What is the difference between ace inhibitor and arb




















One limitation of this report is that details on follow-up duration are not provided for all databases in the study. Nevertheless, these findings reinforce a growing recognition that ACE inhibitors and ARBs have similar efficacy in preventing complications of hypertension and that ARBs have fewer adverse effects. Chen R et al. Comparative first-line effectiveness and safety of ACE angiotensin-converting enzyme inhibitors and angiotensin receptor blockers: A multinational cohort study.

Hypertension Sep; Hypertension Sep In an observational study, new users of angiotensin-receptor blockers had similar cardiovascular outcomes and fewer side effects.

Comment One limitation of this report is that details on follow-up duration are not provided for all databases in the study. Citation s : Chen R et al. Disclosures Disclosures for Allan S. Brett, MD, at time of publication Nothing to disclose.

Topics Hypertension. Answers are drawn from an approved set of evidence-based resources and undergo peer review. The complete database of evidence-based questions and answers is copyrighted by FPIN.

This series is coordinated by John E. Delzell, Jr. Want to use this article elsewhere? Get Permissions. Read the Issue. Sign Up Now. Previous: Benzodiazepines and Alzheimer Disease.

Next: Vesicular Rash in a College Student. Angiotensin Receptor Blockers. Feb 1, Issue. Evidence Summary A meta-analysis of 20 clinical trials involving , patients examined the effect of ACE inhibitors and ARBs in patients with hypertension. Read the full article.

Get immediate access, anytime, anywhere. Choose a single article, issue, or full-access subscription. Earn up to 6 CME credits per issue. Purchase Access: See My Options close. Best Value! In my medical practice, I try to make sure patients with HFrEF, hypertension, chronic kidney disease, and coronary artery disease with left ventricular dysfunction receive an inhibitor of the renin-angiotensin-aldosterone system.

I prefer ARBs because patients tolerate them better. Most antihypertensive agents increase the risk of incident gout, except for calcium channel blockers and losartan. The addition of beta-blockers and mineralocorticoid receptor blockers to ACE inhibitors or ARBs is associated with a further decrease in the mortality risk for patients with HFrEF, 20—22 but some patients cannot tolerate these combinations or optimized doses of these medications because of worsening hypotension or increased risk of developing acute kidney injury or hyperkalemia.

This combination may be useful in nondiabetic patients with proteinuria refractory to maximum treatment with 1 class of these agents, but it is associated with an increased risk of hyperkalemia or acute kidney injury in patients with diabetic nephropathy without improving rates of the clinical outcomes of death or cardiovascular events.

I avoid combining direct renin inhibitors with ACE inhibitors or ARBs, since this combination has been contraindicated by the US Food and Drug Administration due to lack of reduction in target-organ damage and an associated increased risk of hypotension, hyperkalemia, and kidney failure, and a slight increase in the risk of stroke or death in patients with diabetic nephropathy.

Neprilysin is a membrane-bound endopeptidase that degrades vasoactive peptides, including B-type natriuretic peptide and atrial natriuretic peptide. Very importantly, an ACE inhibitor cannot be used together with valsartan-sacubitril due to increased risk of angioedema and cough. Interestingly, a network meta-analysis showed that the combination of valsartan-sacubitril plus a mineralocorticoid receptor blocker and a beta-blocker resulted in the greatest mortality reduction in patients with HFrEF.



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