ライフサイエンスコーパス: statin therapy

1 high-density cholesterol >=100 mg/dl despite statin therapy.

2 ixed dyslipidemia taking maximally-tolerated statin therapy.

3 Eligibility for primary prevention statin therapy.

4 creased coronary heart disease when added to statin therapy.

5 ute to the benefits of adding ezetimibe to a statin therapy.

6 nt of diabetes mellitus; or by use/nonuse of statin therapy.

7 re likely to benefit from primary prevention statin therapy.

8 adverse reactions to, and may not tolerate, statin therapy.

9 mmol per liter) or higher who were receiving statin therapy.

10 acute coronary syndrome (ACS) when added to statin therapy.

11 s, potentially impacting guideline-indicated statin therapy.

12 ervational cohorts and 1 randomized trial of statin therapy.

13 or benefit from the addition of ezetimibe to statin therapy.

14 olerance and in those with high adherence to statin therapy.

15 Secondary analysis was performed based on statin therapy.

16 sidered by the investigator to be related to statin therapy.

17 ersus without diabetes mellitus (DM) despite statin therapy.

18 tabilization among patients taking intensive statin therapy.

19 nscriptomics in patients receiving high-dose statin therapy.

20 icans as newly eligible for consideration of statin therapy.

21 mation about both the efficacy and safety of statin therapy.

22 .69, I(2) = 0%) was significantly altered by statin therapy.

23 om the addition of a nonstatin to background statin therapy.

24 rt of 4,957 patients, of whom 2,294 received statin therapy.

25 period, all patients were offered open-label statin therapy.

26 States, may be potentially preventable with statin therapy.

27 those individuals who will benefit most from statin therapy.

28 yndromes are improved in patients already on statin therapy.

29 y, compared with those not receiving chronic statin therapy.

30 vely, were not receiving ATP-III recommended statin therapy.

31 ed pravastatin and 84% assigned placebo took statin therapy.

32 sease (PD), and is usually an indication for statin therapy.

33 CV-coinfected veterans had an indication for statin therapy.

34 tially avoid the myotoxicity associated with statin therapy.

35 a recent acute coronary syndrome on optimal statin therapy.

36 f treatment access, adherence, or concurrent statin therapy.

37 ol reduction in patients, including those on statin therapy.

38 fy individuals who meaningfully benefit from statin therapy.

39 esterol levels in patients who are receiving statin therapy.

40 mic stroke; of these, 71% were discharged on statin therapy.

41 may receive less net benefit from aspirin or statin therapy.

42 y one-half of candidates as not eligible for statin therapy.

43 als who derive greater clinical benefit from statin therapy.

44 baseline and after a minimum of 2 months of statin therapy.

45 agement defined new eligibility criteria for statin therapy.

46 ls older than 55 years who were eligible for statin therapy.

47 n in patients with (60%) or without baseline statin therapy.

48 ended statin eligibility and higher rates of statin therapy.

49 n in patients already receiving maximum-dose statin therapy.

50 sterol >=100 mg/dL despite maximum tolerated statin therapy.

51 election of patients for use or avoidance of statin therapy.

52 nce of benefit for the addition of niacin to statin therapy.

53 in dyslipidemic PLHIV on maximally-tolerated statin therapy.

54 % CI: 1.48 to 3.94 ml/min/1.73 m(2)) through statin therapy.

55 to benefit from the addition of ezetimibe to statin therapy.

56 Alirocumab or ezetimibe added to statin therapy.

57 t, regardless of the intensity of background statin therapy.

58 cian-patient discussion before initiation of statin therapy.

59 d atherogenic lipoproteins despite intensive statin therapy.

60 btilisin/kexin type 9 [PCSK9] inhibitors) to statin therapy.

61 te benefit from the addition of ezetimibe to statin therapy.

62 election of patients for use or avoidance of statin therapy.

63 ecent ACS and dyslipidemia despite intensive statin therapy.

64 emia who are receiving guideline-recommended statin therapy.

65 report having previously never been offered statin therapy (18.6% versus 13.5%; P<0.001), declined s

66 ding 150928 (29.6%) receiving high-intensity statin therapy, 232293 (45.6%) receiving moderate-intens

67 rapy (18.6% versus 13.5%; P<0.001), declined statin therapy (3.6% versus 2.0%; P<0.001), or discontin

68 232293 (45.6%) receiving moderate-intensity statin therapy, 33920 (6.7%) receiving low-intensity sta

69 f 126139) for those receiving high-intensity statin therapy, 4.8% (9703 of 200709) for those receivin

70 0709) for those receiving moderate-intensity statin therapy, 5.7% (1632 of 28765) for those receiving

71 9 were more likely to be receiving intensive statin therapy (56%, 36%, 25%, and 13% in the fourth thr

72 re less likely than men to be prescribed any statin therapy (67.0% versus 78.4%; P<0.001) or to recei

73 9%-46.7%) of adults would be recommended for statin therapy according to ACC/AHA guidelines and 39.1%

74 he population studied, 42% were eligible for statin therapy according to the 2013 American College of

75 nd characteristics of adults recommended for statin therapy according to the ACC/AHA and ESC/EAS guid

76 fit from the use of ezetimibe in addition to statin therapy after acute coronary syndrome has been pu

77 syndrome and dyslipidemia despite intensive statin therapy, alirocumab decreased the risk of stroke,

78 a recent acute coronary syndrome on optimal statin therapy, alirocumab improves cardiovascular outco

79 d atherogenic lipoproteins despite intensive statin therapy, alirocumab was associated with large abs

80 ns to statin therapy compared with receiving statin therapy alone in persons who have or are at high

81 poprotein (LDL) cholesterol levels more than statin therapy alone.

82 ical therapy (SMT) with no LDL apheresis and statin therapy alone.

83 elium-dependent dilatation; however, whether statin therapy alters skin sympathetic nervous system ac

84 Further, whether chronic statin therapy alters skin sympathetic outflow or its re

85 ing for age, sex, body mass index, HbA1c and statin therapy, an increase in 25(OH)D of 1 nmol/L was a

86 compared between 716 individuals who started statin therapy and 4,874 persistent nonusers.

87 ; 42% of patients were taking high-intensity statin therapy and 45% received >1 LDL-lowering medicati

88 derstanding the anti-inflammatory effects of statin therapy and have consistently demonstrated on-tre

89 contemporary population that includes potent statin therapy and low low-density lipoprotein cholester

90 nd a graded association between intensity of statin therapy and mortality in a national sample of pat

91 as a graded association between intensity of statin therapy and mortality, with 1-year mortality rate

92 iations point to pathways of LDL response to statin therapy and possibly to mechanisms of statin-depe

93 ficantly different among those who continued statin therapy and those who discontinued (OR, 0.98; 95%

94 d other risk factors, who had been receiving statin therapy and who had a fasting triglyceride level

95 of 28765) for those receiving low-intensity statin therapy, and 6.6% (4868 of 73728) for those recei

96 herapy, 33920 (6.7%) receiving low-intensity statin therapy, and 92625 (18.2%) receiving no statins.

97 tion predicts coronary events, is reduced by statin therapy, and change at 1 year is associated with

98 red sufficient to warrant primary prevention statin therapy, and the decision not to include choleste

99 H patients were discharged on high-intensity statin therapy, and the vast majority had elevated LDL-C

100 evention when clinical decisions to initiate statin therapy are uncertain.

101 Index Spectrum cohort (n = 888), we identify statin therapy as a key covariate of microbiome diversif

102 isease (CVD) to identify adults eligible for statin therapy as primary prevention.

103 ipidemia would not have been recommended for statin therapy at 40 years of age under current national

104 ar death; 93% of the patients were receiving statin therapy at baseline.

105 eriod of 78 weeks, alirocumab, when added to statin therapy at the maximum tolerated dose, significan

106 ted LDL cholesterol levels despite receiving statin therapy at the maximum tolerated dose.

107 owed for up to 12 months; 96% were receiving statin therapy at the time of enrollment.

108 identified fewer younger adults eligible for statin therapy at the time of their MI than the 2013 gui

109 irectly considering the expected benefits of statin therapy based on the available randomized, contro

110 et a guideline indication for high-intensity statin therapy based on the PCE versus only 10% to 15% u

111 Patients initiating statin therapy between 2005 and 2009 without a previous

112 density lipoprotein cholesterol <70 mg/dL or statin therapy), blood pressure control (<140 mm Hg syst

113 d with incident CVD in individuals on potent statin therapy but not at baseline.

114 Asymptomatic subjects eligible for statin therapy by risk score were enrolled in a prospect

115 Compared with individuals recommended for statin therapy by the ESC/EAS guidelines but not the ACC

116 ARRs of major cardiovascular events by statin therapy can be accurately estimated for individua

117 zed trials have suggested that perioperative statin therapy can prevent some of these complications.

118 However, among those not considered statin therapy candidates at 55 years of age, there rema

119 vention studies that assessed the effects of statin therapy compared with a placebo or no treatment a

120 Statin therapy compared with addition of ezetimibe or PC

121 tion in plasma ADMA concentrations following statin therapy compared with placebo (WMD: -0.104 muM, 9

122 and risks of adding nonstatin medications to statin therapy compared with receiving statin therapy al

123 rence to the 2016 USPSTF recommendations for statin therapy, compared with the 2013 ACC/AHA guideline

124 respectively, in subjects receiving chronic statin therapy, compared with those not receiving chroni

125 prevention (CARE and PROVE IT-TIMI 22) with statin therapy, comprising a total of 48,421 individuals

126 rved ASCVD event rates >7.5% who may warrant statin therapy considerations.

127 Apolipoprotein B100 was downregulated by statin therapy, consistent with it mechanism of action (

128 The absolute benefits of statin therapy depend on an individual's absolute risk o

129 Adding ezetimibe to statin therapy did not increase discontinuation risk.

130 bempedoic acid added to maximally tolerated statin therapy did not lead to a higher incidence of ove

131 In this trial, perioperative statin therapy did not prevent postoperative atrial fibr

132 g enough will become eligible for risk-based statin therapy due to age alone.

133 In this study, initiation of statin therapy during childhood in patients with familia

134 ly for two doses, with or without concurrent statin therapy); each dose cohort included four to eight

135 Statin therapy eligibility was determined using the 2013

136 e benefits of reduction in ASCVD events from statin therapy exceed adverse events.

137 When added to statin therapy, ezetimibe resulted in incremental loweri

138 564 patients with atherosclerotic disease on statin therapy followed for a median of 2.2 years.

139 nts with atherosclerotic disease who were on statin therapy, followed up for a median of 2.2 years.

140 s decision pathway (ECDP) on the role of non-statin therapies for low-density lipoprotein (LDL)-chole

141 lood cholesterol recommends consideration of statin therapy for adults with an estimated 10-year athe

142 3 ACC/AHA guideline advises consideration of statin therapy for an estimated 10-year risk of atherosc

143 oke, data on the real-world effectiveness of statin therapy for clinical and patient-centered outcome

144 nes suggest preventive interventions such as statin therapy for individuals with a high estimated 10-

145 rt Association recommendations on initiating statin therapy for primary prevention of ASCVD (net 221

146 Data are limited regarding statin therapy for primary prevention of atherosclerotic

147 ividuals, aged 45 to 75 years, who initiated statin therapy for primary prevention of cardiovascular

148 r disease (CVD) and help guide initiation of statin therapy for primary prevention of CVD.

149 deration of initiation or intensification of statin therapy for primary prevention to mitigate the in

150 st benefit from the addition of ezetimibe to statin therapy for secondary prevention after ACS.

151 nical ASCVD with or without comorbidities on statin therapy for secondary prevention.

152 tial underutilization of and nonadherence to statin therapy for secondary prevention.

153 and the public make informed decisions about statin therapy for the prevention of heart attacks and s

154 to translate the average relative effect of statin therapy from trial data to the individual patient

155 iffer in how they identify adults in need of statin therapy; furthermore, it is unclear how this diff

156 scle-related symptoms that are attributed to statin therapy generally resolve rapidly when treatment

157 ardiovascular disease-we compared the use of statin therapy, guideline-recommended statin dosing, and

158 ddition of evolocumab to maximally tolerated statin therapy had no impact on patient-reported cogniti

159 Statin therapy had no significant effect on the composit

160 In blinded randomised controlled trials, statin therapy has been associated with few adverse even

161 Relative risk reduction with statin therapy has been consistent across nearly all sub

162 Statin therapy has been shown to reduce vascular disease

163 estinal cholesterol absorption inhibitor, to statin therapy has recently shown clinical benefits in t

164 Alirocumab added to intensive statin therapy has the potential to reduce death after a

165 Patients with elevated triglycerides despite statin therapy have increased risk for ischemic events,

166 at have been shown to be caused by long-term statin therapy-ie, adverse effects of the statin-are myo

167 y prevention patients may be recommended for statin therapy if high CAD PRS were considered a guideli

168 style and nonlipid risk factor modification, statin therapy improves cardiovascular disease outcomes

169 rol for 24 to 104 weeks, added to background statin therapy in 8 trials.

170 tions would be associated with initiation of statin therapy in an additional 15.8% (95% CI, 14.0%-17.

171 The short-term efficacy of statin therapy in children is well established, but long

172 We report a 20-year follow-up study of statin therapy in children.

173 ommends moderate-intensity to high-intensity statin therapy in eligible patients.

174 Nevertheless, statin therapy in general, and high-intensity statin the

175 The putative benefit of statin therapy in MM should be corroborated in prospecti

176 d to more definitively determine the role of statin therapy in older adults for primary prevention of

177 Since the evidence regarding statin therapy in PAH has not been conclusive, we assess

178 t been conclusive, we assessed the impact of statin therapy in PAH through a systematic review and me

179 tatin therapy in general, and high-intensity statin therapy in particular, is underused in patients w

180 ion/stroke with the addition of ezetimibe to statin therapy in patients at higher risk on the basis o

181 ating that additional clinical evaluation of statin therapy in patients on dialysis undergoing arteri

182 proved cardiovascular outcomes when added to statin therapy in patients stabilized after acute corona

183 Continuing established statin therapy in patients who develop dengue is safe.Ch

184 Addition of ezetimibe to statin therapy in patients with a recent acute coronary

185 end in-hospital initiation of high-intensity statin therapy in patients with acute coronary syndromes

186 led trials specifically designed to evaluate statin therapy in patients with cancer.

187 Our findings suggest a potential role for statin therapy in patients with MM.

188 ASCVD risk-reduction interventions including statin therapy in patients with PAD are warranted.

189 ssing likely benefit with ezetimibe added to statin therapy in post-ACS patients.

190 es among guideline recommendations for using statin therapy in primary prevention.

191 ient interactions concerning prescription of statin therapy in primary prevention.

192 omatic adverse events that are attributed to statin therapy in routine practice are not actually caus

193 l benefits from the addition of ezetimibe to statin therapy in subjects with acute coronary syndromes

194 t show a statistically significant effect of statin therapy in the improvement of 6MWD, pulmonary art

195 between all-cause mortality and intensity of statin therapy in the Veterans Affairs health care syste

196 We compared the relative efficacy of statin therapy in those at high genetic risk (top quinti

197 dividuals recommended for primary prevention statin therapy, including many younger adults with high

198 n randomized controlled trials investigating statin therapy, including moderate-intensity statin plus

199 Medical prevention with antithrombotic and statin therapies is a mainstay of treatment to prevent a

200 At current prices, the addition of PCSK9i to statin therapy is estimated to provide an additional qua

201 ch is needed to determine whether lipophilic statin therapy is feasible for prevention of HCC.

202 Statin therapy is indicated in the secondary prevention

203 Statin therapy is known to increase blood glucose levels

204 yopathy (one of which might progress, if the statin therapy is not stopped, to the more severe condit

205 High-intensity statin therapy is recommended for the secondary preventi

206 Therefore, initiation of statin therapy is recommended for these individuals.

207 e heart attacks or strokes that may occur if statin therapy is stopped unnecessarily can be devastati

208 assessment in those below this threshold for statin therapy is unclear.

209 ntervention Trial Evaluating Rosuvastatin]), statin therapy led to a greater relative risk reduction

210 A combination of women being offered statin therapy less frequently, while declining and disc

211 of PCSK9 with evolocumab on a background of statin therapy lowered LDL cholesterol levels to a media

212 heterozygous FH, moderate- to high-intensity statin therapy lowered the risk for CAD and mortality by

213 monoclonal antibodies to maximally tolerated statin therapy may be cost effective in very high-risk a

214 ggerated claims about side-effect rates with statin therapy may be responsible for its under-use amon

215 Statin therapy may cause symptomatic adverse events (eg,

216 Lowering of LDL-C levels by statin therapy modestly increases the risk of type 2 dia

217 0.001), whereas both LIST (n = 1,726) and no-statin therapy (n = 224) associated with PAV progression

218 viduals, of whom 8794 subsequently initiated statin therapy (new initiators) and 44,269 did not (non-

219 either evolocumab or placebo in addition to statin therapy, no significant between-group difference

220 sess the long-term effects of treatment with statin therapy on all-cause mortality, cause-specific mo

221 Here we assess the potential effect of statin therapy on cancer risk using evidence from human

222 ional risk factors to evaluate the effect of statin therapy on cardiovascular events.

223 s, and outcome and the impact of concomitant statin therapy on cortisol profiles in 80 steroid naive

224 This study addresses the evidence of statin therapy on ICH and other clinical outcomes in pat

225 We investigated the impact of statin therapy on influenza vaccine effectiveness (VE) a

226 of this study was to determine the effect of statin therapy on lipoproteins and their protein cargo b

227 sought to determine the molecular effects of statin therapy on multiple metabolic pathways.

228 The impact of statin therapy on plasma asymmetric dimethylarginine (AD

229 then assessed longitudinally the effects of statin therapy on primary murine fistula patency and mat

230 elderly persons to evaluate the influence of statin therapy on the immune response to vaccination.

231 During high-intensity statin therapy, on-treatment levels of LDL-C and atherog

232 hese drugs as add-ons to maximally tolerated statin therapy or for those with statin intolerance.

233 tes mellitus (OR, 0.93 [95% CI, 0.74-1.19]), statin therapy (OR, 0.88 [95% CI, 0.68-1.14]), or cardia

234 e was not affected by ACE inhibitor therapy, statin therapy, or the combination of the two.

235 89.9% of non-FH patients were discharged on statin therapy (p = 0.82).

236 orrespond with increased recommendations for statin therapy per the American College of Cardiology/Am

237 ecent ACS and dyslipidemia despite intensive statin therapy, polyvascular disease is associated with

238 Compared with beneficiaries not on statin therapy pre-hospitalization, multivariable adjust

239 ting inclusion criteria, 210 (12.5%) were on statin therapy prior to MI and were excluded.

240 ent guideline-based treatment thresholds for statin therapy prior to their MI.

241 However, statin therapy reduced non-calcified plaque volume and h

242 poprotein cholesterol (LDL-C) with intensive statin therapy reduces progression of coronary atheroscl

243 e evidence from randomised trials shows that statin therapy reduces the risk of major vascular events

244 Addition of ezetimibe to statin therapy reduces the risk of recurrent cardiovascu

245 Our findings suggest that prescription of statin therapy should be accompanied by a careful consid

246 mong those who continued versus discontinued statin therapy, suggesting the potential for indication

247 Statin therapy, supported by a broad evidence base, has

248 atherogenic lipoproteins, despite intensive statin therapy, targeting LDL-C levels of 25 to 50 mg/dL

249 hyl-glutaryl-coenzyme A reductase inhibitor (statin) therapy than middle-aged and older adults.

250 ascular disease who were receiving intensive statin therapy, the use of anacetrapib resulted in a low

251 at high risk of ASCVD already on background statin therapy, there was minimal evidence for improved

252 e greater relative and absolute benefit from statin therapy to prevent a first coronary heart disease

253 ese results do not support the initiation of statin therapy to prevent AKI following cardiac surgery.

254 es in heart transplant recipients undergoing statin therapy to statin-naive patients.

255 uation of statins is advised, but initiating statin therapy to treat COVID-19 is as yet unsubstantiat

256 For patients receiving statin therapy unchanged from baseline, at week 208, the

257 9%-52.9%) of adults would be recommended for statin therapy under ACC/AHA guidelines compared with 47

258 ), patients with hyperlipidemia eligible for statin therapy under National Cholesterol Education Prog

259 he ACC/AHA guidelines, those recommended for statin therapy under the ACC/AHA guidelines only had les

260 enic and inflammatory macrophage response to statin therapy, using the fibrin-targeted, near-infrared

261 dual-antiplatelet therapy, and 71% high-dose statin therapy versus 0.8%, 1.6%, and 31% among T2MI2012

262 Predicted 10-year ARR by statin therapy was <2% for 13% of the patients.

263 3 studies, the absolute risk reduction with statin therapy was 3.6% (95% CI, 2.0-5.1) among those in

264 use of moderate-intensity to high-intensity statin therapy was 62.1% (before publication of the guid

265 In this cohort study of US veterans with MM, statin therapy was associated with a reduced risk of bot

266 Statin therapy was associated with a reduction in MACE a

267 This study aimed to assess whether statin therapy was associated with a reduction in major

268 OPS trial participants at high genetic risk, statin therapy was associated with a relative risk reduc

269 A recent meta-analysis demonstrated that statin therapy was associated with a risk of diabetes.

270 Statin therapy was associated with decreased risk of all

271 statins at the time of admission, discharge statin therapy was associated with lower risk of major a

272 Starting statin therapy was associated with numerous lipoprotein

273 In this study, statin therapy was associated with reduced influenza VE

274 eased CVD risk but without prior CVD events, statin therapy was associated with reduced risk of all-c

275 n patients and their doctors were aware that statin therapy was being used and not when its use was b

276 oembolism was 0.85 (0.73-0.99; p=0.038) when statin therapy was compared with placebo or no treatment

277 The benefit of statin therapy was consistent across multiple sensitivit

278 (Maximally tolerated statin therapy was defined as the highest intensity stat

279 Intensity of statin therapy was defined by the 2013 American College

280 In community-dwelling elderly Australians, statin therapy was not associated with any greater decli

281 g of ACS, evolocumab added to high-intensity statin therapy was well tolerated and resulted in substa

282 Statin therapy was well tolerated, with a low incidence

283 the NHANES population who were eligible for statin therapy, we applied treatment algorithms from the

284 cebo-controlled trial of evolocumab added to statin therapy, we prospectively assessed cognitive func

285 rovement in 6-min walking distance (6MWD) by statin therapy (weighed mean difference [WMD]: -6.08 m,

286 alized ARR on major cardiovascular events by statin therapy were calculated for each patient by subtr

287 Women eligible for statin therapy were less likely than men to be treated w

288 after ACS, 18,924 patients on high-intensity statin therapy were randomized to alirocumab or placebo

289 ic lipoprotein levels despite high-intensity statin therapy were randomized to alirocumab or placebo

290 me and residual dyslipidemia despite optimal statin therapy were randomly assigned to alirocumab or p

291 benefit less than other patient groups from statin therapy, which inhibits cholesterol synthesis.

292 s and 177 088 participants from 25 trials of statin therapy with 20 962 major vascular events were in

293 followed by shared decision making regarding statin therapy with a physician.

294 servational and randomised studies comparing statin therapy with control (placebo or no treatment) in

295 hile they were receiving maximally tolerated statin therapy with or without additional lipid-lowering

296 were on high-intensity or maximum-tolerated statin therapy, with a baseline low-density lipoprotein

297 rs, and 86% qualified for ACC/AHA risk-based statin therapy, with high sensitivity (96%) but low spec

298 Despite intensive statin therapy, with or without ezetimibe, many patients

299 controlled trial of primary prevention with statin therapy (WOSCOPS [West of Scotland Coronary Preve

300 er findings that emerge about the effects of statin therapy would not be expected to alter materially