Addition of an angiotensin receptor blocker to full-dose ACE-inhibition: controversial or common sense?

• Published in: European heart journal Vol. 26; no. 22; pp. 2361 - 2367
• Main Authors: van de Wal, Ruud M.A., van Veldhuisen, Dirk J., van Gilst, Wiek H., Voors, Adriaan A.
• Format: Journal Article
• Language: English
• Published: Oxford Oxford University Press 01.11.2005; Oxford Publishing Limited (England)
• Subjects: Ace-inhibitor; Adrenergic beta-Antagonists - therapeutic use; Angiotensin II Type 1 Receptor Blockers - therapeutic use; Angiotensin receptor blockade; Angiotensin-Converting Enzyme Inhibitors - therapeutic use; Antihypertensive Agents - therapeutic use; Biological and medical sciences; Cardiology. Vascular system; Cardiovascular disease; Diabetic Nephropathies - drug therapy; Drug Synergism; Drug Therapy, Combination; Dual blockade; Heart Failure - drug therapy; Humans; Hypertension - complications; Hypertension - drug therapy; Medical sciences; Myocardial Infarction - drug therapy; Renin angiotensin system; Risk Factors; Addition; Cardiovascular disease; Angiotensin receptor blockade; Dual blockade; Phlebology; Posology; System; Rerun angiotensin system; Angiotensin; Ace-inhibitor; Circulatory system; Cardiology; Dose; ACE inhibitor; Biological receptor
• ISSN: 0195-668X; 1522-9645
• DOI: 10.1093/eurheartj/ehi454

Both angiotensin-converting enzyme (ACE)-inhibitors and angiotensin receptor blockers (ARBs) interfere with the activity of the renin–angiotensin system (RAS) in a different way. Theoretically, one might expect beneficial effects when they are used in combination, as a more complete suppression of the RAS can be achieved. But can this additional effect still be seen in patients on full-dose ACE-inhibition? Several controlled trials demonstrated that combination therapy can have additional benefits in hypertensive patients, in chronic heart failure patients, and in both diabetic and non-diabetic nephropathy patients. However, the clinical benefit was not always as pronounced as expected and not every patient will benefit from dual blockade of the RAS. There is some evidence of a less pronounced effect of combination therapy when a full dose of the ACE-inhibitor is given. However, it is well known that ACE-inhibitors cannot completely suppress the formation of angiotensin II, in particular, when the RAS is activated. Indeed, clinical trials indicated that add-on therapy with an ARB was especially of use when the RAS remained activated despite full-dose ACE-inhibitor treatment. In summary, combination of a full-dose ACE-inhibitor and an ARB can be a rational choice in selected patients.