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Plasma asymmetric dimethylarginine in patients with acute decompensation of chronic heart failure
  1. Ingebjorg Seljeflot
  1. Correspondence to Dr Ingebjorg Seljeflot, Center for Clinical Heart Research, Department of Cardiology, Oslo University Hospital, Ullevål, PB 4956 Nydalen, N-0424 Oslo, Norway; ingebjorg.seljeflot{at}ous-hf.no

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The implications of abnormal endothelial function in the pathophysiology and prognosis in patients with chronic heart failure (CHF) has been extensively discussed.1–3 Endothelial dysfunction may affect the cardiovascular system in different ways, such as impairment of peripheral perfusion, an adverse effect of vascular remodelling, reduced compliance of the failing left ventricle and consequently impaired left ventricular dysfunction.4

Endothelial dysfunction has been attributed to reduced production of endothelial nitric oxide (NO) production, and thus affects vasoreactivity and smooth muscle cell growth, platelet reactivity and leucocyte adhesion to the endothelium.

Reduced production and bioavailability of NO can be caused by several mechanisms, one being increased production and/or accumulation of the amino acid asymmetric dimethylarginine (ADMA). ADMA is an endogenous competitive inhibitor of nitric oxide synthase (NOS),5 and is synthesised by methylation of proteins containing l-arginine, which is the substrate of NOS. Availability of arginine may also limit NO synthesis, and arginine can be depleted or reduced by arginase activity.6 The ratio between l-arginine and ADMA has therefore been claimed to be of great importance, at least in chronic disease states. ADMA has been shown to increase oxidative stress by the uncoupling of electron transport between NOS and l-arginine,5 resulting in increased production of radical oxygen species, an important feature in both acute and CHF, probably directly influencing cardiac remodelling.7 Worsening of heart failure is also accompanied by increased oxidative …

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