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Circulating endothelial cells and stroke: influence of stroke subtypes and changes during the course of disease.

Woywodt, Alexander; Gerdes, Stefan; Ahl, Bjoern; Erdbruegger, Uta; Haubitz, Marion; Weissenborn, Karin.
J Stroke Cerebrovasc Dis; 21(6): 452-8, 2012 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-21852153


Circulating endothelial cells (CECs) are a novel and valuable marker of endothelial damage in a variety of vascular disorders. There is limited information as to CEC counts and the time course of CECs in subtypes of stroke.


We studied 49 patients with stroke (18 with atherothrombotic infarction in the territory of the middle cerebral artery, 16 with cardioembolic stroke, and 15 with lacunar stroke). We also included 16 healthy controls and 64 disease controls. CECs were isolated and enumerated with lectin-augmented CD146-driven immunomagnetic isolation. Neurologic deficit was assessed with the European Stroke Scale (ESS) and the National Institutes of Health Stroke Scale (NIHSS). Recovery was assessed with the modified Rankin scale (mRS).


Healthy controls had low numbers of CECs (median, 8 cells/mL; mean, 9 cells/mL; range, 0-16 cells/mL; n = 16). Patients with stroke had markedly elevated numbers of CECs at presentation. Patients with atherothrombotic infarction had 32 cells per milliliter (mean, 42 cells/mL; range, 24-116 cells/mL; n = 18; P < .001 when compared to controls). Patients with lacunar stroke had 68 cells per milliliter (mean, 68 cells/mL; range, 8-144 cells/mL; n = 15; P < .001 when compared to controls). Patients with cardioembolic stroke had 46 cells per milliter (mean, 54 cells/mL; range, 24-116 cells/mL; n = 16; P < .001 when compared to healthy controls). There was a tendency towards higher numbers of CECs in lacunar stroke. The number of CECs peaked at day 7 in patients with atherothrombotic infarction and came back to normal at day 90. In contrast, CECs in patients with acute lacunar stroke and cardioembolic stroke decreased progressively until day 90.


CECs are markers of endothelial damage and/or repair in stroke. Differences during the course of disease are likely to reflect different pathophysiology.
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