6533b7d4fe1ef96bd126272e

RESEARCH PRODUCT

Symmetric dimethylarginine serum level as a new marker of left ventricular ejection fraction in patients with acute myocardial infarction

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Purpose: Asymmetric dimethylarginine (ADMA) is a by-product of protein methylation that has been implicated in the prognosis after acute myocardial infarction (MI) and heart failure through Nitric Oxide Synthase (NOS) inhibition. We aimed to investigate whether SDMA – the endogenous symmetrical stereoisomer of ADMA- that has insignificant inhibitory effects on NOS- might be a marker of left ventricular function in acute MI. Methods: Blood samples from 635 consecutive patients hospitalized 1 (23%). Mean LVEF was 55±13%. Mean ADMA, SDMA and L-arg levels were at 0.72±0.42, 0.51±0.44 and 91±54 μmol/L, respectively. Spearman analysis showed that LVEF was correlated negatively with SDMA (r=-0.151, p<0.001), but neither with ADMA (r=-0.015, p=0.72) nor L-arg (r=-0.029, p=0.48). SDMA was strongly associated with age (r=+0.391, p<0.001), creatinine clearance (r=-0.455, p<0.001), CRP (r=+0.151, p<0.001) and homocysteine (r=+0.316, p<0.001). By univariate linear regression analysis, age, Killip on admission, diabetes, admission systolic blood pressure, homocysteine, creatinine clearance, troponin, anterior wall location, STEMI, in addition to SDMA, were significantly associated with LVEF (p<0.001). Backward multivariate analysis including these covariates showed that SDMA remains an independent predictor of LVEF (B=-2.816; SE=1.131, p=0.013), beyond classical determinants of LVEF including age, anterior wall location, prior MI, STEMI and renal function. Conclusion: Our large prospective study showed for the first time that SDMA, but ADMA, may be linked to left ventricular function in patients with acute MI, and suggests that such dimethylarginines may probably exert biological activity by other pathways than NOS activity inhibition and beyond renal function.