Rosuvastatin, C-reactive protein, LDL cholesterol, and the JUPITER trial/Authors' reply

[...] it has been suggested that CRP per se might not have a causal role in vascular diseases, but represent a confounding factor or reverse causation.3 In line with this, drug therapy given on a massive scale on the basis of surrogate markers that might not be uniformly linked to an elevated vascular risk could expose some patients to undesired adverse effects without health benefits. The amount of LDL cholesterol accumulating within the intima depends on the cholesterol entering the arterial wall (LDL) and the cholesterol being removed from the arterial wall by reverse cholesterol transport (HDL). Since we know that people who sustain atherothrombotic events despite a normal cholesterol concentration tend to do so in association with a low HDL concentration,2 I submit that, in JUPITER,1 the elevated hsCRP concentration is simply a surrogate for low HDL cholesterol and that patients who benefited from rosuvastatin were those whose LDL: