ライフサイエンスコーパス: ACE inhibitor

1 chronic heart failure, most treated with an ACE inhibitor).

2 ompleted the trial (34 on placebo, 31 on the ACE inhibitor).

3 response to a low-salt diet combined with an ACE inhibitor.

4 expression of ACE, as it is eliminated by an ACE inhibitor.

5 y inhibiting the protease's activity with an ACE inhibitor.

6 MI, even in patients already treated with an ACE inhibitor.

7 after AMI, 98% of whom were treated with an ACE inhibitor.

8 ng enzyme (ACE) used relatively low doses of ACE inhibitors.

9 reversed cortical COX-2 elevation induced by ACE inhibitors.

10 esign of "domain-specific" second-generation ACE inhibitors.

11 ents such as myocardial infarction (MI) like ACE inhibitors.

12 ould be regarded as suitable alternatives to ACE inhibitors.

13 ocker, and 4) angiotensin-converting enzyme (ACE) inhibitor.

14 ) with use of angiotensin-converting enzyme (ACE) inhibitor.

15 dication with angiotensin-converting enzyme (ACE) inhibitors.

16 (0.97; 95% CrI 0.72-1.29), DR inhibitor plus ACE inhibitor (0.99; 95% CrI 0.65-1.57), and DR inhibito

17 as 1.81 (95% CI 0.79-4.13, p=0.162) and with ACE inhibitor 1.73 (0.56-5.32, p=0.342).

18 (0.97; 95% CrI 0.79-1.19), DR inhibitor plus ACE inhibitor (1.32; 95% CrI 0.96-1.81), and DR inhibito

19 increased by angiotensin-converting enzyme (ACE) inhibitors (1.08, 1.02-1.15, p=0.008), angiotensin-

20 omized to either 10 weeks of therapy with an ACE inhibitor (10 mg enalapril) or placebo.

21 included: an ARB (1189 of 14,185, or 8.38%), ACE inhibitor (1618 of 22,941, or 7.05%), calcium-channe

22 Our analysis included 59,316 new users of ACE inhibitors, 47% of whom were black.

23 reatment with angiotensin-converting-enzyme (ACE) inhibitors accounts for one third of angioedema cas

24 y analysis was the association between prior ACE inhibitor (ACE-I) treatment and angio-oedema.

25 ysiological VWF handling might contribute to ACE inhibitors' (ACEi) reno- and cardioprotective effect

26 es with significant in vitro antioxidant and ACE inhibitor activities.

27 ctions exhibited the highest antioxidant and ACE inhibitor activities.

28 terms such as angiotensin-converting enzyme (ACE) inhibitors, adrenaline, allergic myocardial infarct

29 .035) with combination therapy compared with ACE inhibitors alone.

30 o test the hypothesis that beta-blockers and ACE inhibitors alter the risk for severe anaphylaxis and

31 r persistence with therapy for ARBs than for ACE inhibitors, although this evidence was not definitiv

32 hese data suggest that the combination of an ACE inhibitor and a histone deacetylase inhibitor could

33 The use of an ACE inhibitor and a statin did not change the albumin-to

34 assigned in a placebo-controlled trial of an ACE inhibitor and a statin with the use of a 2-by-2 fact

35 ed with monotherapies, the combination of an ACE inhibitor and an ARB failed to provide significant b

36 Conclusions Combination therapy with an ACE inhibitor and an ARB was associated with an increase

37 ACE inhibitor and ARB exposures were defined in aggregat

38 ia or acute kidney injury, although combined ACE inhibitor and ARB treatment had the lowest rank amon

39 Any benefits of combined ACE inhibitor and ARB treatment need to be balanced agai

40 diagnosis were extrapolated; the efficacy of ACE inhibitor and beta-blocker therapy in childhood canc

41 ignificant differences were detected between ACE inhibitor and each of the remaining therapies: ARB (

42 ain selectivity and should help design novel ACE inhibitors and Ac-SDKP analogues that could be used

43 ical trial is necessary to determine whether ACE inhibitors and ARBs also differ with respect to thei

44 explained 87.5% of expenditure variation for ACE inhibitors and ARBs and 56.3% for statins but only 3

45 Several studies have shown that ACE inhibitors and ARBs decrease the incidence of new-on

46 To test whether ACE inhibitors and ARBs differentially affect markers of

47 Because ACE inhibitors and ARBs do not differ in efficacy for re

48 ACE inhibitors and ARBs had similar long-term effects on

49 Available evidence shows that ACE inhibitors and ARBs have similar effects on blood pr

50 erent RAS blockers showed similar effects of ACE inhibitors and ARBs on major cardiovascular and rena

51 This showed that ACE inhibitors and ARBs were associated with reductions

52 significant differences were showed between ACE inhibitors and ARBs with respect to all-cause mortal

53 24 to 0.45 overall and from 0.24 to 0.55 for ACE inhibitors and ARBs, 0.29 to 0.60 for statins, and 0

54 ACE inhibitors and ARBs, alone or in combination, were t

55 Statins, and to a lesser extent ACE inhibitors and ARBs, are associated with improved pn

56 ACE-deficient mice and in mice treated with ACE inhibitors and found that ACE deficiency did not alt

57 emic cardiovascular events, and suggest that ACE inhibitors and MR antagonists may decrease clinical

58 and inhibitors of Ang II synthesis, such as ACE inhibitors and renin inhibitors, are beneficial for

59 An increase in reported allergies to ACE inhibitors and statins is noteworthy.

60 In the 848 patients taking ACE inhibitors and undergoing off-pump cardiac surgery,

61 nts with heart failure who are intolerant to ACE inhibitors and who are on optimal ACE inhibitor ther

62 These studies suggest that ACE inhibitors and/or angiotensin II receptor blockers m

63 ination of an angiotensin-converting-enzyme (ACE) inhibitor and a dihydropyridine calcium-channel blo

64 ination of an angiotensin-converting enzyme (ACE) inhibitor and a histone deacetylase inhibitor would

65 effect of an angiotensin-converting enzyme (ACE) inhibitor and angiotensin receptor blocker (ARB) on

66 g followed by angiotensin-converting enzyme (ACE) inhibitor and beta-blocker therapies after ALVD dia

67 S), including angiotensin converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (AR

68 ectiveness of angiotensin-converting enzyme (ACE) inhibitors and angiotensin II receptor blockers (AR

69 onolactone to angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs)

70 e the role of angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs)

71 Continuing angiotensin converting enzyme (ACE) inhibitors and angiotensin receptor blockers increa

72 emerged that angiotensin-converting-enzyme (ACE) inhibitors and angiotensin-II receptor blockers (AR

73 therapy with angiotensin-converting-enzyme (ACE) inhibitors and angiotensin-receptor blockers (ARBs)

74 g categories: angiotensin-converting-enzyme (ACE) inhibitors and angiotensin-receptor blockers (ARBs)

75 Angiotensin-converting enzyme (ACE) inhibitors and angiotensin-receptor blockers (ARBs)

76 allergies to angiotensin-converting enzyme (ACE) inhibitors and HMG CoA reductase inhibitors (statin

77 reatment with angiotensin converting enzyme (ACE) inhibitors and similar treatment strategies have a

78 benefit from angiotensin-converting-enzyme (ACE) inhibitors and statins, drugs that have not been fu

79 dditional benefit from the combination of an ACE-inhibitor and angiotensin receptor blocker therapy i

80 ACE-inhibitors and angiotensin-receptor blockers remain

81 se was to examine the association of statin, ACE inhibitor, and angiotensin II receptor blocker (ARB)

82 ty at 30 days was 13%; 34% used statins, 30% ACE inhibitors, and 4% ARBs.

83 re-lowering drugs (thiazides, beta-blockers, ACE inhibitors, and angiotensin II receptor antagonists)

84 antihypertensive agents including diuretics, ACE inhibitors, and ARBs.

85 emales and white patients except for NSAIDs, ACE inhibitors, and thiazide diuretics, which were more

86 mice ARBs increased cortical COX-2 more than ACE inhibitors, and this stimulation was attenuated by t

87 h as statins, angiotensin converting enzyme (ACE) inhibitors, and thiazolidinediones (TZDs) providing

88 bitors, angiotensin (Ang)-converting enzyme (ACE) inhibitors, Ang II type 1 receptor antagonists, and

89 interest were angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), a

90 tion, such as angiotensin converting enzyme (ACE) inhibitors, angiotensin receptor blockers (ARBs), b

91 ta-analyses confirm the beneficial effect of ACE-inhibitors, angiotensin-receptor blockers, and diure

92 e interval [CI]: 1.04 to 1.10) and discharge ACE inhibitor/angiotensin receptor blocker (ARB) in LV d

93 in type 1 diabetic subjects not treated with ACE inhibitor/angiotensin receptor blocker who had the T

94 Angiotensin-converting enzyme (ACE) inhibitors/angiotensin II receptor blockers (ARB),

95 dentical to angiotensin I-converting enzyme (ACE) inhibitors, antioxidant, antimicrobial, immunomodul

96 LV assessment and ACE inhibitor/ARB use were associated with reductions in

97 of at least 6 months' duration that compared ACE inhibitors, ARBs, or combination therapy with placeb

98 (95% CI: 1.04 to 1.21) for being adherent to ACE inhibitors/ARBs and beta-blockers only, 0.98 (95% CI

99 Patients adherent to ACE inhibitors/ARBs and statins only had similar mortali

100 Nonadherence to ACE inhibitors/ARBs and/or statins was associated with h

101 tatins only, 1.19 (95% CI: 1.07 to 1.32) for ACE inhibitors/ARBs only, 1.32 (95% CI: 1.21 to 1.44) fo

102 ated the effect of tradeoffs in adherence to ACE inhibitors/ARBs, beta-blockers, and statins on survi

103 >/=65 years of age who had prescriptions for ACE inhibitors/ARBs, beta-blockers, and statins, and sur

104 in patients who were adherent to statins and ACE inhibitors/ARBs.

105 igned to treat cardiovascular disorders, and ACE inhibitors are commonly prescribed.

106 The cardioprotective effects of ACE inhibitors are mediated by blockade of both conversi

107 Angiotensin-converting enzyme (ACE) inhibitors are valuable agents for the treatment of

108 Ang I-converting enzyme (ACE) inhibitors are widely believed to suppress the dele

109 -Blockers and angiotensin-converting enzyme (ACE) inhibitors are widely used cardiovascular drugs.

110 y established angiotensin converting enzyme (ACE) inhibitors as the standard of care in patients with

111 Patients with ACE inhibitor-associated angioedema (defined as swelling

112 gonist would shorten time-to-resolution from ACE inhibitor-associated angioedema.

113 cy of a bradykinin B2 receptor antagonist in ACE inhibitor-associated angioedema.

114 resolution of angiotensin-converting enzyme (ACE) inhibitor-associated angioedema in 1 study of Europ

115 ng ACE inhibitors but not in those receiving ACE inhibitors at 12 months.

116 valuated the comparative effectiveness of an ACE inhibitor-based regimen on a composite outcome of al

117 er outcomes than whites when treated with an ACE inhibitor-based regimen.

118 ACE inhibitor-based therapy was associated with poorer c

119 eated with an angiotensin-converting enzyme (ACE) inhibitor-based regimen, but this has not been eval

120 ed bradycardia, clinically relevant doses of ACE inhibitors, beta-blockade and the funny channel bloc

121 e domain protein with ACE activity) to study ACE inhibitor binding.

122 a decrease in CRP in patients not receiving ACE inhibitors but not in those receiving ACE inhibitors

123 reatments such as aspirin, beta-blockers, or ACE inhibitors but were significantly less likely to rec

124 edications evaluated included beta-blockers, ACE inhibitors, calcium channel blockers, angiotensin re

125 ng II receptor type 1 blocker candesartan or ACE inhibitor captopril markedly attenuated eNOS-derived

126 The ACE inhibitor captopril reduced Ang II levels in the med

127 Treatment with the ACE inhibitor captopril, valsartan, or the combination o

128 of Ac-SDKP in the therapeutic effects of the ACE inhibitor captopril, we used a model of Ang II-induc

129 nase C (PKC)beta inhibitor ruboxistaurin, or ACE inhibitor captopril.

130 ACE inhibitors (captopril, fosinopril and fosinoprilat)

131 eated with an angiotensin converting enzyme (ACE) inhibitor, captopril, to evaluate sensitivity to am

132 evaluated Medicare first-dollar coverage of ACE inhibitors compared with current practice (no covera

133 icular ejection fraction, and intolerance to ACE inhibitors compared with losartan 50 mg daily.

134 the question of whether currently prescribed ACE inhibitors could elevate cerebral Abeta levels in hu

135 domized (21 patients in each arm) to receive ACE inhibitors demonstrated slower MF progression compar

136 Angiotensin I-converting enzyme (ACE) inhibitors derived from foods are valuable auxiliar

137 The ACE inhibitor did not decrease either blood pressure or

138 ut the use of angiotensin-converting enzyme (ACE) inhibitors did modify this risk (ACE users: adjuste

139 and preexisting lung disease, beta-blocker, ACE-inhibitor, diuretic, or antihypertensive medication

140 ed with AD, and second, to determine whether ACE inhibitor drugs might block beta-amyloid degradation

141 However, the combination of aprotinin and ACE inhibitors during off-pump cardiac surgery is associ

142 Exposure to ACE inhibitors during the first trimester cannot be cons

143 o assess the association between exposure to ACE inhibitors during the first trimester of pregnancy o

144 Use of angiotensin-converting-enzyme (ACE) inhibitors during the second and third trimesters o

145 e groups) 0.57 (95% CI 0.46-0.72, p<0.0001); ACE inhibitor (eight groups) 0.67 (0.56-0.80, p<0.0001);

146 nduced hypertension in rats treated with the ACE inhibitor either alone or combined with a blocking m

147 We compared the ACE inhibitor enalapril with the renin inhibitor aliskir

148 Use of the ACE inhibitor enalapril, together with a program of PR,

149 mice with the angiotensin-converting enzyme (ACE) inhibitor enalapril, but not the anti-hypertensive

150 stigate how angiotensin I-converting enzyme (ACE) inhibitors enhance the actions of bradykinin (BK) o

151 ent diabetes is therefore lowest for ARB and ACE inhibitors followed by CCB and placebo, beta blocker

152 ablished that the ARB was as effective as an ACE inhibitor following myocardial infarction.

153 Medicare first-dollar coverage of ACE inhibitors for beneficiaries with diabetes appears t

154 ments such as angiotensin-converting enzyme (ACE) inhibitors for left ventricular (LV) systolic dysfu

155 nfants with only first-trimester exposure to ACE inhibitors had an increased risk of major congenital

156 Thus, high-affinity 99mTc-labeled ACE inhibitor has been designed with potency similar to

157 Furthermore, the effectiveness of ACE inhibitors has been questioned in some populations,

158 In contrast, first-trimester use of ACE inhibitors has not been linked to adverse fetal outc

159 effects on blood pressure control, and that ACE inhibitors have higher rates of cough than ARBs.

160 Angiotensin-converting enzyme (ACE) inhibitors have been associated with severe anaphyl

161 Angiotensin-converting enzyme (ACE) inhibitors have been shown to attenuate left ventri

162 tion setting, angiotensin-converting enzyme (ACE) inhibitors have been shown to be as effective in pa

163 ere not associated with recurrence (adjusted ACE inhibitor HR = 1.2, 95% CI, 0.97 to 1.4; adjusted AR

164 patients over age 80 with indapamide and an ACE-inhibitor if needed can significantly reduce heart f

165 Surprisingly, both ruboxistaurin and ACE inhibitors improved the metabolic gene profile (conf

166 ceptor blockers appear to be as effective as ACE inhibitors in reducing atherosclerotic events, even

167 We identified 209 infants with exposure to ACE inhibitors in the first trimester alone, 202 infants

168 be as effective as, or more effective than, ACE inhibitors in these clinical settings.

169 hus provided clinicians with alternatives to ACE inhibitors in these important clinical syndromes.

170 ic effects of angiotensin-converting enzyme (ACE) inhibitors in patients with CKD; however, whether d

171 icular drug (PPIs, NSAIDs, SSRIs, diuretics, ACE inhibitors) in the 6 months prior to the time of ini

172 Angiotensin-converting enzyme (ACE) inhibitors increase the bioavailability of bradykin

173 phase 2 study, we assigned patients who had ACE-inhibitor-induced angioedema of the upper aerodigest

174 Among patients with ACE-inhibitor-induced angioedema, the time to complete r

175 Treatment with ACE inhibitors induces abundant CD4+FoxP3+ T cells with

176 rolol/bradykinin (the latter increased after ACE inhibitor intake), whereas the substances had no sig

177 hibitors or angiotensin receptor blockers if ACE-inhibitor-intolerant are preferred first-line agents

178 rtension, the cardiac antifibrotic effect of ACE inhibitors is a result of the inhibition of Ac-SDKP

179 platelet, lipid-lowering, beta-blockers, and ACE inhibitors--is associated with improved outcome free

180 .73 m(2) of body-surface area) to receive an ACE inhibitor (lisinopril) and placebo or lisinopril and

181 Angiotensin-converting enzyme (ACE) inhibitors lower Ang II levels by inhibiting conver

182 ed Smad2 phosphorylation 3.2+/-0.9-fold; the ACE inhibitor lowered this to 0.6+/-0.1-fold (P<0.001),

183 to 2.1+/-0.3 (P<0.001, ACE inhibitor versus ACE inhibitor+mAb).

184 b (12.1+/-0.6; P<0.034, ACE inhibitor versus ACE inhibitor+mAb).

185 port the hypothesis that adding an ARB to an ACE inhibitor may have a small additional anti-infarctio

186 Thus, PKCbeta or ACE inhibitors may ameliorate cardiac metabolism and fun

187 s of the currently available and widely used ACE inhibitors may arise from their targeting both domai

188 and its progression to macroalbuminuria, and ACE inhibitors may reduce the excess cardiovascular mort

189 The renoprotective effects of ACE inhibitors may result, in part, from modulation of t

190 These findings suggest that ACE inhibitor-mediated increase in LV BK exacerbates mat

191 nd/or contribute to hereditary angioedema or ACE-inhibitor-mediated angioedema including variations i

192 t statins and angiotensin-converting enzyme (ACE) inhibitors might be beneficial for the treatment of

193 CE and B2 receptors are separately anchored, ACE inhibitors neither enhance activation of chimeric B2

194 When compared with ACE inhibitor, no other RAS blocker used in monotherapy

195 s index, use of antihypertensive medication (ACE inhibitors, non-ophthalmic beta blockers, calcium ch

196 (ARB) and an angiotensin-converting-enzyme (ACE) inhibitor (odds ratio 0.62, 95% CI 0.43-0.90) and a

197 n has a more pronounced effect than ARBs and ACE inhibitors on these diabetes complications and may b

198 The use of an ACE inhibitor or ARB should be considered in patients wi

199 if they had asthma (0.73, 0.58-0.91); or an ACE inhibitor or loop diuretic without appropriate monit

200 Treatment with an ACE inhibitor or receptor blocker, beta-blocker, or calc

201 ckers (90.9% vs. 92.8%), and prescription of ACE inhibitors or ARBs (93.9% vs. 98.7%).

202 The effects of ACE inhibitors or ARBs in placebo-controlled trials were

203 The benefits of ACE inhibitors or ARBs on renal outcomes in placebo-cont

204 no benefit was seen in comparative trials of ACE inhibitors or ARBs on the doubling of creatinine (1.

205 Placebo-controlled trials of ACE inhibitors or ARBs showed greater benefits than comp

206 Patient subgroups for whom ACE inhibitors or ARBs were more effective, associated w

207 <130/85 mm Hg) on established treatment with ACE inhibitors or ARBs were randomized to continue spiro

208 and guidelines now recommend substitution of ACE inhibitors or ARBs with ARNIs in appropriate patient

209 Comparisons of ACE inhibitors or ARBs with other antihypertensive drugs

210 us 18.2% for statins, 42.5% versus 20.8% for ACE inhibitors or ARBs, and 75.1% versus 27.0% for insul

211 and taking stable antidiabetic treatment and ACE inhibitors or ARBs, for at least 8 weeks before stud

212 12 randomized controlled clinical trials of ACE inhibitors or ARBs, identified through a MEDLINE sea

213 out mice were treated for 7 days with either ACE inhibitors or ARBs.

214 al reductions in blood pressure in favour of ACE inhibitors or ARBs.

215 n 300 mg per day or placebo as an adjunct to ACE inhibitors or ARBs.

216 iven in addition to standard care, including ACE inhibitors or ARBs.

217 Blocking AII production with ACE inhibitors or inhibiting AII signaling with AT1R blo

218 rs), in patients treated with beta-blockers, ACE inhibitors or monoamine oxidase inhibitors, in child

219 erapy with an angiotensin-converting-enzyme (ACE) inhibitor or angiotensin II-receptor blocker (ARB).

220 albumin, Hb, angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) use

221 locker and an angiotensin-converting enzyme (ACE) inhibitor or angiotensin-receptor blocker (ARB) for

222 escription of angiotensin converting enzyme (ACE) inhibitor or loop diuretics to those 75 years or ol

223 an adjunct to angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs)

224 ent including angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs).

225 statins, and angiotensin-converting enzyme (ACE) inhibitors or angiotensin-receptor blockers (ARBs)

226 induction by angiotensin-converting enzyme (ACE) inhibitors or AT(1) receptor blockers (ARBs) sugges

227 Thiazide diuretics, ACE-inhibitors or angiotensin receptor blockers if ACE-i

228 OR, 1.0 [95% CI, 0.57-1.9]); CHF with use of ACE inhibitor (OR, 0.98 [95% CI, 0.61-1.6]).

229 with insulin, candesartan (ARB), benazepril (ACE inhibitor), or aliskiren (renin inhibitor).

230 were treated for 12 weeks with enalapril, an ACE inhibitor, or L-158809, an angiotensin II receptor b

231 sion, renal insufficiency, or treatment with ACE inhibitors (p for all interactions > 0.2).

232 enrolled in the Prevention of Events with an ACE inhibitor (PEACE) trial, in which patients with chro

233 cardiovascular events than treatment with an ACE inhibitor plus a thiazide diuretic.

234 therapies: ARB (OR 1.10; 95% CrI 0.90-1.40), ACE inhibitor plus ARB (0.97; 95% CrI 0.72-1.29), DR inh

235 .02; 95% credible interval [CrI] 0.90-1.18), ACE inhibitor plus ARB (0.97; 95% CrI 0.79-1.19), DR inh

236 ment, including beta-adrenergic blockers and ACE inhibitors, potentially exacerbate anaphylaxis or ma

237 val [CI], 0.76-0.87) but comparable rates of ACE inhibitor prescription (0.96; 0.80-1.14).

238 vs 47.3%; P < .001) but comparable rates of ACE inhibitor prescription (71.3% vs 69.7%; P = .40).

239 tion that ACE2 is insensitive to blockade by ACE inhibitors prompted us to define the effect of ACE i

240 s the first in vivo evidence showing that an ACE inhibitor protects human myocardium, possibly via PC

241 inhibitor, alagebrium (1 mg/kg/day), or the ACE inhibitor, quinapril (30 mg/kg/day), for 20 weeks, a

242 Administration of the ACE inhibitor ramipril increased Abeta levels in AD(+)AC

243 (7 trials; 32 559 participants) showed that ACE inhibitors reduce the relative risk (RR) for total m

244 eart failure, angiotensin-converting-enzyme (ACE) inhibitors reduce mortality and hospitalization, bu

245 Most clinical ACE inhibitor(s) (ACEi) have been shown to inhibit both

246 h current practice, first-dollar coverage of ACE inhibitors saved both lives and money (0.23 QALYs ga

247 Likewise, the ACE inhibitor significantly decreased LV monocyte/macrop

248 Angiotensin-converting enzyme (ACE) inhibitors slow renal disease progression and reduc

249 beta-Blockers and ACE inhibitors synergistically aggravate anaphylaxis at

250 ractions with angiotensin-converting enzyme (ACE) inhibitors, the use of aspirin for secondary preven

251 and combination therapy seems no better than ACE inhibitor therapy alone and increases harms.

252 d blood level of ACE observed in patients on ACE inhibitor therapy and elevated blood lysozyme and AC

253 seems to blunt the antiproteinuric effect of ACE inhibitor therapy and increase the risk for ESRD, in

254 ACE inhibitor therapy caused a 1.8-fold increase in plas

255 ase inhibitors could be a useful addition to ACE inhibitor therapy in the treatment of heart failure.

256 In multivariate analysis, ACE inhibitor therapy was an independent indicator of de

257 ved and MF was present as determined on CMR, ACE inhibitor therapy was associated with significantly

258 The primary outcome was not affected by ACE inhibitor therapy, statin therapy, or the combinatio

259 ant to ACE inhibitors and who are on optimal ACE inhibitor therapy.

260 e randomized (1:1) to receive or not receive ACE inhibitor therapy.

261 andomization (1:1) to receive or not receive ACE inhibitor therapy.

262 ed that early angiotensin-converting enzyme (ACE) inhibitor therapy impacts healing after myocardial

263 fect of early angiotensin-converting enzyme (ACE) inhibitor therapy in patients with normal left vent

264 bset of patients most likely to benefit from ACE-inhibitor therapy for cardiovascular protection.

265 as related to outcomes, and the influence of ACE-inhibitor therapy was assessed with formal interacti

266 Adding an ACE inhibitor to standard medical therapy improves outco

267 ACE and B2 receptors can be a mechanism for ACE inhibitors to augment kinin activity at cellular lev

268 M-HF (Prospective Comparison of ARNI With an ACE-Inhibitor to Determine Impact on Global Mortality an

269 The ACE inhibitor-treated group demonstrated a significant r

270 In chronic ACE inhibitor-treated mast cell-sufficient littermates,

271 f conscious mice, we have shown that chronic ACE inhibitor treatment did not suppress Ang II levels i

272 t in the presence or absence of preoperative ACE inhibitor treatment, for both on-pump and off-pump s

273 been shown to return to normal with chronic ACE inhibitor treatment.

274 IBS patients, whereas no association between ACE inhibitor use and IBS was found.

275 ing of lips, tongue, pharynx, or face during ACE inhibitor use and no swelling in the absence of ACE

276 f increase in ACE inhibitor use; however, if ACE inhibitor use increased by only 7.2% (from 40% to 47

277 7) and inpatient (OR, 0.58; 95% CI, .48-.69) ACE inhibitor use was associated with decreased mortalit

278 ibitor use and no swelling in the absence of ACE inhibitor use) were enrolled at Vanderbilt Universit

279 such as blood pressure, lipids, and lack of ACE inhibitor use, but not with sex.

280 ncreased plasma Ang-(1-7) level is linked to ACE inhibitor use, whereas acute HF reduced Ang-(1-7) le

281 to valsartan or placebo depended on baseline ACE inhibitor use.

282 ost sensitive to our estimate of increase in ACE inhibitor use; however, if ACE inhibitor use increas

283 n added to an angiotensin-converting enzyme (ACE) inhibitor, ventricular arrhythmia is unknown.

284 blocked this decrease to 2.1+/-0.3 (P<0.001, ACE inhibitor versus ACE inhibitor+mAb).

285 was blocked by the mAb (12.1+/-0.6; P<0.034, ACE inhibitor versus ACE inhibitor+mAb).

286 61 clinical studies that directly compared ACE inhibitors versus ARBs in adult patients with essent

287 increased risk of renal dysfunction without ACE inhibitor was 1.81 (95% CI 0.79-4.13, p=0.162) and w

288 The use of an ACE inhibitor was associated with a lower incidence of m

289 Monotherapy with an ACE inhibitor was associated with blood-pressure control

290 Similar findings were seen when the ACE inhibitor was replaced by Ac-SDKP.

291 t fair- to good-quality evidence showed that ACE inhibitors were associated with a greater risk for c

292 ACE inhibitors were associated with a slightly increased

293 Infants exposed to ACE inhibitors were at increased risk for malformations

294 Results were similar when patients receiving ACE inhibitors were excluded from the analyses.

295 ntolerance to angiotensin-converting-enzyme (ACE) inhibitors were randomly assigned to losartan 150 m

296 e tolerant to angiotensin-converting-enzyme (ACE)-inhibitors were randomly assigned after a run-in pe

297 NSCEND, 5810 patients who were intolerant to ACE-inhibitors were randomly assigned to oral telmisarta

298 axis after monotherapy with beta-blockers or ACE inhibitors, which was more pronounced when both drug

299 als comparing angiotensin-converting-enzyme (ACE) inhibitors with angiotensin-receptor blockers (ARB)

300 rugs metoprolol (beta-blocker) and ramipril (ACE inhibitor) with the anaphylactic response was determ