Why the study?
Recent studies report potential statin cardiotoxicity, including high-sensitivity cardiac troponin elevation and adverse ultrastructural and molecular myocyte changes, warranting discussion of possible mechanisms.
Do statins exhibit potential cardiotoxic properties in laboratory and experimental models?
Do statins exhibit potential cardiotoxic properties in laboratory and experimental models?
This narrative review highlights emerging laboratory and experimental data suggesting that statins may possess potential cardiotoxic properties, indicated by elevated highly sensitive cardiac troponins and myocyte changes.
May prompt reevaluation of long-term statin safety signals; leaves open clinical translation pending prospective human studies.
Due to the fact that statins are among the most high-demand therapeutic agents used for the treatment and prevention of the most common cardiovascular diseases, a significant amount of research is focused on these drugs. As a result, the study and discovery of new effects in statin drugs continues. Research methods are constantly being improved in terms of their sensitivity and specificity, which leads to a change in ideas. In addition to the main lipid-lowering effect, statins have a number of additional effects, which can be conditionally divided into positive (pleiotropic) and negative (side effects). Moreover, information about many of the pleiotropic effects of statins is controversial and may subsequently change as new data become available. To a large extent, this is due to the introduction of new and the improvement of old methods of study: clinical, laboratory and morphological ones. Recent studies report the possibility of statins having potential cardiotoxic properties, which is expressed by an increase in the concentration of highly sensitive cardiac troponins, as well as various adverse changes in cardiac myocytes at the ultrastructural and molecular levels. This paper discusses possible mechanisms of statin cardiotoxicity. This narrative review is based on an analysis of publications in the Medline, PubMed, PubMed Central and Embase databases. The terms "statins", "troponin", "troponin I", "troponin T" in combination with "cardiotoxicity", "false positive", "mechanisms of increase", "pathophysiological mechanisms", "oxidative stress" and "cardiomyocyte apoptosis" were used to search publications.
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Aleksey M. Chaulin (2022) studied this question.
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