Brain perfusion defects are associated with endothelial dysfunction in cocaine users

Objectives Chronic cocaine consumption induces cortical brain perfusion defects. Vasospasm appears to play a role associated with haemostatic system activation. Endothelial dysfunction (ED), which is involved in vascular damage, is reliably assessed by circulating endothelial cells (CEC). Goal: Investigate ED evidence in patients with recent demonstrated cocaine consumption.

Methods We studied 15 DSM-IV cocaine dependent patientst; 12 male; mean age 31±9 y.o. Basal brain perfusion SPECT with 99mTc-ethylencistein-dimer performed a week after admittance; 13 of them controlled after 4 weeks of strict abstinence. Statistical Parametric Map and Neurostat were used to evaluate hypoperfusion (<66% maximal cortical activity). Whole blood CEC levels were also enumerated.

Results All patients presented focal bilateral perfusion baseline abnormalities, mainly in limbic and fronto temporal areas without significant change after abstinence. CEC were increased at baseline (636±208 cells/ml) and after abstinence (464±172 cells/ml), (p<0.0001 in both) with a significant reduction (p:0.0027). Initial brain hypoperfusion correlated better with CEC levels after a month of abstinence: Global Brain r=0.7694, Global Cortex r=0.7695, Prefrontal r=0.8427 and Cingulate r=0.6365.

Conclusions Cocaine dependent patients had persistant brain hypoperfusion associated to ED after abstinence. These findings support the notion that cocaine-induced endothelial damage may play a pathogenic role in the ischemic vascular damage observed in chronic cocaine users.

Research Support Fondecyt 1080253