Merck/Schering-Plough Pharmaceuticals, a joint venture between Merck and Schering-Plough to develop and market in the US new prescription medicines in cholesterol management has commenced patient enrolment in its large-scale, clinical outcomes trial conducted for Vytorin (ezetimibe/simvastatin).
IMPROVE-IT (Improved Reduction of Outcomes: Vytorin Efficacy International T rial) will evaluate the effectiveness of Vytorin compared to Zocor (simvastatin) alone in treating approximately 10,000 high risk patients with coronary artery disease presenting with "acute coronary syndromes" (ACS). In clinical trials, Vytorin has been shown to be superior to both Lipitor and Zocor in effectively lowering LDL cholesterol.
IMPROVE-IT is a head-to-head study of Vytorin 10/40mg as compared to Zocor 40 mg. The primary endpoint of the trial is the composite of cardiovascular death, myocardial infarction (MI), nonfatal stroke, rehospitalization for ACS or revascularization (occurring 30 days or more after the initial event). The IMPROVE-IT study is designed to lower LDL cholesterol with Vytorin below levels that have been studied in prior large outcomes trials, which demonstrated that lower LDL cholesterol levels led to lower cardiovascular risk.
"This important new trial could add substantially to the body of knowledge concerning how we can reduce the risk of coronary events by managing LDL cholesterol; including a determination of what impact LDL lowering may have in patients who present with ACS. It is important that the medical community continue to investigate how low we should go in reducing LDL cholesterol in an effort to lower residual risk for these patients," said Enrico Veltri, group vice president, Schering-Plough Research Institute.
Acute coronary syndromes are generally caused by the build-up of atherosclerotic plaque (deposits of fat-containing material) in the coronary arteries of the heart. These plaques may tear or rupture, leading to the formation of a blood clot which may partly or completely block the blood flow in a coronary artery, abruptly limiting the supply of oxygenated blood to a portion of heart muscle.