INCREASING ERYTHROCYTE AGGREGABILITY WITH THE PROGRESSIVE GRADES OF CHRONIC VENOUS INSUFFICIENCY - IMPORTANCE AND MECHANISMS

Citation
F. Zuccarelli et al., INCREASING ERYTHROCYTE AGGREGABILITY WITH THE PROGRESSIVE GRADES OF CHRONIC VENOUS INSUFFICIENCY - IMPORTANCE AND MECHANISMS, Journal of Cardiovascular Surgery, 36(4), 1995, pp. 387-391
Citations number
NO
Categorie Soggetti
Cardiac & Cardiovascular System",Surgery
ISSN journal
00219509
Volume
36
Issue
4
Year of publication
1995
Pages
387 - 391
Database
ISI
SICI code
0021-9509(1995)36:4<387:IEAWTP>2.0.ZU;2-E
Abstract
Erythrocyte aggregation (EA) has appeared as the most interesting para meter among theological measurements in chronic venous insufficiency ( CVI). We therefore conducted two different kinds of studies to provide further information about the distribution and mechanisms of EA in CV I. We first analysed EA values in 67 patients, classified according to 3 evolutive groups: 27 patients suffering only from subjective sympto ms of venous disease (grade 1), 19 patients with varicosis and sapheno -femoral incompetence (grade 2), 21 patients with varicosis and trophi c skin changes (grade 3). EA values were also measured in 22 healthy c ontrols. Analysis of EA was performed for equal concentrations of fibr inogen and adjusted for age. EA was significantly higher in CVI. The a ggregation index, related to the kinetics of aggregates formation, ros e significantly even from grade 1 while compared to controls and rose further with the evolutive grades. The same trend was found with the p artial dissociation threshold (i.e. red cells aggregates cohesion). As the measurements were performed at standardized hematocrit and the re sults expressed after fibrinogen levels adjustment, this suggests the involvement of other factors. We subsequently investigated whether red cells from CVI patients aggregate more than those of controls when su spended in the same medium. The results showed that a cellular factor is unlikely to be involved, and that an interaction between red cells and plasma proteins other than fibrinogen could also explain the incre ased EA in CVI.