ADMA--a Possible Marker for Early Therapeutic Outcome in Acute Stroke

Ischemic acute stroke is a leading cause for mortality and invalidity in recent years. Clinical trials show the role of ADMA as endogenous inhibitor of nitric oxide synthase and its connection to acute stroke. An early decrease of serum ADMA levels might help in recovery of the blood stream in patients with acute stroke and non-affective changes in the brain.

We compared 18 patients with acute stroke before and after thrombolysis and 21 patients (without history of cardiovascular disease, diabetes, kidney and liver injury, non-smokers) before and after thrombolysis. All results were compared to 30 healthy persons. Patients were evaluated by NIHSS, with ultrasound, CT and laboratory methods (traditional risk factors and CRP, D-dimmer, homocysteine, and ADMA).

Classic vascular factors showed statistical significance in patients with acute stroke. Serum hsCRP levels and D-dimer in our study showed no connection to acute stroke. We found a statistically significant correlation in patients with stroke between ADMA and homocysteine levels (r = 0.469, p < 0.001). We found no significant difference between basic serum ADMA concentrations in groups with stroke who underwent different treatment (r = -0.449, p < 0.001). In patients with thrombolysis ADMA concentrations are reduced earlier, which also shows that earlier clinical recovery leads to no brain damaging effects.

Through its pathophysiological changes, ADMA might be a predictor for acute stroke (along with already known risk factors) and can be a marker for the outcome of stroke, depending on the treatment.