Catheterization and Cardiovascular Diagnosis 25:2!&30 (1992) zy Lipids and Fatty Acids and Their Relationship to Restenosis Jerome B. Foley, MB, MRCP(UK), Kate Younger, PhD, David Foley, MB, MRCPI, Anthony Kinsella, MSC, FIF, Martin Molloy, MB, FRCR, Peter A. Crean, MB, FRCPI, Gerry Gearty, MB, FRCPI, Michael Gibney, MA, PhD, and Michael J. Walsh, MD, FRCPl One hundred consecutive patients had fasting lipids and percutaneous fat biopsy per- formed at the time of percutaneous transluminal coronary angioplasty to determine if there was an association between restenosis and lipids or fatty acids. Anglographic follow-up and complete lipid and fatty acid results were available in 82 patients. Reste- nosis occurred in 37/82 (45%). Total cholesterol, triglyceride, high density lipoprotein, low density lipoprotein, and apolipoproteins A1 and B were not associated with reste- nosis. There was a significantly lower level of the monounsaturatedfat palmitoleic acid (p < 0.02), a trend towards a lower level of the monounsaturatedfat oleic acid (p < 0.09), and zyxwvutsr a trend towards a higher level of the saturated fat plamitic acid (p < 0.08) in the restenosis group. The polyunsaturated fatty acids were not associated with restenosis. We conclude that lipids are not significantly associated with restenosis, and that lower levels of monounsaturatedfatty aclds may increase the risk of restenosls. Key words: apolipoproteins, angioplasty, percutaneous fat biopsy INTRODUCTION zyxwvutsrq Percutaneous transluminal coronary angioplasty has become established as a safe and effective therapeutic option for the management of ischaemic heart disease. Restenosis, however, which occurs in up to 40% of ini- tially successful procedures, has emerged as the major long term limitation of coronary angioplasty (1-31. The weight of evidence is that restenosis is due to platelet adhesion and activation at the site of the angioplasty, which results in the release of mitogenic and chemotactic substances that cause smooth muscle multiplication and migration into the intima, producing the restenosis lesion PI. Abnormalities of lipid metabolism are associated with atherosclerosis and coronary artery disease zyxwvut [4-61. Their association with restenosis following coronary angio- plasty, however, remains an area of debate. It has been established that a diet high in saturated fatty acids is associated with an increased risk of developing coronary artery disease, while a diet high in polyunsaturated fatty acids is associated with a reduced risk [7-91. In recent years there has been considerable interest in the potential benefit of a diet high in monounsaturated fatty acids which has been shown to result in a reduction in low density lipoprotein, without the reduction in high density lipoprotein seen in a diet low in cholesterol and high in carbohydrate [10,11]. The role of fatty acid intake and metabolism in the pathogenesis of restenosis has not been previously documented. The aim of this study was to determine the role of lipids, apolipoproteins, and fatty acids as predictors of restenosis. METHODS Patient Selection Consecutive patients with stable and unstable angina who had undergone their first successful single lesion angioplasty of a native vessel were prospectively entered into the study after giving informed written consent. Pa- tients with diabetes mellitus or those on lipid lowering drugs were excluded. Patients were classified according to their smoking status at the time of the angioplasty into current smokers, ex-smokers (those who had not smoked for at least 6 months before the angioplasty), and non- smokers. Angina was classified as unstable if it fulfilled one of the three following criteria; (a) angina of less than From Trinity Cardiology and Sir Patrick Dun's Research Laboratory. St James's Hospital, and Institute for Higher Education, Dublin, Ire- land. Received March 29, 1991 ; revision accepted July 3 I, 1991. Address reprint requests to Michael Walsh, MD, FRPCI, Trinity Med- ical School. St James's Hospital, P.O. Box 580, Dublin 8, Ireland. zy 0 1992 Wiley-Liss, Inc.