We read with great interest the report by Tentzeris et al on the influence of high-dose highly efficient statins on short-term mortality in patients with acute coronary syndromes and percutaneous coronary intervention. The investigators mentioned to compare high-dose statin therapy, atorvastatin 80 mg and rosuvastatin 20 mg, with low-dose or no statin therapy. We agree that rosuvastatin is highly efficient; however, 20 mg is not a high dose. Moreover, what about simvastatin 80 mg, which would also be a high-dose statin with moderate intensity, not recommended by the Food and Drug Administration since 2011, the end of including patients in this prospective registry. Therefore, the definition of low-dose statin therapy is vague.

Comparing high-dose statin therapy with low dose and with patients not on statins would be much more informative than including no statin therapy to a low-dose group, which apparently strengthens the effectiveness of a high-dose therapy in statistical analysis. This could also be an explanation for the relatively short-term beneficial effect on all-cause mortality with a significant result in both groups, statistically unadjusted and adjusted, although the number of patients is small in comparison to other statin trials. Moreover, we are astonished about the ethical votum to accept no statin therapy at discharge in patients with an acute coronary syndrome although the European guidelines already stated in 2002 that lipid-lowering therapy should be initiated without delay.

As there was a long period of including patients in the registry, cut-off values and aggressiveness for starting a lipid therapy have substantially changed. Therefore, the results could be driven by patients included in the registry later on as the discretion of the treating physicians to prescribe a statin must have been changed over time.

It is neither mentioned if total cholesterol or low-density lipoprotein cholesterol (LDL-C) was the criterion for initiating statin therapy nor do we know if LDL-C was calculated or measured, which is a big issue in assessing LDL-C. With respect to LDL-C values, there is a huge SD in both groups resulting in a range from 71 to 177 mg/dl in the high-dose statin group. Hence, patients with an LDL-C <100 mg/dl were included in this group, which was not supported by the guidelines.

The main issue why short-term mortality decreases significantly is discussed but remains unanswered. Lipids, inflammatory markers, plaque composition and morphology, and medication have not been assessed during follow-up. Therefore, the effect on patients’ outcome of no, low- or high-dose statin therapy independent of using highly efficient statins or not is still under debate.