(Circulation. 2006;114:e598.)
© 2006 American Heart Association, Inc.
Correspondence |
Department of Neurology, Pammakaristos Hospital, Athens, Greece
I read with great interest the article by Redgrave et al.1 The authors are to be congratulated for the completion of a burdensome work and the excellent presentation of their results. Their contribution to our understanding of carotid atheromatic disease is paramount. However, I would like to ask the authors the following questions. First, in view of the high frequency of cap rupture in unstable plaques, was there any tendency for cap rupture over the midportion of the plaque versus the shoulder regions of the plaque, or vice versa? Previous histological data suggest that, in contrast to the coronaries, carotid plaque rupture seems to occur mostly at the midportion of the plaque rather than at the shoulder area.2 Furthermore, luminal surface changes have been shown to occur in the most severely stenotic regions of both symptomatic and asymptomatic carotid plaques, with surface irregularities being notably absent in areas of the plaque distant from the stenosis.3 In brief, it would be interesting if the authors could identify some histological characteristics of symptomatic carotid atheromata that differ from what is known (or expected) from analogous studies in the coronaries.
Second, did the authors measure the fibrous cap thickness of the unstable plaques? In coronary pathology, caps 65 to 100 µm thick are considered thin, rendering an atheroma unstable. Currently, we do not know the critical cap thickness that renders a carotid plaque vulnerable, and the stroke literature suffers from the (commonly unjustified) extrapolation of data from the coronaries to the carotids. We have recently described an ultrasound method of measurement for the fibrous cap of stenosing (more than 70%) carotid plaques.4 We have demonstrated that carotid plaques with a mean fibrous cap thickness of less than 650 µm are highly likely to be symptomatic. The equivalent value for the minimum cap thickness was less than 460 µm, but its discriminatory accuracy was much lower because the measured values were quite close to the axial resolution of the ultrasound system. Future studies should investigate whether the threshold values proposed by our study4 are corroborated by the largest-ever histological study of symptomatic carotid plaques.1
| Acknowledgments |
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2. Carr S, Farb A, Pearce WH, Virmani R, Yao JS. Atherosclerotic plaque rupture in symptomatic carotid artery stenosis. J Vasc Surg. 1996; 23: 755766.[CrossRef][Medline] [Order article via Infotrieve]
3. Bassiouny HS, Davis H, Massawa N, Gewertz BL, Glagov S, Zarins CK. Critical carotid stenoses: morphologic and chemical similarity between symptomatic and asymptomatic plaques. J Vasc Surg. 1989; 9: 202212.[CrossRef][Medline] [Order article via Infotrieve]
4. Devuyst G, Karapanayiotides T, Ruchat P, Jonasson L, Cuisinaire O, Lobrinus JA, Pusztaszeri M, Kalangos A, Despland PA, Thiran JP, Bogousslavsky J. Ultrasound measurement of the fibrous cap in symptomatic and asymptomatic atheromatous carotid plaques. Circulation. 2005; 111: 27762782.
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J. N. Redgrave, P. Gallagher, J. K. Lovett, and P. M. Rothwell Critical Cap Thickness and Rupture in Symptomatic Carotid Plaques: The Oxford Plaque Study Stroke, June 1, 2008; 39(6): 1722 - 1729. [Abstract] [Full Text] [PDF] |
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