This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Redgrave, J.N. Articles by Gallagher, P.J. Search for Related Content PubMed Articles by Redgrave, J.N. Articles by Gallagher, P.J. Related Collections Carotid endarterectomy Pathophysiology Carotid Stenosis

(Circulation. 2006;114:e599.)
© 2006 American Heart Association, Inc.

Correspondence

Response to Letter Regarding Article, "Histological Assessment of 526 Symptomatic Carotid Plaques in Relation to the Nature and Timing of Ischemic Symptoms: the Oxford Plaque Study"

J.N. Redgrave, MRCP; J.K. Lovett, DPhil; P.M. Rothwell, PhD

Stroke Prevention Research Unit, Department of Clinical Neurology, Radcliffe Infirmary, Oxford, UK

P.J. Gallagher, PhD

Department of Pathology, Southampton General Hospital, Southampton, UK.

We are grateful to Dr Karapanayiotides for raising these 2 important questions in response to our article.¹ First, most histological studies of symptomatic carotid and coronary plaques have taken sections approximating the point of maximal stenosis (ie, the midpoint of the plaque on longitudinal views). We have previously performed a serial longitudinal sectioning study of 26 symptomatic carotid plaques and shown that the vast majority of pathological features, including 87% of ruptures, occur within 3 mm of the maximum stenosis.² In another study of 128 symptomatic carotid plaques, we found that 47 were ulcerated on preoperative angiography, with the ulcer neck at the point of maximum stenosis in 28 (60%) and in the shoulder region in 19 (40%).³ In our recent study of 526 recently symptomatic carotid plaques,¹ we examined transverse sections through the point of maximal stenosis and from 3 mm on either side and found that 60% of plaques showed probable or definite rupture. We have since reexamined the plaques with definite rupture (n=166) to establish the site of rupture in the transverse plane. In all but 1 case, the area of cap rupture could be distinguished from surgical artifact. Of the remaining 165 plaques, the rupture occurred around the midpoint in 90 (55%), at the shoulder region in 65 (39%), between the midpoint and the shoulder in 4 (2%), and at both sites in 6 (4%). Thus, as suggested by Dr Karapanayiotides, midpoint ruptures may well be more common in symptomatic carotid plaques than in culprit coronary plaques.

Second, we did measure thickness of the fibrous cap. In the modified American Heart Association classification of atherosclerotic lesions, Virmani et al⁴ define thin fibrous cap atheroma as less than 65 µm, because this was the 95th percentile mean cap thickness in a series of 41 ruptured coronary plaques. Virmani et al⁴ have suggested that the equivalent value in carotid plaques is much higher (165 µm),⁵ but there are no detailed published data. In our series, we measured cap thickness at its thinnest part and also at the point most representative of the cap as a whole. These parameters were measured reliably in 428 plaques (81%). The median (interquartile range) representative cap thickness was 400 µm (220 to 600 µm), and the minimum cap thickness was 200 µm (100 to 300 µm). However, ruptured plaques had thinner caps than nonruptured plaques (minimum cap thickness: 150 µm [80 to 210 µm] versus 250 µm [180 to 400 µm], P<0.001). Most in vivo imaging techniques have a resolution of 400 to 500 µm and are probably insufficiently sensitive to reliably identify high-risk plaques on the basis of cap thickness alone.

	Acknowledgments

 
Support has been provided by the Guarantors of Brain, the Wellcome Trust, and the Medical Research Council.

Disclosures

None.

	References

Top References

 

1. Redgrave JN, Lovett JK, Gallagher PJ, Rothwell PM. Histological assessment of 526 symptomatic carotid plaques in relation to the nature and timing of ischemic symptoms: the Oxford plaque study. Circulation. 2006; 113: 2320–2328.[Abstract/Free Full Text]
   
2. Lovett JK, Gallagher PJ, Rothwell PM. Reproducibility of histological assessment of carotid plaque: implications for studies of carotid imaging. Cerebrovasc Dis. 2004; 18: 117–123.[CrossRef][Medline] [Order article via Infotrieve]
   
3. Lovett JK, Gallagher PJ, Hands LJ, Walton J, Rothwell PM. Histological correlates of carotid plaque surface morphology on lumen contrast imaging. Circulation. 2004; 110: 2190–2197.[Abstract/Free Full Text]
   
4. Virmani R, Kolodgie FD, Burke AP, Farb A, Schwartz SM. Lessons from sudden coronary death: a comprehensive morphological classification scheme for atherosclerotic lesions. Arterioscler Thromb Vasc Biol. 2000; 20: 1262–1275.[Free Full Text]
   
5. Wasserman BA, Wityk RJ, Trout HH, III, Virmani R. Response to letter by Karapanayiotides et al. Stroke. 2006; 37: 1647.[Free Full Text]
   

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Redgrave, J.N. Articles by Gallagher, P.J. Search for Related Content PubMed Articles by Redgrave, J.N. Articles by Gallagher, P.J. Related Collections Carotid endarterectomy Pathophysiology Carotid Stenosis