Angiotensin receptor blockers for heart failure

Jong, Phillip; Demers, Catherine; McKelvie, Robert S.; Liu, Peter

doi:10.1002/14651858.cd003040

Cited by 4 publications

(2 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…[83] number of smaller studies, a recent meta-analysis failed to demonstrate that ARBs improved survival in CHF when compared with 3.4 CHARM-Added placebo or ACE inhibitor therapy. [84] The combination of an ACE In CHARM-Added, candesartan was superior to placebo at inhibitor and an ARB was superior to ACE inhibitor therapy alone reducing the combined primary endpoint of cardiovascular death at reducing hospitalization but not mortality. There was a trend and hospitalization for heart failure in patients with CHF already towards a reduction in mortality with combined therapy compared receiving an ACE inhibitor.…”

Section: The Val-heft (Valsartan Heart Failure Trial)mentioning

confidence: 99%

“…There was a trend and hospitalization for heart failure in patients with CHF already towards a reduction in mortality with combined therapy compared receiving an ACE inhibitor. [84] 3.6 Tolerability verse effects was significantly greater: [78] of heart failure but no mortality benefit compared with placebo. [84] 3.6 Tolerability verse effects was significantly greater: [78] of heart failure but no mortality benefit compared with placebo.…”

Section: The Val-heft (Valsartan Heart Failure Trial)mentioning

confidence: 99%

See 1 more Smart Citation

Angiotensin Antagonism in Patients with Heart Failure

Cruden

Newby

2004

American Journal of Cardiovascular Drugs

View full text Add to dashboard Cite

Chronic heart failure (CHF) is a major cause of morbidity and mortality in western society. It is now widely accepted that the renin-angiotensin-aldosterone system (RAAS) and, in particular, angiotensin II (A-II) play a key role in the pathophysiology of CHF. Large-scale clinical trials have demonstrated that inhibitors of angiotensin-converting enzyme (ACE), the principal enzyme responsible for A-II production, improve symptoms and survival in patients with CHF. This enzyme is also responsible for the breakdown of the vasodilator hormone bradykinin. Administration of ACE inhibitors is associated with increased plasma bradykinin levels and this is thought to contribute to the vascular changes associated with ACE inhibitor therapy. However, RAAS inhibition with ACE inhibitors remains incomplete because ACE inhibitors do not block the non-ACE-mediated conversion of angiotensin I to A-II. Angiotensin receptor antagonists (angiotensin receptor blockers; ARBs) antagonize the action of A-II at the A-II type 1 (AT(1)) receptor, whilst allowing the potentially beneficial actions of A-II mediated via the A-II type 2 (AT(2)) receptor. Evidence that the clinical benefit demonstrated with ACE inhibitors in patients with CHF may extend to ARBs has only emerged recently. Combination therapy with both an ACE inhibitor and an ARB has a number of potential advantages and has been investigated in several large-scale clinical trials recently. In patients with CHF, first-line therapy should include an ACE inhibitor and a beta-adrenoceptor antagonist. The addition of an ARB provides symptomatic relief but has not been shown to improve survival. Where an ACE inhibitor is not tolerated, treatment with an ARB would seem an appropriate alternative. There is insufficient data to support the routine use of ARBs as first-line therapy in the management of CHF.

show abstract

Section: The Val-heft (Valsartan Heart Failure Trial)mentioning

confidence: 99%

Section: The Val-heft (Valsartan Heart Failure Trial)mentioning

confidence: 99%

Angiotensin Antagonism in Patients with Heart Failure

Cruden

Newby

2004

American Journal of Cardiovascular Drugs

View full text Add to dashboard Cite

show abstract

Angiotensin receptor blockers for heart failure

Heran

Musini

Bassett

et al. 2012

Cochrane Database of Systematic Reviews

View full text Add to dashboard Cite

Cochrane Database of Systematic Reviews Withdrawals due to adverse e ects were higher with ARBs versus placebo when all patients were pooled irrespective of LVEF (RR 1.06 [95% CI 1.01, 1.12]). Authors' conclusionsIn patients with symptomatic HF and systolic dysfunction or with preserved ejection fraction, ARBs compared to placebo or ACEIs do not reduce total mortality or morbidity. ARBs are better tolerated than ACEIs but do not appear to be as safe and well tolerated as placebo in terms of withdrawals due to adverse e ects. Adding an ARB in combination with an ACEI does not reduce total mortality or total hospital admission but increases withdrawals due to adverse e ects compared with ACEI alone.

show abstract