Circulation. 2002;106:2894-2900
Published online before print November 18, 2002, doi: 10.1161/01.CIR.0000042674.89762.20
Published online before print November 18, 2002, doi: 10.1161/01.CIR.0000042674.89762.20
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(Circulation. 2002;106:2894.)
© 2002 American Heart Association, Inc.
Clinical Investigation and Reports |
Neutrophil Infiltration of Culprit Lesions in Acute Coronary Syndromes
From the Department of Cardiology, Osaka City General Hospital (T.N., K.H., A.I.); Departments of Pathology (M.U., R.K., Y.I., M.O.) and Internal Medicine and Cardiology (Y.S., S.E., M.Y., K.T., J.Y.), Osaka City University Graduate School of Medicine, Osaka; and the Department of Cardiovascular Pathology (A.C.W., C.M.L., A.E.B.), Academic Medical Center, University of Amsterdam, the Netherlands.
Correspondence to Anton E. Becker, MD, Department of Cardiovascular Pathology, Academic Medical Center, University of Amsterdam, PO Box 22700, 1100 DE Amsterdam, Meibergdreef 9, 1105 AZ, Amsterdam, the Netherlands. E-mail m.i.schenker{at}amc.uva.nl
Background— Neutrophils in unstable atherosclerotic lesions have not received much consideration, despite accumulating evidence suggesting a link between systemic inflammation and acute coronary syndromes.
Methods and Results— Coronary artery segments were obtained at autopsy from 13 patients with acute myocardial infarction (AMI); 8 had a ruptured and 5 an eroded plaque. Patients (n=45) who had died of noncardiovascular diseases served as reference. Atherectomy specimens were obtained from 35 patients with stable angina pectoris (SAP) and from 32 patients with unstable angina pectoris (UAP). Antibodies against CD66b, elastase, myeloperoxidase, and CD11b identified neutrophils; CD10 identified neutral endopeptidase (NEP). CD66b-positive and NEP-positive neutrophils were counted and expressed as a number per square millimeter of tissue. All specimens with plaque rupture or erosion showed distinct neutrophil infiltration; the number did not differ between ruptured and eroded plaques. However, the number of NEP-positive neutrophils was significantly higher (P<0.0001) in ruptured plaques than in eroded plaques. UAP patients showed neutrophils in 14 of 32 culprit lesions; in SAP only 2 of 35 lesions contained neutrophils. The number of neutrophils and NEP-positive cells in patients with UAP was significantly higher (neutrophils, P<0.0005; NEP-positive cells, P<0.005) than in patients with SAP.
Conclusions— The observations suggest that neutrophil infiltration is actively associated with acute coronary events. The high number of NEP-positive neutrophils in ruptured plaques, compared with eroded plaques, may reflect differences in the underlying pathophysiological mechanisms.
Key Words: myocardial infarction • angina • inflammation • atherosclerosis
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