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Lupus
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The Heart and Antiphospholipid Antibodies in MRL-lpr/lpr Mice

J.L. Vianna

Lupus & Arthritis Research Unit, The Rayne Institute, St Thomas' Hospital, London SE1 7EH

S. Trotter

Department of Cardiovascular Pathology, Royal Brompton National Heart & Lung Hospital, London, UK

M.A. Khamashta

Lupus & Arthritis Research Unit, The Rayne Institute, St Thomas' Hospital, London SE1 7EH

S. Chikte

Department of Cardiovascular Pathology, Royal Brompton National Heart & Lung Hospital, London, UK

E. Olsen

Department of Cardiovascular Pathology, Royal Brompton National Heart & Lung Hospital, London, UK

G.R.V. Hughes

Lupus & Arthritis Research Unit, The Rayne Institute, St Thomas' Hospital, London SE1 7EH

Our objective in this study was to determine possible associations between antiphospholipid antibodies (aPL) and histologically defined heart valve lesions in the MRL-lpr/lpr mouse, a suitable model for the antiphospholipid syndrome (APS). At monthly intervals, from 2 to 6 months of age, three MRL-lpr/lpr mice (two with anticardiolipin antibodies, one without) and two sex- and age-matched Balb/c mice (controls) were sacrificed for histological studies. Serum binding to phospholipids and DNA was studied at this time.

We found thickened heart valves in 68% of MRL-lpr/lpr mice and in 80% of Balb/c mice, and no association with any of the antibodies tested was found. No evidence of coronary vasculitis or thrombi was found in any of the mice studied. Platelet counts in MRL-lpr/lpr mice were significantly lower (640.530 ± 211.818 x 106/ml) than in Balb/c mice (780.0 + 112.5 x 106/ml) (P < 0.05), and no association was found between platelet counts and aPL. In this model of murine APS, aPL bear no importance in heart valve pathology.

Key Words: Antiphospholipid syndrome • Animal models • Anticardiolipin • Lupus

Lupus, Vol. 1, No. 6, 357-361 (1992)
DOI: 10.1177/096120339200100604
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