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https://doi.org/10.11613/BM.2019.010703

Fast skeletal troponin I, but not the slow isoform, is increased in patients under statin therapy: a pilot study

Alessandro Trentini ; Section of Medical Biochemistry, Molecular Biology and Genetics, Department of Biomedical and Specialist Surgical Sciences, University of Ferrara, Ferrara, Italy
Savino Spadaro ; Section of Anesthesia and Intensive Care, Department of Morphology, Surgery and Experimental Medicine, University of Ferrara, Ferrara, Italy
Valentina Rosta ; Section of Medical Biochemistry, Molecular Biology and Genetics, Department of Biomedical and Specialist Surgical Sciences, University of Ferrara, Ferrara, Italy
Maria C Manfrinato ; Section of Medical Biochemistry, Molecular Biology and Genetics, Department of Biomedical and Specialist Surgical Sciences, University of Ferrara, Ferrara, Italy
Carlo Cervellati ; Section of Medical Biochemistry, Molecular Biology and Genetics, Department of Biomedical and Specialist Surgical Sciences, University of Ferrara, Ferrara, Italy
Francesca Dalla Corte ; Section of Anesthesia and Intensive Care, Department of Morphology, Surgery and Experimental Medicine, University of Ferrara, Ferrara, Italy
Stefania Hanau ; Section of Medical Biochemistry, Molecular Biology and Genetics, Department of Biomedical and Specialist Surgical Sciences, University of Ferrara, Ferrara, Italy
Carlo A Volta ; Section of Anesthesia and Intensive Care, Department of Morphology, Surgery and Experimental Medicine, University of Ferrara, Ferrara, Italy
Tiziana Bellini ; Section of Medical Biochemistry, Molecular Biology and Genetics, Department of Biomedical and Specialist Surgical Sciences, University of Ferrara, Ferrara, Italy

Sažetak

Introduction: Statin therapy is often associated with muscle complaints and increased serum creatine kinase (CK). However, although essential in
determining muscle damage, this marker is not specific for skeletal muscle. Recent studies on animal models have shown that slow and fast isoforms
of 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 of
ssTnI 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 Ferrara
Academic Hospital were included in this observational study. Serum activities of CK, aldolase, alanine aminotransferase and myoglobin were determined
by spectrophotometric assays or routine laboratory analysis. Isoforms ssTnI and fsTnI were determined by commercially available ELISAs. The
creatine 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 specifically
increased in those patients using statins (P = 0.009) evidencing the major susceptibility of fast-twitch fibres towards statins. Sub-clinical increase in
fsTnI, but not CK, was more frequent in statin users (P = 0.007). Cardiac markers were not significantly altered by statins confirming the selectivity
of the effect on skeletal muscle.
Conclusions: Serum fsTnI could be a good marker for monitoring statin-associated muscular damage outperforming traditional markers.

Ključne riječi

statin; fast skeletal troponin; slow skeletal troponin; muscle damage; creatine kinase

Hrčak ID:

213857

URI

https://hrcak.srce.hr/213857

Datum izdavanja:

15.2.2019.

Posjeta: 1.147 *