ライフサイエンスコーパス: amlodipine

1 y targeted Ca2+ slow channels (diltiazem and amlodipine).

2 symptoms despite maximum recommended dose of amlodipine.

3 comparison of therapy based on valsartan or amlodipine.

4 il and hydrochlorothiazide or benazepril and amlodipine.

5 and LTM dogs received placebo, atenolol, or amlodipine.

6 the response to bradykinin, enalaprilat and amlodipine.

7 lerotic effects of lovastatin, vitamin E and amlodipine.

8 316 to amlodipine, and 620 to aliskiren plus amlodipine.

9 ent with amlodipine, and after withdrawal of amlodipine.

10 th intracellular calcium mobility similar to amlodipine.

11 ion therapy with 300 mg aliskiren plus 10 mg amlodipine.

12 plus placebo, or 150 mg aliskiren plus 5 mg amlodipine.

13 be treated successfully with octreotide and amlodipine.

14 uppressed by pretreatment with verapamil and amlodipine.

15 0 mg/kg given over first 6 hrs postburn); or amlodipine (0.07 mg/kg, 24 hrs preburn and 30 mins postb

16 gs each at quarter-dose (irbesartan 37.5 mg, amlodipine 1.25 mg, hydrochlorothiazide 6.25 mg, and ate

17 240 bpm, 3 weeks, n=8) or chronic pacing and amlodipine (1.5 mg . kg-1 . d-1, n=8).

18 enalaprilat: -0.7 +/- 0.5% to -26 +/- 1.2%; amlodipine: -1.3 +/- 0.9% to -18 +/- 1.2%; P < 0.05).

19 rug dose (6.5+/-6.1 and 3.4+/-3.9 ng/mL with amlodipine 10 and 5 mg, respectively, and -0.4+/-3.1 and

20 on 72-h electrocardiogram were randomized to amlodipine 10 mg once daily or diltiazem (Adizem XL) 300

21 8, hydrochlorothiazide 12.5 to 25 mg and/or amlodipine 10 mg was added if diastolic blood pressure w

22 mipril 10 mg/d (or irbesartan 300 mg/d), and amlodipine 10 mg/d were randomly assigned to renal dener

23 to treatment with irbesartan (300 mg daily), amlodipine (10 mg daily), or placebo.

24 sover study comparing the calcium antagonist amlodipine (10 mg once daily) versus isosorbide mononitr

25 nal classes III and IV randomized to receive amlodipine (10 mg/day) or placebo.

26 r week despite maximum recommended dosage of amlodipine (10 mg/day) were randomized to 1,000 mg ranol

27 Bradykinin (10(-4) mol/L, -21+/-5%), amlodipine (10(-5) mol/L, -14+/-5%), the ACE inhibitor r

28 Patients were randomized to receive amlodipine, 10 mg; enalapril, 20 mg; or placebo.

29 -13.9 +/- 1.9%, enalaprilat -15.3 +/- 1.6%, amlodipine -11.9 +/- 0.7%; WKY: bradykinin -22.8 +/- 1.0

30 sease was peripheral oedema (benazepril plus amlodipine, 189 of 561, 33.7%; benazepril plus hydrochlo

31 blocker BMS-186295 50 mg.kg-1.d-1 (n = 49), amlodipine 2.5 mg.kg-1.d-1 (n = 48) as a positive contro

32 w-onset heart failure (HF) was higher in the amlodipine (2.5-10 mg/d) and lisinopril (10-40 mg/d) arm

33 Responses to bradykinin (-2+/-6%), amlodipine (-2+/-4%), ramiprilat (-5+/-6%), and thiorpha

34 -22.8 +/- 1.0%, enalaprilat -24.1 +/- 2.0%, amlodipine -20.7 +/- 2.3%; P < 0.05), consistent with le

35 minutes after exercise in patients receiving amlodipine (3.5+/-1.4% versus 2.5+/-1.4%, P=0.014, and 5

36 s with chlorthalidone (-6.5 mm Hg) than with amlodipine (-3.8 mm Hg), lisinopril (-2.4 mm Hg), or dox

37 locker (acebutolol), (3) calcium antagonist (amlodipine), (4) diuretic (chlorthalidone), (5) alpha1-a

38 5%), enalaprilat (-37+/-5% vs. -23+/-5%) and amlodipine (-43+/-13% vs. -16+/-5%; p<0.05 from controls

39 , 62 patients were allocated to receive oral amlodipine 5 mg/day or placebo in addition to their curr

40 a dihydropyridine calcium channel blocker, (amlodipine 5-10 mg/d; n = 217).

41 1:1 ratio to receive benazepril (20 mg) plus amlodipine (5 mg; n=5744) or benazepril (20 mg) plus hyd

42 d fifty dentate patients who had been taking amlodipine, 5 mg per day for at least 6 months, voluntee

43 s from this group of patients indicated that amlodipine, 5 mg per day, did not induce gingival hyperp

44 rticipants were randomly assigned to receive amlodipine, 5 to 10 mg/d (n = 217), ramipril, 2.5 to 10

45 atment with either placebo (582 patients) or amlodipine (571 patients) for 6 to 33 months, while thei

46 Stunning occurred more often with ISMN than amlodipine (82% versus 48%).

47 ic relaxation period was less prolonged with amlodipine (93+/-15.5 versus 106.3+/-14.9 ms, P=0.018).

48 bined risk of fatal and nonfatal events with amlodipine (95 percent confidence interval, 24 percent r

49 percent reduction in the risk of death with amlodipine (95 percent confidence interval, 31 percent r

50 ns as cotreatment: a Mg2+-supplemented diet; amlodipine, a CCB; and N-acetylcysteine, an antioxidant.

51 92% (95% CI, 81.7 to 103.7) of baseline with amlodipine, a highly significant between-group effect (P

52 Amlodipine achieved a greater systolic and diastolic blo

53 There was no difference, however, between amlodipine (adjusted hazard ratio [HR], 0.46; 95% confid

54 Amlodipine also increased nitrite production in large co

55 Amlodipine also showed no effect on regression of hypert

56 to examine a large group of patients taking amlodipine and determine the prevalence of gingival hype

57 in Europe (CAPE II) compared the efficacy of amlodipine and diltiazem (Adizem XL) and the combination

58 Both monotherapy with amlodipine and diltiazem (Adizem XL) were effective on s

59 t hospitalized HFPEF and HFREF compared with amlodipine and doxazosin.

60 ed by 4.8/2.5 mm Hg and 4.9/2.4 mm Hg in the amlodipine and enalapril groups, respectively (P<.001 fo

61 ose to null for the peripherally acting drug amlodipine and for other antihypertensive medications.

62 e second phase, atenolol 100 mg was added to amlodipine and isosorbide 5-mononitrate 100 mg to diltia

63 .12) and 1.05 (0.89-1.25), respectively, for amlodipine and lisinopril compared with chlorthalidone,

64 ences in the subacute hemodynamic effects of amlodipine and lisinopril could contribute to the differ

65 Amlodipine and lisinopril lowered BP similarly, but CCA

66 n the clinical composite outcome between the amlodipine and metoprolol groups.

67 we categorized patients into those receiving amlodipine and nonamlodipine CCBs.

68 The binding site for amlodipine and other dihydropyridines is located on the

69 The baseline amlodipine and placebo groups did not differ in demograp

70 disease, there was no difference between the amlodipine and placebo groups in the occurrence of eithe

71 s were undertaken in the treatment groups of amlodipine and placebo, and among those receiving backgr

72 lovastatin, the dihydropyridine Ca2+ blocker amlodipine and the antioxidant vitamin E.

73 In vivo, amlodipine and verapamil suppressed peritoneal macrophag

74 (2+) channel (LTCC) blockers, represented by amlodipine and verapamil, are widely used antihypertensi

75 /6.6 mm Hg for valsartan, 11.6/6.5 mm Hg for amlodipine) and at no time point was there a between-gro

76 re to less brain-penetrant dihydropyridines (amlodipine) and more brain-penetrant dihydropyridines (e

77 ertensive therapy (ramipril, metoprolol, and amlodipine) and two levels of BP control.

78 Of these, 442 were taking nifedipine, 181 amlodipine, and 186 diltiazem.

79 iabetes (7.5% with chlorthalidone, 5.6% with amlodipine, and 4.3% with lisinopril), or no diabetes at

80 lly allocated to aliskiren, 315 allocated to amlodipine, and 617 allocated to aliskiren plus amlodipi

81 were randomly assigned to aliskiren, 316 to amlodipine, and 620 to aliskiren plus amlodipine.

82 obtained at baseline, during treatment with amlodipine, and after withdrawal of amlodipine.

83 The effects of glyceryl trinitrate (GTN), amlodipine, and atenolol were studied in nine normal vol

84 140/80 mm Hg in those given chlorthalidone, amlodipine, and lisinopril.

85 n of assigned study medications (irbesartan, amlodipine, and placebo) on progressive renal failure an

86 g, angiotensin-converting enzyme inhibitors, amlodipine, and statins) can restore or maintain endogen

87 diltiazem (Adizem XL) and the combination of amlodipine/atenolol and diltiazem (Adizem XL)/isosorbide

88 ation therapy reduced ischemia further, with amlodipine/atenolol superior to diltiazem (Adizem XL)/is

89 Amlodipine/atenolol was significantly superior during th

90 Despite comparable levels of ischemia, amlodipine attenuated stunning when compared with ISMN.

91 in system blocker, benazepril, combined with amlodipine (B+A) or hydrochlorothiazide (B+H).

92 ear after randomization to atenolol-based or amlodipine-based antihypertensive treatment to assess LV

93 nd stroke events in individuals allocated an amlodipine-based combination drug regimen than in those

94 and 1.3 (SD 12.1) beats/min in atenolol- and amlodipine-based groups, respectively.

95 here was no evidence that the superiority of amlodipine-based over atenolol-based therapy for patient

96 Patients receiving treatment with an amlodipine-based regimen had better diastolic function t

97 d by both treatments, but the effects of the amlodipine-based regimen were more pronounced, especiall

98 We hypothesized that an amlodipine-based regimen would have more favorable effec

99 egimen: atenolol-based regimen, 7.9 +/- 1.8; amlodipine-based regimen, 8.8 +/- 2.0.

100 /- 17 mm Hg, diastolic BP of 82 +/- 9 mm Hg; amlodipine-based regimen, systolic BP of 136 +/- 15 mm H

101 Pressure Lowering Arm (ASCOT-BPLA) compared amlodipine-based regimens with atenolol-based regimens i

102 e was a reduction in TCVP in those allocated amlodipine-based therapy compared with atenolol-based th

103 the efficacy of atenolol-based compared with amlodipine-based therapy in patients with hypertension u

104 lowering with atenolol-based therapy versus amlodipine-based therapy in people with hypertension.

105 on in normal weight than obese patients, but amlodipine-based therapy is equally effective across BMI

106 bjects prescribed dihydropyridines (excludes amlodipine) between 1995 and 2 years prior to the index

107 l and hydrochlorothiazide and benazepril and amlodipine, but rates were significantly lower with bena

108 g) with a combination such as aliskiren plus amlodipine can be recommended.

109 Amlodipine can increase CsA levels

110 Medications included chlorthalidone, amlodipine, carvedilol, cholecalciferol, erythropoietin,

111 In marked contrast, amlodipine caused a dose-dependent increase in nitrite p

112 Amlodipine causes increased blood flow and increased tim

113 ndividuals when comparing chlorthalidone and amlodipine (CHD: CC = 0.86; TC = 0.90; TT = 1.09; P = .0

114 The benazepril-amlodipine combination was superior to the benazepril-hy

115 Thus, in TM patients with cardiac siderosis, amlodipine combined with chelation therapy reduced cardi

116 ause of superior efficacy of benazepril plus amlodipine compared with benazepril plus hydrochlorothia

117 ing were attenuated in patients while taking amlodipine compared with ISMN.

118 ning a renin-angiotensin system blocker with amlodipine, compared with hydrochlorothiazide, was super

119 e-blind 20 or 40 mg fosinopril or 5 or 10 mg amlodipine daily for 4 weeks in a fixed-dose regimen.

120 Addition of bradykinin, enalaprilat, and amlodipine decreased oxygen consumption significantly le

121 Amlodipine did not increase cardiovascular morbidity or

122 ry IVUS, which was repeated after 2 years of amlodipine, enalapril, or placebo therapy.

123 in response to agonist stimulation, whereas amlodipine enhanced P-selectin expression and atenolol i

124 083) while taking a calcium-channel blocker (amlodipine, felodipine, nifedipine, diltiazem, or verapa

125 omly assigned to 80 mg/d valsartan or 5 mg/d amlodipine for 24 weeks.

126 ted renal transplant patients were placed on amlodipine for an average of 6.9 wk and later withdrawn.

127 A 63-year-old male taking amlodipine for his hypertension presented with a 3-week

128 ospitals are routinely switching patients to amlodipine from other CCB for reasons of cost.

129 25.5 per 1000 patient-years) and 789 in the amlodipine group (10.4%, 24.7 per 1000 patient-years; ha

130 552 primary-outcome events in the benazepril-amlodipine group (9.6%) and 679 in the benazepril-hydroc

131 duced risk of the clinical end points vs the amlodipine group (95% confidence interval [CI], 20%-66%)

132 The lower risk of stroke in the amlodipine group (hazard ratio 0.78, 95% CI 0.67-0.90) w

133 l group (P = .08), and no progression in the amlodipine group (P = .31).

134 y, reduced variability in daytime SBP in the amlodipine group (p<0.0001) partly accounted for the red

135 nt lower in the irbesartan group than in the amlodipine group (P<0.001).

136 hereas there was a 0.0126-mm decrease in the amlodipine group (P:=0.007).

137 =0.02) and 23 percent lower than that in the amlodipine group (P=0.006).

138 .008) and 21 percent more slowly than in the amlodipine group (P=0.02).

139 ment were 131.6/73.3 mm Hg in the benazepril-amlodipine group and 132.5/74.4 mm Hg in the benazepril-

140 that variability decreased over time in the amlodipine group and increased in the atenolol group.

141 y disease progression in the benazepril plus amlodipine group compared with 215 (3.7%) in the benazep

142 PM variability in SBP were also lower in the amlodipine group than in the atenolol group (all p<0.000

143 lic blood pressure (SBP) SD was lower in the amlodipine group than in the atenolol group at all follo

144 ema was more frequent in the benazepril plus amlodipine group than in the benazepril plus hydrochloro

145 d less progression of atherosclerosis in the amlodipine group vs placebo (P = .12), with significantl

146 tients (14%) from the initial aliskiren plus amlodipine group, 45 (14%) from the aliskiren group, and

147 However, compared with the amlodipine group, after adjustment for baseline covariat

148 For the amlodipine group, correlation between blood pressure red

149 as compared with 33 percent of those in the amlodipine group, representing a 16 percent reduction in

150 t of the placebo group and 39 percent of the amlodipine group, representing a 9 percent reduction in

151 m the aliskiren group, and 58 (18%) from the amlodipine group.

152 rothiazide group than in the benazepril plus amlodipine group.

153 amin E (Group D) or 1% cholesterol diet plus amlodipine (Group E) for 12 weeks.

154 This report compares the ramipril and amlodipine groups following discontinuation of the amlod

155 The placebo and amlodipine groups had nearly identical average 36-month

156 However, compared with the metoprolol and amlodipine groups, the ramipril group manifested risk re

157 tical in the chlorthalidone, lisinopril, and amlodipine groups.

158 In contrast, amlodipine had a significant effect in slowing the 36-mo

159 Likewise, patients receiving amlodipine had a significantly lower rate of myocardial

160 Amlodipine has no demonstrable effect on angiographic pr

161 t few years a newer calcium channel blocker, amlodipine, has been used with increasing frequency.

162 The effect of a new CCB, amlodipine, has not been established.

163 % confidence interval, 0.94-1.15; P=0.46) or amlodipine (hazard ratio, 0.93; 95% confidence interval,

164 However, both AT1-receptor blockade and amlodipine improved in vivo left ventricular end-diastol

165 il significantly reduced PAI-1 compared with amlodipine in a dose-dependent fashion.

166 The beneficial effect of amlodipine in CHF may be due to a reduction of cytokines

167 determine whether the beneficial effects of amlodipine in heart failure may be mediated by a reducti

168 ce cardiac morbidity and mortality more than amlodipine in hypertensive patients at high cardiovascul

169 were significantly lower with benazepril and amlodipine in overweight patients (hazard ratio 0.76, 95

170 the use of valsartan (ARB) was compared with amlodipine in patients at high cardiovascular disease ri

171 valsartan lowered UAER more effectively than amlodipine in patients with type 2 diabetes and microalb

172 ve effect of chlorthalidone, lisinopril, and amlodipine in preventing HF.

173 the effect of a new calcium-channel blocker, amlodipine, in patients with severe chronic heart failur

174 CsA levels on amlodipine increased an average of 40% above baseline (P

175 pine groups following discontinuation of the amlodipine intervention in September 2000.

176 increased CsA levels after being changed to amlodipine is presented along with a prospective trial t

177 ested whether a combination of aliskiren and amlodipine is superior to each monotherapy in early cont

178 r second-generation dihydropyridines such as amlodipine, isradipine, nicardipine, and felodipine also

179 For amlodipine, IVUS showed evidence of slowing of atheroscl

180 rticipants were randomly assigned to receive amlodipine, lisinopril, or chlorthalidone.

181 9 participants randomized to chlorthalidone, amlodipine, lisinopril, or doxazosin treatments and foll

182 Attack Trial) determined that treatment with amlodipine, lisinopril, or doxazosin was not superior to

183 patients were randomized to chlorthalidone, amlodipine, lisinopril, or doxazosin, providing an oppor

184 done reduced the risk of HFPEF compared with amlodipine, lisinopril, or doxazosin; the hazard ratios

185 red in 29.2% of participants (chlorthalidone/amlodipine/lisinopril) with new-onset HFPEF versus 41.9%

186 Amlodipine lowers plasma IL-6 levels in patients with CH

187 ix cases have been published indicating that amlodipine may also promote gingival hyperplasia; howeve

188 that a portion of the beneficial actions of amlodipine may involve the release or action of NO.

189 Recent studies suggest that amlodipine may reduce mortality in patients with heart f

190 s, patients in the reduction group receiving amlodipine (n = 15) had a significant decrease in MIC co

191 who were lost to follow-up (benazepril plus amlodipine, n=70; benazepril plus hydrochlorothiazide, n

192 halidone; n = 13,860), a calcium antagonist (amlodipine; n = 8174), an angiotensin-converting enzyme

193 Neither amlodipine nor lisinopril is superior to chlorthalidone

194 The effect of amlodipine on cytokine levels in patients with CHF is un

195 eceive treatment with either benazepril plus amlodipine or benazepril plus hydrochlorothiazide.

196 prevalence of gingival overgrowth induced by amlodipine or diltiazem was not statistically significan

197 done reduced the risk of HFREF compared with amlodipine or doxazosin; the hazard ratios were 0.74 (95

198 HF risk decreased with chlorthalidone versus amlodipine or lisinopril use during year 1.

199 e appropriate model showed relative risks of amlodipine or lisinopril versus chlorthalidone during ye

200 isks (95% confidence intervals; P values) of amlodipine or lisinopril versus chlorthalidone were 1.35

201 .05; 95% CI, 0.77-1.42) than participants on amlodipine or lisinopril with incident diabetes (HR rang

202 channel blockers nifedipine, diltiazem, and amlodipine or the ACE inhibitors enalaprilat and ramipri

203 , a dihydropyridine calcium channel blocker (amlodipine) or a beta-blocker (metoprolol) as initial th

204 ic angina taking standard doses of atenolol, amlodipine, or diltiazem, without evident adverse, long-

205 Random assignment to chlorthalidone, amlodipine, or lisinopril.

206 effects of 7 days of treatment with placebo, amlodipine, or lisinopril.

207 d overt nephropathy treated with irbesartan, amlodipine, or placebo in addition to conventional antih

208 Patients were randomized to irbesartan, amlodipine, or placebo, with other antihypertensive agen

209 Treatment with irbesartan, amlodipine, or placebo.

210 essure were complete, created 5006 valsartan-amlodipine patient pairs matched exactly for systolic bl

211 g-regimens (atenolol+/-thiazide-based versus amlodipine+/-perindopril-based therapy) on derived centr

212 ent with 150 mg aliskiren plus placebo, 5 mg amlodipine plus placebo, or 150 mg aliskiren plus 5 mg a

213 In in vitro experiments, both lovastatin and amlodipine preserved SOD activity and reduced the oxidiz

214 mented diet and by N-acetylcysteine, whereas amlodipine prevented Ca2+ loading and an altered redox s

215 The possibility that amlodipine prolongs survival in patients with nonischemi

216 atio, 0.72 [CI, 0.52 to 1.00]; P = 0.048) or amlodipine recipients (hazard ratio, 0.65 [CI, 0.48 to 0

217 ng patients with nonischemic cardiomyopathy, amlodipine reduced the combined risk of fatal and nonfat

218 uctions in central aortic pressures with the amlodipine regimen (central aortic systolic BP, Delta4.3

219 Thus, unlike nifedipine and diltiazem, amlodipine releases NO from blood vessels.

220 ose individuals taking chlorthalidone versus amlodipine remained decreased but less so, whereas it wa

221 Ramipril, compared with amlodipine, retards renal disease progression in patient

222 ihypertensive treatment with benazepril plus amlodipine should be considered in preference to benazep

223 Bradykinin, enalaprilat, and amlodipine significantly suppressed cortical oxygen cons

224 er irbesartan or the calcium-channel blocker amlodipine slows the progression of nephropathy in patie

225 defects in responsiveness to enalaprilat and amlodipine, suggesting that inactivation of NO by supero

226 In the Prospective Randomized Amlodipine Survival Evaluation (PRAISE) trial, we used e

227 nical trials (PRAISE [Prospective Randomized Amlodipine Survival Evaluation], PRAISE-2, MERIT-HF [Met

228 We analyzed data from Prospective Randomized Amlodipine Survival Trial (PRAISE).

229 eriod (blood pressure 4.0/2.1 mm Hg lower in amlodipine than valsartan group after 1 month; 1.5/1.3 m

230 However, in those allocated benazepril and amlodipine, the primary endpoint did not differ between

231 g an absolute risk reduction with benazepril-amlodipine therapy of 2.2% and a relative risk reduction

232 ut inequalities in blood pressure, favouring amlodipine, throughout the multiyear trial precluded com

233 We evaluated whether addition of amlodipine to chelation strategies would reduce myocardi

234 Administration of amlodipine to patients with CAD and normal blood pressur

235 the ability of bradykinin, enalaprilat, and amlodipine to suppress oxygen consumption in tissue from

236 ar systolic pressure in the AT1-blocker- and amlodipine-treated LVH groups (189 +/- 9 and 188 +/- 16

237 1%) placebo-treated patients, in 110 (16.6%) amlodipine-treated patients (hazard ratio [HR], 0.69; 95

238 AT1-blocker-treated (11.0 +/- 1.7 mm Hg) and amlodipine-treated rats (11.5 +/- 1.8 mm Hg) and was sim

239 zed in both the AT1-blocker-treated rats and amlodipine-treated rats.

240 ectively, both P<0.05) and were reduced with amlodipine treatment (2108+/-199 and 480+/-74, respectiv

241 +/-2, P<0.05) and increased with concomitant amlodipine treatment (29+/-2, P<0.05).

242 +/-1, P<0.05) and was increased with chronic amlodipine treatment (52+/-1, P<0.05).

243 rsus 3.1+/-0.3, P<0.05) and was reduced with amlodipine treatment (6.6+/-1.1, P<0.5).

244 lower after lisinopril treatment than after amlodipine treatment (P = .03).

245 Amlodipine treatment did not cause any serious adverse e

246 Chronic amlodipine treatment in this model of developing CHF pro

247 Neither amlodipine treatment nor aspirin or warfarin use altered

248 w during treadmill exercise, whereas chronic amlodipine treatment normalized LV stroke volume and imp

249 This study examined the effects of chronic amlodipine treatment on left ventricular (LV) pump funct

250 scular resistance was lower (P = .016) after amlodipine treatment than after lisinopril treatment.

251 Amlodipine treatment was associated with reduced cardiov

252 reduced by 50% from CHF values with chronic amlodipine treatment.

253 ity or major cardiovascular events, although amlodipine use was associated with fewer cases of unstab

254 IVUS) substudy of the CAMELOT (Comparison of Amlodipine Versus Enalapril to Limit Occurrences of Thro

255 y lower at 26 weeks in patients treated with amlodipine versus placebo (p = 0.007 by the Wilcoxon sig

256 a decrease in strokes in patients receiving amlodipine versus those receiving placebo (hazard ratio,

257 Other outcomes included comparisons of amlodipine vs enalapril and enalapril vs placebo.

258 s usual BP goal; ramipril vs metoprolol; and amlodipine vs metoprolol.

259 r was incidence of cardiovascular events for amlodipine vs placebo.

260 rimary end point comparison for enalapril vs amlodipine was not significant (HR, 0.81; 95% CI, 0.63-1

261 Amlodipine was similar to chlorthalidone in reducing CHD

262 ntihypertensive therapy with benazepril plus amlodipine was superior to benazepril plus hydrochloroth

263 Amlodipine was the most commonly prescribed calcium-chan

264 and decreased to baseline (P = 0.001) after amlodipine was withdrawn, despite no significant change

265 odipine, and 617 allocated to aliskiren plus amlodipine were available for analysis.

266 gnificant differences between fosinopril and amlodipine were found for short-term changes in tissue p

267 odipine, whereas the effects of atenolol and amlodipine were not additive.

268 GTN neutralized the proactivatory effects of amlodipine, whereas the effects of atenolol and amlodipi

269 in the groups given lovastatin, vitamin E or amlodipine with a high cholesterol diet.

270 ly in rabbits given lovastatin, vitamin E or amlodipine with a high cholesterol diet.

271 lence of overgrowth induced by diltiazem and amlodipine, with estimates of 74% and 3.3%, respectively

272 Amlodipine, with its intrinsically long half-life alone

273 od pressures, regimens based on valsartan or amlodipine would have differing effects on cardiovascula

274 A secondary hypothesis was whether amlodipine would reduce the rate of atherosclerosis in t

275 sked clinical trial designed to test whether amlodipine would slow the progression of early coronary