ライフサイエンスコーパス: ACE inhibitor

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

2 chronic heart failure, most treated with an 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 ng enzyme (ACE) used relatively low doses of ACE inhibitors.

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

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

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

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

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

11 (0.97; 95% CrI 0.72-1.29), DR inhibitor plus ACE inhibitor (0.99; 95% CrI 0.65-1.57), and DR inhibito

12 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).

13 (0.97; 95% CrI 0.79-1.19), DR inhibitor plus ACE inhibitor (1.32; 95% CrI 0.96-1.81), and DR inhibito

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

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

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

17 ications were angiotensin-converting enzyme (ACE) inhibitors (17.9%), antidepressants (17.8%), and li

18 h was found to be associated with the use of ACE inhibitors (2.1% vs. 6.1%; odds ratio, 0.33; 95% CI,

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

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

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

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

23 alysis of COVID-19 cohorts has revealed that ACE inhibitors (ACEIs) or angiotensin receptor blockers

24 ctions exhibited the highest antioxidant and ACE inhibitor activities.

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

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

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

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

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

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

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

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

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

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

35 ACE inhibitor and ARB exposures were defined in aggregat

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

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

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

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

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

41 It is plausible that the ACE inhibitors and ACE receptor blockers may have the po

42 Both ACE inhibitors and antidepressants showed statistically

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 To test whether ACE inhibitors and ARBs differentially affect markers of

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

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

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

49 The use of ACE inhibitors and ARBs was more common among case patie

50 is large, population-based study, the use of ACE inhibitors and ARBs was more frequent among patients

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

52 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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

68 ugs, mostly angiotensin I converting enzyme (ACE) inhibitors and angiotensin receptor type I (AT(1)R)

69 ful effect of angiotensin-converting-enzyme (ACE) inhibitors and angiotensin-receptor blockers (ARBs)

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

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

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

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

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

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

76 rs (ARBs) and angiotensin-converting-enzyme (ACE) inhibitors and the risk of coronavirus disease 2019

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

78 ACE-inhibitors and angiotensin-receptor blockers remain

79 for ARBs and 0.91 [95% CI, 0.69 to 1.21] for ACE inhibitors), and no association between these variab

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

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

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

83 Because angiotensin II receptor blockers, ACE inhibitors, and mineralocorticoid receptor antagonis

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

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

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

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

88 the relation between previous treatment with ACE inhibitors, angiotensin-receptor blockers, beta-bloc

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 the effect of angiotensin-converting enzyme (ACE) inhibitors, angiotensin-receptor blockers (ARBs), b

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

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

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

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

96 vities of tempe peptides obtained were as an ACE inhibitor, antioxidant, and antithrombotic.

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

98 RVs, and at least 3 months of treatment with ACE inhibitor, ARB, beta blocker, or aldosterone antagon

99 n daily post-operative lisinopril-equivalent ACE inhibitor/ARB dose was >5 mg, the risk of major GIB

100 ACE inhibitor/ARB dose was abstracted from medical recor

101 ACE inhibitor/ARB exposure status was landmarked at 30 d

102 ACE inhibitor/ARB therapy is associated with a protectiv

103 nd Gray hazard models assessed the impact of ACE inhibitor/ARB therapy on major GIB and AVM-related G

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

105 Patients who received an ACE inhibitor/ARB within 30 days post-operatively had a

106 fect are needed to elucidate the efficacy of ACE inhibitors, ARBs, beta blockers, and aldosterone ant

107 After at least 3 months of treatment with ACE inhibitors, ARBs, or aldosterone antagonists, there

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

109 (95% CI: 1.04 to 1.21) for being adherent to ACE inhibitors/ARBs and beta-blockers only, 0.98 (95% CI

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

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

112 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

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

114 >/=65 years of age who had prescriptions for ACE inhibitors/ARBs, beta-blockers, and statins, and sur

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

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

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

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

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

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

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

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

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

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

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

126 ACE inhibitor-based therapy was associated with poorer c

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

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

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

130 ain catalytic activity; it is reversed by an ACE inhibitor but not by an angiotensin II AT1 receptor

131 on reverted to that of the WT enzyme with an ACE inhibitor but not with an angiotensin II type 1 (AT1

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

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

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

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

136 ACE inhibitors (captopril, fosinopril and fosinoprilat)

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

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

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

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

141 Use of ARBs or ACE inhibitors did not show any association with Covid-1

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

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

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

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

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

147 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);

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

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

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

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

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

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

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

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

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

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

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

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

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

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

162 ng potential effects of beta-blockers and/or ACE inhibitors in coexisting venom allergy are inconclus

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

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

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

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

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

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

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

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

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

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

173 t a 30-day course of high-dose captopril, an ACE inhibitor, initiated 1-4 h after total body irradiat

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

175 onic urticaria (mast cell mediator-induced), ACE-inhibitor intake and hereditary angioedema (both bra

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

177 .73 m(2) of body-surface area) to receive an ACE inhibitor (lisinopril) and placebo or lisinopril and

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

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

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

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

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

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

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

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

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

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

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

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

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

191 Routine laboratory monitoring after ACE inhibitor or angiotensin II receptor blocker initiat

192 e identified 75 251 matched pairs initiating ACE inhibitor or angiotensin II receptor blocker therapy

193 otassium tests in the 30 days after starting ACE inhibitor or angiotensin II receptor blocker therapy

194 worsening chronic HF) and treatment with an ACE inhibitor or ARB (i.e., ACE inhibitor or ARB-yes vs.

195 GLT2 inhibitor) versus conventional therapy (ACE inhibitor or ARB and beta blocker) in patients with

196 the control group of the EMPHASIS-HF trial (ACE inhibitor or ARB and beta blocker).

197 tion between prior HF history (p = 0.350) or ACE inhibitor or ARB treatment (p = 0.880) and the effec

198 april irrespective of previous HF history or ACE inhibitor or ARB treatment.

199 lity rank, implantable cardiac defibrillator+ACE inhibitor or ARB+BB+mineralocorticoid receptor antag

200 ntagonist, implantable cardiac defibrillator+ACE inhibitor or ARB+BB, and angiotensin receptor-nepril

201 421 (48%) patients had been treated with an ACE inhibitor or ARB, while 458 (52%) had not been treat

202 r or ARB (i.e., ACE inhibitor or ARB-yes vs. ACE inhibitor or ARB-no) at admission.

203 reatment with an ACE inhibitor or ARB (i.e., ACE inhibitor or ARB-yes vs. ACE inhibitor or ARB-no) at

204 while 458 (52%) had not been treated with an ACE inhibitor or ARB.

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

206 Confirmatory studies of whether adjunctive ACE inhibitor or statin treatment truly can enhance scle

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

208 eached guideline-recommended target doses of ACE inhibitors or ARBs (99 [25%] vs 304 [23%], p=0.61) a

209 However, there was no evidence that ACE inhibitors or ARBs affected the risk of COVID-19.

210 ht be sex differences in the optimal dose of ACE inhibitors or ARBs and beta blockers in patients wit

211 t women with HFrEF might need lower doses of ACE inhibitors or ARBs and beta blockers than men, and b

212 ilure in whom initiation and up-titration of ACE inhibitors or ARBs and beta blockers was encouraged

213 occurred at 100% of the recommended dose of ACE inhibitors or ARBs and beta blockers, but women show

214 try, similar patterns were observed for both ACE inhibitors or ARBs and beta blockers, with women hav

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

216 <130/85 mm Hg) on established treatment with ACE inhibitors or ARBs were randomized to continue spiro

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

218 regarding a potential harmful association of ACE inhibitors or ARBs with in-hospital death in this cl

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

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

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

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

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

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

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

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

227 tment with an angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) aff

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

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

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

231 rmine whether angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARB) w

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

233 consisting of angiotensin-converting enzyme (ACE) inhibitors or angiotensin receptor blockers (ARBs)

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

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

236 nded doses of angiotensin-converting-enzyme (ACE) inhibitors or angiotensin-receptor blockers (ARBs),

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

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

239 about use of angiotensin-converting enzyme (ACEs) inhibitors or angiotensin II receptor blockers (AR

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

241 for ARBs and 0.96 [95% CI, 0.87 to 1.07] for ACE inhibitors) or among patients who had a severe or fa

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

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

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

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

246 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

247 .02; 95% credible interval [CrI] 0.90-1.18), ACE inhibitor plus ARB (0.97; 95% CrI 0.79-1.19), DR inh

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

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

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

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

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

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

254 In healthy young mice, neither the ACE inhibitor ramipril nor the AT1 receptor blocker telm

255 (7 trials; 32 559 participants) showed that ACE inhibitors reduce the relative risk (RR) for total m

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

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

258 beta-Blockers and ACE inhibitors synergistically aggravate anaphylaxis at

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

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

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

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

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

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

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

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

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

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

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

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

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

272 Adding an ACE inhibitor to standard medical therapy improves outco

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

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

275 The ACE inhibitor-treated group demonstrated a significant r

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

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

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

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

280 Angiotensin Converting Enzyme (ACE) Inhibitor treatment (aHR=1.69, 95% CI: 1.18-2.35) w

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

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

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

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

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

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

287 61 clinical studies that directly compared ACE inhibitors versus ARBs in adult patients with essent

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

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

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

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