[Plasma asymmetric dimethylarginine and cystatin C levels in patients with coronary artery disease].

OBJECTIVE

To compare plasma asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase inhibitor, and cystatin C levels in patients with or without coronary artery disease (CAD).

METHODS

We recruited 87 CAD patients (39 with acute myocardial infarction and 48 with unstable angina pectoris) and 51 non-CAD controls. Plasma ADMA was measured by HPLC, cystatin C by particle-enhanced immunonephelometric assay (N Latex cystatin C, Dade Behring) with nephelometer (BNII, Dade Behring). CAD patients were further divided into low cystatin C group (< 1.0 mg/L, 36 cases) and high cystatin C group (> 1.0 mg/L, 51 cases).

RESULTS

(1) The plasma levels of ADMA [(0.47 ± 0.15) µmol/L vs. (0.37 ± 0.15) µmol/L], SDMA [(0.39 ± 0.19) µmol/L vs. (0.28 ± 0.12) µmol/L] and cystatin C [(1.16 ± 0.32) mg/L vs. (0.73 ± 0.16) mg/L] were significantly higher in CAD patients than in controls (all P < 0.05). The plasma L-Arg was significantly lower in CAD patients than in controls [(59.4 ± 19.4) µmol/L vs. (83.7 ± 19.6) µmol/L, P < 0.05]. (2) Plasma ADMA was similar in CAD patients with low cystatin C level and controls [(0.42 ± 0.12) µmol/L vs. (0.39 ± 0.15) µmol/L, P = 0.251] and Plasma ADMA was significantly higher in CAD patients with high cystatin C level than in controls [(0.50 ± 0.17) µmol/L vs. (0.39 ± 0.15) µmol/L, P < 0.05].

CONCLUSION

ADMA levels were significantly increased only in CAD patients with elevated cystatin C levels but not in CAD patients with normal renal function. The reported relationship between coronary heart disease and ADMA may not be direct, but could be secondary due to reduced renal function.