(Circulation. 2008;117:717-719.)
© 2008 American Heart Association, Inc.
Editorial |
From the Division of Vascular and Endovascular Surgery, Brigham and Womens Hospital, Boston, Mass.
Correspondence to Michael S. Conte, Division of Vascular and Endovascular Surgery, Brigham and Womens Hospital, 75 Francis St, Boston, MA 02115. E-mail mconte@partners.org
Key Words: Editorials peripheral vascular disease claudication pharmacology vasodilation
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Peripheral arterial disease (PAD) is a distinct clinical manifestation of atherosclerosis, with an associated long-term risk of coronary and cerebrovascular events that is equivalent to that of a primary diagnosis of myocardial infarction or ischemic stroke.1,2 The prevalence of PAD, as estimated by an abnormal ankle-to-brachial systolic pressure index (ABI <0.9), is closely linked to age, afflicting up to 20% or more of individuals >55 years of age in Western societies.3–5 The majority of patients with PAD are asymptomatic, but recognition of the disease is clinically important because it may be the primary manifestation of systemic atherosclerosis. Indeed, numerous studies have demonstrated a correlation between the global risk of cardiovascular events and ABI, which portends a more dire outcome for those with increasing degrees of hemodynamic compromise in the limb.6,7 The major risk factors for PAD, aside from age, are cigarette smoking, diabetes mellitus, dyslipidemia, hyperhomocysteinemia, and hypertension. Among these, the recent explosion in the worldwide prevalence of diabetes mellitus is of particular concern, particularly because the risk of both mortality and limb loss in diabetic PAD patients is increased several-fold. Thus, a major focus of clinical management in PAD is on secondary prevention, including the aggressive treatment of these risk factors by dietary and behavioral modification, combined with medical therapies. Present evidence suggests that PAD patients should receive lifelong antiplatelet therapy, treatment with a hydroxymethylglutaryl coenzyme A reductase inhibitor (statin), and appropriate antihypertensive therapy, which should probably include an angiotensin-converting enzyme inhibitor.8
Article p 816
Symptomatic PAD, which affects
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