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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
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 techniques such us intravascular ultrasound (IVUS) and MRI, which allow the assessment of the arterial wall and the composition of atheromatous plaques, will be instrumental in the evaluation of total atherosclerosis burden. They will represent a significant step forward in the understanding of plaque vulnerability and should help us move beyond the type of "lumenographic" analysis provided by conventional coronary angiography.
References
Coller BS. Leukocytosis and ischemic vascular disease morbidity and mortality: is it time to intervene? Arterioscler Thromb Vasc Biol. 2005; 25: 658–670.
Kaski JC, Chester MR, Chen L, Katritsis D. Rapid angiographic progression of coronary artery disease in patients with angina pectoris. The role of complex stenosis morphology. Circulation. 1995; 92: 2058–2065.
Zouridakis E, Avanzas P, Arroyo-Espliguero R, Fredericks S, Kaski JC. Markers of inflammation and rapid coronary artery disease progression in patients with stable angina pectoris. Circulation. 2004; 110: 1747–1753.
Avanzas P, Arroyo-Espliguero R, Cosin-Sales J, Quiles J, Zouridakis E, Kaski JC. Multiple complex stenoses, high neutrophil count and C-reactive protein levels in patients with chronic stable angina. Atherosclerosis. 2004; 175: 151–157.
Avanzas P, Arroyo-Espliguero R, Cosin-Sales J, Aldama G, Pizzi C, Quiles J, Kaski JC. Markers of inflammation and multiple complex stenoses (pancoronary plaque vulnerability) in patients with non-ST segment elevation acute coronary syndromes. Heart. 2004; 90: 847–852.
Naruko T, Ueda M, Haze K, van der Wal AC, van der Loos CM, Itoh A, Komatsu R, Ikura Y, Ogami M, Shimada Y, Ehara S, Yoshiyama M, Takeuchi K, Yoshikawa J, Becker AE. Neutrophil infiltration of culprit lesions in acute coronary syndromes. Circulation. 2002; 106: 2894–900.
In response:
Barry S. Coller
The Rockefeller University, New York, NY
I appreciate Drs Kaski, Avanzas, and Arroyo-Espliguero bringing to my attention their interesting studies on the association between leukocyte count, multiple complex coronary artery stenoses, and the rate of coronary disease progression. Their observations add an important dimension to the other associations that have been described between leukocytosis and vascular disease. The article that they cite by Naruko et al1 provides histopathologic support for the presence of neutrophils in atherosclerotic lesions associated with acute coronary syndromes. In addition, since submission of my manuscript, several other studies have been published2,3 or have come to my attention4,5 which provide additional support for an associations of leukocytosis and cardiovascular morbidity and mortality. Thus, collectively, these data provide additional support for the association of leukocytosis and cardiovascular morbidity and mortality, and the potential direct role of leukocytes in the underlying processes of atherosclerosis and thrombosis.
References
Naruko T, Ueda M, Haze K, van der Wal AC, van der Loos CM, Itoh A, Komatsu R, Ikura Y, Ogami M, Shimada Y, Ehara S, Yoshiyama M, Takeuchi K, Yoshikawa J, Becker AE. Neutrophil infiltration of culprit lesions in acute coronary syndromes. Circulation. 2002; 106: 2894–2900.
Margolis KL, Manson JE, Greenland P, Rodabough RJ, Bray PF, Safford M, Grimm RH, Jr., Howard BV, Assaf AR, Prentice R. Leukocyte count as a predictor of cardiovascular events and mortality in postmenopausal women: the Women’s Health Initiative Observational Study. Arch Intern Med. 2005; 165: 500–508.
Patel MR, Mahaffey KW, Armstrong PW, Weaver WD, Tasissa G, Hochman JS, Todaro TG, Malloy KJ, Rollins S, Theroux P, Ruzyllo W, Nicolau JC, Granger CB. Prognostic usefulness of white blood cell count and temperature in acute myocardial infarction (from the CARDINAL Trial). Am J Cardiol. 2005; 95: 614–618.
Sabatine MS, Morrow DA, Cannon CP, Murphy SA, Demopoulos LA, DiBattiste PM, McCabe CH, Braunwald E, Gibson CM. Relationship between baseline white blood cell count and degree of coronary artery disease and mortality in patients with acute coronary syndromes: a TACTICS-TIMI 18 (Treat Angina with Aggrastat and determine Cost of Therapy with an Invasive or Conservative Strategy–Thrombolysis in Myocardial Infarction 18 trial) substudy. J Am Coll Cardiol. 2002; 40: 1761–1768.
Gurm HS, Bhatt DL, Gupta R, Ellis SG, Topol EJ, Lauer MS. Preprocedural white blood cell count and death after percutaneous coronary intervention. Am Heart J. 2003; 146: 692–698.