistently associated with MI and isc

297 stroke among women and Blacks compared with HDL-C.

298 y associated with birthweight outcomes, with HDL-C more strongly associated with healthy birthweight

299 ned the association of genetic variants with HDL-C levels, 28-day survival, 90-day survival, organ dy

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