(Stroke. 1995;26:123-127.)
© 1995 American Heart Association, Inc.
Articles |
Elevated Transcranial Doppler Ultrasound Velocities Following Therapeutic Arterial Dilation
From the Departments of Neurosurgery (C.A.G., A.G., H.H.B., T.K.) and Radiology (C.A.G., P.P.), University of Texas Southwestern Medical Center at Dallas.
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Abstract |
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Background Elevated transcranial Doppler (TCD) velocities seen after cerebral angioplasty are commonly interpreted as evidence of residual or recurrent stenosis but may conceivably arise from hyperemia and require different clinical management.
Summary of Report Four cases of abnormally elevated mean TCD velocities obtained after therapeutic arterial dilation with either balloon angioplasty or intra-arterial administration of papaverine are described. In each case, cerebral angiography revealed a dilated vessel, suggesting that hyperemia and impaired autoregulation were the causes of the high velocities.
Conclusions These examples suggest that high TCD velocities after vessel dilation may be produced by unpredictable amounts of vessel narrowing and flow alteration. Although a normalizing TCD velocity after angioplasty suggests effective vessel dilation, high velocities may be due partly to hyperemia and cannot be interpreted as arising solely from recurrent stenosis.
Key Words: angioplasty • autoregulation • cerebral vasospasm • ultrasonics
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Introduction |
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TopAbstractIntroductionMethodsCase 1Case 2Case 3Case 4DiscussionReferences |
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Although the technique of transcranial Doppler ultrasound (TCD) has enjoyed success in the diagnosis of cerebral arterial vasospasm and stenosis,1 2 there can be difficulties in interpretation of elevated TCD velocities, and correlation to outcome or vessel narrowing is not absolute.3 4 Theoretical calculations predict a good correlation between velocity elevation and degree of stenosis only if one assumes that the change in flow is minimal as the stenosis worsens. The error arising from a decrease in flow has been recognized,5 but a flow increase would drastically alter the relation of velocity to diameter and might significantly confound correct interpretation of TCD velocities.
Hyperemia after subarachnoid hemorrhage (SAH) has been reported6 7 and presumably arises from the associated impairment of autoregulation.8 9 10 11 12 13 This report presents four cases of elevated mean TCD velocities following therapeutic arterial dilation that were believed to be due to hyperemia, illustrating this profound difficulty in TCD interpretation.
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Methods |
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All examinations were performed with the same equipment (Trans-scan, EME) using standard techniques.1 All velocities are mean velocities.
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Case 1 |
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TopAbstractIntroductionMethodsCase 1Case 2Case 3Case 4DiscussionReferences |
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A 47-year-old woman suffered an SAH from a ruptured right posterior inferior cerebellar artery aneurysm. TCD examination on postbleed day 8 revealed a basilar artery (BA) velocity of 129 cm/s with middle cerebral artery (MCA) velocities of 174 and 179 cm/s on the right and left, respectively. At the time of study, hematocrit value was 28, PCO2 was 23 mm Hg, and blood pressure (BP) was 148/74 mm Hg. An angiogram on the same day confirmed diffuse BA spasm. Four days later, the patient's increased somnolence led to another angiogram revealing worsened vasospasm (Fig 1
, top
left), and a balloon angioplasty of the BA was
performed, which achieved clinical improvement and angiographic
dilation (Fig 1, bottom left). A TCD study 4.5 hours later showed a
drop in BA velocity to 57 cm/s with MCA velocities of 184 and 229 cm/s
on the right and left, respectively. Hematocrit,
PCO2, and BP levels at this time were
30, 25, and 145/76, respectively. Five days later, a repeat TCD study
showed elevation of the BA velocity to 162 cm/s (hematocrit, 28;
PCO2, 33; BP, 138/60), and an
angiogram on the same day showed that the middle portion of the BA was
of normal caliber and showed spasm at the basilar tip. Because these
velocities were all obtained from the area of the middle portion of the
BA at a depth of 100 to 110 mm (Table), this combination
of high TCD velocity and angiographic dilation was interpreted as
hyperemia. The TCD waveforms at time of spasm and after angioplasty
were strikingly similar (Fig 1, top right and bottom right).
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Case 2 |
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A 55-year-old woman was found to have focal signs of left MCA spasm after rupture of a left posterior carotid wall aneurysm. On postbleed day 8, TCD velocities in the left MCA, right MCA, and BA were 164, 259, and 86 cm/s, respectively (hematocrit, 30; PCO2, 34; BP, 185/80). Angiography performed that day confirmed left MCA spasm (Fig 2
,
left), and a balloon angioplasty was performed the
following day with good angiographic results (Fig 2, right). TCD
velocity in the left MCA segment 5 hours later remained elevated at 178
cm/s (hematocrit, 29; PCO2, 34; BP,
191/94), and the TCD waveforms before and after angioplasty were of
similar morphology.
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Case 3 |
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A 39-year-old woman was admitted for SAH arising from a ruptured anterior communicating artery aneurysm and developed a left hemiparesis on postbleed day 9. TCD velocities in the right MCA, left MCA, and BA at this time were 217, 139, and 49 cm/s, respectively (hematocrit, 31; PCO2, 46; BP, 140/80). Angiography confirmed severe right MCA spasm (Fig 3
, left), and the
patient underwent balloon angioplasty of the segment with resolution of
hemiparesis (Fig 3, right). MCA velocities 2 hours later were 214 and
175 cm/s on the right and left, respectively. One week later,
angiography again showed dilation of the right MCA, and the right MCA
velocity was 222 cm/s (hematocrit, 29;
PCO2, 34; BP, 120/90). The TCD
waveforms before and after angioplasty were of similar morphology.
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Case 4 |
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A 44-year-old man underwent clipping of an anterior communicating artery aneurysm and developed a right hemiparesis on postbleed day 10. Angiography showed moderate left MCA spasm, and intra-arterial papaverine was administered as part of a separate protocol with subsequent vessel dilation and clinical response (Fig 4
). TCD velocities 40 minutes later were 192, 149, and
37 cm/s in the right MCA, left MCA, and BA, respectively (hematocrit,
31; BP, 220/100).
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Discussion |
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TopAbstractIntroductionMethodsCase 1Case 2Case 3Case 4DiscussionReferences |
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Our emphasis in this article centers on the fact that high TCD velocities may arise from an unpredictable combination of vessel narrowing and flow augmentation, and the reported cases confirm that these theoretical concerns can occur in practice. Originating from a presumed impairment in autoregulation known to occur in SAH8 9 10 11 12 13 along with relative hypertension (as in cases 2 and 4), some degree of hyperemia combined with mild residual narrowing after dilation produced persistently high velocities that might easily be incorrectly interpreted as significant stenosis. This may confound the usefulness of TCD studies in the follow-up of vessel dilation and underlines the difficulty of interpreting high velocities in other settings as well.
The time course of the observed velocity changes deserves comment. In case 1, BA velocity initially decreased and then rose despite preservation of vessel diameter. We believe this represents late impairment of autoregulation but may also be explained by an increase in demand for collateral flow. Although the velocity decreased in case 2 from 259 to 178 cm/s after angioplasty, the associated diameter change (assuming constant flow) would have been only 20%. This is much smaller than that seen in the angiogram, and so we concluded that flow had increased. The velocity elevation in case 3 persisted for 1 week, reflecting a prolonged impairment in autoregulation consonant with the phenomenon of luxury perfusion.
There have been other reports of high TCD velocities after angioplasty. Newell et al14 described the marked fall of TCD velocities in four vessels in two patients after angioplasty, although velocities in one of these vessels rose after 3 days. Another report on five patients receiving angioplasty after aneurysm clipping described a decrease in TCD velocities after angioplasty.15 In a report on one patient with posttraumatic vasospasm, the ratio of MCA to internal carotid artery (ICA) velocity fell after bilateral angioplasties.16 Hurst et al17 reported four patients receiving angioplasties; in two of these patients elevated velocities proved to be due to new areas of vasospasm, and all velocities fell after angiographically successful angioplasty. The elevated velocities in one of these patients, however, were recorded from a dilated MCA segment and so may have represented hyperemia rather than recurrent spasm.
These reports do not fully confirm our findings. However, our four examples came from a retrospective review of 28 cases of vessel dilation with balloon angioplasty or papaverine, suggesting a relatively low rate of occurrence of hyperemia that may have been overlooked because of the low number of patients reported in these prior studies. In addition, patients showing high TCD velocities after dilation who had residual areas of focal stenosis on angiography were not uncommon and were not reported here as examples of hyperemia.
Despite the impediment to flow imparted by a narrowed vessel, there is evidence that significant hyperemia in the setting of cerebral stenosis is not uncommon. Dinh et al6 described the appearance of hyperemia in the MCA distribution measured with 133Xe single-photon emission computed tomography in a case of SAH, and subsequent angiography verified the development of vasospasm in this vessel. Jakobsen et al7 calculated a spasm index defined as MCA velocity divided by regional cerebral blood flow measured with the inhaled 133Xe technique. At least 13 of 146 measurements in 24 patients with SAH showed cerebral blood flow to be greater than 50 (initial slope index), with velocities ranging from approximately 40 to 150 cm/s (spasm index between 0.8 and 2.8). Furthermore, 14 of 56 measurements of arteriovenous oxygen content difference in this population were less than 4.0, confirming the relative hyperemia seen in other studies of SAH.18 19 We speculate that such uncoupling allows cerebral blood flow to increase passively in response to BP, requiring careful control of hypertension and volume rather than standard hypertensive therapy.
This review is retrospective and has several associated limitations. TCD studies were obtained several hours after angioplasty, and the high velocities might conceivably be explained by very fast recurrence. However, the persistence of the velocity elevation and angiographic dilation appearing after 5 to 7 days in cases 1 and 3 argues against quick recurrence. Mistaken insonation of a different, spastic vessel during the postdilation studies or of distal angiographically invisible segments remains a possibility, although the velocities reported here were recorded over lengths of 1 to 2 cm at relatively constant depths by experienced technologists. A further but speculative source of error may arise from the irregularities of the vessel lumen after angioplasty. Indentation in the lumen of the vessel already distorted by both the biological changes associated with vasospasm20 and the mechanical process of angioplasty21 may serve to decrease the cross-sectional area and increase velocity while projecting to a normal size in any angiographic plane.
Although a potential error in our interpretation of the observed high
velocities following arterial dilation would arise from insonation of
sites not affected by the dilation, we do not believe this to be the
case in our examples because the depth of insonation was constant and
correlated to dilated segments on the angiogram (Table
). In case 1, the
depth of 100 mm indicates insonation of the middle portion of the BA.
This site is clearly dilated on the postangioplasty angiogram even
though there is vasospasm more distally. Although there may be residual
distal internal carotid spasm in case 3, the carotid bifurcation was
seen at 69 mm, and the high velocities were seen 7 mm superficial to
that site. We believe the elevated velocities arise from the more
superficial MCA.
The occurrence of hyperemia in the presence of a known stenosis in cases 1 and 3 may seem paradoxical and deserves comment. In case 1, we found evidence of hyperemia in the middle portion of the BA despite a severe stenosis distally. We believe this has two explanations. First, the intervening branches of the BA may feed tissue in which autoregulation is impaired, producing elevated flow in the more proximal BA segments. Second, the exact degree of flow limitation arising from a stenosis can never be derived with certainty from an angiogram, and we speculate that a combination of dysautoregulation of the distal tissues and flow impediment due to the stenosis resulted in a contribution to the high velocity seen proximally. In case 3, we believe that any residual stenosis of the distal carotid segment was in fact not flow limiting, since the neurological exam improved so dramatically with angioplasty. Dysautoregulation-induced hyperemia would therefore not be prevented by this stenosis.
Correlations with waveform shapes have been reported,22 and the ratio of MCA velocity to that in the cervical ICA has also been widely used to distinguish between hyperemia and stenosis.5 We believe, however, that variances in the ICA velocity due to neck position and insonation site can lead to difficulties in this ratio and explain variances noted by others.23 We did not observe any difference in waveform shape before or after angioplasty in our patients.
We believe that the difficulties illustrated by these cases show that the high TCD velocities seen following cerebral angioplasty cannot be taken as firm evidence of restenosis but may instead arise from an unpredictable combination of vessel narrowing and flow alteration. We speculate that the same mechanism of velocity elevation frequently produces the high velocity seen after SAH, accounting in part for the variability corresponding to vessel diameter. These conclusions suggest that although normalization of TCD velocities after angioplasty is reasonable evidence for effective dilation, a high velocity can only be interpreted as an undetermined mixture of hyperemia and vessel narrowing.
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Acknowledgments |
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The authors thank Janice Denniston for preparation of the manuscript.
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Footnotes |
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Reprint requests to Cole A. Giller, PhD, MD, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75235-8855.
Received April 7, 1994; revision received October 3, 1994; accepted October 3, 1994.
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References |
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