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Influence of plasma and erythrocyte factors on red blood cell aggregation in survivors of acute myocardial infarction.
Thromb Haemost. 2004 Feb; 91(2):354-9.TH

Abstract

Increased erythrocyte aggregation (EA) has been observed in patients with ischaemic heart disease (IHD), although most of these studies have been performed in the acute phase when reactant proteins may account for this increase. Little is known about the role played by the erythrocyte itself in this aggregation process. To ascertain the contribution of both plasma and erythrocyte factors to EA in IHD, we investigated the following parameters in 78 survivors of acute myocardial infarction (AMI) and in a well-matched control group of 98 subjects: EA, glucose, total cholesterol (T-Chol), low-density lipoprotein-cholesterol (LDL-Chol), high-density lipoprotein-cholesterol (HDL-Chol), triglycerides, apolipoproteins A(1) and B, protein and functional fibrinogen, plasma sialic acid, membrane sialic acid, and the cholesterol and phospholipid content of the erythrocyte membrane. AMI survivors showed higher glucose (p<0.001), a borderline increase in triglycerides (p = 0.043), and a statistical decrease in Apo A(1) (p= 0.003) relative to controls. EA, functional fibrinogen, and plasma sialic acid were statistically higher in AMI survivors than in controls (p= 0.001; p<0.001; p= 0.011, respectively). Membrane sialic acid content was statistically lower in AMI patients than in controls (p= 0.026). No differences were observed in either membrane cholesterol or phospholipids. Multivariate logistic regression analysis, in which EA was dichotomized as higher or lower than 8.7, demonstrated that triglyceride levels higher than 175 mg/dL (OR= 7.7, p= 0.001) and functional fibrinogen levels higher than 320 mg/dL (OR= 3.7, p= 0.004) were independently associated with a greater risk of erythrocyte hyperaggregability. Our results suggest that plasma lipids, predominantly triglycerides, and fibrinogen may not only enhance the development of ischaemic events by their recognized atherogenic mechanisms, but also by increasing EA.

Authors+Show Affiliations

Hemorheology and Thrombosis Unit, Department of Clinical Pathology, La Fe University Hospital, Valencia, Spain. vaya_amp@gva.esNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

14961164

Citation

Vayá, Amparo, et al. "Influence of Plasma and Erythrocyte Factors On Red Blood Cell Aggregation in Survivors of Acute Myocardial Infarction." Thrombosis and Haemostasis, vol. 91, no. 2, 2004, pp. 354-9.
Vayá A, Falcó C, Réganon E, et al. Influence of plasma and erythrocyte factors on red blood cell aggregation in survivors of acute myocardial infarction. Thromb Haemost. 2004;91(2):354-9.
Vayá, A., Falcó, C., Réganon, E., Vila, V., Martínez-Sales, V., Corella, D., Contreras, M. T., & Aznar, J. (2004). Influence of plasma and erythrocyte factors on red blood cell aggregation in survivors of acute myocardial infarction. Thrombosis and Haemostasis, 91(2), 354-9.
Vayá A, et al. Influence of Plasma and Erythrocyte Factors On Red Blood Cell Aggregation in Survivors of Acute Myocardial Infarction. Thromb Haemost. 2004;91(2):354-9. PubMed PMID: 14961164.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Influence of plasma and erythrocyte factors on red blood cell aggregation in survivors of acute myocardial infarction. AU - Vayá,Amparo, AU - Falcó,Cristina, AU - Réganon,Edelmiro, AU - Vila,Virtudes, AU - Martínez-Sales,Vicenta, AU - Corella,Dolores, AU - Contreras,M Teresa, AU - Aznar,Justo, PY - 2004/2/13/pubmed PY - 2004/10/20/medline PY - 2004/2/13/entrez SP - 354 EP - 9 JF - Thrombosis and haemostasis JO - Thromb Haemost VL - 91 IS - 2 N2 - Increased erythrocyte aggregation (EA) has been observed in patients with ischaemic heart disease (IHD), although most of these studies have been performed in the acute phase when reactant proteins may account for this increase. Little is known about the role played by the erythrocyte itself in this aggregation process. To ascertain the contribution of both plasma and erythrocyte factors to EA in IHD, we investigated the following parameters in 78 survivors of acute myocardial infarction (AMI) and in a well-matched control group of 98 subjects: EA, glucose, total cholesterol (T-Chol), low-density lipoprotein-cholesterol (LDL-Chol), high-density lipoprotein-cholesterol (HDL-Chol), triglycerides, apolipoproteins A(1) and B, protein and functional fibrinogen, plasma sialic acid, membrane sialic acid, and the cholesterol and phospholipid content of the erythrocyte membrane. AMI survivors showed higher glucose (p<0.001), a borderline increase in triglycerides (p = 0.043), and a statistical decrease in Apo A(1) (p= 0.003) relative to controls. EA, functional fibrinogen, and plasma sialic acid were statistically higher in AMI survivors than in controls (p= 0.001; p<0.001; p= 0.011, respectively). Membrane sialic acid content was statistically lower in AMI patients than in controls (p= 0.026). No differences were observed in either membrane cholesterol or phospholipids. Multivariate logistic regression analysis, in which EA was dichotomized as higher or lower than 8.7, demonstrated that triglyceride levels higher than 175 mg/dL (OR= 7.7, p= 0.001) and functional fibrinogen levels higher than 320 mg/dL (OR= 3.7, p= 0.004) were independently associated with a greater risk of erythrocyte hyperaggregability. Our results suggest that plasma lipids, predominantly triglycerides, and fibrinogen may not only enhance the development of ischaemic events by their recognized atherogenic mechanisms, but also by increasing EA. SN - 0340-6245 UR - https://www.unboundmedicine.com/medline/citation/14961164/Influence_of_plasma_and_erythrocyte_factors_on_red_blood_cell_aggregation_in_survivors_of_acute_myocardial_infarction_ L2 - http://www.thieme-connect.com/DOI/DOI?10.1160/TH03-08-0497 DB - PRIME DP - Unbound Medicine ER -