© 2006 European Society of Cardiology
Myocardial regulatory proteins and heart failure
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a Department of Physiology, Faculty of Medicine in Hradec Králové, Charles University in Prague
imkova 870, 500 38 Hradec Králové, Czech Republic
b Department of Pharmacology, Faculty of Medicine in Hradec Králové, Charles University in Prague
imkova 870, 500 38 Hradec Králové, Czech Republic
c Department of Biochemical Sciences, Faculty of Pharmacy in Hradec Králové, Charles University in Prague Heyrovského 1203, 500 05 Hradec Králové, Czech Republic
* Corresponding author. Tel.: +420 49 5816180; fax: +420 49 5436054 E-mail address: adamcova{at}lfhk.cuni.cz
| Abstract |
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Cardiac troponin T (cTnT) and cardiac troponin I (cTnI) are considered to be the most specific and sensitive biochemical markers of myocardial damage. Troponins have been studied in a wide range of clinical settings, including heart failure; however, there are few data on the role of regulatory proteins in the pathogenesis of heart failure, although a few interesting hypotheses have been proposed. A considerable body of evidence favours the view that alteration of the myocardial thin filament is the primary event leading to defective contractility of the failing myocardium, while the changes in Ca2+ handling are a compensatory response. A better understanding of the role of regulatory proteins under different physiological and pathological conditions could lead to new therapeutic approaches in heart failure. Recently, calcium sensitisation has been proposed as a novel method by which cardiac performance may be enhanced via an increase in the affinity of troponin C for calcium but without affecting intracellular calcium concentration. To date, the only calcium sensitizer used in clinical practice is levosimendan.
Key Words: Heart failure Regulatory proteins Cardiac troponin Cardiac marker Calcium sensitizers Myocardial stunning
Received November 9, 2004; Revised July 1, 2005; Accepted September 22, 2005
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