Summary
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 A1 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 A1 (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.
Keywords
Red blood cell aggregation - myocardial infarction - plasma factors - erythrocyte
factors
