Thromb Haemost 2003; 90(06): 1112-1120
DOI: 10.1160/TH03-02-0069
Platelets and Blood Cells
Schattauer GmbH

Platelet factor 4 localization in carotid atherosclerotic plaques: correlation with clinical parameters

Stephanie Pitsilos
1   Departments of Pathology and Laboratory Medicine, Univ. of Pennsylvania, Philadelphia, USA
,
Jennifer Hunt
2   Department of Pathology and Laboratory Medicine, University of Pittsburgh, Pittsburgh, USA
,
Emile R. Mohler
3   Departments of Cardiology, Univ. of Pennsylvania, Philadelphia, USA
,
Anand M. Prabhakar
1   Departments of Pathology and Laboratory Medicine, Univ. of Pennsylvania, Philadelphia, USA
,
Mortimer Poncz
4   Departments of Pediatrics, Univ. of Pennsylvania, Philadelphia, USA
,
Jennine Dawicki
1   Departments of Pathology and Laboratory Medicine, Univ. of Pennsylvania, Philadelphia, USA
,
Tigran Z. Khalapyan
3   Departments of Cardiology, Univ. of Pennsylvania, Philadelphia, USA
,
Megan L.Wolfe
3   Departments of Cardiology, Univ. of Pennsylvania, Philadelphia, USA
,
Ronald Fairman
5   Departments of Surgery, Univ. of Pennsylvania, Philadelphia, USA
,
Marc Mitchell
5   Departments of Surgery, Univ. of Pennsylvania, Philadelphia, USA
,
Jeffrey Carpenter
5   Departments of Surgery, Univ. of Pennsylvania, Philadelphia, USA
,
Michael A. Golden
5   Departments of Surgery, Univ. of Pennsylvania, Philadelphia, USA
,
Douglas B. Cines
1   Departments of Pathology and Laboratory Medicine, Univ. of Pennsylvania, Philadelphia, USA
,
Bruce S. Sachais
1   Departments of Pathology and Laboratory Medicine, Univ. of Pennsylvania, Philadelphia, USA
› Author Affiliations

Financial support: NIH K08 HL04245 (B.S.), P50 HL54500 (D.B.C., M.P.), NIH KO8 HL03974-01 (ERM), Mary L. Smith Charitable Lead Trust (ERM)
Further Information

Publication History

Received 03 February 2003

Accepted after revision 25 May 2003

Publication Date:
05 December 2017 (online)

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Summary

Emerging evidence supports a role for platelets in the progression of atherosclerosis in addition to an involvement in thrombotic vascular occlusion. Platelet Factor 4 (PF4), a chemokine released by activated platelets, stimulates several pro-atherogenic processes. Therefore, we examined the localization of PF4 and the homologous protein, Neutrophil Activating Protein-2 (NAP-2) in lesions representing the evolution of human atherosclerotic plaques. Carotid plaques from 132 patients with critical carotid stenosis and 6 autopsy specimens were studied. Clinical, histologic and immunohistochemical data were analyzed using a χ2-test. PF4 was detected in the cytoplasm of luminal and neovascular endothelium, in macrophages and in regions of plaque calcification. The presence of PF4 in macrophages and neovascular endothelium correlated with lesion grade (p = 0.004; p = 0.044). Staining of macrophages for PF4 correlated with the presence of symptomatic atherosclerotic disease (p = 0.028). In early lesions, PF4 was commonly found in macrophages of early lesions (Grade I/II), whereas NAP-2 was rarely present.

In conclusion, correlation between PF4 deposition, lesion severity and symptomatic atherosclerosis suggests that persistent platelet activation may contribute to the evolution of athero-sclerotic vascular lesions. These studies support the rationale for the chronic use of anti-platelet therapy in patients at risk for developing symptomatic atherosclerosis.