Please note - this EPG Cholesterol Knowledge Centre is for Doctors and other Healthcare Professionals.

Low-density lipoprotein cholesterol (LDL-C) has been shown to be strongly associated with the development of atherosclerosis, Cardiovascular Heart Disease (CHD) and events in patients with established CHD.

The association between LDL-C and the risk of CHD events is considerably increased by other risk factors, such as low high-density lipoprotein cholesterol (HDL-C), smoking, hypertension, diabetes and the metabolic syndrome.¹

Today it is more common to identify the dyslipidaemias by the particular lipoprotein or apolipoprotein that is abnormal. Once dyslipidaemia has been identified it is important to determine the cause where possible.

ATP III recognizes that detection of cholesterol disorders and other coronary heart disease (CHD) risk factors occurs primarily through clinical case finding. 

Risk factors can be detected and evaluated as part of a person’s work-up for any medical problem. A basic principle of prevention is that the intensity of risk-reduction therapy should be adjusted to a person’s absolute risk. Hence, the first step in selection of LDL-lowering therapy is to assess a person’s risk status. Risk assessment requires measurement of LDL cholesterol as part of lipoprotein analysis and identification of accompanying risk determinants.

Statins are the treatment choice in dyslipidaemia. Statins (HMG-CoA reductase inhibitors) are the most effective class of drugs in reducing LDL-C levels and have also been shown to be very effective in improving the overall lipid profiles in patients with dyslipidaemia. The benefits of statin therapy on morbidity and mortality from cardiovascular disease have also been demonstrated in patients with a wide range of LDL-C levels.

Enter the Cholesterol Knowledge Centre

What’s in the Cholesterol Knowledge Centre?

• Cholesterol
• LDL/HDL
• Lipoprotein Metabolism Cycles
• Dyslipidaemia
• Atherosclerosis
  
• CV Risk Factors
• Clinical Manifestation of Atherosclerosis
• Atherosclerosis
• Atherogenesis
• Prevalence and Incidence
• Pathogenesis of Atherosclerotic Plaques
• Plaque Formation
  
• Invasive Imaging Techniques Used to Assess Atherosclerosis
• Non-invasive techniques
  
• Risk Assessment
• Management Guidelines
• NCEP ATP III Management Guidelines
  
• Millimol Converter
• BMI Calculator
• Treatment: Rosuvastatin
• Efficacy
• Safety and Tolerability
• Controlled Clinical trials
• Post-marketing surveillance
• Pharmacoepidemiology
• Fibrates
• Bile Acid Sequestrants
• Nicotinic Acid (Niacin)
• Diet and Exercise
• E-Learning
• Useful Links
• Case Studies
• Angina
• Arrhythmia
• Arteries
• Atheromatous Plaque
• Atherosclerosis
  
• Bile acids
• Cardiovascular Disease (CVD)
• Cardiovascular risk factor
  
• Cerebrovascular accident
• Cerebrovascular Disease (CBVD)
• Cholesterol
  
• Coronary heart disease (CHD)
• Dyslipidaemia
• Endogenous Pathway
• Enzyme
  
• Exogenous Pathway
• Fibrates
• Framingham Study
  
• Global (or total) cardiovascular risk assessment
• Gold standard therapy
• HDL - cholesterol A
• Intermittent claudication
• Ischaemia
• LDL-cholesterol
• LDL-cholesterol
• Lipoproteins
• Modifiable risk factor
• Myocardial Infarction (MI)
• Myocardium
• Nicotinic acid
  
• Non-modifiable risk factor
• Outcome
• Peripheral Vascular Disease (PVD)
• Placebo-control
• Plaque
• Primary Prevention
• Randomised
• Resins
• Risk factor
• Secondary prevention
• Secretion
• Synthesis
• Starting dose
• Statins Drugs
• Titrate
• Toxins
  
• Transient ischaemic attack (TIA)
• Triglyceride

References
1. Wood D et al, for the Joint European Committee, Second Task Force of European and other Societies. Atherosclerosis 1998;140:199–270.