2003; Werner et al. 2005; Fadini et al. 2007; Rouhl et al. 2008), although other studies reported conflicting results (Eizawa et al. 2004; Kunz et al. 2006; Hristov et al. 2007; Xiao et al. 2007). Conversely, statins, estrogen, erythropoietin, angiotensin-converting enzyme inhibitors and physical exercise tend

to increase EPC counts (Werner et al. 2005; Fadini et al. 2007). Clearly, as EPC may play an important role in the pathophysiology of ischemic stroke, it is worthwhile to investigate the variables that influence the levels of these cells. It is possible that these variables have prognostic and therapeutic consequences. Inhibitors,research,lifescience,medical In our study we did not observe an influence of aging or vascular risk factors on EPC counts. Only patients who received prior treatment with statins and specific etiologies were significantly associated with EPC counts. A direct comparison of our study with previous studies is

not possible for several reasons: statin pretreatment was not included as Inhibitors,research,lifescience,medical a variable (Ghani et al. 2005; Chu et al. 2008; Zhou et al. 2009); etiology subtype was not analyzed (Ghani et al. 2005; Inhibitors,research,lifescience,medical Yip et al. 2008; Zhou et al. 2009); the time from stroke onset to time of blood sampling were not restricted to the acute stage (Chu et al. 2008) or was not provided (Ghani et al. 2005); and the number of recruited patients was relatively small (Ghani et al. 2005; Chu

et al. 2008; Inhibitors,research,lifescience,medical Cesari et al. 2009). Additionally, some studies used flow cytometry (Yip et al. 2008; Cesari et al. 2009; Zhou et al. 2009) while others relied on counting colony-forming units (Ghani et al. 2005; Chu et al. 2008). Also, the definition of EPC was variable among the studies (Ghani et al. 2005; Chu et al. 2008; Yip et al. 2008; Zhou et al. 2009). To our knowledge, our study is the largest Inhibitors,research,lifescience,medical to date and the only one that analyzed serial samples at the acute, subacute, and chronic stage of stroke. Statins have several effects that are beneficial for patients with acute ischemic stroke, and are independent of the lipid-lowering properties (Marti-Fabregas et al. 2004). These effects may be mediated by the increase in the mobilization and the improvement of the functional activity of the EPC population, Batimastat that has been demonstrated in vitro and in patients with stable ischemic heart kinase inhibitor Oligomycin A disease (Vasa et al. 2001; Urbich and Dimmeler 2004). Thus, this influence of statins is likely a novel pleiotropic selleck Abiraterone effect. The administration of statins to patients with stable CAD increases the number of EPC (Vasa et al. 2001), but these results were not replicated in patients with chronic stroke (Mohammad et al. 2010). Recently, a study in patients with acute ischemic stroke reported that statin treatment for 4 days may increase circulating EPC levels (Sobrino et al. 2012b).