Search for: [Abstract = "Family history of premature coronary artery disease \(CAD\) is associated with accelerated atherogenesis and excessive risk of coronary events. Endothelial dysfunction, an antecedent of atherosclerotic plaques, is largely dependent on depressed bioavailability of nitric oxide \(NO\).Our aim was to test the hypothesis that asymmetric dimethyl\-L\-arginine \(ADMA\), an endogenous inhibitor of nitric oxide \(NO\) formation, might be elevated in young offspring of patients with early\-onset CAD, and could contribute to subclinical atherosclerosis.We studied 20 healthy subjects \(10 men\/10 women\) aged 19–30 years with a parental history of documented CAD before 60 years of age, and 20 matched controls with no evidence of parental CAD. ADMA and its isomer symmetric dimethylarginine \(SDMA\) were determined by enzyme\-linked immunosorbent assays. Averaged intima\-media thickness \(IMT\) of the common carotid arteries was assessed by B\-mode ultrasound.Demographical, clinical and biochemical characteristics of the both groups were similar. Subjects with a parental history of premature CAD exhibited similar plasma levels of ADMA and SDMA, and significantly elevated carotid IMT. The results did not substantially change upon adjustment for covariates. By multivariate analysis, parental history of premature CAD and LDL\-cholesterol but not ADMA were independent positive IMT predictors.These results suggest th"]

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