Lipid lowering versus revascularization: an idea whose time (for testing) has come.

There is strong evidence that revascularization does not prevent myocardial infarction in patients with stable coronary artery disease (CAD). The anatomic basis for this counterintuitive conclusion seems to be that most myocardial infarctions occur at sites that did not previously exhibit an angiographically significant stenosis. These angiographic observations are further supported by thallium studies in stable CAD that demonstrate that the site of stress-induced ischemia is frequently not the site of subsequent myocardial infarction. Since both coronary artery bypass graft surgery and percutaneous transluminal coronary angioplasty are directed at more severe coronary stenoses, we are led to the remarkable conclusion that angiography does not identify, and consequently revascularization therapies do not treat, the lesions that lead to myocardial infarction. The pathology of coronary atherosclerosis provides the basis for understanding why revascularization does not prevent infarction: unstable lesions that cause infarction are not necessarily severely stenotic, and stenotic lesions are not necessarily unstable. In contrast to revascularization, lipid lowering reduces the rate of myocardial infarction by approximately 30% over a period of 5 years. Thus, we might postulate that lipid lowering is the more effective therapy for both prevention of acute myocardial infarction and long-term survival. The health policy and economic implications of this viewpoint, should it emerge in the management of coronary heart disease, are clearly substantial. Consequently, the relative roles of lipid-lowering therapy and revascularization, both alone and together, must now be determined. It is an idea whose time--for testing--has come.