ライフサイエンスコーパス: lipid-lowering

1 sion may be on the rise in an era of intense lipid lowering.

2 e regression of lesions following aggressive lipid lowering.

3 r antiplatelet (17.9% versus 2.7%; P<0.001), lipid-lowering (19.2% versus 4.8%; P<0.001), and blood p

4 eptide DualAG exhibits superior weight loss, lipid-lowering activity, and antihyperglycemic efficacy

5 blocker, and 20% to 25% were not receiving a lipid-lowering agent at 90 days after the index test.

6 The only lipid-lowering agent currently available that specifical

7 The recent FIELD study demonstrated that the lipid-lowering agent fenofibrate significantly reduces t

8 alpha ligand that has been widely used as a lipid-lowering agent in the treatment of hypertriglyceri

9 emission tomography, changes in aspirin and lipid-lowering agent use was greater after computed tomo

10 that compared statins with another statin or lipid-lowering agent were excluded.

11 or antiplatelets/anticoagulants (p<0.05) and lipid-lowering agents (p<0.001) and were maintained at 1

12 , mechanical ventilation, gastrostomy tubes, lipid-lowering agents and symptom management.

13 Additional lipid-lowering agents are needed to fulfill an unmet med

14 Further trials of lipid-lowering agents beyond statins will be required in

15 equently, thyromimetic drugs hold promise as lipid-lowering agents if adverse effects can be avoided.

16 ted to the lipid pathway, and the effects of lipid-lowering agents on reducing the incidence of OA.

17 Guidelines recommend combining additional lipid-lowering agents with a complementary mode of actio

18 rugs [NSAIDs] or aspirin, 17 hormones, and 7 lipid-lowering agents).

19 torial risk reduction with statins and other lipid-lowering agents, antihypertensive therapies, and a

20 Subsequent use of statin, other lipid-lowering agents, aspirin, and angiotensin-converti

21 IV infection include lifestyle modification, lipid-lowering agents, insulin sensitizers, and treatmen

22 clinical investigation of ASBT inhibitors as lipid-lowering agents.

23 l need for more effective and well tolerated lipid-lowering agents.

24 the component profiles of BV contributed the lipid lowering and antioxidant effects on HFCD fed hamst

25 There was no correlation between lipid lowering and EAT regression.

26 disease is well founded, derived from their lipid lowering and pleiotropic effects.

27 The use of both lipid-lowering and antidiabetic medications rose in the

28 k factors, eGFR, cardiovascular history, and lipid-lowering and antihypertensive drug treatments.

29 h diet treatment only and non-adjustment for lipid-lowering and antihypertensive drugs did not introd

30 tients with diet only and non-adjustment for lipid-lowering and antihypertensive drugs resulted in ma

31 or a number of hepatic diseases due to their lipid-lowering and antiinflammatory properties.

32 ecific agonist may afford a new strategy for lipid-lowering and CVD risk reduction.

33 ng mysteries, such as how AKT might regulate lipid-lowering and glucose-lowering pathways that become

34 s, including genes encoding drug targets for lipid lowering, and identify previously unidentified rar

35 ated a significant benefit for antiplatelet, lipid-lowering, and beta-blocker therapy in both the CAB

36 of and adherence to common antihypertensive, lipid-lowering, and hypoglycemic medications.

37 Improving prescription of lipid-lowering, anticoagulant, and antihypertensive drug

38 Lipid-lowering, anticoagulant, and antihypertensive drug

39 our study, over half of people eligible for lipid-lowering, anticoagulant, or antihypertensive drugs

40 Drugs were considered under-prescribed when lipid-lowering, anticoagulant, or antihypertensive drugs

41 t and cardiovascular medication prescribing (lipid-lowering, antiplatelet, renin-angiotensin system d

42 ase subtilisin/kexin type 9 (PCSK9) is a new lipid-lowering approach.

43 ients with type 2 diabetes mellitus from the Lipid Lowering Arm of the Anglo Scandinavian Cardiac Out

44 In the Lipid-Lowering Arm of the Anglo-Scandinavian Cardiac Out

45 In ASCOT Lipid-Lowering Arm, the relative statin effect in preven

46 T [Anglo-Scandinavian Cardiac Outcomes Trial-Lipid-Lowering Arm] and JUPITER [Justification for the U

47 oximately 30 years ago ushered in the era of lipid lowering as the most effective way to reduce risk

48 cardiovascular disease requiring additional lipid lowering beyond dietary measures and statin use.

49 Aside from their well-known lipid-lowering capacities, statins exert pleiotropic eff

50 latory effects that are independent of their lipid-lowering capacity and may be beneficial as therape

51 Fenofibrate (FF) is a common lipid-lowering drug and a potent agonist of the peroxiso

52 By activating PPARalpha, the lipid-lowering drug fenofibrate reverses dyslipidemia an

53 Both the lipid-lowering drug lovastatin and the Rac1-specific inh

54 d a decrease in monthly antihypertensive and lipid-lowering drug prescriptions during the coverage ga

55 The lipid-lowering drug simvastatin decreases portal pressur

56 characterized regarding plasma lipid status, lipid-lowering drug treatment, and variants at the LPA g

57 nt of glioblastoma cells with fenofibrate, a lipid-lowering drug with multiple anticancer activities.

58 rlier studies have shown that gemfibrozil, a lipid-lowering drug, has anti-inflammatory properties.

59 em), a Food and Drug Administration-approved lipid-lowering drug, in increasing the expression of IL-

60 zil, a Food and Drug Administration-approved lipid-lowering drug, in up-regulating the expression of

61 cell DNA from 991 Whites in the Genetics of Lipid Lowering Drugs and Diet Network Study was followed

62 nondiabetic participants in the Genetics of Lipid Lowering Drugs and Diet Network study, divided int

63 In the GOLDN (Genetics of Lipid Lowering Drugs and Diet Network) study, higher ABC

64 dchip in 991 participants of the Genetics of Lipid Lowering Drugs and Diet Network.

65 Fibrates are lipid lowering drugs and found as ligands for peroxisome

66 ntihypertensives, antithrombotic agents, and lipid-lowering drugs (relative risk, 0.55 [95% confidenc

67 sin II receptor blockers, beta-blockers, and lipid-lowering drugs also increased among both sexes.

68 Also, lipid-lowering drugs fenofibrate and niacin reduced live

69 inhibitors) are the most prescribed class of lipid-lowering drugs for the treatment and prevention of

70 ention drug clinically indicated: 16,028 had lipid-lowering drugs indicated, 3,194 anticoagulant drug

71 ncomitant treatment of lomitapide with other lipid-lowering drugs is generally safe.

72 Statins are one of the lipid-lowering drugs that help in reducing cholesterol l

73 Statins are widely used lipid-lowering drugs with immunomodulatory properties th

74 ents: 49% (7,836/16,028) were not prescribed lipid-lowering drugs, 52% (1,647/3,194) were not prescri

75 ity assessment of conduit and target vessel, lipid-lowering drugs, antithrombotic therapy, and cessat

76 substantial increase in antihypertensive and lipid-lowering drugs, blood pressure management remained

77 of 8 study drug classes for detailed drugs (lipid-lowering drugs, gastroesophageal reflux disease dr

78 led and nondetailed drugs in 8 drug classes (lipid-lowering drugs, gastroesophageal reflux disease dr

79 brate, Food and Drug Administration-approved lipid-lowering drugs, in up-regulating TPP1 in brain cel

80 re not using an antihypertensive medication, lipid-lowering drugs, or a glucose-lowering treatment.

81 ein cholesterol (LDL-c) >/=130 mg/dL, and no lipid-lowering drugs.

82 isk factors, and use of antihypertensive and lipid-lowering drugs.

83 ed as proxies to study the efficacy of these lipid-lowering drugs.

84 ght, weight, and use of antihypertensive and lipid-lowering drugs.

85 ipidemia, nearly half of whom were receiving lipid-lowering drugs.

86 dds ratio [OR], 1.60 [95% CI, 1.50 to 1.71]; lipid-lowering drugs: OR, 1.59 [CI, 1.50 to 1.68]).

87 These findings were independent of the lipid-lowering effect and the use of protease inhibitors

88 Rosuvastatin showed a superior lipid-lowering effect compared to fluvastatin in stable

89 Its lipid-lowering effect is additive to that of existing dr

90 In addition, lipid-lowering effect of PB-NLCs/G5-PEG was studied.

91 y system to improve oral bioavailability and lipid-lowering effect of PB.

92 The lipid-lowering effect of pravastatin was accompanied by

93 improve the oral bioavailability and plasma lipid-lowering effect of probucol (PB) by constructing a

94 We have aimed to assess the lipid-lowering effect of rosuvastatin as compared with f

95 of cardiovascular events, not only via their lipid-lowering effect, but also due to their anti-inflam

96 Coformulated TDF/FTC has an intrinsic lipid-lowering effect, likely attributable to TDF.

97 the lipid-neutral emtricitabine (FTC), has a lipid-lowering effect.

98 ureus fermented red rice contributing to the lipid-lowering effect.

99 Polydextrose (PDX), a soluble fiber has lipid lowering effects.

100 lism and beta-cell functionality through its lipid-lowering effects in a diet-induced obesity model.

101 an impact on clinical outcomes beyond their lipid-lowering effects.

102 After lipid lowering, favorable changes in plaque composition

103 We show that phenoxyauxin herbicides and lipid-lowering fibrates inhibit human but not rodent T1R

104 Peroxisome proliferators, such as the lipid-lowering fibrates that function as agonists for pe

105 patic Sort1 under diabetic conditions and by lipid-lowering fish oil and fenofibrate.

106 Durable strategies to address gaps in lipid lowering for secondary prevention are essential to

107 of hard exudates and severity of DME in the lipid-lowering group compared with placebo (hard exudate

108 al Decrease in End Points Through Aggressive Lipid-Lowering (IDEAL) study.

109 cholesterol supports the need for intensive lipid lowering in patients with PAD.

110 g CVD and are renowned for their pleiotropic lipid-lowering independent effects.

111 regression occurs in these mice upon plasma lipid lowering induced by a change in diet and the resto

112 mited number of clinical studies, reveal the lipid-lowering, insulin-sensitizing, antihypertensive, a

113 ing the cost-effectiveness of pharmaceutical lipid-lowering interventions published since January 201

114 Lipid-lowering is an intervention that reduces atheroscl

115 In patients on usual dose lipid-lowering medication (n = 1,910) there was a 6% red

116 The copayment increase adversely affected lipid-lowering medication adherence among veterans, incl

117 e-in-difference approach compared changes in lipid-lowering medication adherence during the 24 months

118 ined the impact of the copayment increase on lipid-lowering medication adherence.

119 t models that were adjusted for the use of a lipid-lowering medication after baseline, these associat

120 .80 (95% confidence interval, 0.73-0.88) for lipid-lowering medication and 0.82 (95% confidence inter

121 In patients not using lipid-lowering medication at baseline (n = 2,153), a 0.1

122 sus 96.9% (AOR, 1.48; 95% CI, 1.35-1.63), or lipid-lowering medication for low-density lipoprotein le

123 L-C) in relation to the use and intensity of lipid-lowering medication in patients with clinically ma

124 ociations with lipid levels and incidence of lipid-lowering medication or abnormal lipid levels.

125 verage who had continuous medication gaps in lipid-lowering medication use and antihypertensive use i

126 The prevalence of lipid-lowering medication use increased from 3.4% (95% C

127 on the association of blood lipid levels and lipid-lowering medication use with AF risk.

128 -of-pocket cost (copay), clinical diagnoses, lipid-lowering medication use, and low-density lipoprote

129 an triglyceride levels and the prevalence of lipid-lowering medication use.

130 ication at recruitment and 1% were receiving lipid-lowering medication).

131 We excluded 1,100 participants (16%) on lipid-lowering medication, 87 (1.3%) without low-density

132 cholesterol, systolic blood pressure, use of lipid-lowering medication, and smoking status.

133 %) of patients who reported currently taking lipid-lowering medication, full implementation of the US

134 ar risk, whereas in patients using intensive lipid-lowering medication, HDL-C levels are not related

135 diovascular disease, and maximally tolerated lipid-lowering medication, LA effectively lowered the in

136 fest vascular disease using no or usual dose lipid-lowering medication, low plasma HDL-C levels are r

137 d after adjusting for the lipid fraction and lipid-lowering medication.

138 ied prescriptions for statins and non-statin lipid lowering medications filled after BE diagnosis and

139 on between Barrett's esophagus and nonstatin lipid-lowering medications (P = .452).

140 rsus 67.0% (AOR, 2.42; 95% CI, 2.23-2.61) or lipid-lowering medications 94.8% versus 88.0% (AOR, 1.71

141 individuals who did not have diabetes or use lipid-lowering medications and had complete dietary info

142 No association was found between the use of lipid-lowering medications and incident AF.

143 , and without hormone replacement therapy or lipid-lowering medications at baseline).

144 al cardiovascular disease, and not receiving lipid-lowering medications at baseline, from the Multiet

145 ey had at least 1 continuous episode with no lipid-lowering medications for > or =90 days.

146 Participants taking lipid-lowering medications had an adjusted HR (95% CI) o

147 Self-reported use of lipid-lowering medications increased from 8.0% to 13.4%

148 alcium after participants who were receiving lipid-lowering medications or had clinically abnormal li

149 the original sample (n = 926), those taking lipid-lowering medications or who had diabetes (n = 168)

150 Statins are commonly prescribed lipid-lowering medications that significantly reduce the

151 erent if the proportion of days covered with lipid-lowering medications was > or =80%.

152 Use of statins and other lipid-lowering medications was ascertained by reviewing

153 association of the use of statins and other lipid-lowering medications with AF was estimated in 13 0

154 2042 (5.3%) were treated only with nonstatin lipid-lowering medications, and 6573 (17.0%) were untrea

155 rts, reveal population-specific responses to lipid-lowering medications, and aid in the development o

156 terol, high-density lipoprotein cholesterol, lipid-lowering medications, and income, individuals in t

157 , age, sex, race/ethnicity, LDL cholesterol, lipid-lowering medications, and smoking, were increased

158 In analyses before alterations in lipid-lowering medications, total cholesterol decreased

159 Among adults not receiving lipid-lowering medications, trends in lipids were simila

160 without baseline CHD, excluding subjects on lipid-lowering medications, triglycerides >400 mg/dl, or

161 nd no association between EAC and non-statin lipid-lowering medications.

162 ssess trends in use of statins and nonstatin lipid-lowering medications.

163 risk factor modification and use of multiple lipid-lowering medications.

164 crease in the percentage of adults receiving lipid-lowering medications.

165 (0.66-1.25) compared with those taking other lipid-lowering medications.

166 eated or undertreated despite growing use of lipid-lowering medications.

167 tal Decrease in Endpoints Through Aggressive Lipid Lowering) (n = 7,461) trials.

168 recent interest has been piqued by putative lipid-lowering neutraceuticals like red yeast rice (Mona

169 The effect of lipid lowering on the incidence of deep venous thrombosi

170 Aspirin, lipid-lowering or antihypertensive therapy, and interim

171 s; body mass index; use of antihypertensive, lipid-lowering, or anticholinergic medication; and apoli

172 thways may mediate the anti-inflammatory and lipid-lowering properties of statin therapy.

173 Beyond these well known lipid-lowering properties, they possess broad-reaching e

174 matory effects that are independent of their lipid-lowering properties.

175 have beneficial effects independent of their lipid-lowering properties.

176 ng matters, and whether ever more aggressive lipid-lowering provides a safe, long-term mechanism to p

177 However, the optimal postoperative lipid-lowering regimen remains unknown and should be the

178 al Decrease in End Points Through Aggressive Lipid Lowering), SPARCL (Stroke Prevention by Aggressive

179 le disorders, especially those caused by the lipid-lowering statin family of drugs, but also myopathi

180 In addition to lipid lowering, statins have pleiotropic effects that im

181 In addition, 22.6% were receiving nonstatin lipid-lowering therapies and 20.8% had repeated LDL-C te

182 Lipid-lowering therapies and LDL-C testing patterns by p

183 esterol (LDL-C) >/=70 mg/dL on their current lipid-lowering therapies at baseline.

184 ngiotensin-converting enzyme inhibitors, and lipid-lowering therapies in eligible patients, adoption

185 Hypoglycaemic and lipid-lowering therapies may have a role in the treatmen

186 (NASH) and the effects of hypoglycaemic and lipid-lowering therapies on NAFLD/NASH.

187 Many patients on lipid-lowering therapies remain unable to achieve target

188 icipants who were not receiving any baseline lipid-lowering therapies, 3,714 (66%) had LDL-C </= 130

189 Despite the use of currently available lipid-lowering therapies, a significant proportion of pa

190 H) when administered concurrently with other lipid-lowering therapies, including apheresis.

191 Despite statins and additional lipid-lowering therapies, many HeFH patients fail to ach

192 Statins, frequently prescribed in lipid-lowering therapies, seem to have additional benefi

193 initiation of aspirin and intensification of lipid-lowering therapies.

194 ctors influence the effectiveness of dietary lipid-lowering therapies.

195 ymptomatic dyslipidemia who may benefit from lipid-lowering therapies.

196 such as when evaluating reimbursement of new lipid-lowering therapies.

197 g individuals prescribed antihypertensive or lipid-lowering therapies.

198 re profoundly altered in HCV-positive men by lipid lowering therapy (change in HR with lipid-lowering

199 (Reduction in YEllow Plaque by Aggressive Lipid LOWering Therapy [YELLOW]); NCT01567826).

200 Lipid lowering therapy significantly reduces this risk,

201 Current lipid lowering therapy was maintained from 6 weeks befor

202 is protein has become a major new target for lipid lowering therapy.

203 ncreases in cholesterol to levels warranting lipid lowering therapy.

204 current or prospective molecular targets of lipid-lowering therapy (ie, HMGCR, PCSK9, ABCG5/G8, LDLR

205 ho would require a PCSK9 inhibitor when oral lipid-lowering therapy (LLT) is intensified first.

206 nsity to high-intensity statin and nonstatin lipid-lowering therapy (LLT) were analyzed before (Septe

207 ow-up was investigated in relation to use of lipid-lowering therapy (LLT).

208 tween 2007 and 2011 for statin and nonstatin lipid-lowering therapy (niacin, fibrates, bile acid sequ

209 upport continuation of intensive combination lipid-lowering therapy after an initial CV event.

210 antly in association with intensification of lipid-lowering therapy after CCTA in all patient subgrou

211 somewhat lower vascular risk should receive lipid-lowering therapy and also how intensive statin tre

212 benefits were significant both for those on lipid-lowering therapy and for those not, and both for m

213 ent CHD in participants who had not received lipid-lowering therapy at baseline (HR = 1.05, 95% CI: 0

214 Lipid-lowering therapy decreases cardiac death and ather

215 Lipid-lowering therapy does not improve kidney outcomes

216 ial hypercholesterolaemia and were on stable lipid-lowering therapy for at least 4 weeks, with a fast

217 by lipid lowering therapy (change in HR with lipid-lowering therapy for TC >240 mg/dL from 1.82 to 1.

218 ent in dyslipidemic adult patients on stable lipid-lowering therapy in 9 countries.

219 examining potential benefits of combination lipid-lowering therapy in individuals with CKD are neede

220 is review investigates the potential role of lipid-lowering therapy in its management.

221 nd efficacy of the continuation of intensive lipid-lowering therapy in very higher-risk patients resu

222 Nonstatin lipid-lowering therapy is adjunctive therapy for high-ri

223 Following a myocardial infarction, lipid-lowering therapy is an established intervention to

224 h-risk patients, these results indicate that lipid-lowering therapy is being applied much more succes

225 Lipid-lowering therapy is costly but effective at reduci

226 Lipid-lowering therapy is not widely used in persons wit

227 We studied the effect of lipid-lowering therapy on LDL permeability and degradati

228 o 2.6 mmol per liter) if they were receiving lipid-lowering therapy or 50 to 125 mg per deciliter (1.

229 Aggressive lipid-lowering therapy over a 3-month period is associat

230 After titration of background lipid-lowering therapy per cardiovascular risk, 901 pati

231 rs, the odds of physician intensification of lipid-lowering therapy significantly increased for those

232 Nonstatin lipid-lowering therapy use was more common among men and

233 holesterol levels <70 or >/=190 mg/dl, prior lipid-lowering therapy use, or incomplete 5-year follow-

234 Median age at initiation of lipid-lowering therapy was 39 years, and median age at F

235 Use of nonstatin lipid-lowering therapy was less common at older age, amo

236 with diabetes mellitus or who were receiving lipid-lowering therapy were excluded.

237 ication, patients were started on background lipid-lowering therapy with diet alone or diet plus ator

238 Lipid-lowering therapy with ezetimibe plus simvastatin i

239 aggravates dyslipidemia, thus necessitating lipid-lowering therapy with fluvastatin, pravastatin, or

240 discharge, patients should receive intensive lipid-lowering therapy with high doses of a statin, as t

241 Lipid-lowering therapy with statins is cost-effective fo

242 iants associated with a positive response to lipid-lowering therapy, and variants in CYP4F2 and VKORC

243 Lipid-lowering therapy, antihypertensive drugs, and anti

244 dent CHD in participants who did not receive lipid-lowering therapy, as well as in those with LDL-C c

245 hen LDL-c is reduced by more than 30% during lipid-lowering therapy, blood glucose monitoring is sugg

246 Among those not on any lipid-lowering therapy, low-density lipoprotein choleste

247 or earlier diagnosis of FH and initiation of lipid-lowering therapy, more consistent use of guideline

248 otensin II receptor blocker (ACE-I/ARB), and lipid-lowering therapy, respectively, than privately ins

249 s likely to receive 3 particular treatments (lipid-lowering therapy, smoking cessation counseling, an

250 , including enzyme replacement therapy, oral lipid-lowering therapy, stem-cell transplantation, and l

251 model, while correcting for the use of other lipid-lowering therapy, thrombocyte aggregation inhibito

252 ve been a number of retrospective studies of lipid-lowering therapy, which suggested that statins mig

253 chronic kidney disease, alcohol intake, and lipid-lowering therapy.

254 2 mmol per liter) if they were not receiving lipid-lowering therapy.

255 to very low levels when added to background lipid-lowering therapy.

256 mbers of patients receiving standard of care lipid-lowering therapy.

257 patients using no, usual dose, or intensive lipid-lowering therapy.

258 osuvastatin 40 mg daily) or standard-of-care lipid-lowering therapy.

259 rnative to LDL-C for risk stratification and lipid-lowering therapy.

260 sease who were receiving maximally tolerated lipid-lowering therapy.

261 coronary artery disease on statins and other lipid-lowering therapy.

262 are treated with statins, nonstatins, or no lipid-lowering therapy.

263 the statin treatment, and using alternative lipid-lowering therapy.

264 ients, most of whom are receiving inadequate lipid-lowering therapy.

265 e, LDL-cholesterol concentration, and use of lipid-lowering therapy.

266 side-effect profile), with or without other lipid-lowering therapy.

267 ey were more likely to be taking aspirin and lipid-lowering therapy; and they had a greater prevalenc

268 Statin therapy is the mainstay of lipid-lowering therapy; however, many patients, particul

269 However, in patients using intensive lipid-lowering treatment (n = 2,046), HDL-C was not asso

270 cholesterolaemia receiving stable background lipid-lowering treatment and not on apheresis, evolocuma

271 Patients discontinued all lipid-lowering treatment except ezetimibe and/or apheres

272 s familial hypercholesterolaemia, on optimum lipid-lowering treatment for at least 6 weeks, and with

273 f Cardiology (ESC) guidelines both recommend lipid-lowering treatment for primary prevention based on

274 Screening can detect FH in children, and lipid-lowering treatment in childhood can reduce lipid c

275 the long-term benefits or harms of beginning lipid-lowering treatment in childhood.

276 Proportions of individuals qualifying for lipid-lowering treatment per guidelines, proportions of

277 In the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (

278 The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (

279 formed in data from the Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (

280 (Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial [

281 ipants from the ALLHAT (Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial)

282 The ALLHAT (Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial)

283 analysis of the ALLHAT (Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial),

284 eers with raised cholesterol who were not on lipid-lowering treatment.

285 scular disease receiving maximally tolerated lipid-lowering treatment.

286 holesterolaemia in the absence of concurrent lipid-lowering treatment.

287 individuals' responsiveness to conventional lipid-lowering treatment.

288 Conventional lipid-lowering treatments are modestly effective.

289 The role of lipid-lowering treatments in renoprotection for patients

290 ide levels below 4.5 mmol/L after washout of lipid-lowering treatments.

291 al Decrease in End Points Through Aggressive Lipid Lowering trial (IDEAL; n=8888) confirmed adequate

292 tients from the Scottish Aortic Stenosis and Lipid Lowering Trial Impact on Regression (SALTIRE) stud

293 al Decrease in End Points Through Aggressive Lipid Lowering) trial, 239 of 3,737 patients randomized

294 We conducted six parallel, multinational lipid-lowering trials enrolling 4300 patients with hyper

295 Lipid-lowering was induced by microsomal triglyceride tr

296 oss, caloric reduction, glucose control, and lipid lowering, were compared upon chronic dosing in die

297 cardial Infarction 22) trial, more intensive lipid lowering with high-dose atorvastatin reduced the f

298 ation > or = 30 days) compared with moderate lipid lowering with pravastatin.

299 ids from atherosclerotic lesions upon plasma lipid lowering without significantly affecting the remod

300 pids and Vascular Inflammation by Aggressive Lipid Lowering [YELLOW II]; NCT01837823).