ライフサイエンスコーパス: statin therapy

1 creased coronary heart disease when added to statin therapy.

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

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

4 States, may be potentially preventable with statin therapy.

5 those individuals who will benefit most from statin therapy.

6 yndromes are improved in patients already on statin therapy.

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

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

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

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

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

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

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

14 tially avoid the myotoxicity associated with statin therapy.

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

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

17 fy individuals who meaningfully benefit from statin therapy.

18 esterol levels in patients who are receiving statin therapy.

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

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

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

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

23 als who derive greater clinical benefit from statin therapy.

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

25 agement defined new eligibility criteria for statin therapy.

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

27 relative and absolute clinical benefit from statin therapy.

28 eneficial and harmful pleiotropic effects of statin therapy.

29 Among 7,248 eligible subjects, 46% received statin therapy.

30 ollment criterion in any randomized trial of statin therapy.

31 low-intensity statin therapy (LIST), and no-statin therapy.

32 oadened the scope of candidates eligible for statin therapy.

33 iovascular risk to determine eligibility for statin therapy.

34 The majority of these patients also receive statin therapy.

35 with >/=2 healthcare visits per year and on statin therapy.

36 CAM1-5 imaging sensitivity using a reference statin therapy.

37 yocardial infarction is early high-intensity statin therapy.

38 , reduced LDL-C levels in patients receiving statin therapy.

39 rm adherence to aspirin, exercise, diet, and statin therapy.

40 -C goal of <70 mg/dl, even with high-potency statin therapy.

41 ontrols with patients with hyperlipidemia on statin therapy.

42 th familial hypercholesterolemia (FH) during statin therapy.

43 density lipoprotein cholesterol after potent statin therapy.

44 poprotein B, and the influence of background statin therapy.

45 herapy, treatment targets, and monitoring of statin therapy.

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

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

48 ervational cohorts and 1 randomized trial of statin therapy.

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

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

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

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

53 tabilization among patients taking intensive statin therapy.

54 nscriptomics in patients receiving high-dose statin therapy.

55 icans as newly eligible for consideration of statin therapy.

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

57 .69, I(2) = 0%) was significantly altered by statin therapy.

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

59 Eligibility for primary prevention statin therapy.

60 y; atorvastatin patients only) when added to statin therapies.

61 apolipoprotein B (apoB) levels achieved with statin therapy; 2) the proportion of patients not reachi

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

63 232293 (45.6%) receiving moderate-intensity statin therapy, 33920 (6.7%) receiving low-intensity sta

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

65 0709) for those receiving moderate-intensity statin therapy, 5.7% (1632 of 28765) for those receiving

66 9 were more likely to be receiving intensive statin therapy (56%, 36%, 25%, and 13% in the fourth thr

67 Among 38,153 patients allocated to statin therapy, a total of 6,286 major cardiovascular ev

68 9%-46.7%) of adults would be recommended for statin therapy according to ACC/AHA guidelines and 39.1%

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

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

71 intraoperative renal oximetry), prevention (statin therapy, acetylsalicylic acid, N-acetylcysteine,

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

73 of initiating, intensifying, and maximizing statin therapy after acute myocardial infarction are unk

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

75 t reclassification index for eligibility for statin therapy among 40- to 75-year-old subjects from th

76 were 377,311 patients (32.4%) not receiving statin therapy and 259,143 (22.6%) receiving nonstatin t

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

78 ; 42% of patients were taking high-intensity statin therapy and 45% received >1 LDL-lowering medicati

79 ssess the impact of statin dose, duration of statin therapy and baseline ADMA concentrations as poten

80 ls of atherogenic lipoproteins achieved with statin therapy and cardiovascular disease risk.

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

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

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

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

85 show suboptimal use of early high-intensity statin therapy and overall lipid control following myoca

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

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

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

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

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

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

92 deline-recommended lipid levels on high-dose statin therapy; and 3) the association between very low

93 ls of atherogenic lipoproteins achieved with statin therapy are highly variable, but the consequence

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

95 s cardiovascular event rates, and the use of statin therapy as an adjunct to diet, exercise, and smok

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

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

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

99 After adjustment, statin therapy at discharge was associated with a lower

100 Statin therapy at discharge was not associated with incr

101 Both the presence and intensity of statin therapy at discharge were strongly associated wit

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

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

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

105 fectiveness of measuring CAC and prescribing statin therapy based on the resulting score under a rang

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

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

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

109 e number of adults who would be eligible for statin therapy by 12.8 million, with the increase seen m

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

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

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

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

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

115 Statin therapy compared with addition of ezetimibe or PC

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

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

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

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

120 It is often accompanied by statin therapy, connective tissue diseases, cancer, and

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

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

123 Reductions in cystatin C with statin therapy correlate with reductions in inflammatory

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

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

126 of trial participants assigned to high-dose statin therapy did not reach an LDL-C target <70 mg/dl.

127 -C, non-HDL-C, and apoB levels achieved with statin therapy displayed large interindividual variation

128 Statin therapy does not influence the plasma cortisol pr

129 Statin therapy downregulated novel proteins concerned wi

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

131 ut these cannot be fully exploited with oral statin therapy due to low systemic bioavailability.

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

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

134 that the guideline succeeds in prioritizing statin therapy, expanding the focus to atherosclerotic c

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

136 564 patients with atherosclerotic disease on statin therapy followed for a median of 2.2 years.

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

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

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

140 3 ACC/AHA guideline advises consideration of statin therapy for an estimated 10-year risk of atherosc

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

142 d gain in lifespan (utility) from initiating statin therapy for each age group, sex, and cardiovascul

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

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

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

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

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

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

149 nt of cholesterol expand the indications for statin therapy for the prevention of cardiovascular dise

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

151 ber of U.S. adults receiving or eligible for statin therapy from 43.2 million (37.5%) to 56.0 million

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

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

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

155 ng trial participants treated with high-dose statin therapy, >40% did not reach an LDL-C target <70 m

156 Statin therapy had no significant effect on the composit

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

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

159 Statin therapy has been shown to reduce vascular disease

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

161 s (CaI) in patients receiving high-intensity statin therapy (HIST), low-intensity statin therapy (LIS

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

177 These findings support the use of intensive statin therapy in post-MI patients and provide estimates

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

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

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

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

182 s, the risk-benefit balance of discontinuing statin therapy in the acute setting of ICH should be car

183 In terms of the benefit of statin therapy in the four randomised trials, we noted a

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

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

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

187 the long-term efficacy on cIMT and safety of statin therapy in young children.

188 Those who would be newly eligible for statin therapy include more men than women and persons w

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

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

191 17 proteins were upregulated by statin therapy, including proteins concerned with cytosk

192 Statin therapy influences not only low-density lipoprote

193 arrived on submaximal statins, 26% had their statin therapy intensified, with modest site variability

194 Accurate assignment of statin therapy is a major public health issue.

195 Ongoing statin therapy is associated with a lower daily risk of

196 Given that more intense statin therapy is associated with better outcomes, chang

197 critical illness, whereas discontinuation of statin therapy is associated with increased delirium.

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

199 e of the clinician-patient discussion before statin therapy is initiated.

200 Statin therapy is known to increase blood glucose levels

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

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

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

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

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

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

207 tensity statin therapy (HIST), low-intensity statin therapy (LIST), and no-statin therapy.

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

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

210 ite JUPITER participants treated with potent statin therapy, Lp(a) was a significant determinant of r

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

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

213 Statin therapy may cause symptomatic adverse events (eg,

214 ormance measures to include the intensity of statin therapy may improve care.

215 re frequent healthcare visits and the use of statin therapy may improve hypertension control in all a

216 ng the initiation of the metastatic cascade, statin therapy may represent an effective approach to ta

217 Adherence to statin therapy (measured as the proportion of days cover

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

219 Whether statin therapy modifies this association is poorly under

220 0.001), whereas both LIST (n = 1,726) and no-statin therapy (n = 224) associated with PAV progression

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

222 For these patients, initiating statin therapy of an appropriate intensity to reduce ASC

223 ssociated with the presence and intensity of statin therapy, older age, male sex, hypertension, and b

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

225 No significant effects of statin therapy on arterial inflammation of the aorta wer

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

227 o-controlled trial to evaluate the effect of statin therapy on inflammatory markers during HIV infect

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

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

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

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

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

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

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

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

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

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

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

239 Basing statin therapy recommendations on a 10-year fixed risk t

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

241 Statin therapy reduces low-density lipoprotein (LDL) cho

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 locumab added to moderate- or high-intensity statin therapy resulted in additional LDL-C lowering.

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

246 ctions in coronary heart disease events with statin therapy stratified by genetic risk.

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

248 cardiovascular disease who are not receiving statin therapy, the percentage who would be eligible for

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

250 monoclonaL Antibody Inhibition Combined With Statin thErapy-Thrombolysis In Myocardial Infarction 57)

251 CAC may have the potential to help match statin therapy to absolute CVD risk.

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 elines for dyslipidemia emphasize allocating statin therapy to those at the highest absolute atherosc

256 of cardiovascular disease risk, intensity of statin therapy, treatment targets, and monitoring of sta

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

258 9%-52.9%) of adults would be recommended for statin therapy under ACC/AHA guidelines compared with 47

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

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

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 The proportion of patients assigned to statin therapy was 15% higher under the GACR.

264 3 studies, the absolute risk reduction with statin therapy was 3.6% (95% CI, 2.0-5.1) among those in

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

266 ates) confirmed that a higher probability of statin therapy was associated with a higher probability

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

268 Statin therapy was associated with a reduction in MACE a

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

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

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

272 Statin therapy was associated with decreased risk of all

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

274 Starting statin therapy was associated with numerous lipoprotein

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

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

277 ticenter acute myocardial infarction cohort, statin therapy was begun in nearly 90% of patients durin

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

279 Whether to assign a given patient to statin therapy was compared between the NCEP and GACR gu

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

281 The benefit of statin therapy was consistent across multiple sensitivit

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

283 Patients whose statin therapy was discontinued were less likely than st

284 Statin therapy was well tolerated, with a low incidence

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

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

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

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

289 MCs and MDMs from patients with FH receiving statin therapy were more resistant to M. tuberculosis in

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

291 This therapy complements that of statin therapy, which inhibits the synthesis of choleste

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

293 rol concentrations after at least 8 weeks of statin therapy with or without ezetimibe.

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

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

296 raindication, 23% were discharged on maximal statin therapy, with substantial hospital variability (m

297 treatment using evidenced-based intensity of statin therapy without such targets.

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

299 the risk-factor profile, of persons for whom statin therapy would be recommended (i.e., eligible pers

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