Acute myocardial infarction is both an emergency and the beginning of a prolonged period of exceptionally high recurrent cardiovascular risk. Few components of secondary prevention are supported by evidence as consistent as low-density lipoprotein cholesterol (LDL-C) lowering: LDL is causal in atherosclerotic cardiovascular disease, the clinical benefit is proportional to the absolute reduction achieved, and additional benefit persists at concentrations well below historical targets [1–6]. Yet, in everyday practice, the principal obstacle is no longer uncertainty about whether LDL-C should be lowered, but failure to convert an unequivocal therapeutic objective into a reliable care pathway.
