Approximately 70 million people in the U.S. have one or more forms of cardiovascular disease, including coronary heart disease, the leading cause of death in the U.S., responsible for over 479,000 deaths in 2003. Coronary heart disease is caused by deposition of cholesterol in the coronary arteries leading to coronary arteriosclerosis, a condition that may lead to chest pain, heart attack or debilitating and potentially fatal heart disease. At least 13.2 million Americans alive today have suffered from such conditions. In addition, arteriosclerosis can occur in other blood vessels, particularly those supplying blood to the brain, leading to stroke and other cerebrovascular conditions. High levels of low-density lipoproteins (LDL) have been conclusively shown to be a major cause of coronary heart disease.

A series of recent landmark clinical trials using statins (for example Lipitor^® and Zocor^®) confirmed that decreasing high LDL cholesterol reduces the risk of coronary artery disease and stroke. In 1985, the National Cholesterol Education Program (NCEP) was launched with the goal of reducing coronary heart disease by reducing the percentage of Americans with high cholesterol. Treatment guidelines issued by the NCEP have advocated increasingly lower LDL cholesterol treatment targets as new scientific data has emerged. Despite this, it is estimated that in the major pharmaceuticals markets, 300 million people have cholesterol disorders and of these, 180 million remain undiagnosed. It is expected that the number of patients needing cholesterol-lowering therapy will continue to grow because of an aging population and the increasing number of diabetic individuals.

LP(a)

Lipoproteins are proteins which transport fatty substances in the blood stream to and from the liver. One of these lipoproteins is Lp(a), which has a shape similar to blood clotting proteins and may encourage blood to clot when Lp(a) levels are high. Lp(a) has been shown to be an important independent variable for prediction of risk of cardiovascular disease after LDL cholesterol and HDL cholesterol, as demonstrated in patients with coronary heart disease, stroke and premature peripheral vascular disease and in the aging. Epidemiological studies indicate that high levels of Lp(a) are associated with an increased frequency of stroke and coronary heart disease. Large studies confirming the effect of lowering Lp(a) have not yet been conducted and, to date, there are no drugs approved for the treatment of elevated Lp(a) levels. Nevertheless, it is generally believed that lowering Lp(a) could be beneficial and contribute to a further reduction of the incidence of stroke and coronary heart disease.