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(Circulation. 2004;110:1013-1020.)
© 2004 American Heart Association, Inc.

New Drugs and Technologies

Should Angiotensin II Receptor Blockers and Statins Be Combined?

Georg Nickenig, MD

From the Department of Internal Medicine III, University Hospital of the Saarland, Homburg/Saar, Germany.

Correspondence to Prof Dr G. Nickenig, Klinik Innere Medizin III, Universitätskliniken des Saarlandes, 66421 Homburg/Saar, Germany. E-mail nickenig@med-in.uni-saarland.de

Received February 24, 2004; revision received June 1, 2004; accepted June 7, 2004.

Key Words: receptors, angiotensin • statins • heart failure • cardiovascular diseases • syndrome X

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

Coronary heart disease (CHD) resulting from atherosclerosis is the single largest killer in the Western world. Approximately 40% of patients with hypertension have hypercholesterolemia, which is central to the pathogenesis of atherosclerosis and cardiovascular disease (CVD).¹ Conversely, hypertension is a significant risk factor in patients with elevated cholesterol.² There is strong synergy between hypertension and hypercholesterolemia in terms of risk factors for the development of CVD.² Both hypertension and hypercholesterolemia result in endothelial dysfunction and consequently the development of atherosclerosis. The recent definition of the metabolic syndrome, characterized by hypertension, elevated cholesterol and triglyceride levels, insulin resistance/dyslipidemia, and central obesity, has brought together these conditions with the notion that they are linked and represent a cluster of factors that are synergistic for CVD.³

The renin-angiotensin system (RAS) contributes importantly to a variety of CVDs and is the target of angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs; Figure 1). RAS is an enzymatic cascade that starts with the cleavage of angiotensinogen by renin to form the inactive peptide angiotensin I. ACE is responsible for converting the inactive angiotensin I to the active moiety angiotensin II, which is the principle effector hormone of the RAS and, through its action on angiotensin II receptors, plays a critical role in maintaining arterial blood pressure (BP) and fluid and electrolyte homeostasis. Although angiotensin II binds to both type I (AT₁) and type II (AT₂) receptor subtypes, the AT₁ receptor mediates most of the cardiovascular effects of angiotensin II, including oxidative . . . [Full Text of this Article]

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