Abstract
Acute coronary syndromes are caused by plaque rupture. The conventional strategy of prevention of plaque rupture has been driven by the “lipid hypothesis”—if lipid levels are optimized to target levels, the risk of coronary events is decreased. Indeed, the hypothesis has been validated by the dramatic success of statin therapy. However, further major reductions in cardiac events is a realistic goal; various mechanistic and small clinical studies show that statins have beneficial effects in addition to their lipid-lowering properties. One of these beneficial effects is stabilization of plaque. Despite billions of dollars spent on randomized clinical trials, optimal therapy for coronary artery disease is yet to be tested. This therapy might include various combinations of the Mediterranean or low-fat diet, endothelial passivation, lipid-lowering drugs, antioxidants, antiplatelet agents and anti-inflammatory agents.
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