Post-transplant hyperlipidaemia: low-dose lovastatin lowers atherogenic lipids with without plasma accumulation of lovastatin

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Abstract
Gullestad L, Nordal K, Forfang K, Ihlen H, Hostmark A, Berg KJ, Cheng H, Schwartz MS, Geiran 0, Simonsen S (Rikshospitalet University Hospital and University of Oslo, Oslo, Norway, and Merck Research Laboratories, West Point, PA, USA). Post‐transplant hyperlipidaemia: low‐dose lovastatin lowers atherogenic lipids without plasma ac‐cumulation of lovastatin. 1 Intern Med 1997; 242: 483‐490. Objectives: The purpose of the present study was twofold. First, to determine the frequency of hyperlipidaemia after heart transplantation (Tx) in relation to values obtained before Tx. Secondly, to examine the effect of low‐dose lovastatin on possible antiatherogenic mechanisms and test the hypothesis that the side‐effects are dose‐dependent. Subjects and design: Retrospective study of the frequency of hyperlipidaemia disturbances in heart transplant patients. In addition, in a prospective study, the safety and efficacy of incremental study, the safety and efficacy of incremental studied, with measurements of its plasma concentration in 24 cyclosporin A treated heart (n = 14) and kidney (n = 10) recipients with total cholesterol >7.5 mmol L‐I. Results: Cholesterol increased markedly after heart transplantation from a pretransplant value of 5.3 (5.0.5.6) mmol L‐‘ to 6.7 (6.4.7.0) mmol L ‐’ after 1 year and then remained constant, but this increase was largely due to a ‘normalization’ since cholesterol decreased significantly during increasing heart failure before transplantation. Treatment with lovastatin decreased total cholesterol by 19% (P < 0.00l), primarily by an effect on IBL cholesterol. HDL cholesterol increased by 15% (P < 0.05), whereas triglycerides remained unchanged. Lovastatin also caused a significant reduction in apolipoprotein B of 16% and lipid peroxidation of 40%. whereas apolipoprotein A‐I, fibperoxidation of 40%. whereas apolipoprotein A‐I, fibcentration of lovastatin was significantly higher in transplant recipients compared with controls, but there was no accumulation during incremental dosing of lovastatin. The drug was well tolerated without significant symptoms or evidence of myopathy. Conclusions: Hyperlipidaemia is common after cardiac transplantation. Treatment with low dose lovastatin is well tolerated and has a favourable effect on atherogenic lipids.

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