Cardiovascular disease (CVD) represents one of the leading causes of morbidity worldwide. In the United States (U.S.), a myocardial infarction (MI) occurs every 40 seconds and a stroke occurs every 40 seconds.1 Nearly 1 in 3 patients with a history of prior ischemic events will experience a recurrent event.2 While cardiovascular (CV) events often seem to arise spontaneously, they are the result of a complex process that occurs over an extended period of time. Despite advances in secondary prevention, many patients with established CVD remain at risk for cardiovascular events. Understanding the science of atherosclerosis is key to mitigating that risk. Additionally, recent ACC/AHA guidelines call for improved patient-physician discussion.
LDL-C is the driver of atherosclerosis and one of the key modifiable risk factors for the development of CVD.3,4 As the risk for CV events is directly related to the absolute level and duration of exposure to LDL-C, effective LDL-C lowering is critical to the reduction of CV risk.3
Many patients with established CVD do not achieve LDL-C goals despite treatment.5 Even those who do achieve recommended goals remain at significant risk for subsequent events.6 An estimated 1 in 3 patients with a history of an ischemic event will experience a recurrent event.2
Cholesterol is essential for many physiological functions and all cells have the ability to synthesize it de novo.7,8,9 Cholesterol levels are tightly regulated to ensure intracellular levels remain constant regardless of changes in circulating LDL-C levels.7 Many lines of evidence indicate that ‘average’ LDL-C levels in American adults today are many times above what is considered physiologically normal.10