Rheological profile in severe and morbid obesity. Preliminary results
Issue title: Selected proceedings of the 12th European Conference on Clinical Hemorheology, 22‐26 June 2003, Sofia, Bulgaria
Article type: Research Article
Authors: Solá, Eva | Vayá, Amparo; | Contreras, Teresa | Falcó, Cristina | Corella, Dolores | Hernández, Antonio | Aznar, Justo
Affiliations: Endocrinology Service, Dr. Peset Hospital, Valencia, Spain | Thrombosis and Hemorheology Unit, La Fe University Hospital, Department of Clinical Pathology, Valencia, Spain | Genetic and Molecular Epidemiology Unit, School of Medicine University of Valencia, Spain
Note: [] Corresponding author: Amparo Vayá, MD, PhD, Thrombosis and Hemorheology Unit, Department of Clinical Pathology, La Fe University Hospital, Avda. de Campanar, 21, 46009 Valencia, Spain. Tel.: +34 963861714; Fax: +34 961973089; E‐mail: vaya_amp@gva.es.
Abstract: The association of hemorheological alterations with morbid obesity remains a question of debate. In order to ascertain whether morbid obese subjects show certain hemorheological alterations which might be involved in the higher thrombotic risk which characterizes these subjects, we determine glucose, plasma lipids, apolipoproteins, fibrinogen, hematocrit, blood viscosity (Brookfield DVIII viscosimeter), both at native and corrected hematocrit of 45%, plasma viscosity (Fresenius capillary viscosimeter), erythrocyte aggregation (Myrenne aggregometer), both at stasis and at 3 s−1 at 45% hematocrit and erythrocyte indexes in 41 morbid obese subjects (32 female, 9 male aged 33±10 years), and in a well matched non‐obese control group (40 female, 15 male, aged 32±10 years). Mean BMI in the morbid obese group was 44.9±6.7 kg/m2 vs 23.5±4.8 kg/m2 in the control group (p<0.001). Morbid obese subjects when compared with the control group showed a statistically higher glucose level (p<0.001), LDL‐cholesterol (p=0.019), triglycerides (p<0.001), apoB (p=0.019), apoB/A1 (p<0.001), fibrinogen (p<0.001), erythrocyte aggregation (p<0.001), and a statistically lower HDL‐cholesterol (p<0.001). No differences between both groups were observed regarding total‐cholesterol, plasma viscosity, blood viscosity and hematocrit (p=0.109; p=0.690; p=0.510; p=0.950), respectively. After the adjustment for BMI, differences in glucose, LDL‐cholesterol, triglycerides, apoB, apoB/A1, and erythrocyte aggregation did not reach the statistical significance, and differences in fibrinogen were borderline significant (p=0.051), showing a direct effect of BMI on the detected differences between obese and non‐obese. Our results suggest that in morbid obese subjects the increased fibrinogen levels and the altered lipid profile associated with their higher BMI, could in addition to its known mechanisms on haemostasis, favour both venous and arterial thrombotic events by enhancing erythrocyte aggregation.
Journal: Clinical Hemorheology and Microcirculation, vol. 30, no. 3-4, pp. 415-418, 2004
