IMPLICATIONS FOR THE PRESENT AND DIRECTION FOR THE FUTURE

Numerous angiographic trials have demonstrated that the atherosclerotic process can be modified through reductions in levels of low-density lipoprotein (LDL) cholesterol. Recent research has focused on other potential modalities by which atheroroma development might be inhibited. These newer strategies include reduction of the oxidative potential of LDL particles through modification of dietary fat intake; prevention of LDL oxidation through the use of antioxidants; and inhibition of monocyte and macrophage function by omega-3 fatty acids and leukotriene-1 antagonists. Inhibition of acyl-coenzyme A:cholesterol acyltransferase (ACAT) may block intestinal cholesterol absorption and reduce synthesis of very-low-density lipoprotein (VLDL), while simultaneously enriching high-density lipoprotein (HDL) cholesterol. Modification of cholesterol ester transfer protein may be associated with improved reverse cholesterol transport or enlarged HDL particles. In the future, a wide variety of therapeutic modalities may be available for use alone or in combination to reverse atherosclerosis or prevent its progression.