Key-words:
Antiplatelet therapy - endovascular treatment - stent-assisted coil embolization -
vertebral artery dissection
Introduction
Ruptured vertebral artery (VA) dissection has a high risk of rapid rebleeding and
must be treated quickly.[[1]] In the treatment of VA, dissection involving the origin of the posterior inferior
cerebellar artery (PICA), the prevention of rebleeding, and the preservation of VA
and PICA patency are challenging. Herein, we first report a staged therapy of ruptured
VA dissection involving PICA, with the preservation of the patency of VA and PICA
without cerebral infarction.
Case Report
A 48-year-old male patient presenting with sudden headache and disturbance of consciousness
was referred. A computed tomography scan revealed subarachnoid hemorrhage (SAH) with
acute hydrocephalus, the World Federation of Neurosurgical Societies Grade IV [[Figure 1]]a. Emergency digital subtraction angiography (DSA) under general anesthesia demonstrated
stenosis and fusiform dilatation of left VA [[Figure 1]]b and [[Figure 1]]c and double origin of PICA[[2]],[[3]] [[[Figure 1]]c,[[Figure 1]]d,[[Figure 1]]e, white arrow]. The diameter of the left VA was 4.2 mm and the diameter of the
main branch of the PICA was 1.2 mm. A diagnosis of ruptured VA dissection involving
PICA was made.
Figure 1: (a) A computed tomography scan on admission shows a massive subarachnoid hemorrhage.
(b) Right vertebral angiography. (c) Left vertebral angiography demonstrates the stenosis
and fusiform dilation of the left vertebral artery. (d) Three-dimensional digital
subtraction angiography reveals double origin of the posterior inferior cerebellar
artery: one from the dilatation itself, and the other from the stenosis proximal to
the dilatation. (e) Coil embolization of the fusiform dilatation with stenting is
performed (arrow; flared ends of the stent). Vertebral artery and posterior inferior
cerebellar artery patency was preserved. (f) Postoperative digital subtraction angiography
(venous phase) showed contrast medium stagnated in the fusiform dilatation. White
arrows (c-e) show double origin of posterior inferior cerebellar artery
First, ventricular drainage was performed on day 0. Endovascular therapy was performed
on day 1 under general anesthesia. For stenting, a Prowler Select Plus microcatheter
(Codman and Shurtleff, Inc., Raynham, MA) was placed into the left VA, using a contralateral
approach. For coil embolization, two Excelsior SL-10 microcatheters (Stryker, Kalamazoo,
MI) were placed into the fusiform dilatation of left VA, using an ipsilateral approach.
Immediately after the two coils were placed, loading doses of aspirin (200 mg) and
clopidogrel (300 mg) were administered. An Enterprise 2 4.0 mm × 30 mm stent (Codman
and Shurtleff, Inc.) was placed over the whole lesion of left VA. Then, coil embolization
was added. Postoperative DSA (venous phase) showed contrast medium stagnated at the
fusiform dilatation [[Figure 1]]f, white arrowhead].
VA and PICA patency was preserved and a postoperative magnetic resonance imaging scan
showed no infarction at the medulla oblongata or PICA territory. After the first treatment,
to monitor the neurological condition, the patient was kept with the awake condition,
under strict control of blood pressure. Dual-antiplatelet therapy (DAPT) continued
with aspirin 100 mg/day and clopidogrel 75 mg/day.
Although rebleeding did not occur, follow-up DSA performed 2 days after the first
treatment showed enlargement just proximal to the coil mass [[[Figure 2]]a, double arrows], but contrast medium still stagnated in the fusiform dilatation
[[[Figure 2]]b, double white arrowheads]. After a plateau of inhibition of platelet aggregation
achieved, a second endovascular therapy was performed 7 days after the first treatment.
Under local anesthesia, an Enterprise 2 4.0 mm × 30 mm stent was placed at the enlargement
of the dissection, and an Enterprise 2 4.0 mm × 39 mm stent was placed to overlap
the two former stents [[Figure 2]]c. We expected a flow-diversion effect with the additional stent placement; thus,
no coils were added.
Figure 2: (a and b) Digital subtraction angiography 2 days after the first treatment demonstrates
the enlargement of the fusiform dilatation (a, double arrows), but contrast medium
remained stagnated (b, double white arrowheads). (c) Two stents were added at the
fusiform dilatation (the second stent) and the left vertebral artery over the two
stents (the third stent) 7 days after the first treatment. (d) Digital subtraction
angiography 4 days after the second treatment demonstrates thrombosis. (e) Digital
subtraction angiography 6 months after the onset shows no regrowth (arrow, flared
ends of the first stent; arrowhead, those of the second stent; and white arrowhead,
those of the third stent). (f) Magnetic resonance angiography 2 years after procedure
shows preservation of left posterior inferior cerebellar artery and no dilatation
of the right vertebral artery
Follow-up DSA on day 12 (4 days after the second treatment) showed thrombosis of the
lesion [[Figure 2]]d. After it was confirmed that repeated DSA performed before the shunt operation
did not show regrowth, DAPT was changed to single-antiplatelet therapy about 1 month
after second treatment due to a lumboperitoneal shunt operation for hydrocephalus.
DSA performed 6 months after the onset did not show regrowth [[Figure 2]]e. Single-antiplatelet therapy has been administered, and the patient has displayed
no neurological deficits over 3 years after the onset [[Figure 2]]f.
Discussion
VA dissection is normally idiopathic and is an uncommon cause of SAH. The rebleeding
rate of ruptured VA dissection has been reported to be as high as 71.4% of cases;
moreover, rebleeding has led to a high mortality rate.[[1]],[[4]] All possible endovascular treatment options for ruptured VA dissection involving
PICA were listed as follows: parent artery occlusion with/without bypass, stent-assisted
coiling, and stenting. Internal trapping or proximal/distal occlusion of parent VA
by coil embolization has become the first-line treatment for ruptured VA dissection;
however, parent artery occlusion for VA dissection involving PICA carries a risk of
severe ischemic complications, even if occipital artery-PICA anastomosis is performed.[[5]],[[6]] In addition, de novo VA dissecting aneurysms after trapping or occlusion of a dissecting
aneurysm in contralateral VA have been reported, likely due to excessive hemodynamic
stress, even if the occlusion side was not the dominant side.[[7]],[[8]] Therefore, preservation of VA and PICA patency in treatment for VA dissection involving
PICA is necessary. To preserve PICA patency, it was reported that an Enterprise stent
was deployed from the PICA to the proximal VA and the segment of dissection was completely
occluded by coils.[[9]] However, evidence detailing the feasibility, use, or safety of Enterprise stents
in small cerebral vessels (<2 mm in diameter) is lacking. We did not use this strategy
in this case, as the diameter of the PICA was 1.2 mm and the PICA had two origins.
We selected the strategy of stent-assisted coiling in the acute stage to prevent rebleeding.
In a review of ruptured and unruptured VA dissection,[[10]] rebleeding was found to occur in 6.9% of ruptured VA dissection treated using stent
placement and coils. This suggests that stent-assisted coiling alone does not completely
eliminate the risk of rebleeding or enlargement of dissection.[[11]] Careful follow-up study is required to check for enlargement of residual dissection
after stent-assisted coiling. On the contrary, due to a delay in aneurysmal occlusion
and high complication rate, treatment using flow diverter stents without coil embolization
may not be suitable for ruptured aneurysms in the acute stage.[[12]],[[13]] In addition, patients with ruptured VA dissection cannot receive premedication
with antiplatelet agents, resulting in more frequent thromboembolic complications.[[11]] Placement of multiple stents or flow diverter stents in the acute stage potentially
risks inducing thromboembolic complications.[[13]] In this case, DAPT continued after the first stent placement. After clopidogrel
achieved a plateau of inhibition of platelet aggregation after 3–7 days,[[14]] two additional Enterprise stents were added to achieve a “flow diversion” effect
because a low-profile visualized intraluminal support (LVIS) stent (MicroVention/Terumo,
Aliso Veijo, CA) was not available in Japan at that time. In an aneurysm model study,[[15]] reduction in the velocity within the aneurysm sac using two Enterprise stents was
not as significant as that achieved using flow diverter stents. Consistent with this
finding, treatment using one Enterprise stent with coil embolization resulted in the
enlargement of the fusiform dilatation, and 4 days after two additional Enterprise
stents were deployed (three Enterprise stents in total), the lesion was thrombosed.
Therefore, at least three Enterprise stents might be needed to achieve the flow diversion
effect.
No protocol has been established for the management of antiplatelet therapy in cases
of stent-assisted coil embolization for ruptured VA dissection. In this case, DAPT
was changed to single-antiplatelet therapy about 1 month after the procedure due to
a shunt operation, since DAPT was a significant risk factor for hemorrhagic complications
associated with ventriculoperitoneal shunt placement.[[16]] In previous studies for unruptured aneurysms, the stent-containing vessel with
incomplete aneurysm occlusion is a risk factor for a delayed thromboembolic event,[[17]] and long-term DAPT did not prevent the incidence of delayed thromboembolic events.[[18]] In this case, due to confirmation of thrombosis of the lesion, single-antiplatelet
therapy has been administered without delayed thromboembolic event, but further studies
are warranted to determine the optimal antiplatelet therapy for ruptured aneurysms.
Conclusion
Preventing rebleeding and preserving VA and PICA patency can be challenging in treatment
of PICA-involved VA dissection. The reported therapy might be a treatment option.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms.
In the form the patient has given his consent for his images and other clinical information
to be reported in the journal. The patient understands that his name and initials
will not be published and due efforts will be made to conceal their identity, but
anonymity cannot be guaranteed.
