Inflammation of the atherosclerotic cap and shoulder of the plaque is a common and locally observed feature in unruptured plaques of femoral and coronary arteries.

-Retrospectively, plaque rupture is often colocalized with inflammation of the cap and shoulder of the atherosclerotic plaque. Local inflammation is therefore considered a potential marker for plaque vulnerability. However, high specificity of inflammation for plaque rupture is a requisite for application of inflammation markers to detect rupture-prone lesions. The objective of the present study was to investigate the prevalence and distribution (local versus general) of inflammatory cells in nonruptured atherosclerotic plaques. The cap and shoulder of the plaque were stained for the presence of macrophages and T lymphocytes in 282 and 262 cross sections obtained from 74 coronary and 50 femoral arteries, respectively. From most cases, 2 atherosclerotic arteries were studied to gain insight into the local and systemic distribution of the inflammatory process. In 45% and 41% of all cross sections, staining for macrophages was observed in the femoral and coronary arteries, respectively. Rupture of the fibrous cap was observed in 2 femoral and 3 coronary artery segments and was always colocalized with inflammatory cells. At least 1 cross section stained positively for CD68 or acid phosphatase in 84% and 71% of all femoral and coronary arteries, respectively. Only 1 femoral and 6 coronary arteries revealed a positive stain for CD68 in all investigated segments. Inflammation of the cap and shoulder of the plaque is a common feature, locally observed, in atherosclerotic femoral and coronary arteries. The high prevalence of local inflammatory responses should be considered if they are used as a diagnostic target to detect vulnerable, rupture-prone lesions.

[1]  P. Ridker,et al.  Inflammation, aspirin, and the risk of cardiovascular disease in apparently healthy men. , 1997, The New England journal of medicine.

[2]  W. Weintraub,et al.  Elevation of C-reactive protein in "active" coronary artery disease. , 1990, The American journal of cardiology.

[3]  A. Becker,et al.  Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology. , 1994, Circulation.

[4]  P. Libby,et al.  The unstable atheroma. , 1997, Arteriosclerosis, thrombosis, and vascular biology.

[5]  J. Fujimoto,et al.  Optical coherence tomography for optical biopsy. Properties and demonstration of vascular pathology. , 1996, Circulation.

[6]  G. V. R. Born,et al.  INFLUENCE OF PLAQUE CONFIGURATION AND STRESS DISTRIBUTION ON FISSURING OF CORONARY ATHEROSCLEROTIC PLAQUES , 1989, The Lancet.

[7]  M J Davies,et al.  Plaque fissuring--the cause of acute myocardial infarction, sudden ischaemic death, and crescendo angina. , 1985, British heart journal.

[8]  M. Davies,et al.  Risk of thrombosis in human atherosclerotic plaques: role of extracellular lipid, macrophage, and smooth muscle cell content. , 1993, British heart journal.

[9]  J. Boyle,et al.  ASSOCIATION OF CORONARY PLAQUE RUPTURE AND ATHEROSCLEROTIC INFLAMMATION , 1997, The Journal of pathology.

[10]  B Hillen,et al.  Relation of arterial geometry to luminal narrowing and histologic markers for plaque vulnerability: the remodeling paradox. , 1998, Journal of the American College of Cardiology.

[11]  B Hillen,et al.  The impact of atherosclerotic arterial remodeling on percentage of luminal stenosis varies widely within the arterial system. A postmortem study. , 1997, Arteriosclerosis, thrombosis, and vascular biology.

[12]  J. Reekers,et al.  Remodeling of De Novo atherosclerotic lesions in femoral arteries: impact on mechanism of balloon angioplasty. , 1995, Journal of the American College of Cardiology.

[13]  V. Fuster,et al.  Macrophage Infiltration in Acute Coronary Syndromes: Implications for Plaque Rupture , 1994, Circulation.

[14]  B Hillen,et al.  Paradoxical arterial wall shrinkage may contribute to luminal narrowing of human atherosclerotic femoral arteries. , 1995, Circulation.

[15]  C. Zarins,et al.  Compensatory enlargement of human atherosclerotic coronary arteries. , 1987, The New England journal of medicine.

[16]  V. Fuster,et al.  Lewis A. Conner Memorial Lecture. Mechanisms leading to myocardial infarction: insights from studies of vascular biology. , 1994, Circulation.

[17]  A. Angelini,et al.  Factors influencing the presence or absence of acute coronary artery thrombi in sudden ischaemic death. , 1989, European heart journal.

[18]  G. Bearman,et al.  Thermal detection of cellular infiltrates in living atherosclerotic plaques: possible implications for plaque rupture and thrombosis , 1996, The Lancet.

[19]  V. Fuster,et al.  Coronary plaque disruption. , 1995, Circulation.