雖然在分子心臟學與介入心?學世大的進步，動脈粥狀硬化仍在美國居患病率及死亡率的首要原因，且遠超過排行基下七項疾病之總數。動脈粥狀硬化?慢性疾病，它不僅是許多?所週知的臨床疾病的初始，例如急性心肌梗塞，研究亦顯示血管硬化的病理也與其他心血管疾病，從高同氨酸症到糖尿病，都有錯綜複雜的關係，例如發炎反應，或氧化傷害，即?這些疾病理變化過程中，扮演了極重要之角色。當發生發炎反應，或氧化傷害時，中間的媒介分子不只使血管?生病變，同時也扮演了預後的因子。由於ADMA具有診斷及預後的指標，因此最近被廣泛接受成?心?血管疾病之新發現的危險因子之一。ADMA是體內一氧化氮合成酵素(NOS)的內源性抑制分子，因此在高血脂、高血壓、高同氨酸症、高血糖及胰島素陰抗的情況之下，血清中的ADMA值是偏高。ADMA會減少抗發炎及抗硬化分子的?生，因此也同時具有診斷及預後之價值。本文將探討ADMA、NOS生化路徑及相互關係之最新研究。

Despite monumental progress in both molecular and interventional cardiology, atherosclerosis remains the leading cause of mortality and morbidity in the US, claiming more lives than the next 7 causes of mortality combined. Not only is this chronic disease the beginning of many familiar downstream clinical manifestations such as acute myocardial infarction, but research has demonstrated that the pathogenesis of atherosclerosis is intricately linked to many other cardiovascular abnormalities, from hyperhomocysteinemia to diabetes mellitus. Inflammation and oxidative stress, for instance, are common mediators for these diseases. Their interrelatedness has elicited much interest in finding a molecular marker with both prognostic and diagnostic values. Asymmetric dimethylarginine (ADMA) is one such molecule, recently gaining wider acceptance as a novel cardiovascular risk factor. As an endogenous competitive inhibitor of nitric oxide synthase (NOS), ADMA is elevated in the plasma of patients with hypercholesterolemia, hypertension, hyperhomocysteinemia, hyperglycemia, and insulin resistance. Not only is plasma ADMA concentration predictive of cardiovascular events, ADMA reduces the production of the anti-inflammatory and anti-atherogenic molecule, nitric oxide. As such, ADMA is both a disease marker and a mediator, whose pathophysiology merits attention. This article reviews the current knowledge of ADMA within the larger context of the NOS pathway.