Ultrasound Evaluation of the Carotid Arteries

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CHAPTER 90 Ultrasound Evaluation of the Carotid Arteries

Leslie M. Scoutt, Jonathan D. Kirsch, Ulrike Hamper

Stroke remains the third leading cause of death and is a major cause of morbidity in the United States.¹ Most strokes are due to thromboembolic events rather than to ischemia or reduced perfusion. Whereas the heart is the number one source, 20% to 30% of strokes are believed to be secondary to embolus from plaque or thrombus at the carotid bifurcation.² Carotid endarterectomy has been convincingly shown in several prospective multicentered, randomized, double-blind trials to significantly reduce the risk of stroke and death in patients with stenoses of the internal carotid artery (ICA) of more than 60% to 70% compared with optimized medical therapy.³^–⁶ However, at the time these trials were published in the 1990s, statin therapy was not a part of the standard medical regimen, and double-blind trials comparing carotid endarterectomy with medical management including statin therapy are currently ongoing.

Thus, the identification of patients with ICA stenoses of 60% to 70% is clearly important for patient management, allowing appropriate referral for carotid endarterectomy. Risk factors for disease at the carotid bifurcation include atherosclerosis, hypertension, diabetes mellitus, hyperlipidemia, hypercholesterolemia, obesity, and smoking. Patients with risk factors for carotid plaque, carotid bruits, and symptoms of stroke or transient ischemic attacks are typically referred for evaluation of the carotid arteries, which can be performed with ultrasonography, computed tomographic angiography, magnetic resonance angiography, or conventional angiography. Of these potential screening modalities, carotid ultrasound examination is the most readily available, least invasive, and least expensive. Numerous studies have shown that when it is performed appropriately, ultrasound examination of the carotid arteries is highly accurate for detection of surgical lesions (i.e., ICA stenoses ≥70%),⁷^–¹⁰ and additional confirmatory studies such as CT angiography, magnetic resonance angiography, and conventional angiography are usually unnecessary except in complex cases with discordant findings or poor visualization. The precise method of grading stenoses of the ICA changed with the publication of the North American Symptomatic Carotid Endarterectomy Trial (NASCET).³ Before the NASCET, the percentage stenosis of the ICA was typically calculated by comparing the width of the residual lumen with the estimated diameter (outer wall to outer wall) of the ICA at the site of the stenosis (Fig. 90-1A). However, because the outer wall of the ICA can be seen on an angiogram only if it is calcified, angiographic measurements of ICA diameter are only estimates in many cases. Hence, this method has significant interobserver and intraobserver variability as well as poor reproducibility. Thus, when the NASCET was designed, the measurement of percentage ICA stenosis was standardized angiographically by comparing the width of the residual lumen at its narrowest point with the diameter of the lumen of the distal normal ICA (beyond any post-stenotic dilation; Fig. 90-1B) because the vessel lumen can be accurately and reproducibly measured on angiographic images. For a given residual lumen, the percentage stenosis is generally higher with the pre-NASCET method of calculating an ICA stenosis.

FIGURE 90-1 Schematic diagrams demonstrating the methods of calculating percentage internal carotid artery stenosis. A, The pre-NASCET or traditional formula for calculation of an ICA stenosis compares the diameter of the residual lumen with the distance between the outer walls of the ICA at the site of stenosis. On angiograms, this method is less accurate than the NASCET method because of difficulty in identifying the outer wall of the ICA. B, Percentage ICA stenosis in the NASCET trial was calculated by comparing the diameter of the residual lumen with the luminal diameter of the distal normal ICA beyond any post-stenotic dilation. This is the currently accepted method of calculating percentage stenosis of the ICA. In general, percentage stenosis is greater when it is calculated by the pre-NASCET or traditional formula than by the NASCET method. CCA, common carotid artery; ECA, external carotid artery; ICA, internal carotid artery.

TECHNICAL REQUIREMENTS

Doppler ultrasound examination of the carotid arteries requires an ultrasound machine with high-resolution gray-scale imaging as well as color Doppler and spectral Doppler capability. A high-frequency 5- to 7.5-MHz linear array transducer should be used to optimize spatial resolution. However, if the carotid arteries are too deep to visualize with the linear array transducer in a patient with a short, thick neck, a lower frequency curved array transducer may be necessary for adequate penetration.

Technique

The examination begins with evaluation of plaque burden. Plaque echotexture should be characterized as hypoechoic, heterogeneous, or echogenic (Fig. 90-2). The surface contour of the plaque should be described as smooth or irregular (Fig. 90-3), and the percentage reduction of the arterial diameter by the plaque should be estimated.

FIGURE 90-2 Carotid plaque: echotexture. A, Color Doppler image demonstrating a large amount of homogeneous hypoechoic plaque causing a “string sign” (arrow) in the left ICA. B, Note focal hypoechoic area (arrow) within a heterogeneous plaque in the left carotid bulb. C, Note homogeneous echogenic shadowing plaque (arrows) in the proximal right ICA. D, Color Doppler image demonstrating homogeneous echogenic shadowing plaque (arrows) in the left proximal ICA.

FIGURE 90-3 Carotid plaque: surface contour. A, Longitudinal gray-scale image of the distal left CCA demonstrating plaque with a smooth surface contour and heterogeneous echotexture. B, Longitudinal gray-scale image reveals a large amount of hypoechoic plaque with a smooth surface contour (arrows) along the posterior and anterior walls of the right ICA and bulb. C and D, Longitudinal gray-scale images of plaque with irregular surface contour from two different patients. Note hypoechoic area within the plaque (arrow in D). E, Longitudinal power Doppler image of the right ICA reveals an irregular residual lumen, indicative of irregular plaque surface.

Optimal evaluation of plaque requires both gray-scale and color or power Doppler imaging in the longitudinal and transverse planes of the entire CCA and ICA as well as the origin of the external carotid artery (ECA). The focal zone should be set at the level of the far wall of the vessel. The use of spatial compounding and harmonic imaging will also improve gray-scale resolution. The gray-scale gain should be adjusted such that plaque and the vessel wall are easily depicted but artifactual echoes are not present within the vessel lumen. If the gain is set too low, plaque will look artifactually hypoechoic. The color gain should be optimized by slowly increasing the gain until color speckles are noted in the surrounding soft tissues. The gain is then decreased until the color pixels are visible only within the vessel lumen. If the gain is set too high, the color pixels will overwrite or “bleed” over plaque, obscuring visualization of the true extent of plaque burden, particularly during systole, and stenoses may be overlooked (Fig. 90-4). If the gain is too low, sensitivity to blood flow will be decreased, and false-positive diagnoses of occlusion or stenosis will be made. The color velocity scale should be adjusted such that color fills the lumen reaching to the vessel wall. Therefore, the color velocity scale may have to be changed slightly as one interrogates the different vessels in the neck. If the scale is set too low, aliasing will occur, making it more difficult to detect flow disturbances at the site of a stenosis. In addition, color motion artifact, which may obscure visualization of the vessel, is more prominent when the velocity scale or pulse repetition frequency is set too low. The wall filter should be set as low as possible without degradation of the image by motion artifact. Angling of the color box will facilitate evaluation of the direction of blood flow, and a straight, small color box will increase sensitivity to flow. If the vessel lumen cannot be visualized because of shadowing from plaque, an approach to the vessel from different angles (including the transverse plane) or use of a curved array transducer may be helpful.

FIGURE 90-4 Color “blooming” artifact. A, Note extensive echogenic, irregularly surfaced plaque in the mid left CCA on a longitudinal gray-scale image. B, On the color Doppler image, however, the color overwrites and obscures the plaque.

Once the gray-scale and color or power Doppler images have been obtained, the sonographer should be able to describe the amount and type of plaque in the carotid arteries as well as the relationship of the ICA and ECA to the carotid bulb. Whereas the degree of stenosis can often be estimated on the gray-scale or color Doppler images, precise quantification of stenosis requires accurate measurement of peak systolic velocity (PSV) in the ICA and CCA on the spectral Doppler tracing.

Spectral Doppler tracings are obtained from longitudinal images with the sample volume placed centrally within the vessel lumen or at the brightest spot in any area of focal color aliasing. To optimize the spectral Doppler tracing, the velocity scale and baseline should be adjusted such that the tracing fills the velocity spectrum or scale. If the scale is too high, the waveform will be too small to easily measure or analyze. However, if the scale is too low, the tracing will be too large, and wraparound or aliasing of the systolic velocity peak will occur, making it impossible to accurately measure PSV. The angle of spectral Doppler insonation should be kept between 45 and 60 degrees to minimize error in the calculation of velocity from the Doppler frequency shift. If at all possible, the angle should be kept constant on follow-up studies. The angle cursor should be placed parallel to the direction of blood flow in the color jet or vessel lumen rather than parallel to the vessel wall. The direction of blood flow will, in fact, parallel to the vessel wall in most cases, but the jet of blood may travel tangentially or obliquely in relationship to the vessel wall if plaque is irregular or asymmetric (Fig. 90-5). In such cases, the angle correction cursor should be placed parallel to the jet of blood as seen on color Doppler imaging. The sample gate should be kept small, between 1.5 and 2.5 mm in width, and placed in the center of the vessel because PSV will be lower near the vessel wall owing to the geometry of laminar flow and drag from the vessel wall. If the sample gate is too wide, a wider range of velocities will be depicted, and there is the potential risk of falsely creating the appearance of spectral broadening and turbulent flow. Finally, the spectral Doppler gain should be optimized; the gain should be increased until background speckles appear on the spectral tracing and then readjusted downward until the background is homogeneously black. Although incorrect spectral Doppler gain settings rarely cause shifts in PSV of more than 20 cm/sec, such variation in the distal CCA can be important when the PSV in the distal CCA is used as the denominator in calculation of the peak systolic velocity ratio (PSVR). Apparent spectral broadening with “fill in” of the spectral envelope can also be spuriously created if the spectral Doppler gain is set too high.

FIGURE 90-5 Angle of insonation. There is a large amount of both hypoechoic and echogenic plaque in the right ICA causing tortuosity and angulation of the vessel lumen in this patient who presented with a carotid bruit. The Doppler angle should be calculated in reference to a vector parallel to the direction of blood flow in the residual lumen (yellow line) rather than parallel to the vessel wall.

Protocol

• Longitudinal gray-scale and color or power Doppler images of the proximal and distal CCA, bifurcation, bulb extending into the ICA, and bulb extending into the ECA

• Transverse gray-scale and color or power Doppler images of the proximal and distal CCA, bulb, bifurcation, proximal ICA, and proximal ECA

• Spectral Doppler tracings from the proximal CCA, distal CCA, proximal ICA, mid ICA, distal ICA, proximal ECA, and mid vertebral artery. PSV is recorded for each segment, and end-diastolic velocity (EDV) is noted if it is more than 100 cm/sec. The PSVR is calculated by dividing the highest PSV in the proximal ICA or area of stenosis by the PSV in the distal CCA. PSV in the distal CCA should always be measured 2 to 3 cm proximal to the level of the carotid bulb. Several measurements, optimally three, of PSV should be obtained and the highest velocity recorded.

Additional gray-scale and color or power Doppler images as well as spectral Doppler tracings should be obtained as necessary wherever extensive plaque burden, vessel narrowing, or color aliasing is seen.

Normal Findings

The normal carotid arteries have a thin, regular echogenic wall without focal areas of calcification, intraluminal plaque, or thrombus. Color should fill the vessel lumen homogeneously with a slight central increase in color intensity consistent with normal parabolic or laminar flow. Where the carotid bulb widens, a helical blood flow pattern or reversal of peripheral flow is a normal finding, particularly in younger patients, and is believed to be due to boundary layer separation.

Normal PSV in the CCA is variable and depends on numerous factors, including cardiac output or stroke volume, heart rate, systolic blood pressure, and age. In general, however, PSV in the normal CCA ranges from 70 to 100 cm/sec and decreases gradually as one samples distally.

The CCA, ICA, and ECA demonstrate distinct characteristic waveform patterns. Whereas all segments of the extracranial carotid arteries normally demonstrate a sharp systolic upstroke and thin spectral envelope, the amount of diastolic flow varies in each vessel, reflecting the oxygen consumption and peripheral vascular resistance of the vascular bed supplied. The ECA, which supplies the muscular bed of the scalp, typically demonstrates completely absent or very low velocity end-diastolic flow. Although the amount of diastolic flow in the ECA may vary from patient to patient, it should be symmetric right to left and less than the diastolic flow in the ICA or CCA (Fig. 90-6). An early diastolic notch followed by a short reversal of flow in early diastole is often seen in the ECA. The ICA, which supplies blood to the brain (high oxygen consumption), has a low-resistance waveform pattern with continuous forward, relatively high velocity diastolic flow (Fig. 90-7). The waveform of the CCA demonstrates an intermediate amount of diastolic flow and often demonstrates a brief reversal of flow in early diastole (Fig. 90-8). The vertebral artery has a waveform pattern similar to that of the ICA, characterized by a sharp systolic upstroke and continuous forward diastolic flow (Fig. 90-9).

FIGURE 90-6 Normal spectral Doppler tracing of the external carotid artery. The ECA has a higher resistance waveform with less diastolic flow than the ICA. Whereas the amount of diastolic flow may vary from patient to patient, it should be symmetric right to left in a given individual. A, This patient has no diastolic flow in the ECA. B, In another patient, a small amount of diastolic flow is present. Reversal of flow in early diastole or an early diastolic notch (arrows) is a normal finding in the ECA. Note sharp systolic upstroke and thin spectral envelope in the spectral tracings of both ECAs.

FIGURE 90-7 Normal spectral Doppler tracing of the internal carotid artery. Note that in comparison to the ECA, there is increased diastolic flow, the systolic peak is slightly blunted, and the spectral envelope is slightly widened in the ICA. The systolic upstroke is sharp, and velocity gradually tapers during diastole.

FIGURE 90-8 Normal spectral tracing of the common carotid artery. The systolic upstroke is sharp in the CCA, and there is an intermediate amount of diastolic flow in comparison to the ICA and ECA. An early diastolic notch may be present, but it is less pronounced than in the ECA.

FIGURE 90-9 Normal spectral tracing of the vertebral artery. The waveform of the normal vertebral artery is similar to the waveform of the ICA.

Differentiation of the ICA from the ECA is critically important to avoid misinterpretation of a stenosis in the ECA as a more clinically significant ICA stenosis. The best method of identifying the ECA is by visualization of branches arising from the vessel (Fig. 90-10A). The ICA virtually never gives rise to branch vessels in the neck. Temporal tapping over the ophthalmic artery will generate sharp, spike-like deflections in the waveform of the ECA during diastole (Fig. 90-10B). However, on occasion, transmitted pulsations to the ICA will be observed after temporal tapping, although the deflections are typically blunted in comparison to the deflections observed in the ECA.⁷^,⁸ In general, the ECA is smaller, is more medial, and has a higher resistance waveform pattern than the larger posterolateral ICA. However, location and vessel size are not reliable criteria for differentiation of the ICA from the ECA in all patients.

FIGURE 90-10 Identification of the external carotid artery. A, Note branches arising from the right ECA on this color Doppler image. Branches almost never arise from the ICA below the skull base. B, Note deflections in the spectral tracing from the right ECA due to temporal tapping. These deflections are most easily seen during diastole. Whereas temporal tapping may occasionally cause similar deflections in the ICA or CCA, they will be smaller and less sharply defined than in the ECA.

Grading Stenoses in the Internal Carotid Artery

Grading of stenosis in the ICA by Doppler velocity criteria is based on the simple precept that flow volume is equal to vessel area multiplied by PSV. Because flow volume is a relative constant, PSV is inversely related to vessel lumen diameter. Therefore, if the vessel diameter decreases, PSV must increase to maintain flow volume. As demonstrated by the Spencer diagram, once the vessel diameter decreases by more than 50%, PSV at the site of the stenosis rises exponentially, and this compensatory increase in PSV maintains flow volume until the stenosis reaches approximately 70%.⁹ When a stenosis exceeds 70%, flow volume will begin to drop despite continued exponential increase in PSV. Once a stenosis in the ICA becomes greater than approximately 96%, the gradient across the stenosis becomes too high for the pressure generated by the combination of myocardial contractility and vessel elasticity to force blood through the residual lumen, and PSV begins to drop until the vessel occludes and velocity is zero.⁹

Numerous studies have attempted to correlate Doppler measurements of PSV, PSVR, and EDV criteria with angiographically calculated percentage stenosis. Widely variable results have been reported.¹⁰^–¹⁴ In general, velocity criteria have a higher accuracy and positive predictive value for high-grade stenoses (>70%) and are less reliable for accurate grading of more moderate stenoses (<50%).¹²^,¹⁴ Criteria are probably both machine (possibly even transducer) and laboratory specific and therefore should be validated for each laboratory and machine upgrade if possible. Studies have also demonstrated that vascular laboratories cannot reliably differentiate stenoses in the ICA by 10% increments.¹²^,¹⁴ Accuracy is best achieved by focusing on whether a stenosis is greater than or less than a specific percentage stenosis. In most institutions, carotid endarterectomy is recommended in patients with ICA stenosis of more than 70%. Hence, most vascular laboratories categorize ICA stenoses as less than 50%, 50% to 69%, 70% to 96%, and more than 96%.

A meta-analysis published by Grant and colleagues ¹² found that accuracy varied little over a wide range of threshold values for PSV and PSVR, although the sensitivity and specificity were inversely proportional. Hence, the authors recommend that if the Doppler examination is to be used as a screening test, lower thresholds with higher sensitivity should be used. However, if the Doppler examination is intended as a diagnostic test without anticipating confirmation by some angiographic imaging modality, then specificity should be emphasized and higher thresholds are recommended.¹²

In 2002, the Society of Radiologists in Ultrasound (SRU) convened a multidisciplinary panel of experts, including both radiologists and vascular surgeons, to develop a consensus for grading of ICA stenoses by Doppler ultrasonography. The published recommendations of this consensus conference are as follows ¹³:

PSV < 125 cm/sec and PSVR < 2.0 suggest a stenosis < 50%

PSV between 125 and 230 cm/sec and PSVR between 2.0 and 4.0 are most consistent with a stenosis of 50% to 69% (Fig. 90-11)

PSV > 230 cm/sec, PSVR > 4.0, and EDV > 100 cm/sec indicate a stenosis of ≥70% to 96% (Figs. 90-12 and 90-13)

FIGURE 90-11 ICA stenosis, 50% to 69%. A, Longitudinal color Doppler image of the right ICA in a patient with a right carotid bruit reveals echogenic plaque and a stenosis at the origin of the right ICA. Note color mosaic just distal to the narrowing of the vessel lumen indicative of increased velocity of flow in the post-stenotic jet. B, Spectral tracing reveals a PSV of 195 cm/sec just distal to the stenosis. C, PSV in the right CCA is 96 cm/sec. PSVR is approximately 2 : 1. By SRU criteria, this corresponds to a moderate stenosis of 50% to 69%.

FIGURE 90-12 ICA stenosis, 70% to 96%. A, Longitudinal duplex Doppler image of the right ICA in a 73-year-old man presenting with a transient ischemic attack demonstrates that the diameter of the proximal right ICA is narrowed approximately 80%. PSV is 305 cm/sec at the site of the stenosis. B, Spectral tracing of the distal right CCA demonstrates a PSV of 85 cm/sec, yielding a PSVR close to 4 : 1. By SRU criteria, these velocity measurements are consistent with a stenosis of the right ICA of more than 70%, which was confirmed by a CT angiogram.

FIGURE 90-13 ICA stenosis, 70% to 96%. Longitudinal color Doppler image of the proximal right ICA (A) demonstrates a marked degree of narrowing over a long segment from heterogeneous, largely hypoechoic plaque in a 68-year-old woman presenting with a stroke. By visual inspection, the percentage diameter reduction is estimated at nearly 90%. Spectral Doppler tracing reveals a PSV of 523 cm/sec in the stenosis (B), with a PSV of 58 cm/sec in the distal CCA (C). PSVR is 9 : 1. Although it is not possible to accurately classify stenoses at 10% increments by Doppler velocity criteria, these measurements are well above the SRU threshold for a stenosis of 70% or more, and therefore the degree of stenosis is likely in the higher range, approximately 90% diameter reduction, as suggested by the color Doppler image.

Once an ICA stenosis becomes greater than an approximately 96% diameter reduction, PSV velocity begins to drop (Fig. 90-14) until the vessel occludes and the velocity reaches zero.⁹ Hence, the panel also recommended that the estimation of diameter reduction by plaque on gray-scale and color Doppler imaging be correlated with the velocity-based estimate of percentage stenosis.¹³

FIGURE 90-14 ICA stenosis, greater than 96%. Transverse (A) and longitudinal (B) color Doppler images reveal a tight stenosis (arrow) at the origin of the right ICA. Spectral Doppler tracing of the right CCA (C) demonstrates a high-resistance waveform with absent diastolic flow and reduced PSV (37 cm/sec) in comparison to the left CCA (D), which has a PSV of 73 cm/sec and a normal amount of diastolic flow. A high-resistance waveform in the CCA suggests a distal high-grade stenosis or occlusion. However, maximum PSV in the right ICA is only 189 cm/sec (E). By SRU criteria, this PSV corresponds to only a 50% to 69% stenosis. However, once the percentage diameter reduction exceeds approximately 96%, PSV at the site of a stenosis will drop. Furthermore, PSVR in this patient is more than 5 : 1, which indicates a stenosis of more than 70% by SRU criteria, confirming a tighter stenosis. Color Doppler images and careful waveform analysis of the proximal and distal vessels are required to differentiate between a high-grade (nearly occlusive) and a more moderate stenosis that may have the same PSV.

Pitfalls: Technique

Incorrect Choice of Doppler Angle

An incorrect Doppler angle or a Doppler angle that is too high will introduce error into the calculation of PSV. An angle above 60 degrees will result in a falsely elevated PSV (Fig. 90-15). The correct Doppler angle should be calculated in reference to a vector parallel to the vessel lumen or direction of blood flow, which will not necessarily be parallel to the vessel wall in the case of extensive, irregular plaque (see Fig. 90-5).

FIGURE 90-15 Effect of Doppler angle on calculated PSV. Three duplex Doppler images are presented of the right ICA at the same location. When the Doppler angle (yellow circles) is 44 degrees (A), PSV is calculated at 131 cm/sec. However, with a Doppler angle of 60 degrees (B), PSV is 190 cm/sec; and when the Doppler angle is 70 degrees (C), PSV is calculated at 266 cm/sec. Thus, an incorrect Doppler angle or variations in Doppler angle from examination to examination can introduce significant error into the measurement of PSV.

Incorrect Gain

If the color gain is set too high, the color will bleed over the vessel wall, obscuring plaque and stenosis (see Fig. 90-4). If the color gain is set too low, the color will not reach the vessel wall and will falsely create the appearance of hypoechoic plaque. If the gray-scale gain is set too low, plaque will appear falsely hypoechoic. Incorrect spectral Doppler gain can also cause slight increase or decrease in measurement of PSV (see earlier).

Pitfalls: Pathology

Tortuous Carotid Artery

When the carotid arteries are tortuous, most commonly in elderly patients, PSV can be elevated without an underlying stenosis (Fig. 90-16). This is due in part to a true increase in PSV as the blood accelerates around the curves but is also likely due to difficulty in assigning a correct Doppler angle along the curved vessel, which results in an overestimation of PSV due to incorrect Doppler angle. Hence, the sonographer should use caution before diagnosing a carotid stenosis solely on the basis of elevation of PSV in a tortuous vessel without evidence of plaque or vessel narrowing. A true stenosis should cause post-stenotic turbulence in addition to an increase in PSV.

FIGURE 90-16 Tortuous ICA. A, Color Doppler image demonstrates a tortuous right ICA. B, Duplex Doppler tracing demonstrates a PSV of 186 cm/sec. By SRU criteria, this corresponds to a 50% to 69% stenosis. However, no stenosis was noted on gray-scale or color Doppler imaging. Increased PSV is due to tortuosity of the vessel.

Heart Rate

Heart rate affects both PSV and EDV. PSV will be relatively elevated and EDV will be artificially low in patients with bradycardia. Conversely, in patients with fast heart rates, PSV will be relatively low because of decrease in stroke volume. However, because velocity normally decreases during diastole, EDV will be artificially elevated in patients with tachycardia because of shortening of diastole. Common causes of tachycardia include stress, medications, and thyrotoxicosis. Ventricular conduction defects, medications (including common cardiac drugs such as afterload reducers like propranolol), and hypothyroidism may result in brachycardia. Hence, measurement of PSV and grading of ICA stenoses in patients with cardiac arrhythmias may be problematic. For example, PSV will be increased in the beat after a compensatory pause as a result of relative bradycardia and decreased during a premature ventricular contraction as a result of relative tachycardia (Fig. 90-17). Recommended general guidelines for measurement of PSV in patients with cardiac arrhythmias include the following:

1 Avoid measurement of PSV in a premature ventricular contraction or after a compensatory pause.

2 Measurements should be made at a similar point during the arrhythmia in each vessel segment if the arrhythmia is regular.

3 In the case of an extremely irregular heartbeat, consistently measuring either the most normal appearing cardiac cycle or choosing the highest or lowest PSV in each vessel segment is reasonable. However, a markedly irregular heartbeat does introduce a measure of unreliability to the Doppler criteria.

FIGURE 90-17 Effect of heart rate and arrhythmia on PSV. Note variability of PSV in a patient with a premature ventricular contraction and compensatory pause. PSV is decreased during the premature ventricular contraction (long arrow, relative tachycardia) and increased in the beat that follows the compensatory pause (short arrow, relative bradycardia).

Long-Segment or Synchronous Involvement

Coexistent disease in the carotid arteries will also make PSV Doppler criteria less reliable. Synchronous disease in the CCA, or tandem lesions, will result in a decrease in PSV for a given percentage stenosis in the ICA. Hence, the entire CCA and ICA must be evaluated, not just the carotid bifurcation. Most ICA stenoses are less than 2 cm in length. However, if a stenosis is unusually long (>2 cm), PSV often drops (possibly because of increased in-flow resistance), although diastolic velocity may remain high (Fig. 90-18). Prior radiation therapy, carotid dissection, arteritis, or fibromuscular dysplasia should be considered when a long-segment stenosis is noted, although diffuse atherosclerosis may also be the cause.

FIGURE 90-18 Long-segment stenosis. Gray-scale (A) and color Doppler (B) longitudinal images of the right ICA reveal a long-segment high-grade stenosis and extensive hypoechoic plaque (short arrows, residual lumen in A). However, spectral Doppler tracing (C) reveals a maximum PSV of only 120 cm/sec. By SRU criteria, this corresponds to a less than 50% stenosis. However, PSV is artifactually reduced because of the length of the stenosis.

Contralateral Carotid Disease

A high-grade carotid stenosis or occlusion will increase PSV in the contralateral side, especially at the site of a stenosis. Hence, if the PSV seems more elevated than one would expect given the amount of visualized plaque and if the vessel is not tortuous, one should be suspicious of contralateral disease (Fig. 90-19). The degree of increase in velocity is unpredictable and may differ in the CCA and ICA in a given patient. Hence, the use of PSVR may not adequately compensate.¹⁵^,¹⁶

FIGURE 90-19 Effect of contralateral occlusion on PSV. A, Longitudinal color Doppler image reveals that the left proximal CCA (arrows) is occluded. B, PSV is elevated in the mid right CCA (129 cm/sec) and was even more elevated proximally (160 cm/sec; not shown). C, PSV is 269 cm/sec in the right ICA. By SRU criteria, this corresponds to a stenosis of more than 70%. However, on color Doppler imaging (D), there is only a small amount of plaque noted (arrow) in the right ICA consistent with a stenosis of less than 50%. Furthermore, PSVR is approximately 2 : 1, which corresponds to a stenosis of only 50%. PSV is artificially elevated in the right CCA and ICA because of the occlusion of the left CCA.

Measurements of PSV remain the basis for grading of stenoses of the ICA on Doppler ultrasound examination. However, given the pitfalls in measuring PSV as well as limitations in the applicability of PSV criteria in all patients, the final assessment of an ICA stenosis should always correlate velocity criteria with both gray-scale and color Doppler estimation of plaque burden and waveform analysis of the CCA and ICA. In addition to confirming the presence of a stenosis, abnormalities of the CCA and ICA waveforms can reflect distal or proximal cardiovascular disease not directly assessable by Doppler interrogation.

ULTRASOUND ASSESSMENT OF PLAQUE

Ultrasound evaluation of plaque requires gray-scale and color Doppler imaging in both longitudinal and transverse planes. Such images can be used to estimate percentage diameter reduction by plaque and correlated with PSV measurements. In addition, the echotexture and surface contour of the plaque should be assessed. Plaque should be characterized as hypoechoic or echogenic (see Fig. 90-2) with either a smooth or irregular surface (see Fig. 90-3). Prospective studies have shown that hypoechoic, irregular plaque is associated with an increased risk of neurologic events and increased rate of plaque progression.¹⁷^,¹⁸

Whereas echogenic plaque is readily depicted on gray-scale imaging, hypoechoic plaque may not be visible. However, on color Doppler imaging, hypoechoic plaque is readily observed as a signal void (Fig. 90-20). Similarly, surface irregularities are often best seen when outlined by color Doppler flow (Fig. 90-21). Although a pit deeper than 2 mm in a plaque raises concern for ulceration (Fig. 90-22), Doppler ultrasonography is not highly accurate in identifying plaque ulceration. Indentations or divots in plaque identified on color Doppler imaging can, in fact, be endothelialized and therefore not be true ulcers. The same limitation is true for angiography, and plaque ulceration remains primarily a histologic diagnosis. Color Doppler imaging, although necessary for the depiction of hypoechoic plaque, does not eliminate the need for gray-scale evaluation as color blooming, particularly during systole, may overwrite and obscure plaque, thereby causing an underestimation of plaque burden (see Fig. 90-4). Gain settings are important also on gray-scale imaging. If the gain is set too low, plaque will appear falsely hypoechoic, raising unnecessary concern. The percentage diameter reduction is usually best depicted on longitudinal images. However, if the plaque is irregular or eccentric, if there are numerous foci of plaque, or if the vessel lumen is tortuous, transverse images can be extremely helpful, ensuring that the longitudinal image is truly midline and not too lateral or off axis. If the longitudinal image is obtained over an eccentric focus of plaque or too close to the vessel wall, the degree of stenosis will be overestimated. If the vessel lumen is obscured by shadowing from calcified, echogenic plaque, imaging from different planes (i.e., anteriorly or posteriorly), power Doppler imaging, or use of a lower frequency transducer may help visualize the vessel lumen. On occasion, transverse images will eliminate or avoid shadowing from plaque. If the shadowing from plaque obscures the vessel lumen for less than 1 cm, standard PSV criteria can still be used to estimate percentage stenosis because the high-velocity jet caused by a stenosis will persist for approximately 1 cm. However, if more than 1 cm of the vessel length is obscured by shadowing from plaque, the maximal focal elevation of PSV in the post-stenotic jet may be missed, and therefore the use of Doppler velocity criteria to assess carotid stenosis is limited. In such cases, follow-up with CT angiography, magnetic resonance angiography, or conventional angiography is appropriate.

FIGURE 90-20 Hypoechoic plaque. A, Longitudinal gray-scale image does not demonstrate the hypoechoic plaque in the left carotid bulb. B, However, the hypoechoic plaque (arrow) is clearly outlined by color flow on the color Doppler image.

FIGURE 90-21 Irregular plaque. Longitudinal gray-scale (A) and color Doppler (B) images of the left carotid bulb demonstrate flow (arrow) undermining a focus of echogenic, shadowing plaque.

FIGURE 90-22 Ulcerated plaque. Gray-scale (A) and color Doppler (B) images demonstrating a divot or pit (arrow) within a large area of echogenic plaque with an irregular surface. This probably represents an ulcer.

The length of the stenosis should also be considered. Most ICA stenoses are relatively short. If a long-segment stenosis is observed, PSV will be less than expected, although diastolic velocity will remain high (see Fig. 90-18). The relative decrease in PSV is likely due to in-flow resistance. Causes of long-segment stenosis include radiation therapy, carotid dissection, and arteritis (including fibromuscular dysplasia).

Thickening of the wall of the CCA, termed fibrointimal thickening, has recently been described as a risk factor for cardiovascular disease (Fig. 90-23).¹⁹^,²⁰ Normal wall thickness is likely to be related to race and gender. Measurements should be obtained from the far wall of the CCA or ICA on a magnified image. However, there are technical limitations to accurate measurement and reproducibility of such a thin structure as the vessel wall, and further research in this area continues.

FIGURE 90-23 Fibrointimal thickening. A and B, Longitudinal gray-scale images demonstrate diffuse hypoechoic, somewhat irregular thickening of the posterior wall of the CCA in two patients with fibrointimal thickening.

WAVEFORM ANALYSIS OF THE CAROTID ARTERIES

The spectral Doppler waveform of the carotid arteries provides more information than merely a measure of PSV. Analysis of the contour or morphology of the waveform will reveal physiologic information concerning the distal cerebral circulation as well as the heart and more proximal vessels, which cannot be directly visualized on ultrasound examination. The presence of proximal or distal cardiovascular disease can thus be deduced. In addition, changes in the Doppler waveform may also provide clues to uncommon iatrogenic disease in the neck, such as carotid dissections, pseudoaneurysms, and arteriovenous fistulas. Albeit somewhat arbitrarily, abnormalities of the Doppler waveform can be subdivided for the purpose of analysis and description into changes that primarily affect systole, diastole, or the entire cardiac cycle.

Abnormalities of the Systolic Peak

Stenoses in the carotid vessels are the most common cause of changes in the configuration of the systolic peak. Although the focus of the carotid ultrasound examination is generally on the increase in PSV and EDV in an ICA stenosis, broadening of the spectral envelope, fill-in of the spectral window, and turbulence (random forward and backward flow) also occur. However, the outer contour of the systolic peak remains normal with a sharp systolic upstroke. The presence of such changes can help differentiate elevation of PSV due to a stenosis from an increase in PSV due to tortuosity of the vessel or systemic cause of increased PSV, such as hypertension, thyrotoxicosis, bradycardia, or aortic regurgitation (the water-hammer pulse; see later). Conversely, a global decrease in PSV can be seen in patients with hypotension, shock, tachycardia, thoracic aortic aneurysm, or decreased cardiac output (stroke volume) due, for example, to myocardial ischemia, poor myocardial contractility, cardiomyopathy, left ventricular aneurysm, or pericardial effusion.

Parvus Tardus Waveform

A parvus (diminished) tardus (delayed) waveform occurs distal to a severe proximal stenosis.²¹^,²² The parvus tardus waveform is characterized by decreased PSV and a delayed, more horizontal systolic upstroke with rounding or blunting of the systolic peak. The parvus tardus waveform phenomenon becomes more pronounced the more distal to the stenosis that the vessel is sampled. Hence, it is important to sample the ICA as distally as possible. In addition, the pattern of distribution of the parvus tardus waveform within the vessels in the neck helps pinpoint the location of the proximal stenosis. For example, if only the left CCA, ECA, and ICA have a parvus tardus waveform and if a sharp systolic upstroke is present in the right CCA, right ICA, and both vertebral arteries, the stenosis is likely to be at the level of the origin of the left CCA from the aortic arch. However, involvement of the bilateral CCAs, ICAs, and vertebral arteries is most likely indicative of a stenosis at the level of the aortic valve (Fig. 90-24).²³

FIGURE 90-24 Aortic stenosis. Note tardus parvus waveform on spectral tracings of the right CCA (A), left CCA (B), and left vertebral artery (C). The delay in systolic acceleration is even more pronounced in the right (D) and left (E) ICAs. This 79-year-old woman has severe aortic stenosis with a mean aortic valve gradient of 58 mm Hg and valve area of 0.73 cm².

Pulsus Bisferiens Waveform

Rarely, two systolic peaks of similar velocity with an interposed midsystolic retraction or deceleration may be observed (Fig. 90-25). This has been termed pulsus bisferiens (Latin, “beat twice”). Whereas this has been described in the literature as most commonly associated with aortic regurgitation (particularly if it coexists with aortic stenosis) and hypertrophic cardiomyopathy,²⁴ it may more likely be a result of changes in compliance of the vessel wall. In our experience, a bifid systolic peak may be seen in healthy, athletic young individuals or in elderly patients without known underlying heart disease.

FIGURE 90-25 Bisferiens waveform. Note prominent midsystolic retraction (arrow) and two systolic peaks. This young patient has neither aortic regurgitation nor known cardiomyopathy. The bisferiens waveform may not be visualized in all vessels and may be visualized only intermittently in some patients.

Pulsus Alternans Waveform

Alternating systolic velocity peaks, pulsus alternans, may be very rarely observed (Fig. 90-26). The cause of this phenomenon is not known. However, intrinsic myocardial disease, hypocalcemia, and impairment of venous return have been postulated as possible causes.²⁵

FIGURE 90-26 Pulsus alternans. Note oscillating peak systolic velocities in this 69-year-old man with history of atrial fibrillation, global hypokinesis, and ejection fraction of 30%. The patient had a middle cerebral artery infarct.

Abnormalities of Diastolic Flow

The normal ECA demonstrates a characteristic high-resistance waveform pattern with little or no diastolic flow and an early diastolic notch. Although the amount of diastolic flow may vary from individual to individual, the diastolic flow pattern should be symmetric right to left in the same individual. When the ipsilateral ICA is occluded, “internalization” of the ECA may occur, and a lower resistance waveform pattern with increased diastolic flow and asymmetric to the contralateral ECA may be observed (Fig. 90-27).²²^,²⁶ This phenomenon is incompletely understood but probably reflects the development of low-resistance collateral pathways. Occlusion of the ipsilateral CCA may sometimes result in a similar waveform pattern in the ECA but with reversed flow if the ICA is reconstituted at the level of the carotid bulb by retrograde flow from the ECA (Fig. 90-28). In such cases, the ECA and ICA waveforms may also demonstrate a delay in systolic upstroke.

FIGURE 90-27 Internalization of the ECA. Color Doppler image (A) from an 83-year-old woman presenting with a stroke demonstrates no evidence of blood flow in the right ICA. Spectral Doppler tracing of the right ECA (B) demonstrates increased diastolic flow in comparison to the left ECA (C). This phenomenon is termed internalization of the ECA.

FIGURE 90-28 Occlusion of the common carotid artery. A, Spectral tracing of the proximal left CCA from an 81-year-old woman with history of left CCA occlusion demonstrates a high-resistance waveform pattern with absent end-diastolic flow, reversed early diastolic flow, and reduced PSV. B, Gray-scale image demonstrates plaque (arrow) in the left bulb and distal CCA. E, external carotid artery. C, Color flow image demonstrates occlusion of the distal left CCA. Flow is present in the ICA and ECA. There is also a small amount of regurgitant retrograde flow into the distal left CCA below the carotid bulb above the occlusive plaque or thrombus. D, Spectral Doppler tracing of the left ECA reveals reversed flow toward the transducer away from the head with increased diastolic flow. Spectral Doppler tracings of the proximal (E) and distal (F) left ICA reveal that the ICA is reconstituted from reversed flow in the left ECA and demonstrates flow toward the head with a slight delay in systolic upstroke and prominent diastolic flow.

A high-resistance waveform pattern with diminished, absent, or reversed diastolic flow is an abnormal finding in the CCA or ICA suggestive of increased peripheral vascular resistance or a distal vascular occlusion or high-grade stenosis. When PSV is significantly reduced, this appearance has been described as a “knocking” waveform pattern.²² A unilateral knocking waveform pattern in the CCA is most commonly observed proximal to a distal high-grade stenosis or occlusion of the ICA or intracerebral vasculature (Figs. 90-28 and 90-29). The reversal of diastolic flow and decrease in PSV become more pronounced the closer to the obstructing lesion that the vessel is sampled. On occasion, a unilateral knocking waveform can be seen in the setting of distal vasospasm, arteritis, or carotid dissection. However, in the case of a carotid dissection, the sampled vessel will typically appear quite narrow over a long segment, and the echogenic dissection flap may also be seen on gray-scale images (see later). Bilateral high-resistance waveform patterns in the ICAs may indicate increased intracranial pressure, diffuse intracerebral vasospasm, or arteritis (Fig. 90-30).

FIGURE 90-29 Knocking waveform pattern. Note asymmetry in the spectral waveforms of the normal right CCA (A) and left CCA (B). The left ICA has a high-resistance waveform with reduced or absent diastolic flow. PSV, however, is normal. Duplex Doppler interrogation of the proximal left ICA (C) and mid left ICA (D) reveals a classic knocking waveform pattern with extremely low PSV and absent diastolic flow. PSV is 24 cm/sec in the proximal left ICA and 10 cm/sec in the mid left ICA. PSV decreases as one samples more distally in the left ICA. This is due to complete occlusion of the distal left ICA demonstrated on the sagittal color Doppler image (E, arrows).

FIGURE 90-30 Increased intracranial pressure. A, Spectral tracing of the right ICA from a 75-year-old woman with a large right hemispheric stroke reveals a knocking waveform with decreased PSV (24 cm/sec) and absent end-diastolic flow. B, Longitudinal color Doppler image demonstrates that the right ICA is widely patent. Magnetic resonance angiography (not shown) demonstrated occlusion of the right middle cerebral artery. Duplex Doppler interrogation reveals markedly reduced flow, both systolic and diastolic, in the left ICA (C), which was widely patent. Note that there is actually more diastolic flow in the left ECA (D) than in the ICA. These findings are due to increased intracranial pressure from the large right middle cerebral artery stroke. Axial CT images of the brain reveal both transtentorial (E) and uncal (F) herniation as well as the large middle cerebral artery stroke. Note midline shift and compression of the left lateral ventricle as well as obliteration of the right lateral ventricle (E).

When a high-resistance waveform pattern is noted in the proximal CCAs bilaterally and PSV is increased, aortic regurgitation is the usual cause. The precise diastolic flow pattern depends on the severity of the aortic regurgitation: diastolic flow may be reversed only in early diastole and associated with normal end-diastolic flow; early reversal of diastolic flow may be noted with absent end-diastolic flow; or in severe cases, reversed flow may be seen throughout diastole (Fig. 90-31).²² This waveform pattern is the Doppler equivalent of the water-hammer pulse detected on physical examination in patients with severe aortic regurgitation. Typically, only moderate to severe aortic regurgitation will disturb the common carotid arterial waveform. The change in diastolic flow pattern and increase in PSV are more pronounced the more proximally one samples the CCA. The waveform pattern in the ICA or even distal CCA will normalize, depending on the severity of the aortic regurgitation. This is a bilateral phenomenon.

FIGURE 90-31 Aortic regurgitation. Note increased PSV, flow reversal in early diastole, and absent diastolic flow in the right (A) and left (B) CCAs in a patient with severe aortic regurgitation. Waveforms in the distal ICAs were normal bilaterally.

Abnormal Waveform Patterns Involving the Entire Cardiac Cycle

Diffusely complex carotid artery waveform patterns affecting the entire cardiac cycle are typically the result of iatrogenic or traumatic conditions. Although uncommon, carotid dissections, pseudoaneurysms, arteriovenous fistulas, and the presence of an intra-aortic balloon pump may be diagnosed by a combination of gray-scale appearance and characteristic waveform.

Dissections of the internal carotid arteries occur most commonly in the setting of trauma from compression of the ICA on the spine. However, spontaneous dissections may occur, particularly in patients with predisposing risk factors, such as Marfan syndrome, Ehlers-Danlos syndrome, fibromuscular dysplasia, cystic medial necrosis, hypertension, and drug abuse. Dissections may also extend into the CCAs from an aortic dissection. Dissection of the ICA is the most common cause of stroke in young patients, exclusive of cardiac disease. Additional presenting symptoms of carotid dissection include acute onset of headache and Horner syndrome.

Carotid Dissection

In patients with carotid dissection, an echogenic intraluminal flap may be observed on longitudinal or transverse gray-scale images (Fig. 90-32A,B). Flow in both the true and false lumens may be detected on Doppler imaging, albeit with different velocities and waveform patterns (Fig. 90-32C). The spectral Doppler waveform pattern is highly variable, probably related to the length of the dissection, diameter of the lumen, fenestration of the dissection flap, coexisting involvement of aortic dissection, and whether the true or false lumen is sampled (Fig. 90-32D,E). The waveform may be irregular with low-velocity spikes and flutters, making it difficult to distinguish systole from diastole. If the false lumen is thrombosed or if only intramural hematoma is present, gray-scale and color flow imaging will simply reveal a long, smoothly marginated stenosis. The thickening of the arterial wall is typically hypoechoic and may spiral or smoothly taper the distal arterial lumen (Fig. 90-33).²⁷ A long-segment tapering intraluminal hematoma may create an extremely narrowed lumen with a string sign on color Doppler imaging. In such cases, the waveform may be indistinguishable from a carotid stenosis; the clues to dissection are the length and smoothness of the stenosis, absence of coexistent plaque, and clinical setting. A high-resistance pulsatile but dampened waveform with little or no diastolic flow may be noted proximally in such cases.²⁷^–²⁹

FIGURE 90-32 Carotid dissection. Transverse (A) and longitudinal (B) gray-scale images of the left mid CCA from a 36-year-old man with Marfan syndrome and a type A aortic dissection reveal a thin dissection flap. C, Longitudinal color Doppler image reveals flow in the true lumen (red) and reversed flow in the false lumen (blue). D, Spectral Doppler tracing from the true lumen demonstrates a slight delay in systolic upstroke and reduced diastolic flow. E, The waveform in the false lumen is extremely irregular, and flow direction is reversed.

FIGURE 90-33 Intramural hematoma due to carotid dissection. This 22-year-old patient presented with a left neck hematoma and pain after a motor vehicle accident. Color Doppler image demonstrates markedly hypoechoic circumferential “thickening” of the wall of the CCA consistent with an intramural hematoma or thrombosed false lumen. Note that the vessel lumen is narrowed over a long segment.

(From Scoutt LM, Lin FL, Kliewer M. Waveform analysis of the carotid arteries. Ultrasound Clin 2006; 1:133-159.)

Carotid Pseudoaneurysm

Pseudoaneurysms arising from the carotid arteries occur most commonly in the CCAs as a result of inadvertent needle sticks during attempts to place an internal jugular central line. However, pseudoaneurysms may also occur in the setting of other forms of penetrating trauma (including drug abuse), blunt trauma, infection, cystic medial necrosis, invasion of the carotid artery by malignant neoplasm, and after carotid endarterectomy. On gray-scale and color Doppler imaging, pseudoaneurysms are easily recognized as an outpouching from the carotid artery. The degree of color fill-in will depend on the amount of intraluminal thrombus (Fig. 90-34A,B). Spectral Doppler interrogation will reveal a “to-and-fro” pattern within the neck, if it is narrow, with flow toward the pseudoaneurysm in systole and back toward the carotid artery during diastole (Fig. 90-34C). If the neck is wide, the waveform will be randomly irregular and turbulent.

FIGURE 90-34 Pseudoaneurysm of the common carotid artery. A, Gray-scale image of the left neck from a 50-year-old man with neck swelling after placement of a central line reveals a mass (cursors) representing a largely thrombosed pseudoaneurysm. B, Color Doppler image demonstrates the neck arising from the CCA with a small focus of color aliasing (long arrow) indicating increased velocity. There is a small amount of flow (short arrows) with a yin-yang pattern at the base of the pseudoaneurysm. C, Spectral tracing from the neck of the pseudoaneurysm reveals a classic to-and-fro waveform pattern above the baseline in systole and below the baseline in diastole.

Arteriovenous Fistula

Arteriovenous fistulas involving the carotid arteries typically occur secondary to trauma or malignant invasion. Color Doppler interrogation may demonstrate the connection between the artery and the vein (Fig. 90-35A,B). Color aliasing due to high-velocity flow within the arteriovenous fistula may be observed, and a color bruit due to tissue reverberation secondary to the high-velocity flow may be seen in the surrounding soft tissues. Spectral Doppler interrogation will reveal a low-resistance waveform pattern characterized by an increase in both peak systolic and end-diastolic flow in the feeding artery. However, the carotid artery distal to the arteriovenous fistula will have a normal waveform pattern. Pulsatile high-velocity flow will be observed in the draining vein (Fig. 90-35C).

FIGURE 90-35 Common carotid artery to internal jugular fistula. Sagittal (A) and transverse (B) color Doppler images from a 46-year-old woman with right upper extremity swelling after attempted central line placement demonstrate a connection (arteriovenous fistula, arrow) between the right internal jugular vein (red) and CCA (blue). C, Spectral Doppler tracing from the right internal jugular vein reveals pulsatile flow.

Intra-aortic Balloon Pump

Placement of an intra-aortic balloon pump results in a characteristic waveform in the carotid arteries with “double systolic peaks.” Inflation of the balloon during early diastole causes a second peak of forward flow, increasing flow to the coronary arteries—an intended effect of the balloon pump. Deflation of the balloon at the end of diastole results in a short flow reversal (Fig. 90-36). The intra-aortic balloon pump may be set at different ratios. If it is set at a 1 : 1 ratio, the pump is activated during every cardiac cycle. When the pump is set at a 1 : 2 ratio, the balloon pump is triggered to inflate only every second cardiac cycle. Whereas placement of an intra-aortic balloon pump results in an increase of total volume of forward blood flow during systole, PSV is normally decreased. Therefore, carotid stenoses cannot be graded by only using absolute PSV criteria in patients with intra-aortic balloon pumps, and more reliance must be placed on the color Doppler and gray-scale images.

FIGURE 90-36 Intra-aortic balloon pump. Note second peak of forward flow (long arrow) resulting from inflation of the intra-aortic balloon pump in early diastole in this patient with ischemic cardiomyopathy. Deflation of the balloon results in a transient reversal of flow (short arrow) at the end of diastole.

THE VERTEBRAL ARTERY

In most patients, only the midportion of the vertebral artery in the neck can be directly examined with Doppler ultrasound. However, the presence of distal or proximal disease can occasionally be deduced by analysis of the spectral waveform of the vertebral artery.³⁰ The normal vertebral artery waveform is symmetric right to left and similar to the waveform of the ICA with a sharp systolic upstroke and continuous forward diastolic flow (see Fig. 90-9).

Asymmetrically increased PSV in a vertebral artery may indicate a proximal stenosis. However, the vertebral arteries are often asymmetric in size, and hence an increase in PSV in one vertebral artery may be simply due to compensatory flow. Increased flow in the vertebral artery may also be noted in the setting of an ipsilateral ICA occlusion. Proximal stenosis of the vertebral artery may also cause a unilateral tardus parvus waveform in the upper to mid vertebral artery. Bilateral tardus parvus waveforms in the vertebral arteries associated with tardus parvus waveforms in the carotid arteries suggest aortic stenosis. A high-resistance waveform pattern with low PSV and absent diastolic flow may indicate a distal stenosis or occlusion of the basilar artery or increased intracranial pressure.³⁰

Subclavian Steal Syndrome

Patients with subclavian steal due to a proximal stenosis in the subclavian artery may present with vertigo, syncope, headaches, transient ischemic attacks, visual disturbances, and hearing loss. However, patients may be completely asymptomatic.³¹ In patients with complete subclavian steal, reversed flow will be noted in the vertebral artery on Doppler interrogation (Fig. 90-37A). Doppler interrogation of the ipsilateral subclavian artery will demonstrate increased PSV medially and a tardus parvus waveform distally in the axillary and brachial arteries (Fig. 90-37B,C). A “pre-steal” waveform characterized by a sharp midsystolic retraction or deceleration has been described by Kliewer and associates³² (Fig. 90-38). The depth of the midsystolic retraction depends on the severity of the proximal subclavian stenosis. However, all pre-steal waveforms will demonstrate two systolic peaks. The first is narrow with a sharp upstroke and sharply pointed peak. The second systolic peak is usually of lower velocity and broader as well as rounder in contour. With deeper midsystolic retractions, it may be more difficult to differentiate the second peak from diastole. Provocative maneuvers, such as exercising the hand or inflating a blood pressure cuff above systolic arterial pressure until the hand is mildly symptomatic (usually 3 to 5 minutes), then releasing the cuff and immediately re-evaluating the vertebral artery waveform, can convert a pre-steal waveform into a complete steal or deepen the midsystolic retraction (Fig. 90-39).³² Grant and colleagues³³ have described a similar waveform pattern in the right common carotid and internal carotid arteries in patients with high-grade stenoses of the innominate artery.

FIGURE 90-37 Subclavian steal. A, Spectral Doppler tracing of the left vertebral artery reveals reversed flow heading toward the transducer away from the head. B, Note increased PSV of 336 cm/sec in the proximal left subclavian artery in a patient with a left subclavian artery stenosis causing a subclavian steal phenomenon.

FIGURE 90-38 Pre-steal vertebral artery waveform. A, Note midsystolic retraction (arrow) in the left vertebral artery in a patient with a moderate left subclavian stenosis on October 6, 2006. B, By June 9, 2008, the midsystolic retraction (arrow) had deepened, and there was transient flow reversal. C, Spectral Doppler tracing of the origin of the left subclavian artery at that time demonstrated a PSV of 266 cm/sec, consistent with a high-grade stenosis.

FIGURE 90-39 Subclavian steal—provocative maneuvers. In some cases, provocative maneuvers will deepen the midsystolic retraction in a pre-steal waveform, causing a transient reversal of midsystolic flow or complete flow reversal in the vertebral artery. A, Left vertebral artery waveform obtained at rest in an 83-year-old woman who has a known left subclavian stenosis demonstrates a prominent midsystolic retraction with transient reversal of flow (arrow). This is a pre-steal waveform, type 4. B, After inflation of blood pressure cuff on the left arm and subsequent rapid deflation, there is conversion of the pre-steal waveform to a complete steal, with reversal of blood flow throughout the cardiac cycle. Inflation of the blood pressure cuff causes mild hypoxia in the distal arm. Deflation of the cuff induces relative hyperemia in the distal arm and increases blood flow across the subclavian stenosis, resulting in a complementary pressure drop and change in direction of blood flow in the ipsilateral vertebral artery toward the now lower pressure subclavian artery.

(From Kliewer MA, Hertzberg BS, Kim DH, et al. Vertebral artery Doppler waveform changes indicating subclavian steal physiology. AJR Am J Roentgenol 2000; 174:816-819. Reprinted with permission from the American Journal of Roentgenology.)

CONCLUSION

Doppler interrogation of the carotid arteries is a highly accurate, readily accessible, inexpensive, and noninvasive method of diagnosis of high-grade (>70%) stenosis of the ICA. With careful attention to technique, longitudinal color and power Doppler images provide morphologic information similar to an angiogram unless the image is degraded by shadowing from calcified plaque. Gray-scale and color Doppler images are important for identification of hypoechoic or irregular plaque, which is believed to progress more rapidly and to pose an increased risk of thromboembolic events. Spectral Doppler interrogation provides not only PSV measurements to used grade stenoses of the ICA but also physiologic information that can provide clues to more proximal or distal cardiovascular disease, which in complex cases may be multifactorial (Fig. 90-40). To avoid pitfalls in the estimation of ICA stenoses, PSV criteria should always be correlated with the gray-scale images and analysis of the spectral waveforms. Similarly, an increase in the PSV of the vertebral artery may indicate a proximal stenosis, and changes in the waveform pattern of the vertebral artery may indicate proximal or distal cardiovascular disease, such as a subclavian steal.

FIGURE 90-40 Complex waveform pattern. Spectral Doppler tracings of the right CCA (A), left CCA (B), and left vertebral artery (C) demonstrate bilateral tardus parvus waveforms with a delay in systolic upstroke and rounding of the systolic peak. However, the amount of diastolic flow is asymmetric right to left, with complete absence of diastolic flow in the right CCA. In addition, PSV is reduced, only 44 cm/sec in the right CCA in comparison to 60 cm/sec in the left CCA. D, Power Doppler image demonstrating absence of flow in the right ICA (short arrows). Note flow in ECA and branches (long arrow) and CCA. This patient has aortic stenosis resulting in bilateral tardus parvus waveforms as well as a complete occlusion of the right ICA resulting in a high-resistance waveform (absent diastolic flow) in the right CCA.

KEY POINTS

Carotid ultrasound examination is highly accurate for detection of stenoses of the ICA of more than 70%.

Velocity criteria for grading of ICA stenoses should be validated in individual laboratories and can be chosen to maximize sensitivity or specificity.

The Society of Radiologists in Ultrasound consensus conference ¹³ has proposed that a PSV of more than 230 cm/sec and an ICA/CCA PSV ratio above 4.0 are highly accurate criteria for diagnosis of ICA stenoses of more than 70%.