Macrophage accumulation within the cap of carotid atherosclerotic plaques is associated with the onset of cerebral ischemic events.
OBJECTIVE
Macrophage accumulation is associated with aortic and coronary plaque instability. The macrophage content of carotid plaques removed at carotid endarterectomy (CE) was assessed, and the relevance to the onset of ipsilateral cerebral ischemic events (CIE) was examined.


METHODS
Carotid plaques from patients undergoing CE were examined (group I, symptomatic stenoses, n = 28; group II, high-grade asymptomatic stenosis, n = 7). The plaques were stained with monoclonal antimacrophage antibody (HAM56), and the interval since the last CIE was recorded. The percentage area of the cap, shoulder, and entire sclerotic region was quantified by computerized planimetry.


RESULTS
The macrophage content of the cap, shoulder, and sclerotic region in all 35 plaques was 1.14% (interquartile range, 0.56 to 3.86), 1.03% (0.51 to 2.15), and 0.49% (0.27 to 0.63), respectively (cap vs sclerotic, P <.01; shoulder vs sclerotic, P <. 01; cap vs shoulder, P =.23). In 18 plaques that were removed less than 180 days after the last CIE, the macrophage content of the cap, shoulder, and entire sclerotic region was 2.41% (0.95 to 4.81), 0. 83% (0.40 to 2.52), and 0.53% (0.38 to 0.71), respectively (cap vs sclerotic, P =.01; cap vs shoulder, P =.01). The content in the cap of these plaques was greater than in plaques removed more than 180 days after symptoms, or asymptomatic plaques (n = 17; 0.62% [0.44 to 1.25], P =.01). The cap macrophage content was inversely related to the time since the last CIE (r = -0.414, P =.029).


CONCLUSIONS
In patients requiring CE, macrophage accumulation was maximal within the cap of carotid plaques and greatest in plaques removed less than 180 days after the last CIE. These findings and the inverse relationship between macrophage content and the interval since symptoms support the hypothesis that macrophage accumulation is associated with plaque instability.
Husain
T
T
Department of Pathology, The Leeds Teaching Hospitals NHS Trust, Leeds, United Kingdom.
Abbott
C R
CR
Scott
D J
DJ
Gough
M J
MJ
D000368:Aged; D000369:Aged, 80 and over; D000911:Antibodies, Monoclonal; D001161:Arteriosclerosis / Q000473:pathology* / Q000601:surgery; D015415:Biomarkers / Q000032:analysis; D016893:Carotid Stenosis / Q000473:pathology* / Q000601:surgery; D002561:Cerebrovascular Disorders / Q000453:epidemiology* / Q000209:etiology; D016894:Endarterectomy, Carotid; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008264:Macrophages / Q000473:pathology*; D008297:Male; D008875:Middle Aged; D012044:Regression Analysis; D012307:Risk Factors
D000911:Antibodies, Monoclonal; D015415:Biomarkers; C096893:HAM-56 antibody