Monocyte count is an underlying marker of lacunar subtype of hypertensive small vessel disease M. Gomis Cortina a , A. Rodrı ´guez Campello a , J. Jime ´nez Conde a , A. Ois a , A. Voustianiouk b , M. J. Te ´ llez a , E. Cuadrado a and J. Roquer a a Stroke Unit, Neurology Department, Hospital del Mar, Departament de Medicina de la Universitat Auto ´noma de Barcelona, Barcelona, Spain; and b Neurology Department, Mount Sinai School of Medicine, New York, NY, USA Keywords: deep intracerebral hemor- rhage, lacunar infarct, monocyte count Received 6 December 2007 Accepted 25 March 2008 Background: In the hypertensive small vessel disease (HSVD), it remains unclear why some patients develop lacunar infarcts (LIs) whilst others develop deep intracerebral hemorrhages (dICHs). Inflammation might be related to LI, and leukocyte and monocyte counts are regarded as an inflammatory marker of ischemic stroke. Objective: We investigated the relationship between leukocyte and monocyte counts determined in the first 24 h after stroke onset in HSVD patients. Methods: We prospectively studied 236 patients with first acute stroke because of HSVD (129 LI and 107 dICH). We analyzed demographic data, vascular risk factors, and white blood cell count subtypes obtained in the first 24 h after stroke. Results: The multivariate analysis showed that LI subtype of HSVD was correlated with hyperlipidemia (P < 0.0001), a higher monocyte count (P = 0.002), and showed a trend with current smoking (P = 0.051), whereas dICH subtype was correlated with low serum total cholesterol (P = 0.003), low serum triglycerides (P < 0.0001), and high neutrophil count (P = 0.050). Conclusions: In patients who developed HSVD-related stroke, high monocyte count, current smoking, and hyperlipidemia are prothrombotic factors related to LI, whereas low cholesterol and triglyceride values are related to dICH. Monocyte count might be an inflammatory risk marker for the occlusion of small vessels in hypertensive patients. Introduction The term hypertensive small vessel disease (HSVD) includes two distinct entities that occur in the same structures, lacunar infarcts (LI) and deep intracerebral hemorrhages (dICH). Fisher [1] distinguished in autopsies two different underlying vascular pathologies for small vessel disease (SVD): lipohyalinosis and microatheromatosis. Lipohyalinosis was present mainly in patients with small, multiple and asymptomatic lacunae, and this type of vessel lesion is most commonly associated with dICH [2–5]. Microatheromatosis was found mainly in patients with single, large, and symp- tomatic lacunae, being the second most common cause of LI. Hypertension is the major risk factor for LI and dICH but it fails to account for much of the risk. Inflammation was shown to play an important role in lacunar infarctions [6]. Several markers of inflamma- tion, such as leukocyte and monocyte counts, have been identified as predictors of ischemic stroke [7]. Studies demonstrate that leukocyte count independently pre- dicts ischemic risk [8–10], mainly in the atheroesclerotic group. Studies also demonstrated that monocyte count is a better marker for proinflammatory state in carotid atherosclerosis than leukocyte count [11–13]. Our aim was to analyze differences between LI and dICH patients in demographic data, vascular risk fac- tors, and on leukocyte count determined in the first 24 h after the stroke onset. We sought to determine whether increase in leukocyte or monocyte count might be related to the development of clinical LI in patients with acute HSVD stroke. Methods Study population From January 2001 to February 2006, 2193 consecutive patients with acute stroke were admitted to our hospital and enrolled in the stroke register. We selected the consecutive patients with the diagnosis of primary intracerebral hemorrhages and with the diagnosis of LI. A total of 284 patients had primary intracerebral Correspondence: Meritxell Gomis Cortina, MD, Stroke Unit, Neurology Department, Hospital del Mar-IMIM, Departament de Medicina de la Universitat Auto´noma de Barcelona, Passeig Marı´tim 25-29, 08003 Barcelona, Spain (tel.: +34 93 248 3234; fax: +34 93 248 3376; e-mail: 92571@imas.imim.es). Ó 2008 The Author(s) Journal compilation Ó 2008 EFNS 671 European Journal of Neurology 2008, 15: 671–676 doi:10.1111/j.1468-1331.2008.02145.x