Monocyte count is an underlying marker of lacunar subtype of hypertensive small vessel disease.

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.

Association of lacunar infarcts with small artery and large artery disease: a comparative study.

OBJECTIVES: Patients with lacunar infarcts (LI) and ipsilateral large artery disease (LAD) greater than 50% must be classified according to the Trial of ORG 10172 in Acute Stroke Treatment (TOAST) criteria as strokes of undetermined etiology. The purpose of this study was to compare the vascular risk factors, clinical symptoms, and outcome characteristics of LI associated with LAD with those patients with LI who fulfilled the TOAST criteria of small artery disease (SAD). METHODS: Among 1754 consecutive first ever stroke patients admitted to our department, we analyzed age, gender, vascular risk factors (hypertension, diabetes, ischemic heart disease, arterial peripheral disease, hypercholesterolemia, smoking, alcohol, or illicit drug use), clinical data (motor or sensitive deficit and presence of dysarthria), and outcome (hospitalization length, in-hospital medical complications rate, need of rehabilitation, treatment at discharge, in-hospital mortality, and modified Rankin Scale at discharge) of those patients classified as LI associated with LAD as compared with those with SAD. RESULTS: After a strict application of the TOAST criteria, we found 144 patients with LI associated with SAD and 73 patients with LI associated with LAD. Univariate analysis showed statistical differences in gender (OR: 0.46; 95% CI: 0.23-0.89; P = 0.014), past history of ischemic heart disease (OR: 0.32; 95% CI: 0.13-0.78; P = 0.004), and smoking (OR: 0.56; 95% CI: 0.31-1.04; P = 0.048). After logistic regression analysis only ischemic heart disease (OR: 0.31; 95% CI: 0.11-0.78; P = 0.013), and gender (OR: 0.51; 95% CI: 0.28-0.98; P = 0.05) showed statistical differences. During the follow-up, six patients (all with LI associated with LAD) experienced stroke recurrences (OR: 0.32; 95% CI: 0.26-0.39; P < 0.001). CONCLUSIONS: 1) There are no differences in clinical presentation and in-hospital outcome between patients with LI associated with SAD and patients with LI associated with LAD. 2) Risk factors are very similar in both groups, and the only differences observed (gender and ischemic heart disease) are related to the atherosclerotic factor. 3) Stroke recurrence seems to be more frequent in LI associated with LAD than in LI associated with SAD, but large follow-up studies are needed to be able to decide whether clinical recurrence of stroke allows to differentiate both clinical entities.