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J Am Coll Cardiol, 2007; 50:2440, doi:10.1016/j.jacc.2007.09.023 (Published online 11 December 2007).
© 2007 by the American College of Cardiology Foundation
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CORRESPONDENCE: LETTER TO THE EDITOR

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Brendan Doyle, MB and Noel Caplice, MD, PhD*

* University College Cork, Center for Research in Vascular Biology, Biosciences Institute, Cork, Co. Cork, Ireland. (Email: n.caplice{at}ucc.ie).

We thank Dr. Folts for his interest in our paper (1). The hypothesis that a pressure gradient between the parent vessel and the plaque microvasculature might contribute to plaque rupture is intriguing. One potential limitation of the hypothesis is the assumption that pressure in the plaque microvasculature will be near that of the vasa vasorum and that the latter is near that of systemic pressure. Under normal circumstances, one would expect that the intraluminal pressure within plaque microvessels would be somewhat lower than that of the systemic circulation, similar to the progressive step-down in pressure observed from systemic arteries to the capillary bed. To what extent this physiologic decrease in intraluminal pressure matches the drop in lateral blood pressure of the parent vessel beyond a tight stenosis is uncertain. We suspect that deficiencies in the integrity of the microvasculature remain the primary predisposing factor to intraplaque hemorrhage, but further studies of Dr. Folk’s hypothesis would be of great interest.


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  1. Doyle B, Caplice N. Plaque neovascularization and antiangiogenic therapy for atherosclerosis J Am Coll Cardiol 2007;49:2073-2080.[Abstract/Free Full Text]




This Article
Right arrow Full Text (PDF)
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j.jacc.2007.09.023v1
50/25/2440-a    most recent
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