To the Editor,
The study by Akyea et al1 raises a number of issues. First, the authors have not presented any all-cause mortality data. This is of vital importance when evaluating a preventative measure; not only is preventing death from particular causes relevant but overall mortality must be reduced for effectiveness to be claimed.
The ‘lack of response’ in over half of the patients demonstrates the problem seen with oversimplification of physiology. Low-density lipoprotein (strictly speaking not LDL-cholesterol) is a group of compounds of up to seven different subclasses with significantly different properties which can vary between patients.2 LDL in the form of small, dense LDL (sdLDL) is associated with elevated levels of apoliporotein B and is more directly linked, particularly in its oxidised form, to the development of arteriosclerosis, whereas other LDL particles of greater size (and lower density) are less likely to lead…