The lipoproteins (LPs) have historically been the focus of research into the causes of atherosclerosis and coronary artery disease.
They are still important to our understanding, though we now know that many other biological systems are also involved.
Because so many different factors – some still unknown – are involved in the development of atherosclerosis and CAD, it is difficult to accurately predict an individual’s risk for a heart attack. However, if someone suffers from extreme derangements or disorders, the risk is vastly increased and easier to predict.
The good news is that, for the majority of the population, preventative lifestyle interventions reduce the risk of future illness can to a great extent.
Armed with information about lipoproteins, techniques were developed to measure HDL (“good”) and LDL (“bad”) cholesterol separately. Further research also began to illuminate the biological and other factors which determine the levels of these two plasma lipoproteins.
Levels of LDL cholesterol are directly linked to those of another protein – apoB – which is almost entirely carried by LDL. So, instead of measuring LDL cholesterol, scientists realised that measurement of apoB would give similar (but not identical) information.
It was also discovered that the LDL packages themselves became smaller and denser in certain disorders, including hypertriglyceridaemia (the medical term for raised triglyceride levels).
There is evidence that these forms of LDL are more likely to cause atherosclerosis than the normal version. They are called small-dense LDL or sd-LDL.