This Article Full Text Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kaski, J. C. Articles by Coller, B. S. Search for Related Content PubMed PubMed Citation Articles by Kaski, J. C. Articles by Coller, B. S. Pubmed/NCBI databases Medline Plus Health Information Coronary Artery Disease Related Collections Pathophysiology

(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:e112.)
© 2005 American Heart Association, Inc.

Letters to the Editor

Neutrophil Count and Complex Lesions in Patients With Coronary Artery Disease

Juan Carlos Kaski

Department of Cardiac and Vascular Sciences, St. George's Hospital Medical School, London, UK

Pablo Avanzas

Division of Invasive Cardiology, Hospital Universitario Central de Asturias, Oviedo, Spain

Ramón Arroyo-Espliguero

Division of Cardiology, Hospital General Universitario, Guadalajara, Spain

An extract of the first 250 words of the full text is provided, because this article has no abstract.

To the Editor:

In a recent article, Coller¹ reviews the role of leukocytosis in vascular disease morbidity and mortality. Despite the exhaustive nature of the review, we were concerned that the author failed to address an issue of major importance, namely the relationship between neutrophil count and the presence of vulnerable atheromatous plaques in patients with coronary artery disease.

Acute coronary syndromes result mainly from occlusive coronary artery thrombosis at sites of plaque fissure, rupture, or superficial erosion. At angiography, disrupted or ulcerated plaques often appear as "complex" stenoses with rough contours or "filling defects" suggestive of intracoronary thrombosis. Complex stenoses are at a higher risk of rapid progression than smooth lesions,² and we have recently shown that markers of both inflammation and macrophage activation predict rapid coronary artery disease progression in patients with chronic stable angina.³

In angiographic studies in patients with chronic stable angina, we have shown that neutrophil count is an independent predictor of the presence of multiple complex stenoses irrespective of coronary artery disease extent.⁴ Moreover, in patients with acute coronary syndromes, neutrophil count is also associated with coronary artery disease complexity.⁵ Furthermore, neutrophil infiltration of culprit lesions with release of elastase and myeloperoxidase has been implicated in the pathogenesis of atherosclerosis.⁶ These findings are important, as it has been shown that the presence of multiple complex coronary plaques is associated with adverse prognosis in patients with coronary artery disease. Neutrophil count may have also a predictive role in CSA patients in the clinical setting. New . . . [Full Text of this Article]

Barry S. Coller

The Rockefeller University, New York, NY

This article has been cited by other articles:

				K. Quinn, M. Henriques, T. Parker, A. S. Slutsky, and H. Zhang Human neutrophil peptides: a novel potential mediator of inflammatory cardiovascular diseases Am J Physiol Heart Circ Physiol, November 1, 2008; 295(5): H1817 - H1824. [Abstract] [Full Text] [PDF]

				S. Heptinstall, J. R. Glenn, A. Johnson, B. Myers, A. E. White, and L. Zhao Leukocytosis, Vascular Disease, and Adenine Nucleotide Metabolism Arterioscler Thromb Vasc Biol, February 1, 2006; 26(2): e22 - e23. [Full Text] [PDF]