Parental history of premature coronary artery disease does not affect plasma levels of asymmetric dimethylarginine in young healthy adults

Abstract

Family history of premature coronary artery disease (CAD) is a risk factor of atherogenesis and adverse coronary events. The aim of the study was to establish whether asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide formation, might be elevated in the asymptomatic offspring of patients with early‑onset CAD and whether it might contribute to subclinical atherosclerosis. We studied 20 healthy subjects (10 men and 10 women) aged from 19 to 30 years with a parental history of documented CAD before 60 years of age, and 20 controls with no evidence of parental CAD. ADMA and its isomer, symmetric dimethylarginine (SDMA), were determined by enzyme‑linked immunosorbent assays. Mean intima‑media thickness (IMT) of the common carotid arteries was assessed by B‑mode ultrasound. Characteristics of the 2 groups were similar, except for insignificant tendencies towards higher low‑density lipoprotein (LDL) cholesterol (P = 0.07) and estimated glomerular filtration rate (eGFR) (P = 0.06) in the group with a positive family history. Compared with controls, subjects with a parental history of premature CAD had increased IMT (0.54 ±0.05 vs. 0.48 ±0.05 mm; P <0.001) and similar levels of ADMA (0.66 ±0.17 vs. 0.74 ±0.15 μmol/l; P = 0.14) and SDMA (0.49 ±0.07 vs. 0.50 ±0.07 μmol/l; P = 0.61). The results did not change substantially on adjustment for LDL cholesterol and eGFR. In a multivariate analysis, parental CAD (P = 0.005) and LDL cholesterol (P = 0.06), but not ADMA, were independent positive IMT predictors. Our preliminary data suggest that elevated ADMA is not a part of the proatherogenic risk profile in the young adult offspring of patients with premature CAD.