Vascular Medicine. Thomas Zeller

alt=""/> Slightly altered velocity criteria have been described (by Armstrong et al. 2007, among others), partly due to reduced wall compliance in the stent area and loss of the luminal dilation (“bulb”) often (but not always) located in the internal carotid artery orifice area.

      External carotid artery

      There is no established classification of stenosis grades for external carotid artery stenoses based on maximum velocities. In addition to general stenotic characteristics (see under internal carotid artery stenoses), the peak velocity ratio can be used.

      The differential diagnosis should include distal arteriovenous malformations in the afferent areas for branches of the external carotid artery, as well as dural fistulas; flow acceleration/aliasing is then seen over long stretches and not only focally in the “stenotic area.”

      

      Table 1.1–4 Stenosis grades after stent angioplasty in the internal carotid artery.

	> 70%	> 50%
PSV (cm/s)	> 350	> 225
ICA–CCA ratio	> 4.75	> 2.5

      CCA, common carotid artery; ICA, internal carotid artery; PSV, peak systolic velocity.

      Fig. 1.1–9 An aneurysm in the internal carotid artery. A typical “coffeebean” fragmented color pattern in an internal carotid artery aneurysm, with relative stenosis in the outflow area.

      Fig. 1.1–10 Stenosis of the external carotid artery. A typical undulation phenomenon is seen in the external carotid artery, with evidence of moderate stenosis.

      In cases of occlusion of the external carotid artery, side branches are often collateralized via the corresponding external carotid artery branches on the contralateral side or branches of the thyrocervical trunk or costocervical trunk.

      Subclavian artery

      See section A 4.1.

      Vertebral artery

      For findings involving the subclavian steal effect/syndrome, see section A 4.1.

      There is no established classification of stenosis grades based on maximum velocities for vertebral artery stenoses. The criteria mentioned in connection with the internal carotid artery can be used, but it should be noted that minor flow disturbances in the obtusely angled orifice area of the vertebral arteries must be regarded as physiological. The velocities given should be lower, as the physiological maximum systolic flow velocity is approximately 60–100 cm/s. Values above 100 cm/s must be regarded as suspicious. The critical velocity after which the presence of a > 50% stenosis must be assumed is 120 cm/s (Baumgartner et al. 1999). The peak velocity ratio may also be used.

      Differential diagnoses in cases of flow acceleration in the vertebral artery, with a risk of overestimating stenoses:

      

Inadequate perfusion of the contralateral vertebral artery (e.g., due to aplasia, hypoplasia, stenosis, occlusion, dissection) with hyperperfusion of the artery being examined

      

Hyperperfusion of the vertebral arteries when collaterals via the posterior communicating branch are compensating for obstructive carotid processes

      

Arteriovenous malformations in the vertebrobasilar flow area

      

Measurement of the relevant parameters, e.g., after extrasystoles, with a compensatory pause, or in cases of absolute arrhythmia after a longer RR interval, or with an increased ejection volume in patients with aortic insufficiency or marked bradycardia

      Differential diagnoses in cases of flow deceleration in the vertebral artery, with a risk of underestimating stenoses:

      

Distal vertebrobasilar flow obstruction (high pulsatility, and reduced diastolic flow in particular)

      

Hypoplasia or dilatory arteriopathy in the vertebral artery

      

Marked cerebral microangiopathy or raised intracranial pressure with disturbed distal outflow (with identical bilateral findings)

      

When measurements are carried out during hemodynamically compromising tachycardic heart action

      

In cases of proximal high-grade flow obstructions

      Findings in occlusions of the extracranial vertebral artery:

      

Vessel not identifiable (in continuous-wave mode, occlusion may only be suspected, however)

      

Possible hyperperfusion of the contralateral vessel

      

Arterial lumen definitely demonstrated on duplex ultrasound, without PW Doppler or color signals

      

Demonstration of distal inflow collaterals possible

      Findings in occlusions of the intracranial vertebral artery:

      

Markedly increased extracranial pulsatility, with reduced diastolic flow in one vertebral artery that may amount to pendular flow (caution: outflow into a dilated PICA may lead to a normal Doppler signal when there is a distal vertebral artery occlusion)

      

Possible hyperperfusion of the contralateral artery

      

Course of the vertebral artery not capable of being imaged transnuchally

      

      Vertebral artery compression syndrome (often suspected, but actually a rare finding) characterized by:

      

Rotatory vertigo and nystagmus

      

Capable of being reproducibly triggered by head rotation

      

Can be stopped by a return movement

      

Clear