Abstract
IntroductionStatin 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 methodsA 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.ResultsAmong 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.ConclusionsSerum fsTnI could be a good marker for monitoring statin-associated muscular damage outperforming traditional markers.
Highlights
Statin therapy is often associated with muscle complaints and increased serum creatine kinase (CK)
Among the non-specific markers, only CK was significantly higher in statin users (P = 0.027)
Fast and slow skeletal troponin I and statin use of statins on muscle is the increase in circulating creatine kinase (CK), where values greater than 1950 U/L are considered a reason for concerns [7]
Summary
Statin therapy is often associated with muscle complaints and increased serum creatine kinase (CK). As every drug, statins come with adverse effects among which the most acknowledged is muscle toxicity, manifesting with mild muscle complaints such as muscle weakness, cramps, fatigue and only in rare severe cases, rhabdomyolysis [2]. The frequency of such adverse effects is fairly low, ranging from 0.1% for severe events to 1015% complaints of mild event; these drugs are perceived with a favourable safety profile considering that an impairment of muscular performance do not occur [3,4,5,6]. Fast and slow skeletal troponin I and statin use of statins on muscle is the increase in circulating creatine kinase (CK), where values greater than 1950 U/L (ten times the upper limit for normal values) are considered a reason for concerns [7]. In the past they have been extensively used for diagnosis of myocardial infarction, they have been replaced by more specific cardiac markers such as the MB isoform of CK (CK-MB) and, cardiac troponin I (cTnI), which is a more sensitive and specific marker [14,15]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
