Vertebral artery stenosis or occlusionAndrey писал(а):...Вопрос такой - подходят ли критерии 2-х и более кратного увеличения скорости кровотока для определения гемодинамически значимой экстравазальной компрессии (как например при обычных стенозах)? Нужно ли какое-то дообследование если нет симптоматики?
Most vascular laboratories simply determine the presence
and direction of blood flow in the midcervical
vertebral artery (VA) without an extensive exploration
of the VA origin and its terminal portion. Compared
to carotid imaging, fewer validation studies are available
for detection and quantification of the VA lesions
[152-168]. However, VA stenoses, occlusions and
dissections are increasingly being recognized as potential
causes or risk factors for posterior circulation
ischemia [152,162,169]. VA stenosis occurs more
often in V3-V4 segments, followed by the origin of
the vertebral artery (VO), and midcervical section
(V1-V2) [170]. Direct assessment of the V3 segment
with ultrasound is not possible [170]. Therefore, the
diagnosis of vertebral obstruction at this level is based
on finding indirect proximal signs (i.e. increased
flow pulsatility and different waveforms between two
sides) or distal signs (poststenotic turbulence, blunted
waveform). Diagnostic criteria for direct assessment
of the V4 segment will be presented below in the
section on the criteria for 'Intracranial stenosis'.
During extracranial duplex examination, the
assessment of the vertebral artery should include scanning
the midcervical portion and attempts to visualize
the proximal VA and its origin whenever possible.
Diagnostic criteria for VA stenosis derived from
previous studies [152-168] and our own experience
include:
1 focal significant PSV velocity increase with a ratio
between prestenotic and stenotic segments of l/> 2;
2 presence of a structural lesion, turbulence or
spectral narrowing; and
3 indirect pre- or poststenotic signs (abnormal
pulsatility and waveforms).
Our criteria for VA stenoses do not include a PSV
cut-off since tortuosity of the proximal VA segment,
compensatory velocity increase with ICA lesions [171]
and VA dominance may produce relatively high velocities.
The keys to diagnosis of the VA stenosis with
> 50% diameter reduction are the terms 'focal' and
'significant'. The velocity increase should be found
over a relatively short (usually 1-2 cm) segment of the
VA with normal or decreased pre- and poststenotic
velocities. This increased velocity should at least
double the velocities found in other segments of the
same VA. A hypoplastic VA is more likely to have low
velocity and greater pulsatility over longer arterial
segments particularly with changes in hemorheology
[172].
Derived from previous studies [152-168], diagnostic
criteria for VA occlusion include:
1 flow void area and absent pulsed Doppler signals in
a segment or entire VA stem;
2 hypoechoic vessel lumen (acute and subacute
occlusion); and
3 hyperechoic vessel lumen (chronic occlusion).
Occasionally, a segmental VA occlusion can be found
[173] due to tremendous capacity of the vertebral
artery to compensate via muscular collaterals. In
these cases, patent distal and particularly terminal VA
segments are found carrying antegrade low-resistance
flow, often with delayed systolic upstroke. The latter
should be differentiated from a proximal lesion of
the subclavian artery. Therefore, incomplete assessment
of the VA stem can miss a short segmental
occlusion.
Andrei V. Alexandrov, MD, RVT
Cerebrovascular Ultrasound in Stroke Prevention and Treatment
