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Official Journal of the , the International Union of Phlebology and the
Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,899
Online ISSN 1827-1839
Belch J., McLaren M., Hanslip J., Hill A., Davidson D.
From the University Department of Medicine, Ninewells Hospital & Medical School and Department of Neurology, Dundee Royal Infirmary, Dundee, Scotland
Objectives. Thrombotic stroke is a common disorder with considerable mortality and morbidity. Risk factors for stroke include cigarette smoking, hypertension and hyperlipidaemia and these have been linked to abnormalities of haemorrheology and coagulation such as increased fibrinogen. Other haemorrheological abnormalities have also been documented. These include an elevation in the white blood cell (WBC) count. The aim of our study was to evaluate plasma fibrinogen, WBC aggregation and the release of free radicals in thrombotic stroke.
Experimental design. Thirty-four patients with thrombotic stroke were enrolled in the study. The data were compared to 58 matched controls.
Setting. This study was carried out in Ninewells Hospital, Dundee on patients previously admitted to the medical wards with acute stroke.
Measures. Plasma fibrinogen, WBC aggregation and plasma malondialdehyde (MDA) were measured in this study.
Results. As expected, the stroke patients have a significantly higher fibrinogen level (4.3±1.2 g/dl versus 3.1±0.6, p<0.001). WBC aggregation is also increased in the patient group (47.5±10.4% versus 42.7±10.6, p=0.036), as is plasma MDA (8.6±2.0 µmol/l versus 7.1±1.07, p<0.001). The factor VIII von Willebrand factor antigen measured as a marker as vascular damage was also significantly higher in the patient group (251±87% versus 182±64, p<0.001). There was also a statistically significant correlation between fibrinogen level and WBC aggregation, and fibrinogen and MDA. These are both statistically significant p=0.012 and p<0.001 respectively.
Conclusions. We believe our study suggests that enhanced WBC aggregation/adhesion with release of free radicals may be another mechanism whereby fibrinogen exerts its known detrimental effect in stroke development. This may allow planning of therapeutic strategies as yet undeveloped.