directed through a 200 pm quartz fiber optic) by delivering

Laser therapy for arteriosclerosis: current reviewDavid J. Dries, Marc E. Pollock and John EugeneDepartment of Surgery, University of California, Irvine101 City Drive South, Orange, California 92668IntroductionShortly after the ruby laser was introduced, in 1959, a study for the use of this rubylaser for the in -vitro dissolution of arteriosclerotic plaque was performed.) With subse-quent advances in laser technology and with refined delivery techniques, laser applicationsto the treatment of arteriosclerosis in the coronary arteries and peripheral vascular sys-tem is a reality. This report reviews the disease process, arteriosclerosis, and the ef-forts towards laser treatment of this disease. We conclude with a review of the technicalbarriers to the routine application of laser energy in arteriosclerotic cardiovasculardisease and the progress being made to overcome these obstacles.ArteriosclerosisCardiovascular diseases remain the chief cause of death in Western society and have beenthe focus of research and treatment efforts for decades.2 Arteriosclerosis is the majorcause of stroke and myocardial infarction implicated in most deaths due to cardiovasculardisease. The earliest sign, the fatty streak, is a flat lipid -rich lesion containingmacrophages and smooth muscle cells. These primary changes of arteriosclerosis may befound as early as childhood. Progression of fatty streaks to the next lesion, the fibrousplaque, has been demonstrated in serial studies of coronary arteries in children growing toyoung adulthood. Fibrous plaques contain increased smooth muscle cells with variousamounts of intracellular and extracellular lipid surrounded by a connective tissue matrixand fibrous cap. Deeper portions of these lesions may contain necrotic debris, crystals ofcholesterol and calcium. Progressive accumulation of calcium and other debris along withhemorrhage into the substance of a plaque marks evolution from advanced to complex arterio-sclerosis and the replicative capability of plaque cells is diminished in comparison tonormal endothelial cells of the arterial wall.Several factors appear to be at work in the development of plaques. The initial injuryappears to involve the endothelium. Chemical injury to the endothelium (as can occur withhypercholesterolemia) may allow adherence of platelets and subsequent involvement of bloodborne monocytes with growth factor release from various cell types causing smooth muscleproliferation and macrophage accumulation characteristic of early atherosclerosis. Directstimulation of endothelium as can occur with hypertension, diabetes mellitus or cigarettesmoking may also induce smooth muscle accumulation with subsequent plaque formation. Me-chanical injury causing segmental removal of endothelium is another way to allow plateletand monocyte accumulation with subsequent plaque formation at the site of injury.The clinical presentation of arteriosclerotic lesions has been reviewed by DeBakey andcoworkers in over 13,000 patients treated over a 35 year period.3 They noted that occlusivedisease due to arteriosclerosis could be classified according to anatomic distribution intoone of five patterns: (1) the coronary arterial bed, (2) the major branches of the aortic