scholarly journals Maximally Recommended Doses of Angiotensin-Converting Enzyme (ACE) Inhibitors Do Not Completely Prevent ACE-Mediated Formation of Angiotensin II in Chronic Heart Failure

Circulation ◽  
2000 ◽  
Vol 101 (8) ◽  
pp. 844-846 ◽  
Author(s):  
Ulrich P. Jorde ◽  
Pierre V. Ennezat ◽  
Jay Lisker ◽  
Vanarani Suryadevara ◽  
Jason Infeld ◽  
...  
Keyword(s):  
Heart Failure ◽  
Angiotensin Ii ◽  
Chronic Heart Failure ◽  
Angiotensin Converting Enzyme ◽  
Ace Inhibitors ◽  
Converting Enzyme

Valsartan in Chronic Heart Failure

2005 ◽  
Vol 39 (3) ◽  
pp. 460-469 ◽  
Author(s):  
Toni L Ripley
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Angiotensin Converting Enzyme ◽  
Ace Inhibitors ◽  
Angiotensin Receptor Blockers ◽  
Elevated Serum ◽  
Receptor Subtype ◽  
Converting Enzyme ◽  
Angiotensin Receptor ◽  
Data Support

OBJECTIVE: To evaluate the evidence for valsartan in the treatment of heart failure and determine its need for formulary inclusion. DATA SOURCES: OVID and PubMed databases were searched (1983–June 2004) using the key words angiotensin-receptor blocker, heart failure, valsartan, Diovan, and angiotensin-converting enzyme inhibitor. Only English-language literature was selected. STUDY SELECTION AND DATA EXTRACTION: Pharmacology and pharmacokinetic evaluations for valsartan were selected. Prospective, randomized clinical trials investigating the use of valsartan and other angiotensin-receptor blockers (ARBs) in chronic heart failure were evaluated. DATA SYNTHESIS: Valsartan, a selective antagonist for angiotensin receptor subtype 1, is the first ARB to be approved for use in chronic heart failure. Clinical trial data support valsartan as an alternative to angiotensin-converting enzyme (ACE) inhibitors in ACE inhibitor—intolerant patients with chronic heart failure. 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. Although further study is needed, differences in effectiveness among races may exist with use of valsartan; however, at this time, valsartan is recommended as an alternative to ACE inhibitors regardless of race. Candesartan and losartan have been studied in similar settings. Candesartan's data support its use in heart failure; however, losartan's data have been less consistent. CONCLUSIONS: Valsartan is a safe and effective alternative for heart failure patients intolerant of ACE inhibitors. Valsartan has not been shown to be safe and effective when used in combination with ACE inhibitors.

Use of Angiotensin-Converting Enzyme Inhibitors in Heart Failure

1994 ◽  
Vol 10 (4) ◽  
pp. 156-163 ◽  
Author(s):  
Bisrat Hailemeskel ◽  
Vlncent F. Mauro
Keyword(s):  
Heart Failure ◽  
Angiotensin Ii ◽  
Ejection Fraction ◽  
Angiotensin Converting Enzyme ◽  
Ace Inhibitors ◽  
Current Data ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibitors ◽  
Reduced Ejection Fraction ◽  
English Language Journal

Objective: To review the literature discussing the use of angiotensin-converting enzyme (ACE) inhibitors in the treatment of heart failure. Data Sources: English-language journal articles. Study Selection: Representative articles discussing the effects of ACE inhibitors on hemodynamics, symptoms, and survival. Data Extraction: Studies selected for review in the text were based on study design and clinical endpoints. Data Synthesis: Heart failure results in a series of compensatory responses that, although effective acutely, are ultimately maladaptive. A major mediator in this process is angiotensin II. The production of angiotensin II is dependent on the ACE. Inhibition of this enzyme by ACE inhibitors results in fewer symptoms, improved hemodynamic function, and prolonged survival in patients with heart failure. Conclusions: ACE inhibitors are beneficial in improving the survival of patients with symptomatic heart failure and of patients who have recently had an acute myocardial infarction (MI) and subsequently have a reduced ejection fraction. There appears to be no advantage for immediately initiating ACE-inhibitor therapy within the first few hours of an MI episode. With respect to patients with a reduced ejection fraction without symptoms of heart failure, current data suggest that ACE inhibitors delay the onset of symptoms of heart failure, reduce the need for hospitalization, and may possibly improve survival.

Angiotensin-converting enzyme inhibition restores the diffusing capacity for carbon monoxide in patients with chronic heart failure by improving the molecular diffusion across the alveolar capillary membrane

1999 ◽  
Vol 96 (1) ◽  
pp. 17-22 ◽  
Author(s):  
Marco GUAZZI ◽  
Piergiuseppe AGOSTONI
Keyword(s):  
Heart Failure ◽  
Chronic Heart Failure ◽  
Angiotensin Converting Enzyme ◽  
Enzyme Inhibition ◽  
Angiotensin Converting Enzyme Inhibition ◽  
Converting Enzyme ◽  
Converting Enzyme Inhibition ◽  
Group 2 ◽  
Alveolar Capillary ◽  
Group 1

Conductance of alveolar capillary membrane (DM) and capillary blood volume (VC) are the subcomponents of the pulmonary diffusing capacity for carbon monoxide (DLco). In chronic heart failure, stress failure of the membrane provides a mechanism for reduced DM and subsequent impairment of DLco. Angiotensin-converting enzyme inhibition improves DLco in patients with chronic heart failure. This study was aimed at investigating which of the two subcomponents of DLco is affected by angiotensin-converting enzyme inhibitors. Twenty-seven patients with NYHA class II to III chronic heart failure (group 1) and 13 age- and sex-matched normal subjects underwent pulmonary function testing with determination of DM and VC, while receiving placebo and 48 ;h and 1 and 2 months after starting enalapril treatment (10 ;mg twice daily). Nine similar patients (group 2) received isosorbide dinitrate (40 ;mg thrice daily) for a month then enalapril for another month, and underwent pulmonary function testing at 48 ;h and 1 month after starting treatments. Effects of angiotensin-converting enzyme inhibition in normal controls were not significant in the short- or mid-term. In group 1 patients, the only change observed at 48 ;h was a reduction in VC (probably due to a decrease in capillary pulmonary pressure). There was a marked increase in DM to a similar extent at 1 and 2 months, resulting in a significant improvement in DLco despite a decrease in VC. In group 2 patients, nitrates failed to improve DLco and DM, whereas enalapril was as effective as in group 1. These observations suggest a modulatory effect of angiotensin-converting enzyme inhibition on the membrane function which emerges gradually and persists over time and is probably dissociated from changes in pulmonary capillary pressure and VC. Chronic heart failure disturbs the alveolar capillary interface and increases gas diffusion resistance; angiotensin-converting enzyme inhibition restores the diffusive properties of the membrane and gas transfer, and protects the lung when the heart is failing.

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