Key result
Statin treatment during the acute phase of ischaemic stroke was associated with a higher EPC increment (24.0 vs 6.0 CFU-EC) and an increased likelihood of an EPC increment ≥4 CFU-EC (OR 13.1; P=0.004).
Why the study?
Does atorvastatin 20 mg/day increase circulating endothelial progenitor cells in patients with acute ischaemic stroke?
Cohort (n=48)
Does atorvastatin 20 mg/day increase circulating endothelial progenitor cells in patients with acute ischaemic stroke?
Statin treatment during the acute phase of ischaemic stroke is associated with an increase in circulating endothelial progenitor cells, which correlates with a higher probability of good clinical outcome.
Answers are grounded in this paper and cite their sources.
Early statin use may enhance EPC increments in acute ischaemic stroke; hypothesis-generating and requires confirmation in randomized trials.
BACKGROUND AND PURPOSE: Endothelial progenitor cells (EPCs) have been suggested to be a therapeutic option in ischaemic stroke. Our aim was to study whether statin treatment during acute phase could increase circulating EPCs after acute ischaemic stroke. METHODS: We studied 48 patients with a first-ever non-lacunar ischaemic stroke (<12 h from stroke onset). Sixteen patients received statin treatment (20 mg atorvastatin/day) during the first 4 days. We defined the EPC increment during the first week as the difference in the number of early outgrowth colony-forming unit-endothelial cell (CFU-EC) between day 7 and at admission (previous to atorvastatin treatment). Serum levels of vascular endothelial growth factor and active matrix metalloproteinase 9 (determined by ELISA), and nitric oxide metabolites (NOx) (determined by high-performance liquid chromatography) were measured at admission, 24 and 72 h, and day 7. RESULTS: Colony-forming unit-endothelial cells were similar at baseline between patients treated (n = 16) and non-treated (n = 32) with statins (10.1 ± 3.9 vs. 7.9 ± 6.9 CFU-EC, P = 0.223). However, patients treated with statins showed a higher EPC increment (24.0 ± 17.3 vs. 6.0 ± 17.8 CFU-EC, P = 0.002) during the first week. An EPC increment ≥ 4 CFU-EC predicted with the highest sensitivity (88%) and specificity (92%) the probability of good outcome (area under the curve 0.903, P < 0.0001). Statin treatment (OR, 13.1; CI 95%, 2.2-76.9, P = 0.004) was independently associated with an EPC increment ≥ 4 CFU-EC after adjustment for confounder factors, but this association was lost when adjusting for NOx levels. CONCLUSIONS: Statin treatment for 4 days may increase circulating EPC levels, probably by NO-related mechanisms.
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Sobrino et al. (2012) conducted a cohort in ischaemic stroke (n=48). Statin treatment (atorvastatin) vs. Non-treated with statins was evaluated on EPC increment during the first week (OR 13.1, 95% CI 2.2-76.9, p=0.004). Statin treatment during the acute phase of ischaemic stroke was associated with a higher EPC increment (24.0 vs 6.0 CFU-EC) and an increased likelihood of an EPC increment ≥4 CFU-EC (OR 13.1; P=0.004).
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