Published Online
on August 2, 2004

A more recent version of this article appeared on August 17, 2004

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Submitted on November 18, 2003
Revised on March 23, 2004
Accepted on April 9, 2004

Troponin I Isoform Expression in Human and Experimental Atrial Fibrillation

Victor L.J.L. Thijssen PhD^*, Jannie Ausma PhD, Luisa Gorza MD, Huub M.W. van der Velden PhD, Maurits A. Allessie MD, PhD, Isabelle C. Van Gelder MD, Marcel Borgers PhD, and Guillaume J.J.M. van Eys PhD

From the Cardiovascular Research Institute Maastricht, University Maastricht, Maastricht, Netherlands (V.L.J.L.T., J.A., M.A.A., M.B., G.J.J.M.v.E.); Department of Biomedical Sciences, University of Padova, Padova, Italy (L.G.); Department of Medical Physiology, University Medical Centre Utrecht, Utrecht, Netherlands (H.M.W.v.d.V.); and Department of Cardiology, Thoraxcenter University Hospital, University of Groningen, Groningen, Netherlands (I.C.V.).

^* To whom correspondence should be addressed. E-mail: v.thijssen{at}path.unimaas.nl.

Background--Atrial fibrillation (AF) is accompanied by re-expression of fetal genes and activation of proteolytic enzymes. In this study both aspects were addressed with respect to troponin I (TnI) isoform expression.

Methods and Results--Western blotting and real-time reverse transcription-polymerase chain reaction were used to study TnI isoform expression in patients with paroxysmal or chronic AF and in goats after 1, 2, 4, 8, and 16 weeks of AF. In addition to cardiac TnI (cTnI), low expression of slow-twitch skeletal TnI (ssTnI) protein was found in 60% of patients in sinus rhythm or paroxysmal AF and in 8% of patients with chronic AF. In adult goat atrium, ssTnI protein expression was undetectable. Calcium-dependent degradation of cTnI protein was found in 1 or 2 of 6 animals after 1 to 4 weeks of AF. Although always low, ssTnI mRNA levels were significantly higher in patients who expressed ssTnI protein than in those who did not. Relative ssTnI mRNA expression was significantly lower in patients with paroxysmal AF and chronic AF than in those in sinus rhythm. In goats there was a tendency toward higher relative levels of ssTnI at the onset of AF followed by a normalization when AF had become sustained.

Conclusions--Atrial re-expression of ssTnI during paroxysmal AF in patients and during the first 2 weeks of pacing-induced AF in goats does not seem to be part of the process of AF-associated cardiomyocyte dedifferentiation but seems to result from transient cardiomyocyte stress at the onset of AF.

Key words: atrial fibrillation • troponin I • myocytes, cardiac • gene expression • atrium

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