This is the Scientific Surgery Archive, which contains all randomized clinical trials in surgery that have been identified by searching the top 50 English language medical journal issues since January 1998. Compiled by Jonothan J. Earnshaw, former Editor-in-Chief, BJS
Cyclo‐oxygenase 1 and 2 expression is augmented in symptomatic carotid plaques. BJS 2001; 88: 602-603.
Published: 6th December 2002
Authors: S. M. Wijeyaratne, C. R. Abbott, S. Homer Vanniasinkam, A. I. D. Mavor, M. J. Gough
Background
Macrophage accumulation and increased metalloproteinase levels within carotid plaques are associated with plaque instability. Production of the latter by macrophages and vascular smooth muscle cells (VSMCs) is promoted by prostaglandins synthesized following the action of cyclo‐oxygenase (COX) on arachidonic acid.
Method
Expression of the isoenzymes COX‐1 and COX‐2 was assessed in carotid plaques removed from 12 asymptomatic patients and 11 patients who had had a neurological event within 30 days of carotid endarterectomy. Patients were matched for age, sex, risk factors and degree of stenosis. For each plaque, paraffin sections obtained at 3‐mm intervals throughout its length were stained with goat antihuman antibodies to COX‐1 and COX‐2. The percentage of the area that stained positively was determined within the cap, shoulder regions and sclerotic component of the plaques (computerized planimetry).
Results
The median (interquartile range) percentage area staining for COX‐1 (symptomatic versus asymptomatic) was: cap 8·37 (4·38–13·65) versus 1·07 (0·31–4·51) per cent, P < 0·0006; shoulder 11·76 (3·02–29·48) versus 1·41 (0·73–2·70) per cent, P < 0·0026; sclerotic component 0·08 (0·02–0·54) versus 0·06 (0·04–0·24) per cent, P < 0·4. Values for COX‐2 were: cap 9·62 (4·87–12·50) versus 0·27 (0·02–2·41) per cent, P < 0·0001; shoulder 11·45 (2·34–24·16) versus 0·44 (0·02–2·97) per cent, P < 0·0038; sclerotic component 1·36 (0·24–2·61) versus 0·06 (0·02–0·49) per cent, P < 0·0081. Further, COX‐2 expression was greater than COX‐1 staining in the sclerotic component of the plaques (P < 0·05, Mann–Whitney U test).
Conclusion
Plaques that had recently become symptomatic exhibited increased COX‐1 and COX‐2 expression, particularly in the cap and shoulder regions. Such changes would increase macrophage and VSMC metalloproteinase production (collagenolysis) and reduce collagen synthesis by VSMCs. Such events are likely to promote plaque instability or rupture. These findings suggest that COX‐1 and COX‐2 inhibitors might have a therapeutic role in the prevention of further neurological events. © 2001 British Journal of Surgery Society Ltd
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