Asstent-assisted coiling (SAC) and flow diverters (FDs) became popular for the treatment of acutely ruptured wide-necked intracranial aneurysms, dual antiplatelet therapy (DAPT) was frequently utilized during the acute phase of aneurysmal subarachnoid hemorrhage (SAH).1–3In SAC, the DAPT is used to prevent acute and delayed ischemic events due to stent-induced thromboembolism. While DAPT is effective in reducing the incidence of ischemic events in most cases,4it has the potential to cause hemorrhagic complications in the acute phase of SAH.
DAPT could complicate the management of hemorrhagic complications during endovascular treatment (EVT) since the coagulation capacity of the patients is significantly reduced. Moreover, there is usually a debate about the adverse effect of DAPT in other neurosurgical procedures, such as external ventricular drain (EVD) placement or removal, decompressive craniectomy, and any other craniotomies, which are common in the management of SAH.5,6
In this study, we evaluated the safety of DAPT in the setting of acute aneurysmal SAH based on a propensity score matching (PSM) study comparing hemorrhagic and ischemic complications between patients treated with SAC or FDs and requiring DAPT and patients treated with coiling but no antiplatelet regimen.
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This study was designed as a retrospective observational study reviewing all patients who had been admitted to our hospital for aneurysmal SAH between 2012 and 2022. It was approved by ethical board review of the local medical school. Written informed consent was waived given the retrospective nature of the study. The study inclusion criteria were as follows: 1) aneurysmal SAH, and 2) acutely ruptured aneurysms treated with SAC, FDs, FD-assisted coiling, or coiling (including the remodeling technique) within 2 weeks of rupture. Exclusion criteria were as follows: 1) ruptured aneurysms associated with other vascular abnormalities, such as arteriovenous malformations; 2) pregnant patients; 3) aneurysms treated by other modalities, and 4) incomplete clinical or imaging data.
Two expert neurointerventionists reviewed the clinical and imaging data on 938 ruptured aneurysm cases, 127 of which had received DAPT (DAPT group) because of treatment with SAC, FDs, or FD-assisted coiling and 811 of which had been treated with coiling and no antiplatelet therapy (non-DAPT group). As the primary analysis on the whole cohort showed significant skewing of baseline data between the two groups (including aneurysm location, p = 0.007; World Federation of Neurosurgical Societies [WFNS] grade,22p = 0.015; modified Fisher grade on CT scan, p = 0.007; and aneurysm size, p = 0.027), the decision was made to extract two matched groups using PSM. Using SPSS version 27 (IBM Corp.), PSM (1:1 matching) was performed to adjust the potential difference between the groups with respect to age, sex, aneurysm location (anterior communicating artery, internal carotid artery, middle cerebral artery, vertebrobasilar artery, A1, posterior cerebral artery, and pericallosal artery), WFNS grade, modified Fisher grade on CT scan, and aneurysm size, with a matching accuracy of 0.02. After propensity scoring, 192 matched patients were included, with 96 patients in each group (Fig. 1).
Flow diagram of patient selection according to PSM. AVM = arteriovenous malformation.
Antiplatelet Regimen
For all patients, after the insertion of a 6-Fr sheath, 5000 IU of heparin was administered for the transradial approach and 3000 IU for the transfemoral approach, followed by an infusion of 1000 IU of heparin for every hour into the procedure. In the DAPT group, patients received a loading dose of dual antiplatelets, including 300 mg clopidogrel plus 325 mg acetylsalicylic acid (ASA) or 180 mg ticagrelor plus 325 mg ASA, before anesthesia induction. Immediately after delivery of the stent, 180 µg/kg eptifibatide was injected intravenously, and the same dose was repeated after an interval of 10 minutes. After the procedure, an infusion of eptifibatide (2 µg/kg/min, maximum dose of 7.5 mg/hour) was administrated and continued for 6–12 hours in patients on clopidogrel plus ASA and for 4–6 hours in patients on ticagrelor plus ASA. DAPT was started 4–6 hours after the procedure. The DAPT included 75 mg clopidogrel plus 80 mg ASA daily or 90 mg ticagrelor twice a day plus 80 mg ASA daily. Before January 2017, we used clopidogrel plus ASA as our DAPT regimen; however, after January 2017, the combination of ticagrelor and ASA was the main DAPT regimen. We did not use any test for evaluating the efficacy of antiplatelets. The DAPT was continued for 3–6 months and then was converted to single antiplatelet therapy, including ASA 160 mg daily, for another 6–9 months. We did not administer ASA or any other antiplatelets for patients in the non-DAPT group during or after the procedure.
SAH Management and Endovascular Procedure
All patients were managed according to a single standardized protocol. On admission, CT studies were performed for all patients to evaluate the pattern of SAH, intraparenchymal hematoma, hydrocephalus, and the severity of cerebral edema. The pattern of SAH was defined according to the modified Fisher classification.23An EVD was immediately placed for patients who had WFNS grade IV or V on admission or whose condition deteriorated to WFNS grade IV or V during hospitalization. An EVD was fixed at 10–15 cm H2O, and continuous drainage was preferred. If a patient had an intraparenchymal hematoma with significant mass effect or midline shift, a decompressive craniectomy was considered. All patients with a WFNS grade IV or V were put on deep full sedation until the aneurysm was secured and intracranial pressure (ICP) was controlled. The appropriate method of aneurysm treatment was decided by a multidisciplinary team including a neurovascular neurosurgeon and neuro-interventionist. After discussing the intended benefits and potential risks with the patients and/or their next of kin, informed consent was obtained for the operation. All endovascular procedures were performed by our senior endovascular neurosurgeon (H.B.) with the patient under general anesthesia. Based on their architecture, the aneurysms were secured with coiling alone, coiling with balloon remodeling, SAC, Y-SAC, FDs, or FD with coiling. During the endovascular procedure, if the aneurysm ruptured, the bleeding was halted by reversing the heparinization and continuing the coiling procedure. CT scanning was performed in the angio-suite to assess the gravity of the bleeding. If there was any sign of high ICP or hydrocephalus, loading doses of mannitol or hypertonic saline were administered and an EVD was placed even in patients who had received the loading dose of DAPT and the bolus dose of eptifibatide. A maintenance dose of eptifibatide was not administered to patients in whom an EVD had been placed after EVT. If any clot formed during the EVT, it was treated with intraarterial and/or intravenous thrombolysis using eptifibatide. Prophylactic enoxaparin was administered subcutaneously to all the patients.
In cases in which an EVD had been placed, it was maintained for at least 7–10 days, and the patient was gradually weaned from it if there was no evidence of hydrocephalus, vasospasm, or cerebral edema. The EVD was converted to a ventriculoperitoneal shunt (VPS) if the patient did not tolerate weaning from the EVD. For the VPS procedure, DAPT was not stopped, but prophylactic enoxaparin was ceased for 3–4 days. For other neurosurgical procedures, such as decompressive craniectomy and intracranial hemorrhage evacuation, DAPT was not halted, and only prophylactic enoxaparin was discontinued for 3–4 days.
Complications were divided into intracranial and extracranial events. Intracranial complications were ischemic or hemorrhagic events. The ischemic events included any evidence of ischemia on follow-up brain CT or MRI and were classified as significant if they were accompanied by any new neurological deficit or required operation. The hemorrhagic events included any evidence of new intracranial hemorrhage on follow-up brain CT. They were recorded as major if they resulted in any new neurological deficit or required operation.
Clinical and Imaging Follow-Up
The clinical outcomes were assessed by an interventional neuroradiology fellow at the time of discharge and during the follow-up visits at 3, 6, and 12 months. Patient outcomes according to the modified Rankin Scale (mRS) were recorded and categorized into two groups: favorable, mRS score 0–2; and poor, mRS score 3–6.24Imaging follow-up was conducted at 6–12 months with MRI and MRA/cerebral angiography. Immediate and follow-up occlusion outcomes according to the Raymond-Roy Occlusion Classification were recorded.
Statistical Analysis
连续variables were reported as the mean and standard deviation if they had a normal distribution and as the median and interquartile range if they were skewed. The categorized variables were defined by numbers and percentages. Using SPSS version 27 (IBM Corp.), we utilized the Student t-test, Mann-Whitney U-test, chi-square test, and Fisher’s exact test for statistical analysis and the comparison between the DAPT group and the non-DAPT group, as appropriate. Using the binary regression test, we applied univariate and multivariate analyses to define the predictive factors for complications and outcomes. A cutoff of p < 0.1 in the univariate analysis was used for inclusion in the multivariate analysis. A p value < 0.05 was considered statistically significant.
Results
Table 1shows the baseline clinical and imaging characteristics of both groups. There was no significant difference in these baseline characteristics between the two groups except for the size of the aneurysm neck (p < 0.001).
Admission characteristics of patients with aneurysmal SAH
| Variable | Non-DAPT Group | DAPT Group | p Value |
|---|---|---|---|
| No. of patients | 96 | 96 | |
| Age in yrs | 57.50 (45.50–64.75) | 58.0 (49.0–64.75) | 0.760* |
| Female | 63 (65.6) | 63 (65.6) | >0.99 |
| Aneurysm location | 0.825 | ||
| ICA | 30 (31.3) | 30 (31.3) | |
| MCA | 14 (14.6) | 16 (16.7) | |
| ACoA | 28 (29.2) | 28 (29.2) | |
| A1 segment | 3 (3.1) | 5 (5.2) | |
| Pericallosal artery | 3 (3.1) | 2 (2.1) | |
| Vertebrobasilar artery | 18 (18.8) | 15 (15.6) | |
| WFNS grade | 0.374 | ||
| I | 56 (58.3) | 56 (58.3) | |
| II | 18 (18.8) | 18 (18.8) | |
| III | 6 (6.3) | 1 (1.0) | |
| IV | 13 (13.5) | 17 (17.7) | |
| V | 3 (3.1) | 4 (4.2) | |
| Modified Fisher grade | 0.516 | ||
| 1 | 39 (40.6) | 47 (49.0) | |
| 2 | 9 (9.4) | 5 (5.2) | |
| 3 | 39 (40.6) | 34 (35.4) | |
| 4 | 9 (9.4) | 10 (10.4) | |
| ICH | 7 (7.3) | 8 (8.3) | 0.788 |
| Aneurysm size in mm | 5.5 (3.93–7.6) | 6.0 (3.58–8.7) | 0.906* |
| Aneurysm neck size in mm | 2.1 (1.7–3.5) | 4.0 (3.0–5.93) | <0.001* |
ACoA = anterior communicating artery; ICA = internal carotid artery; ICH = intracranial hemorrhage; MCA = middle cerebral artery.
Values are expressed as median (interquartile range) or number (%), unless indicated otherwise. Boldface type indicates statistical significance.
Mann-Whitney U-test.
In 37 patients (19.3%), an EVD was placed, including 17 (17.7%) in the non-DAPT group and 20 (20.8%) in the DAPT group (Table 2). In the DAPT group, 2 patients required EVD placement in the angio-suite immediately after EVT and both had received the loading dose of dual antiplatelets and eptifibatide. None of these patients had EVD-related hemorrhage. During hospitalization, 9 EVDs were converted to VPSs because of weaning failure. There was no significant difference between the two groups with respect to neurosurgical procedures.
Surgical and endovascular procedures among patients with aneurysmal SAH
| Variable | Non-DAPT Group | DAPT Group | p Value |
|---|---|---|---|
| No. of patients | 96 | 96 | |
| Neurosurgical procedure | |||
| EVD | 17 (17.7) | 20 (20.8) | 0.583 |
| VPS | 3 (3.1) | 6 (6.3) | 0.497* |
| Decompressive craniectomy | 0 (0.0) | 1 (1.0) | 0.565* |
| Transradial approach | 3 (3.1) | 22 (22.9) | <0.001 |
| Endovascular procedure | <0.001 | ||
| Coiling | 96 (100.0) | 0 (0.0) | |
| SAC | 0 (0.0) | 64 (66.7) | |
| Y-SAC | 0 (0.0) | 18 (18.8) | |
| FD | 0 (0.0) | 11 (11.5) | |
| FD w/ coils | 0 (0.0) | 3 (3.1) | |
| Rescue stent | 0 (0.0) | 3 (3.1) | 0.246 |
Values are expressed as number (%), unless indicated otherwise. Boldface type indicates statistical significance.
Fisher’s exact test.
Table 3shows periprocedural complications. During EVT, the aneurysm was perforated in 12 patients (6.3%). This intraprocedural perforation was associated with death in 4 (33.3%) of the 12 patients. There was no significant difference between the DAPT and non-DAPT groups with respect to the rate of death and poor prognosis associated with the intraprocedural perforation (33.3% vs 33.3% and 33.3% vs 50%, respectively). Parent artery/stent thrombosis occurred in 9 patients (9.4%) in the DAPT group, leading to cerebral ischemia in 2 (22.2%) of the patients. In the others, thrombosis was completely resolved with intraarterial and intravenous thrombolysis and stent delivery.
Periprocedural complications and clinical and imaging outcomes
| Variable | Non-DAPT Group | DAPT Group | p Value |
|---|---|---|---|
| Rebleeding before EVT | 7 (7.3) | 3 (3.1) | 0.331* |
| Hydrocephalus | 11 (11.5) | 11 (11.5) | >0.99 |
| Infection | 5 (5.2) | 6 (6.3) | 0.756 |
| Intraprocedural perforation | 6 (6.3) | 6 (6.3) | >0.99 |
| Coil immigration | 4 (4.2) | 1 (1.0) | 0.364* |
| Parent artery/stent thrombosis | 0 (0.0) | 9 (9.4) | 0.003* |
| Cerebral ischemia | 15 (15.6) | 11 (11.5) | 0.399 |
| Rebleeding after EVT | 1 (1.0) | 3 (3.1) | 0.621* |
| Cerebral vasospasm | 21 (21.9) | 15 (15.6) | 0.355 |
| EVD-related ICH | 1 (1.0) | 8 (8.3) | 0.035 |
| Minor/insignificant ICH | 1 (1.0) | 7 (7.3) | 0.302 |
| Subdural hematoma | 0 (0.0) | 1 (1.0) | 0.565 |
| Significant extracranial hemorrhage | 9 (9.4) | 15 (15.6) | 0.190 |
| GI bleeding | 7 (7.3) | 12 (12.5) | 0.156 |
| Bleeding from thoracostomy | 2 (2.1) | 3 (3.1) | 0.465* |
| Immediate complete/near-complete aneurysm occlusion | 83 (86.5) | 81 (84.4) | 0.683 |
| Favorable outcome (mRS scores 0–2) | 76 (79.2) | 80 (83.3) | 0.460 |
| Death | 10 (10.4) | 11 (11.5) | 0.817 |
Values are expressed as number (%), unless indicated otherwise. Boldface type indicates statistical significance.
Mann-Whitney U-test.
Cerebral vasospasm and ischemia were nonsignificantly more common in the non-DAPT group (p = 0.355 and p = 0.399, respectively). The incidence of rebleeding after EVT was slightly higher in the DAPT group than in the non-DAPT group, but the difference was not significant (3.1% vs 1.0%, p = 0.621). The 3 post-EVT rebleeding events in the DAPT group occurred in the patients who had been treated with FDs alone. Of these 3 patients, 1 died (33.3%) and the 2 others (66.7%) were discharged with favorable outcomes. One of them required decompressive craniectomy while she was on the DAPT regimen; the procedure was not complicated by any hemorrhagic complication.
An EVD was associated with a higher rate of hemorrhagic events in the DAPT group than in the non-DAPT group (8/20 [40.0%] vs 1/17 [5.9%], p = 0.023). However, most hemorrhagic complications were insignificant and took place in the cerebral parenchyma around the EVD track. None of them required operation. One patient developed an acute subdural hematoma on the same side as the EVD. There was no hemorrhagic complication following VPS placement. All the VPSs were placed in a track different from the EVD.
Table 3shows the incidence of extracranial hemorrhagic events. All gastrointestinal (GI) bleedings were managed with medical treatment. GI endoscopy was performed for the patients who were on DAPT, and the regimen was not halted for these patients. Univariate analysis showed that the predictive factors of EVD-related hemorrhage were older age (OR 1.071, 95% CI 1.006–1.140, p = 0.031), WFNS grades III–V (OR 32.667, 95% CI 3.958–269.595, p < 0.001), major infection including ventriculitis and meningitis (OR 10.938, 95% CI 2.306–51.871, p < 0.001), thick SAH (OR 1.108, 95% CI 1.036–1.186, p = 0.001), cerebral ischemia (OR 5.855, 95% CI 1.461–23.463, p = 0.021), and a DAPT regimen (OR 8.636, 95% CI 1.059–70.454, p = 0.035). In the multivariate analysis, the predictive factors for EVD-related hemorrhage were WFNS grades III–V (OR 14.567, 95% CI 1.359–156.191, p = 0.027) and a DAPT regimen (OR 9.539, 95% CI 1.033–88.064, p = 0.047).
The immediate complete/near-complete occlusion rate was not different between the two groups at the end of the procedure (Table 3). Of the 192 patients, 156 (81.3%) were discharged with a favorable outcome. The favorable outcome and death rates were not different between the DAPT and non-DAPT groups.Table 4shows the predictive factors of poor prognosis (mRS scores 3–6) in the univariate and multivariate analyses. Multivariate analysis revealed that cerebral ischemia, rebleeding before securing the aneurysm, extracranial hemorrhage, and cerebral vasospasm were the only predictive factors of a poor outcome.
Predictive factors of poor prognosis (mRS scores 3–6) in univariate and multivariate analyses
| Factor | OR | 95% CI | p Value |
|---|---|---|---|
| Univariate analysis | |||
| Age | 1.020 | 0.989–1.051 | 0.208 |
| Male | 1.727 | 0.729 - -3.929 | 0.189 |
| Anterior circulation | 0.597 | 0.195–1.829 | 0.457 |
| WFNS grades III–V | 9.571 | 4.268–21.465 | <0.001 |
| Thick SAH | 7.581 | 2.981–19.277 | <0.001 |
| DAPT | 0.760 | 0.397–1.575 | 0.460 |
| Rebleeding before securing aneurysm | 12.310 | 2.007–50.400 | <0.001 |
| Stent/FD | 0.760 | 0.367–1.575 | 0.460 |
| Hydrocephalus | 9.232 | 3.546–24.034 | <0.001 |
| EVD | 12.250 | 5.285–28.392 | <0.001 |
| Infection | 14.571 | 3.641–58.310 | <0.001 |
| Intraop perforation | 3.433 | 1.023–11.526 | 0.036 |
| Intraop thrombosis | 3.775 | 0.960–14.841 | 0.065 |
| Cerebral vasospasm | 2.750 | 1.213–6.232 | 0.013 |
| Cerebral ischemia | 14.614 | 5.716–37.362 | <0.001 |
| Rebleeding after treatment | 1.457 | 0.147–14.429 | 0.567 |
| Hematoma-related EVD | 10.200 | 2.461–43.055 | 0.002 |
| Extracranial hemorrhage | 2.500 | 0.976 - -6.404 | 0.050 |
| Multivariate analysis | |||
| Cerebral ischemia | 40.532 | 6.797–241.688 | <0.001 |
| Rebleeding before securing aneurysm | 22.172 | 2.941–167.181 | <0.001 |
| Extracranial hemorrhage | 4.493 | 1.089–18.541 | 0.038 |
| Cerebral vasospasm | 0.133 | 0.20–0.891 | 0.038 |
Boldface type indicates statistical significance.
Discussion
Given the trend of using stents and FDs for the treatment of acutely ruptured wide-necked intracranial aneurysms, requiring a DAPT regimen in the setting of SAH, we conducted this retrospective PSM study to assess the hemorrhagic risk of a DAPT regimen and the regimen’s potential advantage in cerebral vasospasm and ischemia in the setting of aneurysmal SAH. Our study demonstrated that a DAPT regimen increased the EVD-related hemorrhage rate without influencing the clinical outcome of patients. Moreover, there tended to be a lower incidence of cerebral ischemia and vasospasm in the DAPT group, but the difference between the two treatment groups was not statistically significant.
While several studies have reported the feasibility and the advantage of EVT using a stent or FDs for acutely ruptured wide-necked aneurysms, the risks of a DAPT regimen were usually emphasized because of the possibility of hemorrhagic events, especially following other neurosurgical procedures.7–9Approximately 10%–20% of patients with aneurysmal SAH require EVD placement for the management of high ICP and hydrocephalus.7,9Moreover, approximately the same percentage of this population requires VPS placement,5and 6% requires decompressive craniectomy.9In previous studies, the rate of EVD-related hemorrhage has varied between 0% and 60% following placement of an EVD in patients who have received antiplatelets.6,7,10,11In a meta-analysis, Cagnazzo et al.7reported EVD-related hemorrhage in 21% of patients who had received antiplatelet therapy, a significantly higher rate compared with that in patients who had not received antiplatelet therapy. Similarly, our patients in the DAPT group had a higher incidence of EVD-related hemorrhage than those in the non-DAPT group (40.0% vs 5.9%, p = 0.023). However, the majority (87.5%) were minor hemorrhages that occurred mostly around the EVD track. Comparably, several studies have demonstrated that most EVD-related hemorrhages in the setting of antiplatelet therapy are small without any neurological effects and are usually discovered on routine CT scanning.7,9,12In 2 patients, we were obliged to place an EVD in the angio-suite immediately after EVT and both had received the loading dose of the DAPT and eptifibatide; however, neither of them had unexpected bleeding during EVD placement and EVD-related hemorrhage on postoperative CT scans. Similarly, Roh et al.9placed 15 EVDs within 4 hours of DAPT administration without significant EVD-related hemorrhage. Conversely, Bruder et al.13reported a higher incidence of EVD-related hemorrhage when the drain was placed after versus before the administration of antiplatelets and anticoagulants. Accordingly, placement of an EVD is recommended before EVT procedures and starting antiplatelets and anticoagulants when it is appropriate. In some cases, however, placement of an EVD after EVT was inevitable especially when the aneurysm was re-ruptured during an operation. So, in these conditions, the EVD should be placed with a meticulous approach, effective coagulation, and one-time insertion of the catheter to prevent subsequent hemorrhage. Furthermore, there is usually the risk of hematoma expansion, especially in the setting of a DAPT regimen. Therefore, frequent examination of the patient is required, as is a repeat CT scan within 48–72 hours after EVD insertion and DAPT administration. In our study, DAPT administration and WFNS grades III–V on admission were the predictive factors for EVD-related hemorrhage. In a meta-analysis, Cagnazzo et al. also reported that older age, high-grade SAH (Fisher grades 3–4 or Hunt and Hess grades III–IV), and DAPT have higher rates of EVD-related hemorrhage.7Therefore, EVD placement requires more vigilance in the setting of high-grade SAH when patients are on a DAPT regimen.
Decompressive craniectomy and VPS placement could have higher risks of intracranial hemorrhage when patients are on an antiplatelet regimen. Hudson et al.5reported 8 hemorrhages (10%) along the track of a VPS proximal catheter in 80 patients, including 7 hemorrhages in patients on DAPT and 1 in a patient not on DAPT. In their study, DAPT was the only predictive factor for VPS-related hemorrhage. Most of these hemorrhages were insignificant, and only 1 patient required VPS revision because of proximal catheter blockage. Conversely, we did not encounter any hemorrhage following placement of a VPS, which could be explained by the limited number of VPSs in our DAPT group (only 6 patients). In addition, our senior residents placed the VPSs with an ultra-careful approach, one-time insertion of the proximal catheter, and meticulous coagulation during the operation.
In their study comparing SAC and no-stent coil embolization (NSC) in the treatment of ruptured intracranial aneurysms, Roh et al.9了得到颅骨切除术病人6s for decreasing ICP, including 4 patients in the SAC group and 2 in the NSC group. None of them showed any evidence of hemorrhagic complications. Similarly, we did not have any hemorrhagic complications following decompressive craniectomy in the patient who was on DAPT.
In our study, we observed a lower incidence of cerebral ischemia and vasospasm in the DAPT group than in the non-DAPT group, although the difference was not statistically significant, possibly because of the study’s small sample size. These findings are in line with several previous publications reporting less delayed cerebral ischemia (DCI) and a better outcome in patients who received antiplatelet therapy.14,15Conversely, in a meta-analysis, Cagnazzo et al.16did not find the benefit of antiplatelet therapy for DCI, although there was a trend toward lower rates of cerebral ischemia in patients treated with EVT and on antiplatelet therapy. Patients on antiplatelet therapy have better clinical outcomes and lower mortality rates. Moreover, Darkwah Oppong et al.15could not find any additional benefit of DAPT for the risk of DCI and a poor clinical outcome in patients with SAH as compared with single antiplatelet therapy.
Stent-induced thromboembolic events are one of the major complications of EVT using a stent or FDs. In our study, the rate of thromboembolic events was significantly higher in the patients treated with a stent or FDs than in those treated with coiling alone despite receiving DAPT. However, most thrombosis was resolved by intraarterial and intravenous thrombolysis, and only 22% of cases led to cerebral ischemia. Several studies have also demonstrated a higher risk of thromboembolic events in SAC procedures compared to coiling alone.9,17,18In the setting of aneurysmal SAH, DAPT can create concern about the risk of rebleeding after securing an aneurysm. While we encountered a slightly higher incidence of aneurysm rebleeding in the DAPT group than in the non-DAPT group, all 3 patients with rebleeding in the DAPT group were treated with FDs alone. Similarly, Alpay et al.19reported a 3% rate of aneurysmal rebleeding after securing a ruptured aneurysm by FDs alone. Different strategies can be applied to reduce the risk of rebleeding following FD placement, including two or more overlapped FDs or adding coils in the ruptured aneurysm as an adjuvant to FDs.19,20
Despite all concerns about using DAPT in the acute phase of SAH, the rate of a favorable clinical outcome was slightly better in the DAPT group than in the non-DAPT group (83% vs 79%) in our study. Similarly, Roh et al.9观察略高的有利outcom率es in the SAC group that received DAPT compared with a coil group that did not receive DAPT. Our study demonstrated that cerebral ischemia remained one of the main predictive factors of a poor prognosis along with rebleeding before securing the aneurysm. Furthermore, extracranial hemorrhage, including GI bleeding, is the other predictive factor of a poor prognosis and could easily complicate the management of patients with SAH. Our patients in the DAPT group had approximately twice the rate of GI bleeding than those in the non-DAPT group. The DAPT regimen could complicate the treatment of extracranial bleeding, including GI bleeding, by reducing the coagulation capacity of patients and the effectiveness of medical treatment. Moreover, halting DAPT could rapidly increase the rate of stent-induced thromboembolic events. Therefore, the rapid and appropriate management of extracranial bleeding is vital to save patients with aneurysmal SAH.21
虽然PSM我们的研究的价值和增加its results, the study’s retrospective nature has its own limitations and biases. Also, the relatively small size of the population may have affected the results. Furthermore, it is a single-center, single-surgeon study, which could limit the generalizability of its results. In addition, EVT is the preferred approach for securing aneurysms at our center, even in wide-necked aneurysms, which can bias the choice of treatment.
Conclusions
The results of this study suggest that a DAPT regimen may be safe in patients within the acute phase of SAH. While EVD-related hemorrhage is more common with DAPT, it is usually insignificant and does not affect clinical outcome. Moreover, DAPT may reduce the risk of cerebral ischemia and vasospasm following SAH. However, a large, randomized, multicentric clinical trial could better clarify the safety and efficacy of DAPT in the setting of SAH.
Disclosures
The authors report no conflict of interest concerning the materials or methods used in this study or the findings specified in this paper.
Author Contributions
Conception and design: Qoorchi Moheb Seraj, Ebrahimnia, Gorji, Sasannejad, Zabihyan, Mowla. Acquisition of data: Qoorchi Moheb Seraj, Mirbolouk, Vaezi, Ebrahimnia, Gorji, Najafi, Pahlavan Shamsi, Sadeghian Shahi, Kheradmand. Analysis and interpretation of data: Baharvahdat, Mowla. Drafting the article: Baharvahdat, Qoorchi Moheb Seraj, Najafi, Mowla, Kheradmand. Critically revising the article: Baharvahdat, Mirbolouk, Sasannejad, Zabihyan, Mowla. Reviewed submitted version of manuscript: Baharvahdat, Qoorchi Moheb Seraj, Sasannejad. Approved the final version of the manuscript on behalf of all authors: Baharvahdat. Statistical analysis: Baharvahdat, Qoorchi Moheb Seraj. Administrative/technical/material support: Sasannejad. Study supervision: Baharvahdat, Zabihyan.
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5 ↑
HudsonJS,NagahamaY,NakagawaD,et al.Hemorrhage associated with ventriculoperitoneal shunt placement in aneurysmal subarachnoid hemorrhage patients on a regimen of dual antiplatelet therapy: a retrospective analysis.J Neurosurg.2018;129(4):916–921.
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6 ↑
LenschowM,von SpreckelsenN,TelentschakS,KabbaschC,GoldbrunnerR,GrauS.Ventriculostomy-related intracranial hemorrhage following surgical and endovascular treatment of ruptured aneurysms.Neurosurg Rev.2022;45(4):2787–2795.
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7 ↑
CagnazzoF,Di CarloDT,PetrellaG,PerriniP.Ventriculostomy-related hemorrhage in patients on antiplatelet therapy for endovascular treatment of acutely ruptured intracranial aneurysms. A meta-analysis.Neurosurg Rev.2020;43(2):397–406.
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8
ZhangX,ZuoQ,TangH,et al.Stent assisted coiling versus non-stent assisted coiling for the management of ruptured intracranial aneurysms: a meta-analysis and systematic review.J Neurointerv Surg.2019;11(5):489–496.
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9 ↑
RohH,KimJ,BaeH,et al.Comparison of stent-assisted and no-stent coil embolization for safety and effectiveness in the treatment of ruptured intracranial aneurysms.J Neurosurg.2020;133(3):814–820.
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10 ↑
CagnazzoF,CappucciM,DargazanliC,et al.Treatment of distal anterior cerebral artery aneurysms with flow-diverter stents: a single-center experience.AJNR Am J Neuroradiol.2018;39(6):1100–1106.
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11 ↑
QinG,PangG,ZhongS,ChenH,TangX,LanS.Increased risk of ventriculostomy-associated hemorrhage in patients treated with antiplatelet agents for stent-assisted coiling of ruptured intracranial aneurysms.Br J Neurosurg.2021;35(3):270–274.
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12 ↑
QinG,PangG,ZhongS,ChenH,TangX,LanS.Increased risk of ventriculostomy-associated hemorrhage in patients treated with antiplatelet agents for stent-assisted coiling of ruptured intracranial aneurysms.Br J Neurosurg.2021;35(3):270–274.
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13 ↑
BruderM,SchussP,KonczallaJ,et al.Ventriculostomy-related hemorrhage after treatment of acutely ruptured aneurysms: the influence of anticoagulation and antiplatelet treatment.World Neurosurg.2015;84(6):1653–1659.
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14 ↑
NagahamaY,AllanL,NakagawaD,et al.Dual antiplatelet therapy in aneurysmal subarachnoid hemorrhage: association with reduced risk of clinical vasospasm and delayed cerebral ischemia.J Neurosurg.2018;129(3):702–710.
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15 ↑
Darkwah OppongM,GembruchO,PierscianekD,et al.Post-treatment antiplatelet therapy reduces risk for delayed cerebral ischemia due to aneurysmal subarachnoid hemorrhage.开云体育app官方网站下载入口.2019;85(6):827–833.
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16 ↑
CagnazzoF,DerrazI,LefevrePH,et al.Antiplatelet therapy in patients with aneurysmal SAH: impact on delayed cerebral ischemia and clinical outcome. A meta-analysis.AJNR Am J Neuroradiol.2019;40(7):1201–1206.
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17 ↑
PiotinM,BlancR,SpelleL,et al.Stent-assisted coiling of intracranial aneurysms: clinical and angiographic results in 216 consecutive aneurysms.Stroke.2010;41(1):110–115.
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18 ↑
ZhangG,WuY,WeiY,et al.Stent-assisted coiling vs. coiling alone of ruptured tiny intracranial aneurysms: a contemporary cohort study in a high-volume center.Front Neurol.2022;13:1076026.
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19 ↑
AlpayK,HinkkaT,LindgrenAE,et al.Finnish flow diverter study: 8 years of experience in the treatment of acutely ruptured intracranial aneurysms.J Neurointerv Surg.2022;14(7):699–703.
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20 ↑
MadaelilTP,MoranCJ,CrossDTIII,KansagraAP.Flow diversion in ruptured intracranial aneurysms: a meta-analysis.AJNR Am J Neuroradiol.2017;38(3):590–595.
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21 ↑
YasudaH,MatsuoY,SatoY,et al.Treatment and prevention of gastrointestinal bleeding in patients receiving antiplatelet therapy.World J Crit Care Med.2015;4(1):40–46.
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22 ↑
TeasdaleGM,DrakeCG,HuntW,et al.A universal subarachnoid hemorrhage scale: report of a committee of the World Federation of Neurosurgical Societies.J Neurol Neurosurg Psychiatry.1988;51:1457.
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23 ↑
FronteraJA,ClaassenJ,SchmidtJM,et al.Prediction of symptomatic vasospasm after subarachnoid hemorrhage: the modified Fisher scale.开云体育app官方网站下载入口.2006;59(1):21–26.
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24 ↑
van SwietenJC,KoudstaalPJ,VisserMC,SchoutenHJ,van GijnJ.Interobserver agreement for the assessment of handicap in stroke patients.Stroke.1988;19(5):604–607.
