Does it Make Sense to Combine Statins with Other Lipid-Altering Agents Following AIM-HIGH, SHARP and ACCORD?
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STATIN DRUGS (MB CLEARFIELD, SECTION EDITOR)
Does it Make Sense to Combine Statins with Other Lipid-Altering Agents Following AIM-HIGH, SHARP and ACCORD? Willibald Hochholzer & Robert P. Giugliano
Published online: 16 December 2012 # Springer Science+Business Media New York 2012
Abstract Hypercholesterolemia is one of the main risk factors for the development of atherosclerotic diseases. Multiple clinical trials of lipid-lowering agents have demonstrated that lowering cholesterol effectively reduces the risk of cardiovascular events and death. Currently, treatment with 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (“statins”) is the most commonly used approach, given their superior efficacy relative to other cholesterol lowering agents. However, not all patients on statin monotherapy achieve target cholesterol levels, and even when cholesterol lowering is successful, significant residual cardiovascular risk remains. There is increasing interest in developing combination cholesterol-modifying therapies that may augment the treatment effect and minimize the side effects of statins. Although there is currently no evidence that any of the potential therapy combinations can improve clinical outcome compared to statin monotherapy alone, results of several large ongoing trials will help to clarify this important field. Keywords Lipids . Cholesterol . Cardiovascular risk . Lipid lowering therapy . Statins . Niacin . Fibrate . Ezetimibe . Omega-3 fatty acids . Cholesterol ester transfer protein inhibitors . Proprotein convertase subtilisin kexin type 9 inhibitors
This article is part of the Topical Collection on Statin Drugs W. Hochholzer Universitaets-Herzzentrum Freiburg · Bad Krozingen, Suedring 15, 79189 Bad Krozingen, Germany e-mail: [email protected] R. P. Giugliano (*) TIMI Study Group, Cardiovascular Division, Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School, 350 Longwood Ave., First Floor, Boston, MA 02115, USA e-mail: [email protected]
Introduction Hyperlipidemia is one of the main risk factors for the development of atherosclerosis, which includes coronary heart disease (CHD), cerebrovascular disease, and peripheral arterial disease [1–4]. In particular, low-density lipoprotein cholesterol (LDL-C) plays a central role in the pathophysiology of atherosclerosis, and levels>200 mg/ dL are strongly associated with a higher risk for CHD [5, 6]. Oxidized LDL-C, together with pro-inflammatory mediators produced by enzymes binding to LDL-C, triggers inflammatory processes leading to the development of atherosclerotic atheroma and plaque rupture [7]. Multiple clinical trials of lipid-lowering agents have demonstrated that lowering LDL-C effectively reduces the risk of cardiovascular events and death in patients with and without CHD [1, 8•]. Therefore, lowering LDL-C is a major cornerstone for both primary and secondary prevention of cardiovascular events. Epidemiological studies have also suggested that low levels of high-density lipoprotein cholesterol
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