Background : Acute coronary syndromes (ACS) are characterized by partial or total occlusion of one or more coronary vessels caused by atherosclerosis. Dyslipidemia plays a major role in atheroma formation. Objectives : We collected three-month follow-up data to assess the outcomes of the therapy prescribed at hospital discharge. We studied the lipid profile of patients hospitalized for ACS and any ongoing lipid lowering therapy. Methods : We collected data on the lipid profile of patients hospitalized for ACS at L. Sacco Hospital in Milan from January 2024 to May 2025, noting risk factors, ongoing therapies, LDL levels at admission. At three months, we repeated a lipid profile to evaluate the efficacy of the prescribed lipid lowering therapy in terms of guideline-directed targets. We also noted any adverse event related to lipid-lowering therapy and the incidence of MACEs. Results : In our population, only 48% reported dyslipidemia, whereas 68% were confermed by laboratory tests. Moreover, 38% had history of at least one ACS event. At admission, LDL was off target in 78.1% of those at extremely high risk, 92% in those at very high risk, 68.8% in those at high risk, 62.5% in those at moderate risk, and 39.1% in those at low risk. Mean LDL level at hospital admission was 100,85 ± 43,36 mg/dL. Also, 49% were already on lipid-lowering therapy but only 37% of these had LDL levels at target. Therapy prescribed at discharge included statins (49%) or statins plus ezetimibe (37%). Only 6% received other lipid-lowering agents. At three months, 63.5% of patients were not at target (mean LDL 61,66 ± 27,25 mg/dL) and 4.5% reported therapy-related side effects. Failure to reach the LDL target was due in 59.5% of cases to inadequate therapy at discharge, but lower than predicted potency of properly prescribed drugs was accounted in the remaing 40.5% with a mean deviation from the target value of 13.46 mg/dL and a maximum deviation of 65 mg/dL. Conclusions : Dyslipidemia is often underestimated and undertreated in patients presenting with ACS. Suboptimal LDL values at hospitalization (primary prevention) and at follow-up (secondary prevention) may be attributable to inadequacy of screening, lack of use of new non-statin drugs, therapeutic inertia, or the short follow-up. Our data differ from the literature in terms of discrepancy between the predicted and actual LDL values obtained through lipid-lowering therapy, a finding which requires further investigations.