The major observation of this study is that atorvastatin 80 mg significantly influences the lipid parameters already within one or two days, if administered in the first-line therapy of ACS. Furthermore, we have shown that an acute effect of intensive atorvastatin therapy on HDL-C and TG is opposite to long-term treatment: we have observed an acute decrease in HDL-C and an acute increase in TG levels.
Current evidence for the acute effect of statins on lipid levels in ACS patients is poor. Present results are in cagreement with our previous study showing rapid reduction of TC and LDL-C after administration of fluvastatin 80 mg in ACS patients . A decrease of TC and LDL-C has been reported also by Michelena et al.  after three days of high-dose simvastatin therapy in stable high-risk patients, by Zhou et al.  after one-week atorvastatin therapy of ACS patients, by Marchesi et al.  after one-week atorvastatin therapy in women with hypercholesterolemia, and by Li et al.  after two weeks of simvastatin treatment in patients with dyslipidemia. On the other hand, Tsunekawa et al.  did not observe any difference in blood lipids after a three-day therapy with cerivastatin in elderly diabetic patients; this discrepancy can be at least partly explained by the low dose of cerivastatin (0.15 mg/day) as well as by different patient's characteristics.
In our previous study we observed only an insignificant trend to acute decrease in HDL-C as a result of fluvastatin 80 mg treatment in ACS patients and the TG level in this study was not changed ; this discordance with the present observation may be explained by the less potent lipid-lowering effect of fluvastatin in comparison with atorvastatin, as well as by the smaller sample size and shorter follow-up. In other studies focusing on the short-term effect of statins on the lipid profile that were carried out with stable patients and on lipid levels measured after three to fourteen days of therapy HDL-C and TG were not significantly changed [14–17]. We have no clear explanation for the marked increase in TG levels in our study, despite the fact that the baseline sample was mostly taken in non-fasting conditions whereas the D1 and D2 samples were fasting.
The major limitation of the present study is the absence of control group. It has been, however, recently reported that the spontaneous changes in lipid profile during the first days of ACS in patients managed according to current recommendations are only borderline or statistically not significant ; it can be, therefore, anticipated that the lipid profile in statin non-users will be similar to the baseline levels. Another limitation comes from the small size of the studied population; however, the observed changes in lipid levels are statistically highly significant. Furthermore, we have determined the lipid profile in non-fasting patients in the baseline and then in fasting conditions in D1 and D2. Non-fasting lipid measurements were, however, used also in other studies focusing on the rapid effect of statins [6, 12, 14] and we did not observe TG levels high enough to interfere with the analysis of other lipid parameters; moreover, surprisingly, we have found that after administration of atorvastatin the fasting TG levels were higher than the non-fasting baseline value.
It can be concluded that intensive atorvastatin therapy initiated at admission of patients with ACS has a prompt acute effect on the lipid profile and that this effect differs from the long-term statin treatment. Further research is, however, needed to confirm and explain these results.