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(Stroke. 2003;34:2581.)
© 2003 American Heart Association, Inc.
Original Contributions |
Cardiovascular Research Foundation, Lenox Hill Heart & Vascular Institute of New York, New York, NY
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
| Introduction |
|---|
In patients with carotid artery stenosis requiring revascularization, the mere presence of calcified atheroma in this specific arterial location has chronically
sensitized
the carotid baroreceptors to very small changes in carotid artery tension. (The thicker and more calcified the wall, the more rapid and efficient pressure/energy transmission it allows.) Therefore, external manipulation of this area during surgery, as well as the transmission of the luminal distention through the arterial wall during balloon inflation and stent expansion, can produce a hypotensive response. This phenomenon varies with (1) the intensity of manipulation or distention of the artery and (2) plaque burden and plaque composition (thickness and calcification).
Development of significant hypotension has been linked with neurological complications after carotid stent procedures.1,2
Persistent profound hypotension
was defined as a >40 mm Hg decrease in arterial pressure without evidence of hypovolemia, with a systolic pressure <90 mm Hg at the end of the procedure and lasting at least 1 hour1; in the other study,
severe hypotension
was defined as a pressure drop of at least 50 mm Hg.2 Lower levels of hypotension were inconsequential in relation to the patients neurological status.
This phenomenon
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