ライフサイエンスコーパス: pravastatin

1 common disease risk modifiers (metformin and pravastatin).

2 ) compared with moderate lipid lowering with pravastatin.

3 8.0% vs. 10.5%, p=0.017) compared with 40 mg pravastatin.

4 was assessed in the absence and presence of pravastatin.

5 d in HRPTEC pretreated and co-incubated with pravastatin.

6 tional hibernating myocardium improves after pravastatin.

7 HRPTEC were co-incubated with BKV and pravastatin.

8 ates of human OATP1B1 and -1B3, rifampin and pravastatin.

9 rolled in a study comparing atorvastatin and pravastatin.

10 tase, the target enzyme that is inhibited by pravastatin.

11 reductions in cholesterol when treated with pravastatin.

12 on of coronary atherosclerosis compared with pravastatin.

13 48% of patients treated for six months with pravastatin.

14 All patients received pravastatin.

15 lead mainly to the ineffective epimer 6-epi-pravastatin.

16 ctable differences, favoring simvastatin and pravastatin.

17 relevant statins-atorvastatin (0.2 mg/kg) or pravastatin (0.2 mg/kg)-to mice during inflammatory arth

18 statin used, atorvastatin (0.51; 0.41-0.64), pravastatin (0.40; 0.28-0.58), and simvastatin (0.33; 0.

19 to atorvastatin 10 mg, simvastatin 20 mg, or pravastatin 10 mg followed by 80 mg, 80 mg, and 40 mg, r

20 splant recipients received either open-label pravastatin 20 mg daily (n = 24) or simvastatin 10 mg da

21 Eleven patients received pravastatin (20 mg/d) in addition to LDA+LMWH at the ons

22 valuate the relative effects of low doses of pravastatin (20 mg/day) and simvastatin (10 mg/day) on i

23 Simvastatin (10 mg/day) and pravastatin (20 mg/day) are associated with similar bene

24 ) before and 24 h after fetal treatment with pravastatin (25 mg i.v.).

25 To test the effect of pravastatin, 3,000 IEQ/kg were transplanted into dogs th

26 atin 80 mg versus 4.2% of patients receiving pravastatin 40 mg (hazard ratio [HR] = 0.72; 95% confide

27 educed by 16% with atorvastatin 80 mg versus pravastatin 40 mg (n = 464 vs. n = 537, respectively; p

28 ficacy events with atorvastatin 80 mg versus pravastatin 40 mg (n = 739 vs. n = 877, respectively; ra

29 ved atorvastatin 80 mg, while 19.4% received pravastatin 40 mg (p < 0.001).

30 quent primary end point events compared with pravastatin 40 mg after ACS.

31 /dl and CRP <2 mg/l, and only 5.8% allocated pravastatin 40 mg and 26.1% allocated atorvastatin 80 mg

32 We addressed the relative efficacy of pravastatin 40 mg and atorvastatin 80 mg daily to reduce

33 Conclusion Pravastatin 40 mg combined with standard SCLC therapy, a

34 zed patients to either atorvastatin 80 mg or pravastatin 40 mg daily.

35 ACS and randomized to atorvastatin 80 mg or pravastatin 40 mg daily.

36 s, and therefore total events, compared with pravastatin 40 mg during the 2-year follow-up.

37 osite event rate of 9.6% versus 13.1% in the pravastatin 40 mg group (HR = 0.72; 95% CI, 0.58 to 0.89

38 While atorvastatin 80 mg was superior to pravastatin 40 mg in terms of achieving the dual goals o

39 ACS) randomized to atorvastatin 80 mg versus pravastatin 40 mg in the PROVE IT-TIMI 22 (Pravastatin o

40 f intensive LLT with atorvastatin 80 mg over pravastatin 40 mg occurred in statin-naive ACS patients

41 l and no history of myocardial infarction to pravastatin 40 mg once daily or placebo for 5 years.

42 total of 6595 men were randomized to receive pravastatin 40 mg once daily or placebo for an average o

43 to 3 were randomly assigned to receive daily pravastatin 40 mg or placebo, combined with up to six cy

44 hs after MI or unstable angina to placebo or pravastatin 40 mg per day.

45 ute coronary syndrome patients randomized to pravastatin 40 mg versus atorvastatin 80 mg).

46 t to Prevent Heart Attack Trial (ALLHAT-LLT; pravastatin 40 mg versus usual care) and Collaborative A

47 igned patients (1:1) to pitavastatin 4 mg or pravastatin 40 mg with matching placebos once daily oral

48 rvastatin 80 mg) or moderate statin therapy (pravastatin 40 mg).

49 ty (P<0.001), whereas Lp-PLA2 rose 3.6% with pravastatin 40 mg/d (P<0.001).

50 tients randomized to atorvastatin 80 mg/d or pravastatin 40 mg/d after ACS in the PROVE IT-TIMI 22 (P

51 g were randomized to atorvastatin 80 mg/d or pravastatin 40 mg/d and followed up for 12 months.

52 5 to 64 years, who were randomly assigned to pravastatin 40 mg/d or placebo.

53 tensive (atorvastatin 80 mg/d) and moderate (pravastatin 40 mg/d) lipid-lowering therapy.

54 omized in a double-blind, parallel design to pravastatin 40 mg/day (prava40), atorvastatin 10 mg/day

55 were randomized to atorvastatin 80 mg/day or pravastatin 40 mg/day and were followed for a mean of 24

56 mized study of atorvastatin 80 mg/day versus pravastatin 40 mg/day for 1 year in a clinical trial des

57 to hypercholesterolemic patients already on pravastatin 40 mg/day, the combination was well tolerate

58 lower survival and more adverse effects than pravastatin 40 mg/day.

59 inical trial designed to test the effects of pravastatin (40 mg once daily) on cardiovascular risk.

60 lind randomized trials comparing placebo and pravastatin (40 mg once daily).

61 of, or risk factors for, vascular disease to pravastatin (40 mg per day; n=2891) or placebo (n=2913).

62 Pravastatin (40 mg/day) was used in the former and atorv

63 (atorvastatin, 80 mg) and moderate therapy (pravastatin, 40 mg) in patients after ACS.

64 y (atorvastatin, 80 mg) or standard therapy (pravastatin, 40 mg).

65 avastatin (68%) and 88 patients treated with pravastatin (70%) reported treatment-emergent adverse ev

66 ntrolled, parallel-group trial that compared pravastatin (80 mg) to a placebo administered once daily

67 High-dose pravastatin (80 mg/day) administered to hypercholesterol

68 In the intent-to-treat population, pravastatin (80 mg/day) significantly lowered the mean L

69 Our data suggest that pravastatin, acting through depletion of caveolin-1, pre

70 Pravastatin administration from E6.5, which increases pl

71 al/neonatal outcomes in women with APS given pravastatin after the onset of preeclampsia and/or IUGR

72 C-reactive protein decreased 5.2% with pravastatin and 36.4% with atorvastatin (P<.001).

73 Only 11% allocated pravastatin and 44% allocated atorvastatin achieved the

74 Study medication was withdrawn in 3 pravastatin and 7 placebo patients due to creatine phosp

75 During extended follow-up, 85% assigned pravastatin and 84% assigned placebo took statin therapy

76 n both treatment groups (91% for patients on pravastatin and 92% for patients on simvastatin).

77 on of this finding in a meta-analysis of all pravastatin and all statin trials showed no overall incr

78 f this study was to determine the effects of pravastatin and atorvastatin on markers of oxidative str

79 n OATP1B1 and -1B3 substrates rifampicin and pravastatin and demonstrated a reduced liver-to-plasma r

80 our current study, we show that simvastatin, pravastatin and fluvastatin can induce PTEN expression i

81 n, and cerivastatin) (CYP3A4-MET) or others (pravastatin and fluvastatin) (non-CYP3A4-MET).

82 Both statins, hydrophilic pravastatin and hypdrophobic simvastatin caused redistri

83 Patients who received both pravastatin and LDA+LMWH exhibited increased placental b

84 Finally, the safe use of pravastatin and pioglitazone was demonstrated in patient

85 tal and nonfatal cancers was similar between pravastatin and placebo groups.

86 LIPID initially compared pravastatin and placebo over 6 years in 9014 patients wi

87 Pravastatin and rosuvastatin were associated with reduce

88 ents were randomized in a crossover study of pravastatin and simvastatin.

89 cardiovascular benefit with the addition of pravastatin and zoledronic acid.

90 analysis of a representative type I statin (pravastatin) and four type II statins (fluvastatin, ceri

91 significant in patients using atorvastatin, pravastatin, and simvastatin.

92 r and low for monotherapy with atorvastatin, pravastatin, and simvastatin; combined statin-fibrate us

93 s were divided into three groups: CsA, CsA + pravastatin, and syngeneic.

94 Similarly, pravastatin, another cholesterol-lowering drug, suppress

95 Simvastatin and pravastatin are inhibitors of 3-hydroxy-3-methylglutaryl

96 ater white matter hyperintensity load in the pravastatin arm (P=0.046).

97 designed to establish the noninferiority of pravastatin as compared with atorvastatin with respect t

98 ucing P. chrysogenum yielded more than 6 g/L pravastatin at a pilot production scale, providing an ef

99 ee sustained release compartments containing pravastatin, atenolol, and ramipril.

100 Atorvastatin, but not pravastatin, attenuated the antiplatelet activity of clo

101 contrast, four of the five dogs treated with pravastatin became normoglycemic (<150 mg/dL) and mainta

102 ctors and did not relate to the magnitude of pravastatin benefit.

103 Simvastatin, but not pravastatin, binds to the inserted domain of leukocyte f

104 We also demonstrated that pravastatin, by down-regulating TF expression on monocyt

105 The cholesterol-lowering blockbuster drug pravastatin can be produced by stereoselective hydroxyla

106 Oral administration of D-4F together with pravastatin caused lesion regression in old apoE null mi

107 tion to the binding affinity of fluvastatin, pravastatin, cerivastatin, and atorvastatin is the entro

108 the preceding 10 days and compared 40 mg of pravastatin daily (standard therapy) with 80 mg of atorv

109 In diabetic participants with low LDL-C, pravastatin decreased CHD events from 34% to 22% (relati

110 We also demonstrated that simvastatin and pravastatin decreased TF and PAR2 expression on neutroph

111 Pravastatin decreased TnI levels by 0.003 ng/ml versus p

112 is of lymphocytes from patients treated with pravastatin demonstrated a 90.1+/-27.3% (n=10, P=0.009)

113 Neither pitavastatin nor pravastatin depend on cytochrome P450 for primary metabo

114 Pravastatin depresses the fetal cardiovascular and metab

115 Fetal exposure to pravastatin did not affect fetal basal cardiovascular fu

116 Simvastatin, but not pravastatin, dissociates EBV latent membrane protein 1 f

117 We provide evidence that pravastatin dramatically decreased caveolin-1 expression

118 We also found that atorvastatin and pravastatin each reduced systemic leukocyte activation,

119 No benefit was found for pravastatin, either in all patients or in several subgro

120 Pravastatin, fluvastatin and pitavastatin are considered

121 patieNts and TREatment with PItavastatin vs pravastatin for Dyslipidemia) randomised, double-blind,

122 vity, producing the pharmacologically active pravastatin form.

123 tment or were treated daily with 20 mg/kg of pravastatin from days -2 to 14.

124 Pravastatin given for 3 years reduced the risk of corona

125 In addition, pravastatin globally lowered levels of lipoprotein subcl

126 ); LDL cholesterol was 110+/-30 mg/dL in the pravastatin group (-27.2%; P<0.001).

127 of coronary atherosclerosis occurred in the pravastatin group (2.7%; 95% confidence interval [CI], 0

128 nd four events in three patients (2%) in the pravastatin group (cerebrovascular accident, arterioscle

129 +/-0.021 mm), whereas CIMT was stable in the pravastatin group (change of 0.025+/- 0.017 mm; P=0.03).

130 gressed more in the atorvastatin than in the pravastatin group (median, -3.38% vs. -0.83%, p = 0.025)

131 252 patients to the pitavastatin (n=126) or pravastatin group (n=126).

132 and upper respiratory tract infection in the pravastatin group (n=14, 11%).

133 significant in the atorvastatin, but not the pravastatin group (p < 0.001 and p = 0.2, respectively).

134 p (P=0.27), nor did on-treatment LDLc in the pravastatin group (P=0.12).

135 point at two years were 26.3 percent in the pravastatin group and 22.4 percent in the atorvastatin g

136 r (2.46 mmol per liter) in the standard-dose pravastatin group and 62 mg per deciliter (1.60 mmol per

137 as reduced to 110 mg/dL (2.85 mmol/L) in the pravastatin group and to 79 mg/dL (2.05 mmol/L) in the a

138 cified ALT event definition was lower in the pravastatin group at all times over the 36 weeks of ther

139 n the pitavastatin group and six (5%) in the pravastatin group had virological failure, with no signi

140 % in the atorvastatin group and 26.3% in the pravastatin group, a 16% relative risk reduction (p = 0.

141 Unlike allografts from the pravastatin group, control allografts demonstrated glome

142 eased transforming growth factor-beta in the pravastatin group.

143 oronary disease fell by 24% (p=0.043) in the pravastatin group.

144 aft expression of Bag-1 was increased in the pravastatin group.

145 Both the placebo and pravastatin groups showed small increases in within-pers

146 Pravastatin had a significant effect on normal hepatocyt

147 Pravastatin had no significant effect on cognitive funct

148 Men allocated to pravastatin had reduced all-cause mortality (hazard rati

149 Patients given atorvastatin or pravastatin had similar 1-year event rates.

150 B-598, squalene monooxygenase inhibitor), or pravastatin (HMG-CoA reductase inhibitor).

151 icantly reduced the risk of HF compared with pravastatin (HR 0.32, 95% CI 0.13 to 0.8, p = 0.014).

152 % CI: 1.09 to 3.49; p < 0.001 for trend) and pravastatin (HR: 0.23; 95% CI: 0.10 to 0.53 vs. HR: 1.08

153 most tumor cell lines more effectively than pravastatin in a dose dependent manner.

154 e safety and efficacy of pitavastatin versus pravastatin in adults with HIV and dyslipidaemia.

155 supplemented with de novo data from PROSPER (Pravastatin in Elderly Individuals at Risk of Vascular D

156 ukocyte-platelet actions of atorvastatin and pravastatin in inflammatory arthritis.

157 The LIPID (Long-Term Intervention With Pravastatin in Ischaemic Disease) study randomized patie

158 ents (CARE), and Long-term Intervention with Pravastatin in Ischemic Disease (LIPID) studies collecti

159 follow-up of the Long-term Intervention with Pravastatin in Ischemic Disease (LIPID) trial.

160 ion studies, and Long-term Intervention with Pravastatin in Ischemic Disease study, have indicated th

161 the LIPID trial (Long-Term Intervention With Pravastatin in Ischemic Disease).

162 Here, we investigated the use of pravastatin in LDA+LMWH-refractory APS in patients at an

163 g the protective actions of atorvastatin and pravastatin in reducing local and vascular inflammation,

164 tack) end points in the Prospective Study of Pravastatin in the Elderly at Risk (n=5804 men and women

165 ed 70-82 years from the Prospective Study of Pravastatin in the Elderly at Risk (PROSPER).

166 reatment benefit in the PROspective Study of Pravastatin in the Elderly at Risk (PROSPER).

167 articipants of PROSPER (PROspective Study of Pravastatin in the Elderly at Risk).

168 ely at the elderly--the Prospective Study of Pravastatin in the Elderly at Risk--have added enormousl

169 were recruited into the PROspective Study of Pravastatin in the Elderly at Risk.

170 end point between high-dose atorvastatin and pravastatin in the PROVE IT-TIMI 22 trial.

171 r events up to 2 years, compared to 40 mg of pravastatin, in patients with ACS.

172 As a result, pravastatin increased LAD myocyte nuclear density from 8

173 Pravastatin increased myocytes in mitosis (phospho-histo

174 Thus, the pravastatin-induced enhancement of fetal capillaries wit

175 1732 men and 1101 women participating in the Pravastatin Inflammation/CRP Evaluation Study.

176 Pravastatin is a hydrophilic statin that is selectively

177 tes that during prolonged exposure, 40 mg of pravastatin is well tolerated, with no excess of noncard

178 filing and metabolite identification, taking pravastatin-lactone and N-oxide desloratidine, as exampl

179 n was 31.1% with pitavastatin and 20.9% with pravastatin (least squares mean difference -9.8%, 95% CI

180 Pravastatin lowered LDL cholesterol concentrations by 34

181 Pravastatin lowered low-density lipoprotein cholesterol

182 and similar body mass index (27 kg/m2); and pravastatin lowered their LDL-C by 36 mg/dL (32%) versus

183 Patients assigned pravastatin maintained a significantly lower risk of dea

184 Fetal exposure to pravastatin markedly diminished the fetal femoral vasoco

185 These results suggest that pravastatin may also facilitate better islet graft survi

186 The present study suggests that pravastatin may improve pregnancy outcomes in women with

187 With pravastatin, men with the syndrome had similar risk redu

188 irst to suggest that cholesterol lowering by pravastatin might increase the response of the heart to

189 Pravastatin mobilized circulating CD133(+)/cKit(+) bone

190 re assessed in pigs treated for 5 weeks with pravastatin (n=12) versus untreated controls (n=10).

191 (n=9), lisinopril/P-placebo (n=8), L-placebo/pravastatin (n=9), L-placebo/P-placebo (n=8)] attended a

192 ticipants were randomized and 34 [lisinopril/pravastatin (n=9), lisinopril/P-placebo (n=8), L-placebo

193 romosulphothalein (both OAT4 and OATP2B1) or pravastatin (OATP2B1).

194 rction (MI), and to determine the effects of pravastatin on TnI levels.

195 ipid-lowering regimen consisting of 40 mg of pravastatin or an intensive lipid-lowering regimen consi

196 We evaluated 4162 patients enrolled in the PRavastatin Or atorVastatin Evaluation and Infection The

197 In the PROVE IT-TIMI 22 (Pravastatin or Atorvastatin Evaluation and Infection The

198 prior to enrollment in the PROVE IT-TIMI 22 (Pravastatin or Atorvastatin Evaluation and Infection The

199 gressive Cholesterol Lowering) and PROVE-IT (Pravastatin or Atorvastatin Evaluation and Infection The

200 The PROVE IT-TIMI (Pravastatin or Atorvastatin Evaluation and Infection The

201 (Pravastatin or Atorvastatin Evaluation and Infection The

202 ndrome patients within the PROVE IT-TIMI 22 (Pravastatin or Atorvastatin Evaluation and Infection The

203 s pravastatin 40 mg in the PROVE IT-TIMI 22 (Pravastatin or Atorvastatin Evaluation and Infection The

204 ovascular disease, and the PROVE IT-TIMI-22 (Pravastatin or Atorvastatin Evaluation and Infection The

205 n 40 mg/d after ACS in the PROVE IT-TIMI 22 (PRavastatin Or atorVastatin Evaluation and Infection The

206 disease and Aggrastat to Zocor (A to Z) and Pravastatin or Atorvastatin Evaluation and Infection The

207 The Aggrastat to Zocor (A to Z) and Pravastatin or Atorvastatin Evaluation and Infection The

208 , such as the Heart Protection Study and the Pravastatin or Atorvastatin Evaluation and Infection The

209 The Pravastatin or Atorvastatin Evaluation and Infection The

210 The Pravastatin or Atorvastatin Evaluation and Infection The

211 s-sectional study of 2,885 patients from the Pravastatin or Atorvastatin Evaluation and Infection The

212 In the Pravastatin or Atorvastatin Evaluation and Infection The

213 The Pravastatin or Atorvastatin Evaluation and Infection The

214 Azithromycin and Coronary Events (ACES) and Pravastatin or Atorvastatin Evaluation and Infection The

215 The Pravastatin or Atorvastatin Evaluation and Infection Tri

216 treated with clopidogrel or clopidogrel plus pravastatin or atorvastatin, and in 27 volunteers treate

217 isease who were randomly assigned to receive pravastatin or placebo.

218 ing lipid-lowering therapy with fluvastatin, pravastatin, or atorvastatin.

219 son-years for monotherapy with atorvastatin, pravastatin, or simvastatin was 0.44 (95% confidence int

220 216.0) for combined therapy of atorvastatin, pravastatin, or simvastatin with a fibrate, and to 1035

221 gned to receive moderate treatment (40 mg of pravastatin orally per day) or intensive treatment (80 m

222 ose seen with atorvastatin, simvastatin, and pravastatin over the concurrent timeframe and during the

223 creased from 3.8+/-0.6 to 5.2+/-0.5 mm after pravastatin (P<0.01).

224 ts on placebo (P=0.0019) but not in those on pravastatin (P=0.24).

225 tment with 80 mg of atorvastatin or 40 mg of pravastatin per day and the risk of recurrent myocardial

226 Finally, we found that pravastatin pretreatment significantly attenuated hepato

227 Here we determine whether pravastatin prevents chronic rejection in a rat renal al

228 Atorvastatin and pravastatin produced significant reductions ( approximat

229 Penicillium chrysogenum toward an industrial pravastatin production process.

230 olled trial of known prevention medications (pravastatin, ramipril, aspirin, and a combination B vita

231 In addition, pravastatin reduced levels of several fatty acids but ha

232 Pravastatin reduced the event rate in diabetics to that

233 Among individuals with LDL-C >/=190 mg/dL, pravastatin reduced the risk of coronary heart disease b

234 g 5529 individuals without vascular disease, pravastatin reduced the risk of coronary heart disease b

235 Pravastatin reduced troponin concentration by 13% (10% t

236 was -53.3% and -28.3% with atorvastatin and pravastatin, respectively (p < 0.001).

237 icrog/h) or high (32 microg/h) dose rates of pravastatin resulted in a 4-fold lower liver-plasma rati

238 manner, unlike its parent and other statins (pravastatin, rosuvastatin, simvastatin).

239 It is likely, that pravastatin's inhibitory effect is explained by depletio

240 Pravastatin's pleiotropic effects of reducing intragraft

241 Among individual statins, simvastatin and pravastatin seem safer and more tolerable than other sta

242 A study with pravastatin showed general benefits on both biomarkers a

243 heroma burden, whereas patients treated with pravastatin showed progression of coronary atheroscleros

244 onsistently, the cholesterol-lowering agent (pravastatin sodium) downregulated the expression of RALD

245 th PTIO or by pharmacological drugs, such as pravastatin, sodium benzoate, or gemfibrozil, restored t

246 nopril and absence of lipid differences with pravastatin suggest future studies of these drug classes

247 New cancer diagnoses were more frequent on pravastatin than on placebo (1.25, 1.04-1.51, p=0.020).

248 Post-pravastatin, the circulatory (5.8 +/- 1.5 mmHg (ml min(-

249 By contrast, in patients treated with pravastatin, the increased risk with shorter telomeres w

250 ated that in patients treated initially with pravastatin, the peak high-frequency power fraction duri

251 patients, 194 received atorvastatin and 226 pravastatin; the median low-density lipoprotein change w

252 s with changes in lipid levels observed with pravastatin therapy during a 24-week period.

253 urse of improved myocardial perfusion during pravastatin therapy is delayed compared to lipids.

254 Compared with moderate pravastatin therapy, intensive atorvastatin therapy was

255 Changes in lipid levels in response to pravastatin therapy.

256 ficantly associated with reduced efficacy of pravastatin therapy.

257 dyslipidemia during the first six months of pravastatin therapy.

258 imaging (MPI) during the first six months of pravastatin therapy.

259 In human atheroma, 3 months' use of statin (pravastatin) therapy reduced the content of oxidized LDL

260 Without pravastatin, this number of islets lowered blood glucose

261 This study demonstrates the ability of pravastatin to inhibit chronic rejection in rat renal al

262 Although atorvastatin was more likely than pravastatin to result in low levels of LDL cholesterol a

263 filtration of T cells and macrophages in the pravastatin-treated animals were significantly lower.

264 ible CYP3A mRNA expression was restored when pravastatin-treated cultures were incubated with medium

265 tolerance tests were significantly higher in pravastatin-treated dogs than in controls (P<0.04 at wee

266 lipoprotein cholesterol reductions than did pravastatin-treated patients, a trend toward fewer major

267 he absolute survival benefit from 6 years of pravastatin treatment appeared to be maintained for the

268 r cognitive function in both the placebo and pravastatin treatment arms.

269 Pravastatin treatment combined with LDA+LMWH was also as

270 igated the molecular changes associated with pravastatin treatment compared with placebo administrati

271 or interaction between LDL-C variability and pravastatin treatment for both cognitive and magnetic re

272 In the pravastatin treatment group, one additional patient disc

273 Our aim was to test the benefits of pravastatin treatment in an elderly cohort of men and wo

274 l data demonstrate the widespread effects of pravastatin treatment on lipoprotein subclass profiles a

275 ects were observed as early as 10 days after pravastatin treatment onset.

276 Peritransplant pravastatin treatment reduced the number of autologous i

277 In addition, simvastatin and pravastatin treatment reversed 3MC-mediated alterations

278 ad an increased risk of coronary events, and pravastatin treatment substantially reduced that risk.

279 Risk reduction on pravastatin treatment was unrelated to baseline LDLc (P=

280 with these polymorphisms could be reduced by pravastatin treatment.

281 The median OS (pravastatin v placebo) was 14.6 months in both groups fo

282 The effect of pravastatin versus placebo on coronary heart disease and

283 pared with those without (HR, 0.73 and 0.69; pravastatin versus placebo).

284 e: 128 [1.4%] versus 131 [1.4%] patients for pravastatin versus placebo, respectively).

285 of coronary events and greater benefit from pravastatin versus placebo.

286 signment to either antihypertensive drugs or pravastatin versus usual care did not affect AF/AFL inci

287 nt group or, in a subset of participants, by pravastatin versus usual care.

288 n cholesterol levels were also randomized to pravastatin versus usual care.

289 There was no treatment difference for pravastatin vs P-placebo in total cholesterol, LDL-C, or

290 ong carriers, the absolute risk reduction by pravastatin was 4.89% (95% CI 1.81% to 7.97%) in the CAR

291 The lipid-lowering effect of pravastatin was accompanied by selective changes in lipi

292 However, when pravastatin was added 72 hr after BKV infection it faile

293 BKV particles in the presence and absence of pravastatin was also investigated.

294 Pravastatin was shown to be safe in patients with nonalc

295 e fetuses (n = 6), responses to hypoxia post-pravastatin were evaluated during NO synthesis blockade.

296 Pravastatin when administered with cyclosporine (CsA) ha

297 Treatment with pravastatin, which down-regulates glomerular TF synthesi

298 = simvastatin > atorvastatin = mevastatin > pravastatin, which is similar to the known rank order of

299 tatin decreases LDL cholesterol more so than pravastatin with no increase in adverse effects in heart

300 utchinson-Gilford progeria syndrome received pravastatin, zoledronic acid, and lonafarnib.