Introduction: Statin therapy is often associated with muscle complaints and increased serum creatine kinase (CK). However, although essential indetermining muscle damage, this marker is not specific for skeletal muscle. Recent studies on animal models have shown that slow and fast isoformsof skeletal troponin I (ssTnI and fsTnI, respectively) can be useful markers of skeletal muscle injury. The aim of this study was to evaluate the utility ofssTnI and fsTnI as markers to monitor the statin-induced skeletal muscle damage.Materials and methods: A total of 51 patients (14 using and 37 not using statins) admitted to the intensive care unit of the University of FerraraAcademic Hospital were included in this observational study. Serum activities of CK, aldolase, alanine aminotransferase and myoglobin were determinedby spectrophotometric assays or routine laboratory analysis. Isoforms ssTnI and fsTnI were determined by commercially available ELISAs. Thecreatine kinase MB isoform (CK-MB) and cardiac troponin I (cTnI) were evaluated as biomarkers of cardiac muscle damage by automatic analysers.Results: Among the non-specific markers, only CK was significantly higher in statin users (P = 0.027). Isoform fsTnI, but not ssTnI, was specificallyincreased in those patients using statins (P = 0.009) evidencing the major susceptibility of fast-twitch fibres towards statins. Sub-clinical increase infsTnI, but not CK, was more frequent in statin users (P = 0.007). Cardiac markers were not significantly altered by statins confirming the selectivityof the effect on skeletal muscle.Conclusions: Serum fsTnI could be a good marker for monitoring statin-associated muscular damage outperforming traditional markers.