PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 16380005-0 2005 Valsartan reduces morbidity in people with heart failure receiving a low dose of ACE inhibitor and no beta-blocker. Valsartan 0-9 angiotensin I converting enzyme Homo sapiens 81-84 17061457-4 2006 In the Val-Heft study, valsartan on the top of standard treatment including ACE inhibitors, significantly lowered the cases of AF In hypertensive patients, ARB are more powerful than ACE inhibitors for the prevention of AF In the LIFE study, patients in the losartan arm had 33% less AF than patients from the other arm, despite treatment with atenolol and similar blood pressure reduction. Valsartan 23-32 angiotensin I converting enzyme Homo sapiens 76-79 17061457-4 2006 In the Val-Heft study, valsartan on the top of standard treatment including ACE inhibitors, significantly lowered the cases of AF In hypertensive patients, ARB are more powerful than ACE inhibitors for the prevention of AF In the LIFE study, patients in the losartan arm had 33% less AF than patients from the other arm, despite treatment with atenolol and similar blood pressure reduction. Valsartan 23-32 angiotensin I converting enzyme Homo sapiens 183-186 16129801-11 2005 CRP did not change significantly over time in the placebo group; however, after 12 months, valsartan was associated with a decrease in CRP in patients not receiving ACE inhibitors but not in those receiving ACE inhibitors at 12 months. Valsartan 91-100 angiotensin I converting enzyme Homo sapiens 165-168 16117995-12 2005 CONCLUSIONS: Addition of valsartan therapy to usual care in this model analysis resulted in net cost savings among hypothetical heart-failure patients not receiving ACE inhibitors. Valsartan 25-34 angiotensin I converting enzyme Homo sapiens 165-168 19804097-5 2005 For the treatment of congestive heart failure with left ventricular dysfunction, valsartan offers a reduction in mortality in patients not able to tolerate an ACE inhibitor and in combination with an ACE inhibitor, valsartan reduces morbidity (hospitalization for heart failure). Valsartan 215-224 angiotensin I converting enzyme Homo sapiens 200-203 15857354-6 2005 In the Val-Heft trial, valsartan reduced heart failure hospitalisations when added to conventional therapy including an ACE inhibitor in most patients, but had no effect on mortality. Valsartan 23-32 angiotensin I converting enzyme Homo sapiens 120-123 12791814-13 2003 CONCLUSION: The addition of valsartan to an ACE inhibitor improves cardiac sympathetic nerve activity, left ventricular function, and symptoms in patients with CHF. Valsartan 28-37 angiotensin I converting enzyme Homo sapiens 44-47 16259523-10 2005 The VALIANT (VALsartan In Acute myocardial iNfarction Trial) results suggest that valsartan is as effective as captopril in patients following an acute MI with HF and/or LV systolic dysfunction and may be used as an alternative treatment in ACE inhibitor-intolerant patients. Valsartan 82-91 angiotensin I converting enzyme Homo sapiens 241-244 15215801-12 2004 In patients not taking ACE inhibitors, valsartan was economically attractive, increasing survival while reducing or marginally increasing overall costs. Valsartan 39-48 angiotensin I converting enzyme Homo sapiens 23-26 15687480-7 2005 Clinical trial data support valsartan as an alternative to angiotensin-converting enzyme (ACE) inhibitors in ACE inhibitor-intolerant patients with chronic heart failure. Valsartan 28-37 angiotensin I converting enzyme Homo sapiens 109-112 15687480-8 2005 Valsartan is generally well tolerated, with renal impairment, elevated serum creatinine and potassium levels, and dizziness being the most common adverse effects; consequently, patients experiencing those adverse events while taking ACE inhibitors are likely to experience them with valsartan. Valsartan 0-9 angiotensin I converting enzyme Homo sapiens 233-236 15687480-8 2005 Valsartan is generally well tolerated, with renal impairment, elevated serum creatinine and potassium levels, and dizziness being the most common adverse effects; consequently, patients experiencing those adverse events while taking ACE inhibitors are likely to experience them with valsartan. Valsartan 283-292 angiotensin I converting enzyme Homo sapiens 233-236 15687480-12 2005 CONCLUSIONS: Valsartan is a safe and effective alternative for heart failure patients intolerant of ACE inhibitors. Valsartan 13-22 angiotensin I converting enzyme Homo sapiens 100-103 15686787-10 2005 Total MACE rates revealed significant differences in ACS due to reintervention rates of 22% and 7% under ACE-i and valsartan (p<0.0001). Valsartan 115-124 angiotensin I converting enzyme Homo sapiens 7-10 15686787-11 2005 The administration of 80 mg valsartan after bare metal stent implantation leads to a reduction of in-stent-restenosis compared to ACE-i. Valsartan 28-37 angiotensin I converting enzyme Homo sapiens 130-133 12512757-6 2002 Moreover, post-hoc analysis of the recent Valsartan Heart Failure Trial study suggests that the combination of ACE inhibitor and AR antagonist therapies may have an adverse effect in heart failure when combined with beta-blocker therapy. Valsartan 42-51 angiotensin I converting enzyme Homo sapiens 111-114 12630586-5 2003 Valsartan was recently approved to treat heart failure in patients who cannot be maintained on an ACE inhibitor. Valsartan 0-9 angiotensin I converting enzyme Homo sapiens 98-101 12729848-6 2003 In patients who cannot tolerate ACE inhibitors because of angioedema or severe cough, valsartan can be substituted. Valsartan 86-95 angiotensin I converting enzyme Homo sapiens 32-35 12918546-9 2003 However, in a post-hoc observation an adverse effect on mortality and morbidity was seen in the subgroup receiving valsartan, an ACE inhibitor and a beta-blocker, which raised concern about the potential safety of this specific combination. Valsartan 115-124 angiotensin I converting enzyme Homo sapiens 129-132 12016625-10 2002 For instance, the small subgroup of 366 patients (7%) who were not receiving ACE inhibitors had a 33% reduction in mortality and a 44% decrease in mortality and morbidity, whereas the morbidity and mortality benefit of valsartan observed in the overall trial was no longer significant in patients receiving background ACE inhibitor therapy (relative risk, 0.90; P.10). Valsartan 219-228 angiotensin I converting enzyme Homo sapiens 318-321 12392830-8 2002 RESULTS: Both all-cause mortality and combined mortality and morbidity for patients not treated with ACE inhibitors were significantly reduced in the valsartan treatment group compared with the placebo group (17.3% vs. 27.1%, p = 0.017 and 24.9% vs. 42.5%, p < 0.001, respectively). Valsartan 150-159 angiotensin I converting enzyme Homo sapiens 101-104 12392830-12 2002 Based on these results, valsartan appears to be an effective therapy in ACE inhibitor-intolerant patients. Valsartan 24-33 angiotensin I converting enzyme Homo sapiens 72-75 12417542-9 2002 Concomitant therapy with both ACE inhibitors and beta-blockers significantly reduced the effect of valsartan on BNP but not on NE (P for interaction=0.0223 and 0.2289, respectively). Valsartan 99-108 angiotensin I converting enzyme Homo sapiens 30-33 12016625-11 2002 The larger subgroup of patients receiving both an ACE inhibitor and a beta-blocker at baseline had a statistically significant 42% increase in mortality with valsartan (P.009) and a trend toward an increase in the mortality and morbidity composite (P.10). Valsartan 158-167 angiotensin I converting enzyme Homo sapiens 50-53 12016625-14 2002 Somewhat troublesome is the finding of significant increase in mortality with valsartan in patients receiving both ACE inhibitor and beta-blocker therapy. Valsartan 78-87 angiotensin I converting enzyme Homo sapiens 115-118 14727972-1 2002 Valsartan, an orally active nonpeptide angiotensin II (AII) receptor antagonist with selectivity for the AII type I (AT(1)) receptor subtype, has recently been approved by the US Food and Drug Administration for the treatment of patients with heart failure (New York Health Association class II-IV) who are intolerant of ACE-inhibitor therapy. Valsartan 0-9 angiotensin I converting enzyme Homo sapiens 321-324 11835907-6 2002 The Valsartan in Heart Failure Trial (Val-HeFT) showed that the combination of an ACE inhibitor and an ARB reduced hospitalization for heart failure in patients with congestive heart failure by 27.5%, although no decrease in all-cause mortality was observed. Valsartan 4-13 angiotensin I converting enzyme Homo sapiens 82-85 14727972-5 2002 Among patients not receiving an ACE inhibitor, irrespective of concomitant beta-blocker use, valsartan reduced the risk of mortality and the combined endpoint by 33.1% and 44% compared with placebo; total hospitalizations for heart failure were also significantly lower in the valsartan group (27.6 vs 64.6%). Valsartan 93-102 angiotensin I converting enzyme Homo sapiens 32-35 14727972-6 2002 In the subgroup of patients who were taking an ACE inhibitor and a beta-blocker at baseline (n = 1610), mortality was significantly higher in the valsartan group than in the placebo group. Valsartan 146-155 angiotensin I converting enzyme Homo sapiens 47-50 12093312-9 2002 Recent evidence has indicated that the Ang II type 1 receptor antagonist valsartan is of value when used in patients already receiving either an ACE inhibitor or a beta-blocker, but has also suggested that giving all three drugs together is deleterious. Valsartan 73-82 angiotensin I converting enzyme Homo sapiens 145-148 9767420-2 1998 The results reported in the present study show that modulators of the renin-angiotensin system, such as the angiotensin-converting enzyme (ACE)-inhibitor captopril and the angiotensin II receptor type I antagonist valsartan, have potent inhibitory effects on the lipopolysaccharide (LPS)-stimulated production of pro-inflammatory cytokines tumour necrosis factor (TNF) and interleukin-1 (IL-1) in vitro. Valsartan 214-223 angiotensin I converting enzyme Homo sapiens 108-137 11899501-6 2002 Valsartan had highly favourable effects in patients not receiving ACE inhibitors but an adverse effect in patients receiving both ACE inhibitors and beta-blockers. Valsartan 0-9 angiotensin I converting enzyme Homo sapiens 66-69 11899501-6 2002 Valsartan had highly favourable effects in patients not receiving ACE inhibitors but an adverse effect in patients receiving both ACE inhibitors and beta-blockers. Valsartan 0-9 angiotensin I converting enzyme Homo sapiens 130-133 11759645-8 2001 In a post hoc analysis of the combined end point and mortality in subgroups defined according to base-line treatment with angiotensin-converting-enzyme (ACE) inhibitors or beta-blockers, valsartan had a favorable effect in patients receiving neither or one of these types of drugs but an adverse effect in patients receiving both types of drugs. Valsartan 187-196 angiotensin I converting enzyme Homo sapiens 122-151 11759645-8 2001 In a post hoc analysis of the combined end point and mortality in subgroups defined according to base-line treatment with angiotensin-converting-enzyme (ACE) inhibitors or beta-blockers, valsartan had a favorable effect in patients receiving neither or one of these types of drugs but an adverse effect in patients receiving both types of drugs. Valsartan 187-196 angiotensin I converting enzyme Homo sapiens 153-156 11676153-4 2001 Val-HeFT showed additive benefits of valsartan on standard treatment with ACE inhibitors, diuretics and digitalis in patients with heart failure. Valsartan 37-46 angiotensin I converting enzyme Homo sapiens 74-77 10618583-10 2000 Results from a pilot study suggest that the combination of an ACE inhibitor and valsartan results in a more thorough inhibition of Ang II and an additive improvement in cardiac hemodynamics. Valsartan 80-89 angiotensin I converting enzyme Homo sapiens 62-65 10618584-10 2000 The VALIANT (Valsartan in Acute Myocardial Infarction) trial is testing the hypothesis that interruption of the renin-angiotensin pathway by using the ARB valsartan alone or in combination with an ACE inhibitor will be more effective in saving lives than an ACE inhibitor alone in treating patients at high risk. Valsartan 13-22 angiotensin I converting enzyme Homo sapiens 197-200 9740480-0 1998 Valsartan in heart failure patients previously untreated with an ACE inhibitor. Valsartan 0-9 angiotensin I converting enzyme Homo sapiens 65-68 9740480-1 1998 OBJECTIVE: To evaluate the effect on cardiac hemodynamic parameters of valsartan in patients with chronic stable congestive heart failure previously untreated with ACE inhibitors. Valsartan 71-80 angiotensin I converting enzyme Homo sapiens 164-167 9740480-7 1998 CONCLUSIONS: Valsartan has beneficial effects on cardiac hemodynamics, and is generally well tolerated in patients with congestive heart failure not taking ACE inhibitors. Valsartan 13-22 angiotensin I converting enzyme Homo sapiens 156-159 9767420-2 1998 The results reported in the present study show that modulators of the renin-angiotensin system, such as the angiotensin-converting enzyme (ACE)-inhibitor captopril and the angiotensin II receptor type I antagonist valsartan, have potent inhibitory effects on the lipopolysaccharide (LPS)-stimulated production of pro-inflammatory cytokines tumour necrosis factor (TNF) and interleukin-1 (IL-1) in vitro. Valsartan 214-223 angiotensin I converting enzyme Homo sapiens 139-142 32741197-5 2021 Conclusions: Sacubitril/valsartan should be considered for hemodynamically stable patients with HFrEF (New York Heart Association class II or III), potassium <5.2 mmol/L, without a history of angioedema, and after a 36-hour washout from angiotensin-converting enzyme (ACE) inhibitor or aliskiren, if applicable. Valsartan 24-33 angiotensin I converting enzyme Homo sapiens 237-266 9257084-9 1997 Thus, valsartan is an effective treatment for mild to moderate essential hypertension and may be particularly useful in patients who experience persistent cough during ACE inhibitor therapy. Valsartan 6-15 angiotensin I converting enzyme Homo sapiens 168-171 33847047-2 2021 We hypothesized that sacubitril/valsartan, effective in the treatment of chronic HF, prevents development of HF and reduces cardiovascular death following high-risk AMI compared to a proven ACE inhibitor. Valsartan 32-41 angiotensin I converting enzyme Homo sapiens 190-193 32741197-5 2021 Conclusions: Sacubitril/valsartan should be considered for hemodynamically stable patients with HFrEF (New York Heart Association class II or III), potassium <5.2 mmol/L, without a history of angioedema, and after a 36-hour washout from angiotensin-converting enzyme (ACE) inhibitor or aliskiren, if applicable. Valsartan 24-33 angiotensin I converting enzyme Homo sapiens 268-271 33522140-4 2021 METHODS AND RESULTS: This was a retrospective case-series of PAP changes following transition from angiotensin-converting enzyme inhibitor (ACEI) or angiotensin receptor blocker (ARB) to sacubitril/valsartan in patients with heart failure reduced ejection fraction and a previously implanted CardioMEMS sensor. Valsartan 198-207 angiotensin I converting enzyme Homo sapiens 99-128 32303468-12 2020 CONCLUSIONS: Our analysis supports switching HFREF patients on ACE inhibitor or ARB to sacubitril/valsartan. Valsartan 98-107 angiotensin I converting enzyme Homo sapiens 63-66 32327307-1 2020 BACKGROUND: Sacubitril/valsartan was shown to be superior to enalapril in the Prospective Comparison of angiotensin receptor neprilysin inhibitor with an angiotensin converting enzyme inhibitor to Determine Impact on Global Mortality and Morbidity in Heart Failure (PARADIGM-HF) study. Valsartan 23-32 angiotensin I converting enzyme Homo sapiens 154-183 33004114-1 2020 Sacubitril/valsartan, an angiotensin receptor-neprilysin inhibitor (ARNI), has been shown to reduce the risk of cardiovascular death or heart failure hospitalization and improve symptoms among patients with chronic heart failure with reduced ejection fraction compared to enalapril, the gold standard angiotensin-converting enzyme inhibitor. Valsartan 11-20 angiotensin I converting enzyme Homo sapiens 301-330 30441998-4 2018 The new dual inhibitor sacubitril/valsartan should be considered as more effective substitute of ACE inhibitors/sartans in all stabilised patients. Valsartan 34-43 angiotensin I converting enzyme Homo sapiens 97-100 31521679-2 2019 BACKGROUND: Although therapy with sacubitril/valsartan, a neprilysin inhibitor, improved patients" health status (compared with enalapril) at 8 months in the PARADIGM-HF (Prospective Comparison of ARNI with ACE inhibitor to Determine Impact on Global Mortality and Morbidity in Heart Failure) study, the early impact of ARNI on patients" symptoms, functions, and quality of life is unknown. Valsartan 45-54 angiotensin I converting enzyme Homo sapiens 207-210 32546023-2 2020 Newer medications targeting combining an ARB with a neprilysin inhibitor (ARNI) sacubitril/valsartan have shown benefits in mortality and can be used in place of an ACE inhibitor or an ARB. Valsartan 91-100 angiotensin I converting enzyme Homo sapiens 165-168 31240976-1 2019 Background The angiotensin-receptor neprilysin inhibitor (ARNI) sacubitril/valsartan was shown to be superior to the angiotensin-converting enzyme inhibitor enalapril in terms of reducing cardiovascular mortality in the PARADIGM-HF (Prospective Comparison of ARNI with angiotensin-converting enzyme inhibitor to Determine Impact on Global Mortality and Morbidity in Heart Failure) study. Valsartan 75-84 angiotensin I converting enzyme Homo sapiens 269-298 28720639-6 2017 As recommended by the guidelines, avoiding sacubitril/valsartan use concurrently or within 36 hours of the last dose of an ACE inhibitor or in patients with a history of angioedema is also crucial to minimize angioedema risk and prevent patient harm. Valsartan 54-63 angiotensin I converting enzyme Homo sapiens 123-126 29369824-2 2018 Sacubitril/valsartan (LCZ696) is a novel complex that combines simultaneous neprilysin inhibition and angiotensin II receptor blockade, that has demonstrated significant cardiovascular death or HF hospitalization reduction in the Prospective Comparison of Angiotensin Receptor/Neprilysin Inhibitor (ARNI) With Angiotensin-Converting Enzyme (ACE) Inhibitors to Determine Impact on Global Mortality and Morbidity in Heart Failure (PARADIGM-HF) trial when compared with evidence-based doses of the gold standard ACE inhibitor enalapril. Valsartan 11-20 angiotensin I converting enzyme Homo sapiens 310-339 29369824-2 2018 Sacubitril/valsartan (LCZ696) is a novel complex that combines simultaneous neprilysin inhibition and angiotensin II receptor blockade, that has demonstrated significant cardiovascular death or HF hospitalization reduction in the Prospective Comparison of Angiotensin Receptor/Neprilysin Inhibitor (ARNI) With Angiotensin-Converting Enzyme (ACE) Inhibitors to Determine Impact on Global Mortality and Morbidity in Heart Failure (PARADIGM-HF) trial when compared with evidence-based doses of the gold standard ACE inhibitor enalapril. Valsartan 11-20 angiotensin I converting enzyme Homo sapiens 341-344 29369824-2 2018 Sacubitril/valsartan (LCZ696) is a novel complex that combines simultaneous neprilysin inhibition and angiotensin II receptor blockade, that has demonstrated significant cardiovascular death or HF hospitalization reduction in the Prospective Comparison of Angiotensin Receptor/Neprilysin Inhibitor (ARNI) With Angiotensin-Converting Enzyme (ACE) Inhibitors to Determine Impact on Global Mortality and Morbidity in Heart Failure (PARADIGM-HF) trial when compared with evidence-based doses of the gold standard ACE inhibitor enalapril. Valsartan 11-20 angiotensin I converting enzyme Homo sapiens 509-512 27924184-8 2016 The reported adverse events among patients newly treated with an ACE inhibitor peaked in 2007 to 10 cases per 1000 patients, and gradually decreased to 4.6 cases in 2012, which was the year after the PA requirements for the ARBs valsartan and candesartan were rescinded by the HMO. Valsartan 229-238 angiotensin I converting enzyme Homo sapiens 65-68 28176581-2 2017 On page 55, the first sentence in the angiotensin receptor neprilysin inhibitor section should read: Valsartan with sacubitril is an angiotensin receptor neprilysin inhibitor that has recently been approved for use as a replacement for ACE inhibitors, to further reduce the risk of hospitalisation and death in ambulatory patients with heart failure and an ejection fraction <=35% who remain symptomatic despite optimal treatment with an ACE inhibitor, a beta-blocker and an aldersterone antagonist (Ponikowski et al 2016). Valsartan 101-110 angiotensin I converting enzyme Homo sapiens 236-239 28176581-2 2017 On page 55, the first sentence in the angiotensin receptor neprilysin inhibitor section should read: Valsartan with sacubitril is an angiotensin receptor neprilysin inhibitor that has recently been approved for use as a replacement for ACE inhibitors, to further reduce the risk of hospitalisation and death in ambulatory patients with heart failure and an ejection fraction <=35% who remain symptomatic despite optimal treatment with an ACE inhibitor, a beta-blocker and an aldersterone antagonist (Ponikowski et al 2016). Valsartan 101-110 angiotensin I converting enzyme Homo sapiens 441-444 28905031-5 2016 Use an angiotensin II receptor blocker (ARB) (candesartan or valsartan) if intolerant to ACE inhibitors because of cough or angioneurotic edema. Valsartan 61-70 angiotensin I converting enzyme Homo sapiens 89-92 27638852-0 2016 The association of ACE gene polymorphism with diabetic kidney disease and renoprotective efficacy of valsartan. Valsartan 101-110 angiotensin I converting enzyme Homo sapiens 19-22 27638852-1 2016 INTRODUCTION: To investigate the associations between the insertion/deletion (I/D) polymorphisms in the angiotensin converting enzyme (ACE) gene and susceptibility to diabetic kidney disease (DKD); and the efficacy of valsartan in reducing the urine protein in Type 2 diabetes mellitus (T2DM) patients. Valsartan 218-227 angiotensin I converting enzyme Homo sapiens 104-133 27638852-1 2016 INTRODUCTION: To investigate the associations between the insertion/deletion (I/D) polymorphisms in the angiotensin converting enzyme (ACE) gene and susceptibility to diabetic kidney disease (DKD); and the efficacy of valsartan in reducing the urine protein in Type 2 diabetes mellitus (T2DM) patients. Valsartan 218-227 angiotensin I converting enzyme Homo sapiens 135-138 27638852-11 2016 Furthermore, the ACE I/D polymorphism influenced the renoprotective response to valsartan: Patients with the DD genotype benefitted the most from this treatment. Valsartan 80-89 angiotensin I converting enzyme Homo sapiens 17-20 26873036-4 2016 PARADIGM-HF trial has proved the superiority of sacubitril/valsartan (LCZ696) over ACE inhibitor enalapril to reduce mortality and morbidity of symptomatic HF patients with reduced ejection fraction (HFrEF), setting the grounds for the replacement of ACE inhibitors by sacubitril/valsartan in the management of HFrEF. Valsartan 59-68 angiotensin I converting enzyme Homo sapiens 251-254 21303424-7 2011 RESULTS: Valsartan treatment caused a significant reduction in proteinuria from baseline throughout the study in patients with each genotype of the ACE, AGT and TGFB1 genes. Valsartan 9-18 angiotensin I converting enzyme Homo sapiens 148-151 26873495-2 2016 In the large, randomized, double-blind, PARADIGM-HF trial, sacubitril/valsartan reduced the incidence of death from cardiovascular causes or first hospitalization for worsening heart failure (composite primary endpoint) significantly more than the angiotensin converting enzyme (ACE) inhibitor enalapril. Valsartan 70-79 angiotensin I converting enzyme Homo sapiens 279-282 26642078-1 2016 The PARADIGM-HF study, a large outcome trial in heart failure and reduced ejection fraction (HFrEF), has recently shown improved cardiovascular outcomes with sacubitril/valsartan (Entresto , Novartis), still commonly referred to as LCZ696, compared to ACE-inhibitor therapy, possibly leading us to a new era for heart failure (HF) treatment. Valsartan 169-178 angiotensin I converting enzyme Homo sapiens 252-255 21142805-7 2011 Cough, a common class effect of ACE inhibitors, occurs less frequently with valsartan. Valsartan 76-85 angiotensin I converting enzyme Homo sapiens 32-35 19192258-1 2009 OBJECTIVES: The overall objective of this study was to estimate the costs and outcomes associated with treatment with valsartan for post-myocardial infarction (post-MI) patients with left ventricular systolic dysfunction, heart failure, or both, who are not suitable for treatment with angiotensin-converting enzyme (ACE) inhibitors, compared to placebo. Valsartan 118-127 angiotensin I converting enzyme Homo sapiens 286-315 19192258-1 2009 OBJECTIVES: The overall objective of this study was to estimate the costs and outcomes associated with treatment with valsartan for post-myocardial infarction (post-MI) patients with left ventricular systolic dysfunction, heart failure, or both, who are not suitable for treatment with angiotensin-converting enzyme (ACE) inhibitors, compared to placebo. Valsartan 118-127 angiotensin I converting enzyme Homo sapiens 317-320 19192258-10 2009 CONCLUSIONS: For patients who are not suitable for treatment with ACE inhibitors, valsartan is a viable and cost-effective treatment for their management after an MI. Valsartan 82-91 angiotensin I converting enzyme Homo sapiens 66-69 19205092-0 2008 Combination of amlodipine 10 mg and valsartan 160 mg lowers blood pressure in patients with hypertension not controlled by an ACE inhibitor/CCB combination. Valsartan 36-45 angiotensin I converting enzyme Homo sapiens 126-129 19929036-13 2009 In subgroup analyses, valsartan lost dominance in patients in NYHA II, and in those receiving beta-adrenoceptor antagonists or ACE inhibitors; the mean incremental cost-utility ratio for these groups was 21 240, 129 200, and 36 500 and U20AC;/QALY, respectively. Valsartan 22-31 angiotensin I converting enzyme Homo sapiens 127-130 19929036-15 2009 There are relevant differences among various patient subgroups, and valsartan is expected to be good value for money particularly in the treatment of the most severe and less intensively treated (no ACE inhibitors, no beta-adrenoceptor antagonist) heart failure patients. Valsartan 68-77 angiotensin I converting enzyme Homo sapiens 199-202 19911855-8 2009 The magnitude of these effects is comparable with that demonstrated with angiotensin-converting enzyme (ACE) inhibitors; however, valsartan has a more favourable tolerability profile, with a significantly lower incidence of cough and only rare reports of angio-oedema, both class effects of ACE inhibitor use. Valsartan 130-139 angiotensin I converting enzyme Homo sapiens 104-107 19911855-8 2009 The magnitude of these effects is comparable with that demonstrated with angiotensin-converting enzyme (ACE) inhibitors; however, valsartan has a more favourable tolerability profile, with a significantly lower incidence of cough and only rare reports of angio-oedema, both class effects of ACE inhibitor use. Valsartan 130-139 angiotensin I converting enzyme Homo sapiens 291-294