CORRESPONDENCE: LETTER TO THE EDITOR
Telomerase-Positive Neutrophils: Plaque "Survivors" and Restenosis
David C. Sane, MD*
* Section of Cardiology, Wake Forest University School of Medicine, Medical Center Boulevard, Winston-Salem, North Carolina 27157-1045 (Email: dsane{at}wfubmc.edu).
Narducci et al. (1) recently demonstrated high telomerase activity in polymorphonuclear neutrophilic leukocytes (PMNs) derived from plaques in patients with unstable angina. In contrast, PMNs from stable coronary plaques and peripheral blood samples had minimal telomerase activity. The authors' analysis relied on a novel, though indirect, method of acquiring plaque PMNs; specifically, they studied cells isolated by washing angioplasty balloons. Immunohistochemical techniques confirmed that >90% of adherent cells were neutrophils. We have previously reported a different strategy for analyzing plaque telomerase activity (2). Using tissue acquired from 23 patients undergoing directional coronary atherectomy (DCA), we found that 8 of 23 (35%) were positive for telomerase (2). All but 1 of these patients presented with an acute coronary syndrome. Although the quantification of the telomeric repeat amplification protocol (TRAP) was performed differently in the 2 studies, our results align well with those of Narducci et al. (1), who found high telomerase activity in 6 of 20 (30%) of their patients with unstable angina. Because DCA samples contain cells other than PMNs, such as vascular smooth muscle cells, endothelial cells, and macrophages, the similar rates of TRAP positivity would suggest that PMNs are the major source of telomerase in the unstable plaque. However, additional studies using in situ assays are warranted before this conclusion is firmly established. The infiltration of coronary plaques by PMNs with persistent or reactivated telomerase could promote an exaggerated local inflammatory response and lead to plaque instability. It is also plausible that PMN-derived telomerase activity promotes restenosis (3). Of note in this regard, we found that patients with telomerase-positive DCA tissue were more likely to experience clinical or angiographic evidence of restenosis (2).
Thus, using 2 different strategies, 30% to 35% of unstable coronary plaques have "survivors" or telomerase-positive cells (1,2). Narducci et al. (1) provide strong support that these cells are predominantly PMNs. Their study could provide a novel strategy for identifying patients at increased risk for adverse events, including restenosis.
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1. Narducci ML, Grasselli A, Biasucci LM, et al. High telomerase activity in neutrophils from unstable coronary plaques J Am Coll Cardiol 2007;50:2369-2374.[Abstract/Free Full Text]2. Gupta M, Shogreen MR, Braden GA, White WL, Sane DC. Prevalence of telomerase in coronary artery atherosclerosis J Anti-Aging Med 2000;3:5-24. 3. Welt FG, Rogers C. Inflammation and restenosis in the stent era Arterioscler Thromb Vasc Biol 2002;22:1769-1776.[Abstract/Free Full Text]
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