Stroke. 1996;27:1358-1364
(Stroke. 1996;27:1358-1364.)
© 1996 American Heart Association, Inc.
Transvenous Hemodynamic Assessment of Arteriovenous Malformations and Fistulas
Preliminary Clinical Experience in Doppler Guidewire Monitoring of Embolotherapy
Yuichi Murayama, MD;
Shino Usami, MD, PhD;
Yuichi Hata, MD, PhD;
Fumikiyo Ganaha, MD;
Yuzuru Hasegawa, MD, PhD;
Tohru Terao, MD;
Satoshi Abe, MD, PhD;
Hiroshi Furuhata, MD, PhD
Toshiaki Abe, MD, PhD
the Departments of Neurosurgery (Y.M., S.U., Y. Hasegawa, T.T., S.A., T.A.) and Radiology (Y. Hata, F.G.) and the Medical Engineering Laboratory (H.F.), Jikei University School of Medicine, Tokyo, Japan.
 |
Abstract
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Background and Purpose Transvenous monitoring of blood flow
through intracranial vascular malformations was performed with
an intravascular Doppler guidewire to assess hemodynamic changes
during endovascular embolotherapy.
Methods Flow velocity was assessed in the intracranial venous sinuses of two patients with arteriovenous malformations and seven patients with dural arteriovenous fistulas. In all cases, the Doppler guidewire was positioned in the dural sinuses coaxially through a 2.1F microcatheter. The Doppler guidewire was then advanced to the site of arteriovenous shunting for sampling of venous average peak velocity (APV) and pulsatility index. In two cases, simultaneous feeding artery flow velocity was monitored by transcranial color-coded duplex sonography.
Results Before embolotherapy, the flow pattern in the venous sinuses was pulsatile, with a mean (±SD) APV of 39.0±22.5 cm/s. Total or near-total embolization was achieved in six of the nine cases. After embolization, the flow pattern became less pulsatile and the APV was reduced to a mean of 21.2±14.6 cm/s (P=.0123, one-tailed paired t test). The pulsatility index was used to calculate the maximum minus the minimum peak velocity (MxPV-MnPV). This was reduced from an average of 27.0±8.7 cm/s to 13.5±8.3 cm/s after treatment (P=.0456). A parallel reduction in APV of the feeding arteries was observed with embolization.
Conclusions Preliminary clinical experience indicates that transvenous assessment of two parameters, APV and MxPV-MnPV, is useful in the hemodynamic evaluation of intracranial arteriovenous shunts. This valuable hemodynamic information may be used for objective and quantitative monitoring during embolotherapy of intracranial vascular malformations.
Key Words: cerebral arteriovenous malformations • Doppler • embolization, therapeutic • fistula • hemodynamics
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Introduction
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The treatment of intracranial AVMs and d-AVFs has changed in
recent years from that in which only direct microsurgery is
used to a more frequent use of adjunctive endovascular embolotherapy
in conjunction with conventional surgery. Hemodynamic assessment
of a malformation before and during embolotherapy is increasingly
regarded as an important step in the prevention of treatment
complications. Although specific and effective hemodynamic monitoring
of blood flow during embolotherapy may be desirable, a safe
and reliable monitoring technique is still not available. The
use of several hemodynamic modalities for evaluation of AVMs,
eg, TCD or direct intravascular pressure measurements, has been
attempted previously.
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 However, most of these techniques have focused on only investigating
the hemodynamic characteristics of feeding arteries of the malformation.
Although draining veins are an integral and often quite accessible
component of intracranial vascular malformations, the procurement
of hemodynamic information from draining veins is relatively
uncommon.
12 13 14 15 16 17 18 In this study we obtained preliminary
experience in transvenous blood flow measurements using an intravascular
Doppler guidewire to assess hemodynamic changes during endovascular
embolotherapy of AVMs and d-AVFs in a group of patients. This
method involves access to the draining veins of the malformation
without any disturbance of the nidus or feeding arteries during
transarterial embolization. The hemodynamic information acquired
by this technique may prove useful in (1) monitoring the progression
and effectiveness of embolization procedures, (2) providing
hemodynamic indicators of complications related to embolization,
(3) deciding the successful end point of therapy, and (4) choosing
the most appropriate embolic agents for a particular malformation.
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Subjects and Methods
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After we obtained informed consent from the patients and the
approval of our institutional review committee, a nonconsecutive
group of 9 patients (5 females and 4 males; age range, 15 to
75 years) underwent transvenous monitoring during endovascular
transarterial embolotherapy. Seven of these patients had d-AVFs,
and 2 had AVMs. Their symptoms were headaches in 4 cases, pulsatile
tinnitus in 3, chemosis and exophthalmos in 1, and intracerebral
hemorrhage in 1. Three of the d-AVFs were located in the transverse
sigmoid sinus, 1 in the superior sagittal sinus, 1 in the cavernous
sinus, 1 in the sphenoparietal sinus, and 1 in the inferior
petrosal sinus.
The Doppler guidewire (SmartWire, Cardiometrics) consists of a 12-MHz piezoelectric ultrasonic transducer mounted on the tip of a 175-cm-long flexible and steerable 0.014-inch guidewire. The distal flexible coil portion of the guidewire is 45 cm in length. The ultrasonic beam diverges approximately 14° from the axis of the transducer, with a range gate depth of 4.3 mm and gate integration distance of 1 mm. These specifications produce an estimated axial sample diameter of 2.5 mm and a sample volume of 5 mm.3 The pulsed Doppler signals were processed by a real-time spectrum analyzer (Flomap, Cardiometrics) with the use of a fast Fourier transform at a rate of 100 spectra per second. In all cases, a 4F guiding catheter (Glidecath, Terumo) was placed as cephalad as possible in the internal jugular vein. A Tracker-18 microcatheter (Target Therapeutics) was introduced coaxially into the intracranial dural sinuses. The Doppler guidewire was navigated through the microcatheter and advanced as close as possible to the site of arteriovenous shunting for sampling of venous APV and PI. The PI value was used to calculate the MxPV-MnPV. This parameter was used to analyze the available Doppler spectra. In our analysis, attention was paid to two parameters in particular, APV and MxPV-MnPV, in evaluating the hemodynamic changes as a result of transarterial embolization of the malformation. Additionally, TCCD (Ultramark 9, ATL) was used in two patients for measurement of flow velocity in feeding arteries of the malformation. A 2.25-MHz phased-array probe was used, which allowed the visualization of cerebral arteries with the use of color flow ultrasonography. Knowledge of the angle of insonation was used to determine the correct direction of blood flow velocity.
In one AVM and one d-AVF, feeding artery and draining venous sinus velocities were measured simultaneously during embolization. In three d-AVFs and one AVM, flow velocities in the draining venous sinuses only were measured during embolization. In three d-AVFs, draining venous sinus velocities were measured only after embolization. Statistical analysis (paired one-tailed Student's t test) was performed on the results of the six cases in which preembolization and postembolization velocities were available.
Transarterial embolization was performed in all patients. Silk threads (6-0) and 2-cm-long straight metallic coils were used as embolic agents in most patients. In only one d-AVF case was the cyanoacrylate liquid mixture Eudragit-E (methyl methacrylate, butyl methacrylate, dimethylaminoethyl methacrylate copolymer) used.
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Results
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Satisfactory (total in two patients and near-total in four patients,
as judged by angiography) embolization was achieved in six patients.
Two d-AVFs and one AVM were partially embolized (Table
). In
all patients, the flow pattern of the venous sinus before treatment
was pulsatile (arterial waveform), with a mean APV of 39.0±22.5
cm/s (mean±SD; n=6). After embolization, the flow pattern
became nonpulsatile and the mean APV was reduced significantly
(
P=.0123) to 21.2±14.6 cm/s (Fig 1A
). The mean preembolization
MxPV-MnPV was reduced significantly (
P=.0456) from 27.0±8.7
cm/s to 13.5±8.3 cm/s after embolization (Fig 1B
). The
mean PI was increased slightly from 0.7±0.3 to 0.8±0.3
after embolization (
P=.228; Fig 1C
). There were no complications
during any of the embolization procedures.
Illustrative Cases
Case 1
A 22-year-old woman (patient 1) presented with a history of throbbing headaches. A cerebral angiogram showed a left occipital AVM fed by the left posterior cerebral artery and blood draining into the superior sagittal sinus (Fig 2A). Transarterial embolization was performed with 1-cm-long 6-0 silk threads. During embolization, the flow velocity of the left posterior cerebral artery was monitored by TCCD (Fig 2B), and the flow velocity of the draining venous sinus was measured by a Doppler guidewire positioned in the superior sagittal sinus (Fig 2C). As the embolization proceeded, the sinus APV was reduced to approximately 40 cm/s, and the Doppler spectra approached nonpulsatility. Several previously unseen small arterial branches to surrounding normal brain (proximal to the nidus) were then seen to fill at angiography, in keeping with redistribution of blood flow from the AVM nidus to adjacent territories after embolization (Fig 2D). An amobarbital test was performed and resulted in the patient experiencing visual disturbance. The embolization was terminated at this stage to prevent complications due to overembolization. In comparison of preembolization and postembolization flow velocities, the draining venous sinus APV was decreased significantly from 54 to 36 cm/s, and the postembolization flow pattern became less pulsatile (Fig 2E). MxPV-MnPV was reduced from 16.2 to 14.4 cm/s. The MxPV of the feeding artery was also decreased from 142 to 124 cm/s by embolization (Fig 2F). However, changes in the PI were not as apparent when concomitant angiographic changes were detected. Postembolization vertebral angiography showed almost complete obliteration of the AVM (Fig 2G).
Case 2
A 68-year-old woman (patient 4) with an intracerebral hemorrhage had a cerebral angiogram that showed a left transverse sigmoid sinus d-AVF fed by the left occipital and the left middle meningeal arteries. (Fig 3A). The left sigmoid and transverse sinuses were occluded except for the d-AVF portion. Retrograde venous drainage was observed through a cortical vein to the cavernous sinus and to the right inferior petrosal sinus. The Doppler guidewire was navigated transvenously and positioned in the right inferior petrosal sinus, where Doppler sampling showed spectra with prominent pulsatile patterns (Fig 3B). The left occipital artery feeder was embolized with Eudragit-E; however, the d-AVF remained incompletely embolized because of the persistent blood supply, mainly from the left middle meningeal artery (Fig 3C). The Doppler guidewire monitor showed a transient decrease in flow velocity with a less pulsatile pattern after this initial embolization (Fig 3D). However, within a few minutes the Doppler monitor showed a significant flow increase and a resumed pulsatile pattern before detection of any flow changes on angiography (Fig 3E). Because of this surge in blood flow through the incompletely embolized fistula, the potential for nidus/fistula rupture was feared. This suspected potentially dangerous change in flow dynamics could be detected by transvenous monitoring and was due to persistent supply to the fistula via the middle meningeal artery. The left middle meningeal artery was embolized immediately with 6-0 silk threads, resulting in satisfactory angiographic occlusion of the d-AVF (Fig 3F). After embolization the APV was reduced from 56.0 to 15.0 cm/s, and the Doppler spectra became nonpulsatile (Fig 3G).
|
Discussion
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Various methods of monitoring have been attempted previously
to assess the hemodynamic changes that may occur during endovascular
treatment of intracranial vascular malformations. Examples of
these include TCD and direct intravascular pressure measurement
of participating vessels to a malformation.
4 6 8 9 10 Although
these methods have many advantages, they also possess technical
limitations that make them less than ideal for monitoring the
hemodynamic consequences of endovascular embolotherapy. TCD
is limited by its inability to provide images of the blood vessels
under insonation. Accurate determination of blood velocity in
these vessels is therefore not possible because the angle of
insonation is unknown. Furthermore, Martin et al
19 reported
that velocities derived with the use of TCCD (which allows the
determination of the insonation angle) were significantly greater
than those derived with the use of TCD in all vessels under
investigation. They concluded, however, that correcting for
the angle of insonation when TCCD is used may enable estimation
of blood flow velocities closer to "true" values than those
derived with conventional TCD. Although TCCD has such advantages
over TCD, it also has some limitations as a hemodynamic monitoring
modality.
19 20 21 22 23 24 For example, the size and thickness
of the temporal bone window vary considerably from patient to
patient. Furthermore, the continuous monitoring of flow velocity
would be difficult from a practical perspective during an embolization
procedure. Intravascular pressure measurement in feeding arteries
of a malformation also has limitations as a monitoring technique.
It would be impossible to perform continuous feeding artery
pressure sampling during embolization through the same artery,
especially when adhesive liquid embolic agents are used to occlude
the malformation. In addition, systolic and diastolic pressure
values are different when obtained by different microcatheters
because of varying degrees of attenuation of the peak and trough
of each pressure wave by small-diametered microcatheters. Only
the obtained mean blood pressure is a reliable value. Consequently,
it is also difficult to observe changes in the pressure waveform
induced by embolization. Most previous studies have focused
on embolization monitoring with the use of arterial feeders;
few investigators have reported measurements made with the use
of the draining veins of a malformation.
12 13 14 15 16 17
The Doppler guidewire was initially developed and validated for interventional cardiology applications.25 26 27 28 Recently, clinical use of the Doppler guidewire for neurointerventional procedures has been attempted after the development of a 45-cm-long distal flexible portion to this device. Chaloupka et al29 30 reported that the relationship between flow velocity as measured by the Doppler guidewire and volumetric blood flow was excellent when correlated experimentally in laboratory swine. However, clinical use of the Doppler guidewire has some limitations. Sometimes it is difficult to advance the Doppler guidewire to the feeding arteries of an AVM because of insufficient flexibility of the device within tortuous small-diametered vessels. Furthermore, it would be impossible to use it for continuous monitoring during transarterial embolization. To counteract both these drawbacks, we have investigated the potential transvenous use of the Doppler guidewire as a clinical tool for monitoring of transarterial embolotherapy.
The transvenous use of the Doppler guidewire for assessment of draining vein/sinus hemodynamics has many advantages as a monitoring technique for embolotherapy of vascular malformations. First, the endovascular navigation, manipulation, and positioning of the device and its surrounding microcatheter are much easier and safer (when performed with the necessary care) within the intracranial venous dural sinuses than in small feeding arteries of a malformation. Furthermore, with continuing technological advances in the manufacture of catheters and Doppler guidewires, it may be possible in the future to safely access intracranial pial veins without the risk of iatrogenic trauma. Access through the venous system also allows the procurement of hemodynamic information related to the malformation and its therapy without hindrance to arteries that are likely to be used for the embolization process itself. A further advantage is that when sampling is performed within a dural sinus, it might be possible to quantitatively evaluate the true volumetric blood flow (once the diameter of the sinus is established) because the diameter of the dural sinus does not change significantly with each blood pressure pulsation. This is not the case in feeding arteries where the pulsatile change in vessel diameter precludes or renders inaccurate the estimation of volumetric blood flow. Also apparent from our results is the observation of venous flow velocity changes occurring earlier than angiographic changes consequent to transarterial embolization. The availability of this hemodynamic information was useful in the management of patient 4, in whom potentially dangerous flow surges were induced by the persistent arterial supply from a second unembolized feeder and were detected before any visible angiographic evidence. Thus, transvenous hemodynamic assessment of embolotherapy with the Doppler guidewire may be helpful not only in monitoring the progression and effectiveness of treatment but also in determining the end point of therapy and quantifying flow reduction/cessation through the malformation.
The hemodynamic alterations that are detected transvenously after embolization of a malformation may be manifest in both flow velocity and wave pattern changes. The AVMs and d-AVFs investigated in this study showed significant pulsatile flow and high mean flow velocities within draining venous sinuses. High-flow d-AVFs showed significant differences between MxPV and MnPV. After treatment, the APV decreased to lower than 10 cm/s and the flow pattern became nonpulsatile in cases embolized satisfactorily. It was also observed that with successful outcomes of treatment (ie, total or near-total angiographic obliteration), the difference between MxPV and MnPV was lower than 10 cm/s. From these two parameters, ie, APV and MxPV-MnPV, an appreciation can be obtained for the degree of arteriovenous shunting in a malformation, and the effectiveness of its reduction/elimination with embolization can be ascertained (Fig 4). The APV values of AVMs tended to be higher than those of d-AVFs. Therefore, the acquisition of further experimental and clinical data from malformations of different morphologies may help in understanding the factors that determine the hemodynamic end points and goals of therapy. Our preliminary experience suggests that the technique of transvenous Doppler guidewire monitoring during embolotherapy may be useful because objective and quantitative periembolization hemodynamic changes can be detected in the draining veins earlier than the subjective angiographic changes seen within the nidus or fistula.
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Figure 4. Relationship of APV and MxPV-MnPV values for all patients. Direction of arrow indicates transition in these values consequent to embolization of each malformation. Vertical and horizontal lines represent values of MxPV-MnPV at 10 cm/s and APV at 20 cm/s; postembolization results below these ranges were associated with successful outcomes of treatment.
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In conclusion, transvenous Doppler guidewire assessment of two parameters, APV and MxPV-MnPV, appears useful in the hemodynamic evaluation of AVMs and d-AVFs. This technique may be used for objective and quantitative monitoring during endovascular embolotherapy. Further investigations and clinical experience are necessary to determine the true role of this technique in the analysis of flow dynamics and in monitoring the consequences of endovascular embolotherapy of intracranial vascular malformations.
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Selected Abbreviations and Acronyms
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| APV |
= |
average peak velocity |
| AVM |
= |
arteriovenous malformation |
| d-AVF |
= |
dural arteriovenous fistula |
| MnPV |
= |
minimum peak velocity |
| MxPV |
= |
maximum peak velocity |
| MxPV-MnPV |
= |
maximum minus minimum peak velocity |
| PI |
= |
pulsatility index |
| TCCD |
= |
transcranial color-coded duplex ultrasonography |
| TCD |
= |
transcranial Doppler ultrasonography |
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Acknowledgments
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We wish to express our appreciation to Tarik F. Massoud, MD
(Endovascular Therapy Service, UCLA Medical Center, Los Angeles),
for assistance and advice in preparation of the manuscript.
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Footnotes
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Reprint requests to Yuichi Murayama, MD, Department of Neurosurgery,
Jikei University School of Medicine, 3-25-8 Nishishinbashi,
Minato-ku Tokyo, Japan.
Received March 18, 1996;
revision received April 29, 1996;
accepted April 29, 1996.
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Abstract
Introduction
