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(Hypertension. 2007;50:998.)
© 2007 American Heart Association, Inc.

Brief Reviews

Role of Renin-Angiotensin System Blockade in Atherosclerotic Renal Artery Stenosis and Renovascular Hypertension

From the Divisions of Clinical Pharmacology (D.G.H.) and Nephrology (A.X.G.), University of Western Ontario, London, Ontario, Canada; Stroke Prevention and Atherosclerosis Research Centre (J.D.S.), London, Ontario, Canada; and the Division of Nephrology and Hypertension (S.C.T.), Mayo Clinic College of Medicine, Rochester, Minn.

Correspondence to Daniel G. Hackam, 1400 Western Rd, London, Ontario, Canada N6G 2V2. E-mail dhackam@uwo.ca

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
Current management of atherosclerotic renal artery stenosis (ARAS) remains controversial. A major issue is the condition’s functional significance; specifically, what is the contribution of ARAS to a specified patient’s heart failure, hypertension, or progressive renal disease? Clinicians will often consider whether revascularization of ARAS is likely to alter a patient’s symptoms or prognosis. Yet, even when ARAS is incidentally detected, patients are at high risk for future cardiovascular events and death. This suggests that regardless of the clinical scenario, intensive medical therapy should be provided to all patients in whom ARAS is discovered. Here we review evidence that angiotensin inhibitors (angiotensin-converting enzyme [ACE] inhibitors and angiotensin receptor blockers [ARBs]) may improve the prognosis of ARAS. To place this evidence into context, it is important to first review the prognosis of this condition.

	Cardiovascular Risk Associated With ARAS

 
Natural history studies indicate that patients with ARAS are at high risk for myocardial infarction, stroke, and cardiovascular death (Table 1). In a recent analysis of patients with ARAS, the annual incidence of coronary events, stroke, heart failure, and death was 30%, 18%, 19%, and 17%, respectively.¹ The presence of this disease decreases long-term survival by 2- to 4-fold.^1–3 An impaired prognosis is also evident in healthy patients with incidentally discovered ARAS. In a cohort of unselected community-dwelling Americans older than 65 years of age, baseline ARAS increased the risk of events by 3-fold (hazard ratio [HR]: 2.92; 95% CI: 1.53 to 5.57).⁴ After adjusting for risk factors, renal function, subclinical cardiovascular disease, and medications, the . . . [Full Text of this Article]

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