ライフサイエンスコーパス: statin

1 matched 1:1 with control patients not using statin.

2 e of secondary prevention strategies such as statins.

3 Different daily dosages and types of statins.

4 scharge, 15.4% of beneficiaries discontinued statins.

5 for the propensity to receive high-intensity statins.

6 those receiving high- vs moderate-intensity statins.

7 sclerotic CVD risk and may be considered for statins.

8 atin therapy, and 92625 (18.2%) receiving no statins.

9 Of this group, 53.7% reinitiated statins.

10 in cholesterol (LDL-C) levels despite use of statins.

11 t should be controlled in clinical trials of statins.

12 n venous thromboembolism compared with other statins 0.57 (0.42-0.75; p=0.015).

13 ble participants, 16% started therapy with a statin, 11% with an ACEI/ARB, and 5% with both.

14 associated with taking the highest dosage of statins (80 mg) compared with a lower dosage (40 mg) (HR

15 Although the benefits of statins accrue over time, treatment discontinuation is c

16 High statin adherence over the year following hospital discha

17 th statin intolerance versus those with high statin adherence were 1.50 (95% confidence interval [CI]

18 Compared to beneficiaries with high statin adherence, statin intolerance was associated with

19 erance, and 55,567 patients (52.8%) had high statin adherence.

20 However, whether combination therapy or statin alone resulted in cardiovascular benefit is uncer

21 nd statin treatment strategy compared with a statin alone strategy.

22 Statins also alter neutrophil responses in vitro.

23 health status, (2) quality of care measures: statin and ASA use, (3) healthcare resource utilization:

24 % more likely to report that they are not on statin and aspirin, respectively, had a significantly gr

25 n-titrated intensity, and 66.0% had the same statin and intensity.

26 use of moderate-intensity to high-intensity statin and nonstatin lipid-lowering therapy (LLT) were a

27 Moderate-intensity to high-intensity statin and nonstatin LLT use before and after publicatio

28 use of moderate-intensity to high-intensity statin and nonstatin LLT use in hierarchical logistic re

29 use of moderate-intensity to high-intensity statin and nonstatin LLT.

30 clinical attachment level (CAL) gain in both statin and placebo/no treatment groups.

31 how it varied by the daily dosage or type of statin and whether any protective effect persists after

32 second breast cancer events with the use of statins and antibiotics, respectively, after adjustment

33 competing cytochrome P450 metabolism between statins and commonly used antiretroviral agents.

34 t studies that reported associations between statins and first venous thromboembolism outcomes were i

35 in intolerance was defined as down-titrating statins and initiating ezetimibe therapy, switching from

36 Longitudinally, the effects of statins and of diet and exercise on AT TSHB mRNA were al

37 th different risk thresholds for instituting statins and statin toxicity estimates but depend greatly

38 of age or older with high or low exposure to statins and with drug molecules for black, Hispanic, and

39 ibitors or angiotensin-receptor blockers and statins), and adverse clinical outcomes (emergency depar

40 iated with lower IOP and systemic ACEI, ARB, statin, and sulfonylurea use was associated with higher

41 fficacy of several opiates, antidepressants, statins, and antibiotics.

42 r cells to the antiproliferative activity of statins, and induction of EMT by ZEB1 was sufficient to

43 use of nonsteroidal anti-inflammatory drugs, statins, and multivitamins.

44 ,500 per year) are >100x higher than generic statins, and only a small fraction of their higher cost

45 for ACE inhibitors/ARBs, beta-blockers, and statins, and survived >/=180 days after AMI hospitalizat

46 3-0.93), and 0.86 (0.74-1.01) in patients on statins, angiotensin-converting enzyme inhibitors/angiot

47 We sought to evaluate the extent to which statins are associated with first venous thromboembolism

48 Statins are believed to inhibit Ras signaling and may al

49 HMG-CoA reductase inhibitors such as statins are cholesterol-reducing agents that may provide

50 I receptor blockers (ARB), beta-blockers and statins are recommended after acute myocardial infarctio

51 tatin ameliorated the pathology, implicating statins as potential therapeutics against a subset of pu

52 is C virus (HCV) infection may be prescribed statins as treatment for metabolic/cardiovascular diseas

53 onary CTA was associated with greater use of statins, aspirin, and invasive procedures, and higher co

54 High adherence to high-intensity statins at 6 months and 2 years after discharge was defi

55 , simvastatin 40-<80 mg), and 12.9% low-dose statins (atorvastatin <20 mg, rosuvastatin <10 mg, simva

56 mg, simvastatin 80 mg), 28.6% moderate-dose statins (atorvastatin 20-<40 mg, rosuvastatin 10-<20 mg,

57 Overall, 58.4% received high-dose statins (atorvastatin 40-80 mg, rosuvastatin 20-40 mg, s

58 Efficacy of statin-based therapies in reducing cardiovascular mortal

59 tion population who would be recommended for statins by ACC/AHA guidelines but not by USPSTF recommen

60 men, in whom 184 (63%) were not eligible for statins by either guideline, compared with 549 (46%) men

61 ted significant differences in the effect of statins by type of statin, with rosuvastatin having the

62 frican American individuals not eligible for statins by USPSTF guidelines had a higher ASCVD event ra

63 with a CACS >/=300 Agatston units mostly on statins, CACS correlated with total plaque volume but no

64 owth, and observational studies suggest that statins combined with anticancer therapies delay relapse

65 levels, persons who filled prescriptions for statins continuously for 2 years had a 21% reduced risk

66 These statins decreased neutrophil trafficking to the joint as

67 Examining the patterns of statin discontinuation, reinitiation, and persistence af

68 ntihyperlipidemic adverse event, followed by statin down-titration or discontinuation, or switching b

69 amples was demonstrated with three different statin drugs (atorvastatin, rosuvastatin, and fluvastati

70 these findings, we propose that repurposing statin drugs for topical treatment of DFUs may offer ano

71 ege of Cardiology/American Heart Association statin eligibility criteria to identify individuals at a

72 Statin eligibility increased among all race, education,

73 The 2013 ACC/AHA guidelines increase statin eligibility most among adults with nonwhite race,

74 NHANES) data (2009-2014) were used to assess statin eligibility under the 2016 USPSTF recommendations

75 Statin eligibility was determined per American College o

76 While statin-eligible individuals by USPSTF guidelines did not

77 dent cancer occurred in 125 (15%) of the 812 statin-eligible participants versus 122 (8.8%) of the 1,

78 r mortality occurred in 34 (4.2%) of the 812 statin-eligible participants versus five (0.4%) of the 1

79 r mortality occurred in 49 (6.0%) of the 812 statin-eligible participants versus nine (0.7%) of the 1

80 l advantage compared with moderate-intensity statins, even among older adults.

81 3 patients (27.3%) receiving maximal-potency statins, evolocumab significantly reduced the primary en

82 Experimental studies show that statins exert additive effects with agents, such as cisp

83 for baseline low-density lipoprotein level, statin exposure continued to be associated with a reduct

84 High statin exposure was not associated with a statistically

85 The use of high-intensity statins following hospitalization for MI increased progr

86 The group with intensive LDL-c-lowering statin had an 18% increase in the likelihood of developi

87 treated with maximal doses of high-intensity statins had lower mortality (hazard ratio, 0.90; 95% CI,

88 Statin treatment starts at diagnosis, but no statin has been formally evaluated in, or approved for,

89 Treatment of dyslipidaemia with statins has been challenging in people with HIV because

90 Aspirin and statins have a positive impact on these resolution pathw

91 Statins have been suggested to have a protective effect

92 The statins have been used for 30 years to prevent coronary

93 l-coenzyme A (HMG-CoA) reductase inhibitors (statins) have been the main therapy for lowering LDL-C.

94 031 patients not receiving a maximal-potency statin (HR, 0.85; 95% CI, 0.78-0.93; P = .88 for interac

95 herapy in 35.7% (standard error [SE]: 2.7%), statin in 33.1% (SE: 2.4%), ACEI/ARB in 28.4% (SE: 2.0%)

96 of-pocket (OOP) expenditures associated with statins in a representative US adult population from 200

97 f PCSK9 monoclonal antibodies incremental to statins in on-going clinical end point trials.

98 JUPITER trial (Justification for the Use of Statins in Prevention: An Intervention Trial Evaluating

99 m] and JUPITER [Justification for the Use of Statins in Prevention: An Intervention Trial Evaluating

100 trial (JUPITER [Justification for the Use of Statins in Primary Prevention: An Intervention Trial Eva

101 of statin sensitivity, and the mechanism of statin-induced tumor-specific apoptosis remains unclear.

102 Because statins inhibit the production of isoprenoid intermediat

103 3%) of patients who would be recommended for statin initiation under full implementation of the 2013

104 of acute liver injury (ALI) is increased for statin initiators compared to nonusers in groups classif

105 Regardless of HIV and/or chronic HCV status, statin initiators had a lower risk of ALI and death with

106 Among HIV-monoinfected patients, statin initiators had lower risks of aminotransferase in

107 Among HIV/HCV-coinfected patients, statin initiators had lower risks of aminotransferase le

108 In the setting of chronic HCV alone, statin initiators had reduced risks of aminotransferase

109 ed a cohort study to compare rates of ALI in statin initiators vs nonusers among 7686 HIV/HCV-coinfec

110 of less than 70 or at least 70 mg/dL and by statin intensity (maximal: atorvastatin calcium, 80 mg/d

111 Down-titrating versus reinitiating the same statin intensity (RR, 1.10; 95% CI, 1.05-1.16) and reini

112 ortion of days covered less than 80% for any statin intensity without discontinuation.

113 els were similar across pools, regardless of statin intensity.

114 ratory infections and determine if and how a statin intervention could alter these blunted responses.

115 ard ratios (HR) comparing beneficiaries with statin intolerance versus those with high statin adheren

116 to beneficiaries with high statin adherence, statin intolerance was associated with a 36% higher rate

117 Statin intolerance was defined as down-titrating statins

118 Overall, 1,741 patients (1.65%) had statin intolerance, and 55,567 patients (52.8%) had high

119 ing secondary dyslipidaemia, or a history of statin intolerance, diabetes, or coronary artery disease

120 sease risk, physicians should consider which statin is prescribed to each patient.

121 lation for atrial fibrillation, discharge on statin, lipid management, neurology consultation, Holter

122 Statins lower cholesterol by inhibiting HMG-CoA reductas

123 lted in a sample of 1,475 patients receiving statin matched 1:1 with control patients not using stati

124 Because statins may affect Alzheimer disease risk, physicians sh

125 eroidal antiinflammatory drugs (NSAIDs), and statins may play a role in chemoprevention.

126 we demonstrate that the naturally occurring statin mevastatin reverses FPP's effects and promotes he

127 of less than 70 mg/dL, including 67.3% with statin monotherapy, 18.7% with statins plus ezetimibe, a

128 comparing a total of 10 strategies: saline, statin, N-acetylcysteine (NAC), sodium bicarbonate (NaHC

129 5 +/- 8.1 years of age; 55% female) who were statin naive and free of cancer at baseline from the off

130 older, male, nonwhite, diabetic, overweight, statin naive, and presenting with a first myocardial inf

131 preadmission single-agent or combined use of statins, nonsteroidal anti-inflammatory drugs, or glucoc

132 ALI and death within 18 months compared with statin nonusers.

133 h (HR, 0.36 [95% CI, .28-.46]) compared with statin nonusers.

134 may help determine the beneficial effects of statin on plaque stabilization.

135 Use of statins on adult patients with chronic periodontitis sho

136 ay, reversed the protective actions of these statins on both joint and systemic inflammation.

137 ence demonstrating the beneficial effects of statins on clinical outcomes, the mechanisms underlying

138 However, effect of locally delivered statins on periodontal treatment has not yet been system

139 e to ACE inhibitors/ARBs, beta-blockers, and statins on survival among older people after AMI.

140 ox analyses were used to study the effect of statins on survival.

141 To assess whether the protective effect of statins on the risk of glaucoma varies depending on the

142 enzyme A reductase inhibitors (also known as statins) on colorectal cancer prognosis, investigators r

143 alonate signaling, which can be inhibited by statin or 6-fluoromevalonate treatment.

144 performance were seen in single domains with statin or ACEI/ARB therapy, we did not find consistent e

145 d Trials cohort participants not receiving a statin or ACEI/ARB within 30 days of first neurologic as

146 5 mmol/L or lower, and who were not taking a statin or fibrate, had no history of myocardial infarcti

147 py, we did not find consistent evidence that statins or ACEI/ARB have an effect on global neurocognit

148 ; 95% confidence interval [CI]: 1.8 to 3.9), statins (OR: 2.6; 95% CI: 1.8 to 3.9), ACEI/ARB (OR: 2.6

149 sive drugs (OR: 0.18; 95% CI: 0.06-0.61) and statins (OR: 4.96; 95% CI: 1.60-16.41).

150 use of moderate-intensity to high-intensity statins overall and in the ASCVD cohort, such a trend wa

151 6.6% (4868 of 73728) for those receiving no statin (P < .001).

152 o discontinue a statin reinitiate treatment, statin persistence after reinitiation was low.

153 babilistic sensitivity analysis found that a statin plus PCSK9i strategy had a low probability (<1%)

154 the incremental cost-effectiveness ratio of statin plus PCSK9i therapy was $337729 per quality-adjus

155 ng 67.3% with statin monotherapy, 18.7% with statins plus ezetimibe, and 14% with add-on PCSK9 inhibi

156 en 2007 and 2012 who filled a high-intensity statin prescription (atorvastatin, 40-80 mg, and rosuvas

157 e, comorbidities, not filling high-intensity statin prescriptions before their myocardial infarction

158 roportion of patients filling high-intensity statin prescriptions following myocardial infarction who

159 ctors associated with filling high-intensity statin prescriptions included male sex, filling beta-blo

160 Patients filling statin prescriptions within 30 days of discharge were in

161 and those taking low- or moderate-intensity statins prior to hospitalization (from 27.8% to 62.3% in

162 Statin recommendation under both guidelines was associat

163 isk factors, and there is some evidence that statins reduce cancer mortality.

164 er adding triglyceride-lowering treatment to statin reduces this risk.

165 Although many people who discontinue a statin reinitiate treatment, statin persistence after re

166 mine the associations between treatment with statins, renin-angiotensin system blockers, beta-blocker

167 However, many patients taking statins report muscle-related symptoms that prevent the

168 and reinitiating a different versus the same statin (RR, 1.10; 95% CI, 1.06-1.14) were associated wit

169 f the RAS superfamily are poor biomarkers of statin sensitivity, and the mechanism of statin-induced

170 lthough ectopic expression of HRAS increased statin sensitivity, expression of myristoylated HRAS did

171 Treatment of cells with various statins strongly increased LDLR expression levels but di

172 tion of days covered >/=80% with >/=1 day of statin supply 182 days after reinitiation.

173 ies depending on the daily dosage or type of statin taken.

174 Statins tend to increase Lp(a) levels, possibly contribu

175 modulated with short-term therapies, such as statins, that mitigate cardiovascular risk.

176 for the propensity to receive high-intensity statins, the hazard ratio for mortality was 0.91 (95% CI

177 9 were more likely to be receiving intensive statin therapy (56%, 36%, 25%, and 13% in the fourth thr

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

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

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

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

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

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

184 564 patients with atherosclerotic disease on statin therapy followed for a median of 2.2 years.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

204 The benefit of statin therapy was consistent across multiple sensitivit

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

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

207 232293 (45.6%) receiving moderate-intensity statin therapy, 33920 (6.7%) receiving low-intensity sta

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

209 0709) for those receiving moderate-intensity statin therapy, 5.7% (1632 of 28765) for those receiving

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

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

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

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

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

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

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

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

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

219 Eligibility for primary prevention statin therapy.

220 creased coronary heart disease when added to statin therapy.

221 ers of a reasonable daily dosage and type of statin to use when designing randomized clinical trials

222 t; therefore, there is no basis to prescribe statins to colorectal cancer patients who do not have ca

223 initiating ezetimibe therapy, switching from statins to ezetimibe monotherapy, having International C

224 risk thresholds for instituting statins and statin toxicity estimates but depend greatly on the disu

225 included BIOSTAT-CHF risk scores, LDLR, and statin treatment as covariates, revealed a positive line

226 ngs support the value of early initiation of statin treatment for low-density lipoprotein cholesterol

227 n assist in guiding the decision to initiate statin treatment for primary prevention in older adults

228 Statin treatment inhibiting Rac1 geranylgeranylation red

229 Statin treatment starts at diagnosis, but no statin has

230 rmine the cost-effectiveness of a PCSK9i and statin treatment strategy compared with a statin alone s

231 ase (ASCVD), guidelines recommend optimizing statin treatment, and consensus pathways suggest use of

232 76.6% (95% CI, 75.8-77.5) were eligible for statin treatment, but only 33.2% (95% CI, 32.1-34.3) wer

233 ssion in RacET mice that was diminished with statin treatment.

234 atory drug sulindac and largely prevented by statin treatment.

235 On reinitiation, 27.1% changed statin type, 6.9% up-titrated intensity, 14.4% down-titr

236 Randomized trials of various statin types in hospitalized patients prone to delirium

237 While individuals indicated for statins under both guidelines experienced 9.6 cardiovasc

238 Statin use after diagnosis was not associated with reduc

239 Statin use also decreases the risk of hepatocellular car

240 ntions are needed to increase high-intensity statin use and adherence after myocardial infarction.

241 cal trials to assess the association between statin use and glaucoma.

242 The association between statin use and risk of decompensation, mortality, and HC

243 To examine the association between statin use and the risk of delirium in hospitalized pati

244 Among patients with cirrhosis, statin use decreased the risk of decompensation, mortali

245 Statin use decreases the decompensation rate in both HBV

246 Statin use decreases the risk of decompensation and mort

247 mine trends and predictors of high-intensity statin use following hospital discharge for myocardial i

248 Increases in high-intensity statin use following hospital discharge occurred over th

249 on level, the ACC/AHA guideline for expanded statin use for primary prevention is projected to treat

250 or a myocardial infarction may help increase statin use in high-risk patients.

251 Statin use in the year preceding recurrence was associat

252 Conclusion and Relevance: Statin use increased substantially in the last decade am

253 These findings support our hypotheses that statin use is inversely associated, and diabetes is posi

254 There was no evidence of an effect of statin use on pulmonary embolism.

255 of this study was to determine the effect of statin use on rates of decompensation, mortality, and HC

256 ntion studies suggest a beneficial effect of statin use on venous thromboembolism.

257 Statin use resulted in significant reductions in total,

258 parison between adjunctive locally delivered statin use to mechanical scaling and root planing (SRP)

259 Statin use was associated with a significant decrease in

260 Statin use was associated with intrusive body pain, diff

261 ntative British population in early old age, statin use was associated with lower limb muscle-related

262 this work, we examined whether postdiagnosis statin use was associated with reduced cancer-specific m

263 Statin use was not associated with a reduced rate of col

264 nal cohorts that assessed the association of statin use with venous thromboembolism, deep vein thromb

265 ming of systemic therapy, menopausal status, statin use, and treating centre.

266 on suggested that male sex, current smoking, statin use, elevated creatinine, and higher lipids were

267 Estimated trends in statin use, total expenditure, and OOP share among the g

268 adjusted for age, sex, body mass index, and statin use.

269 ow-density lipoprotein cholesterol level nor statin use.

270 have resulted in a change in high-intensity statin use.

271 Considering the type of statin used, atorvastatin (0.51; 0.41-0.64), pravastatin

272 When considering types of statins used, this reduction was significant in patients

273 s of Alzheimer disease diagnosis for 399 979 statin users 65 years of age or older with high or low e

274 0% of the patients (210/999) were defined as statin users after diagnosis of colon cancer.

275 We noted no significant differences between statin users and non-users in the rates of other AEs, wi

276 =0.03), which were reported more commonly by statin users than by non-users.

277 s, Hispanic patients, and new high-intensity statin users were less likely to take high-intensity sta

278 sion to ICU was 1.04 (95% CI, 0.96-1.13) for statin users, 1.00 (95% CI, 0.90-1.11) for nonsteroidal

279 sive care was 18.0% (95% CI, 17.0-19.0%) for statin users, 21.3% (95% CI, 19.8-22.9%) for nonsteroida

280 Brand-name statins were used by 18.2% of statin users, accounting for 55% of total costs in 2012-

281 rising 3 148 259 participants and 23 RCTs of statins vs placebo or no treatment comprising 118 464 pa

282 n measuring the anti-inflammatory actions of statins.-Walker, M.

283 PROVE-IT, the benefit of adding ezetimibe to statin was enhanced in patients with DM and in high-risk

284 Nonadherence to ACE inhibitors/ARBs and/or statins was associated with higher mortality.

285 All patients not initially receiving a statin were given atorvastatin, 20 mg, and the following

286 Maximal doses of high-intensity statins were associated with a further survival benefit.

287 High-intensity statins were associated with a small but significant sur

288 Brand-name statins were used by 18.2% of statin users, accounting f

289 n that this is in part because a hydrophobic statin with a long half-life is necessary.

290 ned by switching to a low/moderate-intensity statin with a proportion of days covered of at least 80%

291 associated with continuing a high-intensity statin with high adherence after myocardial infarction.

292 h a diagnosis of colon cancer, we associated statin with reduced risk of death from any cause or from

293 placebo-controlled, double-blind trial of a statin with standard-of-care for patients with cancer, s

294 o-controlled trial of an ACE inhibitor and a statin with the use of a 2-by-2 factorial design minimiz

295 Pitavastatin, the only statin with this profile, has not undergone clinical eva

296 sers were less likely to take high-intensity statins with high adherence, and those with dual Medicar

297 tion were more likely to take high-intensity statins with high adherence.

298 ssels in 20 asymptomatic individuals (90% on statins) with no prior history of coronary artery diseas

299 ferences in the effect of statins by type of statin, with rosuvastatin having the lowest risk on veno

300 inuation, or switching between >/=3 types of statins within 1 year after initiation.