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J Am Coll Cardiol, 2007; 50:1911-1912, doi:10.1016/j.jacc.2007.07.055 (Published online 22 October 2007).
© 2007 by the American College of Cardiology Foundation
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CORRESPONDENCE: LETTER TO THE EDITOR

Can Critically Short Telomeres Cause Functional Exhaustion of Progenitor Cells in Postinfarction Heart Failure?

Hisko Oeseburg, MSc, B. Daan Westenbrink, MD, Rudolf A. de Boer, MD, PhD, Wiek H. van Gilst, PhD, Dirk J. van Veldhuisen, MD, PhD, FACC and Pim van der Harst, MD, PhD*

* University Medical Center Groningen, University of Groningen, Hanzeplein 1, 9700RB Groningen, the Netherlands (Email: p.van.der.harst{at}thorax.umcg.nl).

With great interest we read the article of Kissel et al. (1) on the selective functional exhaustion of progenitor cells in patients with ischemic cardiomyopathy (ICM) compared with nonischemic dilated cardiomyopathy. As stated by the authors, obviously this clinical study cannot disclose the potential mechanisms underlying the functional impairment of progenitor cells. However, circumstantial evidence for a very reasonable explanation for the selective exhaustion of (progenitor) cells in ICM could have been easily obtained. Cells with telomeres reaching a critical length become genomically unstable, become apoptotic, or enter replicative senescence (2,3). We recently reported in this Journal that telomere length is reduced in patients with congestive heart failure but was selectively reduced further in patients with ICM, as compared with patients with nonischemic dilated cardiomyopathy (4). Moreover, as Kissel et al. (1) observed a relationship with progenitor cell function and New York Heart Association functional class, we observed a relationship with telomere length and New York Heart Association functional class. Consequently, we speculate that patients with advanced ICM are likely to have critically short telomeres in their progenitor cells, leading to functional exhaustion (2). Considering the fact that the group of Kissel et al. (1) has the know-how and ability to perform in-depth research on telomeres, we are surprised that these potentially very relevant mechanisms were not taken into account (5). We strongly advocate probing this potentially very relevant mechanism in future studies.


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  1. Kissel CK, Lehmann R, Assmus B, et al. Selective functional exhaustion of hematopoietic progenitor cells in the bone marrow of patients with postinfarction heart failure J Am Coll Cardiol 2007;49:2341-2349.[Abstract/Free Full Text]
  2. Blackburn EH. Switching and signaling at the telomere Cell 2001;106:661-673.[CrossRef][ISI][Medline]
  3. Wong JM, Collins K. Telomere maintenance and disease Lancet 2003;362:983-988.[CrossRef][ISI][Medline]
  4. van der Harst P, van der Steege G, de Boer RA, et al. Telomere length of circulating leukocytes is decreased in patients with chronic heart failure J Am Coll Cardiol 2007;49:1459-1464.[Abstract/Free Full Text]
  5. Spyridopoulos I, Haendeler J, Urbich C, et al. Statins enhance migratory capacity by upregulation of the telomere repeat-binding factor TRF2 in endothelial progenitor cells Circulation 2004;110:3136-3142.[Abstract/Free Full Text]

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Ioakim Spyridopoulos, Christine K. Kissel, Stefanie Dimmeler, and Andreas M. Zeiher
J. Am. Coll. Cardiol. 2007 50: 1912-1913. [Full Text] [PDF]




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