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Q J Med 2001; 94: 327-332
© 2001 Association of Physicians

Dyslipidaemia in patients with malignant-phase hypertension

E. Edmunds1, M.J. Landray1,2, F.L. Li-Saw-Hee1, B.A. Hughes2, D.G. Beevers1 and G.Y.H. Lip1,

1 From the University of Birmingham Division of Medical Sciences, City Hospital and 2 Queen Elizabeth Hospital, Birmingham, UK

Received 27 February 2001 and in revised form 6 April 2001

Low-density lipoprotein (LDL) consists of a heterogeneous group of particles of differing size, density and electrophoretic mobility, smaller particles being more atherogenic. A high proportion of small LDL particles is an independent risk factor for cardiovascular disease. We hypothesized that patients with malignant phase hypertension (MHT), the most severe form of hypertension, would demonstrate a more atherogenic LDL subfraction profile than either non-malignant hypertension (NMHT) or normotensive controls. We compared 16 patients with MHT to 41 patients with untreated NMHT and 45 normotensive controls. LDL subfraction profile was measured by disc polyacrylamide gel electrophoresis using a validated scoring system to calculate the mean size (locus) and heterogeneity (spread) of LDL subfraction mobilities. A higher LDL locus indicates a greater proportion of small LDL subfractions. LDL cholesterol levels were similar in all three groups (p=0.23). High-density lipoprotein cholesterol (HDL-C) levels were significantly lower (p<0.001) and serum triglyceride concentrations significantly higher (p=0.02) in the MHT group, compared to normotensive controls. LDL locus was greater in the NMHT group than in the normotensive controls and intermediate in the MHT group (p=0.008). There was no significant difference in LDL spread (p=0.26). Serum triglyceride concentrations were not significantly higher after adjusting for confounding variables. MHT is associated with an abnormal lipid profile, characterized by low HDL-cholesterol concentration. This dyslipidaemia may be partly responsible for the vascular complications and the poor prognosis of these patients.

Address correspondence to Dr G.Y.H. Lip, Haemostasis, Thrombosis and Vascular Biology Unit, City Hospital NHS Trust, Dudley Road, Birmingham B18 7QH. e–mail: g.y.h.lip{at}bham.ac.uk


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