ライフサイエンスコーパス: pravastatin

1 common disease risk modifiers (metformin and pravastatin).

2 ctable differences, favoring simvastatin and pravastatin.

3 ) compared with moderate lipid lowering with pravastatin.

4 8.0% vs. 10.5%, p=0.017) compared with 40 mg pravastatin.

5 was assessed in the absence and presence of pravastatin.

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

7 tional hibernating myocardium improves after pravastatin.

8 HRPTEC were co-incubated with BKV and pravastatin.

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

10 rolled in a study comparing atorvastatin and pravastatin.

11 at lower 10-year risks than simvastatin and pravastatin.

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

13 reductions in cholesterol when treated with pravastatin.

14 on of coronary atherosclerosis compared with pravastatin.

15 48% of patients treated for six months with pravastatin.

16 All patients received pravastatin.

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

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

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

20 rmoxia or hypoxia (14% O(2) ) from day 1 +/- pravastatin (1 mg/kg/d) from day 13 of incubation (term

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

36 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

51 5 to 64 years, who were randomly assigned to pravastatin 40 mg/d or placebo.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

67 Pravastatin administration from E6.5, which increases pl

68 When male mice underwent atorvastatin and pravastatin administration per os for up to 7 mo, only l

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

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

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

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

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

74 mportant compounds such as the medical drugs pravastatin and artemether, and the steroid hormone test

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

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

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

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

79 Both statins, hydrophilic pravastatin and hypdrophobic simvastatin caused redistri

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

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

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

83 Pravastatin and rosuvastatin were associated with reduce

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

85 Here, we have determined the effects of pravastatin and underlying mechanisms on the cardiovascu

86 parameters, but treatment combinations with pravastatin and zoledronic acid significantly improved b

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

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

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

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

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

92 rent treatment combinations with lonafarnib, pravastatin, and zoledronic acid.

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

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

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

96 mpelling evidence for clinical evaluation of pravastatin as adjunctive, host-directed therapy for TB.

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

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

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

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

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

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

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

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

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

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

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

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

113 Pravastatin depresses the fetal cardiovascular and metab

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

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

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

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

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

119 Pravastatin, fluvastatin and pitavastatin are considered

120 myocytes were treated with atorvastatin and pravastatin for 48 h.

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

122 vity, producing the pharmacologically active pravastatin form.

123 the chronically hypoxic chicken embryo with pravastatin from day 13 of incubation, equivalent to ca.

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

125 Pravastatin given for 3 years reduced the risk of corona

126 In addition, pravastatin globally lowered levels of lipoprotein subcl

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

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

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

130 +/-0.021 mm), whereas CIMT was stable in the pravastatin group (change of 0.025+/- 0.017 mm; P=0.03).

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

132 252 patients to the pitavastatin (n=126) or pravastatin group (n=126).

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

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

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

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

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

138 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

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

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

141 % in the atorvastatin group and 26.3% in the pravastatin group, a 16% relative risk reduction (p = 0.

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

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

144 Pravastatin had a significant effect on normal hepatocyt

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

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

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

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

149 % 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

150 ommon statins: atorvastatin (lipophilic) and pravastatin (hydrophilic).

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

170 Pravastatin increased myocytes in mitosis (phospho-histo

171 o 7 mo, only long-term atorvastatin, but not pravastatin, induced elevated serum creatine kinase; swo

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

173 1732 men and 1101 women participating in the Pravastatin Inflammation/CRP Evaluation Study.

174 Atorvastatin, but not pravastatin, inhibits cardiac Akt/mTOR signaling and dis

175 Pravastatin is a hydrophilic statin that is selectively

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

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

178 Pravastatin lowered LDL cholesterol concentrations by 34

179 Pravastatin lowered low-density lipoprotein cholesterol

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

181 Patients assigned pravastatin maintained a significantly lower risk of dea

182 Fetal exposure to pravastatin markedly diminished the fetal femoral vasoco

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

184 Therefore, pravastatin may be a candidate for human clinical transl

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

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

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

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

189 Pravastatin modulated phagosomal maturation characterist

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 el system that permits the direct effects of pravastatin on the developing offspring to be isolated i

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

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

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

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

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

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

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

202 (Pravastatin or Atorvastatin Evaluation and Infection The

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

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

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

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

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

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

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

210 The Pravastatin or Atorvastatin Evaluation and Infection The

211 The Pravastatin or Atorvastatin Evaluation and Infection The

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

213 In the Pravastatin or Atorvastatin Evaluation and Infection The

214 The Pravastatin or Atorvastatin Evaluation and Infection The

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

216 The Pravastatin or Atorvastatin Evaluation and Infection Tri

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

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

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

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

221 216.0) for combined therapy of atorvastatin, pravastatin, or simvastatin with a fibrate, and to 1035

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

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

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

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

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

227 Finally, we found that pravastatin pretreatment significantly attenuated hepato

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

229 Atorvastatin and pravastatin produced significant reductions ( approximat

230 Penicillium chrysogenum toward an industrial pravastatin production process.

231 The data show that pravastatin protected the hypoxic chicken embryo against

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

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

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

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

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

237 equivalent HL-1 cells, atorvastatin, but not pravastatin, reduced mitochondrial oxygen consumption.

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

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

240 tatins, including, atorvastatin, lovastatin, pravastatin, rosuvastatin, and simvastatin.

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

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

243 Pravastatin's pleiotropic effects of reducing intragraft

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

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

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

247 Pravastatin showed the least toxicity in THP-1 and Vero

248 Simvastatin, fluvastatin, and pravastatin showed the most favorable therapeutic index

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

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

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

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

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

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

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

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

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

258 Compared with moderate pravastatin therapy, intensive atorvastatin therapy was

259 Changes in lipid levels in response to pravastatin therapy.

260 ficantly associated with reduced efficacy of pravastatin therapy.

261 dyslipidemia during the first six months of pravastatin therapy.

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

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

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

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

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

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

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

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

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

271 Pravastatin treatment combined with LDA+LMWH was also as

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

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

274 In the pravastatin treatment group, one additional patient disc

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

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

277 Peritransplant pravastatin treatment reduced the number of autologous i

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

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

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

281 with these polymorphisms could be reduced by pravastatin treatment.

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

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

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

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 evaluating the 2-year efficacy and safety of pravastatin, were invited for follow-up, together with t

297 Pravastatin when administered with cyclosporine (CsA) ha

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

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

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