ライフサイエンスコーパス: lipid-lowering

1 protein B antisense oligonucleotide-mediated lipid lowering.

2 e regression of lesions following aggressive lipid lowering.

3 s, to lesion regression following aggressive lipid lowering.

4 might be more relevant than whether to start lipid lowering.

5 ed to demonstrating the clinical benefits of lipid lowering.

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

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

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

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

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

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

12 Fenofibrate, a PPARalpha agonist and lipid-lowering agent, decreases amputation incidence in

13 List prices of lipid-lowering agents (n = 11) increased by 278% and net

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

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

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

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

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

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

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

21 des as monotherapy or as an adjunct to other lipid-lowering agents.

22 chronic inflammation due to their pleotropic lipid lowering and anti-inflammatory properties.

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

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

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

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

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

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

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

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

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

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

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

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

35 Lipid-lowering, anticoagulant, and antihypertensive drug

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

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

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

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

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

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

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

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

44 stimated the absolute and relative impact of lipid lowering as a function of age, age at initiation,

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

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

47 Delaying lipid lowering by 10 years (treatment for 20 years) woul

48 The impact of lipid lowering by proprotein convertase subtilisin-kexin

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

50 Berberine (BBR) is a natural lipid lowering drug that reduces plasma LDL-cholesterol

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

52 C1L1 did not suggest that the use of related lipid-lowering drug classes would affect AD risk.

53 code the protein targets of several approved lipid-lowering drug classes: HMGCR (encoding the target

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

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

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

57 Bempedoic acid is a first-in-class lipid-lowering drug recommended by guidelines for the tr

58 The lipid-lowering drug simvastatin decreases portal pressur

59 As IDOL is a putative lipid-lowering drug target, we investigated the molecula

60 iants indexed expected effects of modulating lipid-lowering drug targets on PD.

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

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

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

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

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

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

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

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

69 bolic diseases in 3 populations (Genetics of Lipid Lowering Drugs and Diet Network, n = 978; Framingh

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

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

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

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

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

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

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

77 Long-term exposure to lipid-lowering drugs might affect Parkinson's disease (P

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

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

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

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

82 artiles of suPAR, including age, sex, use of lipid-lowering drugs, body mass index, diabetes mellitus

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

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

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

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

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

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

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

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

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

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

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

94 The hepatic lipid-lowering effect observed in animals cotreated with

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

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

97 The lipid-lowering effect of pravastatin was accompanied by

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

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

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

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

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

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

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

105 o the mechanisms behind the cholesterol- and lipid-lowering effects of Pu-erh tea, and suggest that d

106 icosapentaenoic acid, appear to exceed their lipid-lowering effects.

107 n about the potential benefits of preventive lipid-lowering efforts during the early midlife period.

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

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

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

111 Immediate initiation of lipid lowering (ie, treatment for 30 years) in 40- to 49

112 the next 30 years is achievable by intensive lipid lowering in individuals in their 40s and 50s with

113 pathways could serve as powerful adjuncts to lipid lowering in the prevention and treatment of cardio

114 determine the optimal time for initiation of lipid lowering in younger adults as a function of expect

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

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

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

118 ssessment and the potential benefit of early lipid-lowering intervention.

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

120 Lipid-lowering is an intervention that reduces atheroscl

121 eventive pharmacotherapies, such as aspirin, lipid-lowering mediations, and cardiometabolic agents.

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

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

124 .80 (95% confidence interval, 0.73-0.88) for lipid-lowering medication and 0.82 (95% confidence inter

125 lemia, but were less likely to be prescribed lipid-lowering medication and angiotensin-converting enz

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

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

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

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

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

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

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

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

134 %) of patients who reported currently taking lipid-lowering medication, full implementation of the US

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

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

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

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

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

140 bitors (17.9%), antidepressants (17.8%), and lipid-lowering medications (16.5%).

141 ompared to 6.5% of patients who did not take lipid-lowering medications (P < 0.01).

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

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

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

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

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

147 Approximately 6% of patients taking lipid-lowering medications had a diagnosis code for NPDR

148 ed time-to-event analyses, patients who took lipid-lowering medications prior to diagnosis of T2DM we

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

150 und consistent evidence that patients taking lipid-lowering medications were less likely to develop N

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

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

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

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

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

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

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

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

159 at can be considered as proxies for specific lipid-lowering medications.

160 atients (37%) were undergoing treatment with lipid-lowering medications.

161 For many, the question of when to start lipid lowering might be more relevant than whether to st

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

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

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

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

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

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

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

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

170 Lipid-lowering recommendations for prevention of atheros

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

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

173 Beyond lipid-lowering, statins exert cardioprotective effects.

174 These findings may have implications for lipid-lowering strategies in patients with SCD, as well

175 g women had a lower probability of receiving lipid-lowering therapies (relative risk [RR]=0.87; 95% c

176 termined potential eligibility for intensive lipid-lowering therapies (very high risk) under the 2018

177 ential growth in terms of antithrombotic and lipid-lowering therapies aimed at mitigating ischemic ev

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

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

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

181 L) cholesterol levels despite treatment with lipid-lowering therapies at maximum tolerated doses, hav

182 l management guidelines recommend additional lipid-lowering therapies for secondary prevention in pat

183 multiple risk enhancers and novel intensive lipid-lowering therapies for secondary prevention.

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

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

186 vel meta-regression analysis of 3 classes of lipid-lowering therapies that reduce triglycerides to a

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

188 hen guideline recommendations for the use of lipid-lowering therapies, including non-statin treatment

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

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

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

192 g individuals prescribed antihypertensive or lipid-lowering therapies.

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

194 ein cholesterol (LDL-C) level with available lipid-lowering therapies.

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

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

197 Lipid lowering therapy significantly reduces this risk,

198 Current lipid lowering therapy was maintained from 6 weeks befor

199 criteria for intensive secondary prevention lipid-lowering therapy (28.3% vs. 40.0% vs. 81.4%, respe

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

201 cutaneous coronary intervention to intensive lipid-lowering therapy (ILLT) comprising single LDL aphe

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

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

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

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

206 een convincingly demonstrated that intensive lipid-lowering therapy (to a low-density lipoprotein cho

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

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

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

210 the authors examined 25,480 subjects free of lipid-lowering therapy and myocardial infarction at stud

211 It therefore currently forms the mainstay of lipid-lowering therapy as recommended by international g

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

213 severe HeFH >=12 years of age and on stable lipid-lowering therapy began subcutaneous evolocumab 420

214 Lipid-lowering therapy does not improve kidney outcomes

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

216 cardiovascular disease and the relevance of lipid-lowering therapy for cardiovascular disease outcom

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

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

219 eline includes recommendations for intensive lipid-lowering therapy in patients at very high risk for

220 dialysis because guidelines do not recommend lipid-lowering therapy in such patients who do not have

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

222 dings reinforce the need for more aggressive lipid-lowering therapy in young FH and non-FH patients p

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

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

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

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

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

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

229 /ACC cholesterol guideline directs intensive lipid-lowering therapy to adults with a very high ASCVD

230 percholesterolemia who were receiving stable lipid-lowering therapy to receive an intravenous infusio

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

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

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

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

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

236 Lipid-lowering therapy with ezetimibe plus simvastatin i

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

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

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

240 lassified as probable or definite FH, use of lipid-lowering therapy, and LDL-C achieved 1-year post M

241 Lipid-lowering therapy, antihypertensive drugs, and anti

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

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

244 dial infarction, and the efficacy of maximum lipid-lowering therapy, it has been suggested that plaqu

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

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

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

248 ercholesterolemia receiving maximum doses of lipid-lowering therapy, the reduction from baseline in t

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

250 e the receipt of maximum doses of background lipid-lowering therapy.

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

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

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

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

255 2 mmol per liter) if they were not receiving 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 hat they are induced in the periphery during lipid-lowering therapy.

263 ed statin therapy with or without additional lipid-lowering therapy.

264 greater while receiving maximally tolerated lipid-lowering therapy.

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

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

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

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

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

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

271 0 to 17 years of age who had received stable lipid-lowering treatment for at least 4 weeks before scr

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 ipants, age 30 to 59 years, not eligible for lipid-lowering treatment recommendation under the most r

278 nts in gene regions representing alternative lipid-lowering treatment targets (PCSK9, LDLR, NPC1L1, A

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

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

281 ute risk reductions for antihypertensive and lipid-lowering treatment were assessed.

282 individuals' responsiveness to conventional lipid-lowering treatment.

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

284 scular disease receiving maximally tolerated lipid-lowering treatment.

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

286 olesterol and modelled its risk reduction by lipid-lowering treatment.

287 Conventional lipid-lowering treatments are modestly effective.

288 ct that statins reduce cancer risk but other lipid-lowering treatments do not.

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

290 Despite the clinical successes of lipid-lowering treatments, atherosclerosis remains one o

291 Along with effective lipid-lowering treatments, the recent success of clinica

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

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

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

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

296 es have not been systematically reported for lipid-lowering trials.

297 In patients aged 75 years and older, lipid lowering was as effective in reducing cardiovascul

298 Lipid-lowering was induced by microsomal triglyceride tr

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).