I’d like to change the focus of the discussion on ICA stenosis evaluation.
I must constantly remind myself that the purpose of the carotid examination:
is to identify those patients that will have atheroembolic stroke from
the rupture of a carotid atheroma (a vascularized tumor often called a
“plaque”) and thus the patients can be saved from stroke with anatomic
Based on stenosis alone (from the ACAS study), only 1/16 of patients
with a “severe stenosis” (> 70% Diameter reduction) will have
carotid atheroma rupture resulting in stroke if the stenosis is not treated
endarterectomy or stent.
A severe stenosis is “hemodynamically significant”, causing EITHER A FLOW
REDUCTION OR PRESSURE REDUCTION.
I believe that the difference between flow reduction and pressure reduction is
the critical difference between an ATHEROMA VULNERABLE TO RUPTURE and a benign
I believe that only a PRESSURE REDUCING stenosis is vulnerable to rupture.
I believe that a flow reducing stenosis is benign.
The key to a pressure reducing stenosis is a disconnected circle of Willis
[[Lal BK, Beach KW, Sumner DS., Intracranial collateralization determines
hemodynamic forces for carotid plaque disruption., J Vasc Surg. 2011
Only about 5% of patients have a disconnected coW.
I believe that a pressure reducing proximal ICA stenosis can be identified by
1. Post stenotic bruit (a diagnostic method which we have discarded as
[Kartchner MM, McRae LP, Morrison FD, Noninvasive Detection and Evaluation of
Carotid Occlusive Disease, Arch Surgery, Vol 106, April 1973, Pages 528-535.]
[Lees RS, Kistner JP Sanders D, Duplex Doppler Scanning and Spectral Burit
Analysis for Diagnosing Carotid Stenosis, Circulation V66, Sup1 August 1982
2. With transcranial coW Doppler examination, finding no flow toward the
ipsilateral ICA/MCA via either the ipsilateral a1ACA or PcomA
a. No flow in the a1ACA or flow away from the ICA/MCA in the a1ACA
b. No flow in the PcomA or flow away from the ICA/MCA in the PcomA
(We often consider TCD to be too difficult, as the TCD examination cannot be
done in about 30% of cases) (but gives this valuable information in the other
70%) (and can be performed with a 2 MHz duplex scanhead available on most
vascular ultrasound systems).
(If there is collateral flow TOWARD the ICA/MCA in the case of a sever
stenosis, either through the anterior coW (reverse flow in the a1ACA)
OR through the posterior coW via the PcomA, then the severe ICA is flow
reducing and benign.
Of severe ICA stenoses, I expect 5% to be pressure reducing
and 95% to be flow reducing.
I expect that the pressure reducing ICA stenoses will result in
Reduced cerebrovascular reserve (for those who want to test that).
I invite all of our friends and our adversaries to test this theory.
Holding my breath in hopes of progress.
------ Original Message ------
Received: Mon, 13 May 2019 08:44:12 PM PDT
From: Larry Needleman <[log in to unmask]>
To: [log in to unmask], [log in to unmask]
Subject: Re: ICA Criteria
Kirk et al.
I agree the plaque is almost always in the first several cms of the
bifurcation. The normal measurements are taken from there. Did someone measure
normal velocities more dismally in the bulb. AMK issue was someone have a DICA
velocity of over 125 cm/s and the reader wished to call it stenosed. The
technologist rightly pointed out there was no stenosis and no plaque there.
The reader said “why not read elevated velocity in the DICA, maybe its hard
to see plaque and the high velocity indicates a stenosis.”
I agree your references did discuss measuring the velocity in stenosis and
they show the PICA is where the stenosis is. The Blackshear article does
mention a normal range for the PICA. Do you know if someone measured the MICA
and DICA in normals and their ranges?
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