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1 bitor, and a component of LCZ696 (sacubitril/valsartan).
2 hese genes was preserved by naloxone but not valsartan.
3 ting the angiotensin II type I receptor with valsartan.
4 ion, a failure prevented by naloxone but not valsartan.
5 ied changes in CRP that were associated with valsartan.
6 r heart failure was significantly lower with valsartan.
7 s a BP-independent antiproteinuric effect of valsartan.
8 as no longer different from that noted after valsartan.
9 s before and after administration of the ARB valsartan.
10 sponse to Ang I was blunted significantly by valsartan.
11 reatment with enalapril than with sacubitril/valsartan.
12 weeks (14% reduction; P=0.03) compared with valsartan.
13 kers of heart failure severity compared with valsartan.
14 d AT1 Ang II receptor blockade (benazeprilat/valsartan, 0.05/3 mg x kg(-1) d(-1)) and rapid pacing (n
15 d AT1 Ang II receptor blockade (benazeprilat/valsartan, 0.05/3 mg x kg(-1) x d(-1)) and rapid pacing
17 ments (systolic/diastolic 11.2/6.6 mm Hg for valsartan, 11.6/6.5 mm Hg for amlodipine) and at no time
18 s 29% lower in patients receiving sacubitril/valsartan (114 [7%] patients) compared with patients rec
19 were randomly assigned to LCZ696 and 152 to valsartan; 134 in the LCZ696 group and 132 in the valsar
20 (455), a combination of aliskiren 150 mg and valsartan 160 mg (446), or placebo (459) for 4 weeks, fo
21 receive once-daily aliskiren 150 mg (n=437), valsartan 160 mg (455), a combination of aliskiren 150 m
22 le-blind treatment with valsartan 80 mg BID, valsartan 160 mg BID, or placebo while receiving their u
25 Compared with placebo, the first dose of valsartan 160 mg resulted in a significantly greater red
26 led trial of angiotensin II receptor blocker valsartan 160 mg twice daily compared with placebo in pa
27 odialysis to placebo, ramipril (5 mg/d), and valsartan (160 mg/d) for 7 days, with a washout period o
28 6 patients were randomly assigned to receive valsartan; 198 were randomly assigned to receive placebo
29 ted with adverse effects similar to those of valsartan; 22 patients (15%) on LCZ696 and 30 (20%) on v
31 mly assigned to enalapril than to sacubitril/valsartan (3.1 vs 2.2 per 100 patient-years; HR, 1.37 [9
32 han to those randomly assigned to sacubitril/valsartan (3.3 vs 2.3 per 100 patient-years; HR, 1.43 [9
33 ing (n=9), (3) AT1 Ang II receptor blockade (valsartan, 3 mg x kg(-1) x d(-1)) and rapid pacing (n=9)
34 9), (2) concomitant AT(1) receptor blockade (valsartan, 3 mg/kg per day) and rapid pacing (n=8), (3)
35 3) concomitant AT1 Ang II receptor blockade (valsartan, 3 mg/kg/d) and rapid pacing (n=9), (4) concom
37 int, the combination of aliskiren 300 mg and valsartan 320 mg lowered mean sitting diastolic blood pr
38 iskiren 300 mg 9.0 mm Hg decrease, p<0.0001; valsartan 320 mg, 9.7 mm Hg decrease, p<0.0001), or with
39 1.2 mm Hg, 95% CI -2.3 to -0.1; p=0.030) and valsartan 320 mg/day (-4.4 mm Hg, -5.4 to -3.3; p<0.0001
40 rdial infarction, to additional therapy with valsartan (4909 patients), valsartan plus captopril (488
41 eated animals with animals treated with oral valsartan (50 mg/kg/d), oral enalapril (10 mg/kg/d), and
42 f therapy, plasma aldosterone was reduced by valsartan 80 mg BID (-52.1 pg/mL; P=0.001) and 160 mg BI
43 omly assigned to double-blind treatment with valsartan 80 mg BID, valsartan 160 mg BID, or placebo wh
45 an 160 mg PO BID, captopril 50 mg PO TID, or valsartan 80 mg PO BID plus captopril 50 mg PO TID betwe
47 th enalapril 10 mg twice daily or sacubitril/valsartan 97/103 mg twice daily (previously known as LCZ
48 (LVEF) </=40%] were randomized to sacubitril/valsartan 97/103 mg twice daily versus enalapril 10 mg t
57 f blood pressure were complete, created 5006 valsartan-amlodipine patient pairs matched exactly for s
58 lity and morbidity in the subgroup receiving valsartan, an ACE inhibitor, and a beta-blocker raises c
59 56% (95% CI, 49.6 to 63.0) of baseline with valsartan and 92% (95% CI, 81.7 to 103.7) of baseline wi
60 or the syntheses of industrial precursors to valsartan and boscalid from chloroarenes with approximat
64 nd/or beta-blocker (BB) were randomized into valsartan and placebo groups and followed for a mean of
68 Small but significant differences between valsartan and placebo were present for change in right v
69 ents on background therapy and randomized to valsartan and placebo, serial recordings of left ventric
73 tensin type 1 receptor blockers losartan and valsartan and the angiotensin-converting enzyme inhibito
74 rtan+LBQ augmented the inhibitory effects of valsartan and the highest doses completely abrogated ang
75 o) combines the angiotensin receptor blocker valsartan and the neprilysin inhibitor prodrug sacubitri
80 artan group died, as did 941 patients in the valsartan-and-captopril group and 958 patients in the ca
81 l, 0.90 to 1.11; P=0.98; hazard ratio in the valsartan-and-captopril group as compared with the capto
85 s effect was proposed after results from the Valsartan Antihypertensive Long-Term Use Evaluation (VAL
86 valuation (VALUE) trial, in which the use of valsartan (ARB) was compared with amlodipine in patients
89 and during follow-up in patients assigned to valsartan at a target dose of 160 mg twice daily or plac
91 CI 670-914], 12 weeks, 605 pg/mL [512-714]; valsartan: baseline, 862 pg/mL [733-1012], 12 weeks, 835
93 ibitory effects of the clinical AT1R blocker valsartan can be identified, whereas blockage of upstrea
95 r mediated, because AT1 receptor antagonists valsartan, candesartan, and losartan inhibited Ang II-in
97 randomly assigned to receive treatment with valsartan, captopril, or the combination; follow-up cont
98 trated consistent improvements in sacubitril/valsartan compared with enalapril through 36 months.
100 u by one year, and persisted to two years in valsartan compared with placebo patients, irrespective o
101 e better in patients treated with sacubitril/valsartan compared with those treated with enalapril, wi
103 e maximum recommended doses of aliskiren and valsartan, compared with each drug alone in patients wit
105 designed to test the hypothesis that the ARB valsartan, either alone or in combination with captopril
106 s, a high potassium intake or treatment with valsartan enhanced AA-induced inhibition of ENaC, an eff
107 of double-blind treatment with nebivolol and valsartan fixed-dose combination (5 and 80 mg/day, 5 and
111 ite endpoint occurred in 810 patients in the valsartan group (10.6%, 25.5 per 1000 patient-years) and
112 group and 0.26% (SD 1.25) in the sacubitril/valsartan group (between-group reduction 0.13%, 95% CI 0
113 weeks in the LCZ696 group compared with the valsartan group (LCZ696: baseline, 783 pg/mL [95% CI 670
115 d by 0.60 (SD 1.4) cm/s from baseline in the valsartan group (p<0.0001) and 0.44 (1.4) cm/s from base
117 ssure 4.0/2.1 mm Hg lower in amlodipine than valsartan group after 1 month; 1.5/1.3 mm Hg after 1 yea
118 .9) mm Hg reduction in blood pressure in the valsartan group and a 9.7 (17.0)/5.5 (10.2) mm Hg reduct
119 in the captopril group (hazard ratio in the valsartan group as compared with the captopril group, 1.
120 ollow-up of 24.7 months, 979 patients in the valsartan group died, as did 941 patients in the valsart
121 esults of Base-Case Analysis: The sacubitril-valsartan group experienced 0.08 fewer heart failure hos
123 ns were persistently lower in the sacubitril/valsartan group than in the enalapril group over the 3-y
124 rtan; 134 in the LCZ696 group and 132 in the valsartan group were included in analysis of the primary
125 onfidence interval for the comparison of the valsartan group with the captopril group was within the
126 the valsartan group, and 37 in the aliskiren/valsartan group), mainly due to lack of therapeutic effe
128 group, 53 in the aliskiren group, 43 in the valsartan group, and 37 in the aliskiren/valsartan group
129 gator reported events 798), 587 (796) in the valsartan group, and 554 (756) in the combination group;
130 nd renal dysfunction were more common in the valsartan group, and cough, rash, and taste disturbance
135 ng-enzyme (ACE) inhibitors or beta-blockers, valsartan had a favorable effect in patients receiving n
136 olled in PARADIGM-HF who received sacubitril/valsartan had a greater long-term reduction in HbA1c tha
137 treated with a beta-blocker or randomized to valsartan had greater odds of being in the HFiEF group,
140 independent randomized clinical trials, the Valsartan Heart Failure Trial (Val-HeFT) (n=4053) and th
145 e of CRP in patients randomized in Val-HeFT (Valsartan Heart Failure Trial) and studied changes in CR
150 ocardial infarction who were enrolled in the Valsartan in Acute Myocardial Infarction (VALIANT) echoc
151 4,703 patients with acute MI enrolled in the VALsartan In Acute myocardial iNfarcTion (VALIANT) trial
152 entation for 1067 patients who had SD in the Valsartan in Acute Myocardial Infarction Trial (VALIANT)
153 as sudden death events in patients from the VALsartan In Acute myocardial infarctioN Trial (VALIANT)
154 events in 14,703 patients randomized in the Valsartan in Acute Myocardial Infarction Trial (VALIANT)
157 0 African-American patients) in the VALIANT (VALsartan In Acute myocardial iNfarcTion) trial were com
166 ration of the Ang II type 1 receptor blocker valsartan inhibited Ang II-induced ABCA1 mRNA repression
172 ure (PARADIGM-HF) trial, in which sacubitril/valsartan (LCZ696) reduced both death and HF hospitaliza
173 sin receptor neprilysin inhibitor sacubitril/valsartan (LCZ696) reduced cardiovascular morbidity and
174 ht to determine if treatment with sacubitril/valsartan (LCZ696) reduces rates of hospital readmission
175 These findings demonstrate that sacubitril/valsartan leads to better HRQL in surviving patients wit
176 ined BP and the same degree of BP reduction, valsartan lowered UAER more effectively than amlodipine
185 There was no significant treatment effect of valsartan on right ventricular ejection fraction, exerci
186 ned to evaluate the BP-independent effect of valsartan on UAER in type 2 diabetic patients with micro
189 achieved blood pressures, regimens based on valsartan or amlodipine would have differing effects on
196 2 months between groups randomly assigned to valsartan or placebo depended on baseline ACE inhibitor
199 improved with either ANG II receptor blocker valsartan or superoxide dismutase/catalase mimetic tempo
201 Treatment with the ACE inhibitor captopril, valsartan, or the combination of captopril plus valsarta
205 onal therapy with valsartan (4909 patients), valsartan plus captopril (4885 patients), or captopril (
210 and Morbidity in Heart Failure), sacubitril/valsartan reduced morbidity and mortality compared with
211 fraction, whether treatment with sacubitril/valsartan reduced NT-proBNP below specific partition val
213 ril did not reduce focal tracer uptake, oral valsartan resulted in partial blockade (infarct-to-remot
214 sartan, or the combination of captopril plus valsartan resulted in similar changes in cardiac volume,
215 of drugs for the treatment of heart failure: Valsartan/sacubitril (formerly known as LCZ696 and curre
216 g clinical trials are evaluating the role of valsartan/sacubitril in the treatment of heart failure w
217 bidity in Heart Failure (PARADIGM-HF) trial, valsartan/sacubitril significantly reduced mortality and
218 identify a PKG-dependent mechanism by which valsartan/sacubitril, a combination drug recently approv
219 We review here the mechanisms of action of valsartan/sacubitril, the pharmacological properties of
221 hat preventive treatment of Tg2576 mice with valsartan significantly reduced AD-type neuropathology a
225 ase were quartile-dependent and greater with valsartan than placebo at virtually all time points.
226 point, however, was 13.2 percent lower with valsartan than with placebo (relative risk, 0.87; 97.5 p
227 e effect of the angiotensin-receptor blocker valsartan, the ACE inhibitor captopril, and the combinat
228 There was no significant effect of 3-year valsartan therapy on systemic right ventricular ejection
230 ith moderate heart failure demonstrated that valsartan therapy taken with either ACEI or BB reversed
231 en improvements in mortality with sacubitril/valsartan, this analysis provides comprehensive assessme
232 to LCZ696 titrated to 200 mg twice daily or valsartan titrated to 160 mg twice daily, and treated fo
233 eive either the angiotensin receptor blocker valsartan (titrated to 320 mg once daily) or matched pla
234 stration of the angiotensin receptor blocker valsartan to intact mice results in a significant reduct
237 Results of Sensitivity Analysis: Sacubitril-valsartan treatment was most sensitive to the duration o
238 ental costs and QALYs gained with sacubitril/valsartan treatment were estimated at $35512 and 0.78, r
243 valuate the cost-effectiveness of sacubitril-valsartan versus angiotensin-converting enzyme inhibitor
244 oup, and 554 (756) in the combination group; valsartan versus captopril, p = 0.651 (0.965); combinati
246 imed to investigate the effect of sacubitril/valsartan versus enalapril on HbA1c and time to first-ti
247 rdiovascular risk factors were randomized to valsartan versus placebo and nateglinide versus placebo
250 e pressor response to Ang I before and after valsartan was also reevaluated in 11 patients after the
251 the placebo group; however, after 12 months, valsartan was associated with a decrease in CRP in patie
252 sin receptor neprilysin inhibitor sacubitril/valsartan was associated with a reduction in cardiovascu
257 sin receptor neprilysin inhibitor sacubitril/valsartan was more effective than the angiotensin-conver
260 we found that only 1 of the candidate drugs, valsartan, was capable of attenuating oligomerization of
263 the Markov model calculated that sacubitril/valsartan would increase life expectancy at an ICER cons
264 is that for the same blood-pressure control, valsartan would reduce cardiac morbidity and mortality m
265 Sensitivity analyses demonstrated sacubitril/valsartan would remain cost-effective vs enalapril.
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