Local Tirofiban Infusion for Remnant Stenosis in Large Vessel Occlusion: Tirofiban ASSIST study

doi:10.21203/rs.3.rs-21801/v1

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Research article

Local Tirofiban Infusion for Remnant Stenosis in Large Vessel Occlusion: Tirofiban ASSIST study

https://doi.org/10.21203/rs.3.rs-21801/v1

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Journal Publication

published 20 Jul, 2020

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Background

Compared to embolic occlusions, intracranial atherosclerotic stenosis (ICAS)-related large vessel occlusions (LVOs) often require rescue treatment following mechanical thrombectomy (MT). Herein, we hypothesized that local tirofiban infusion can be effective and safe for remnant stenosis in LVO during endovascular treatment, and can improve clinical outcomes.

Methods

This observational multicenter registry study (January 2011 to February 2016) included patients with ICAS who underwent endovascular treatment for LVO within 24 hours after stroke onset. An underlying fixed focal stenosis at the occlusion site observed on a cerebral angiography during and after MT was retrospectively determined as a surrogate marker of ICAS. Procedural and clinical outcomes were compared between the tirofiban and non-tirofiban groups.

Results

Patients were older (median, 71 years vs. 63 years, p = 0.015) and the onset to puncture time was longer (median, 395 min vs. 275 min, p = 0.036) in the tirofiban group than in the non-tirofiban group. Final reperfusion success (modified Treatment In Cerebral Ischemic 2b–3) was more frequent (86.4% vs. 42.4%, p = 0.016) and post-procedure parenchymal hematoma type 2 and/or thick subarachnoid hemorrhages were less frequent (5.1% vs. 15.3%, p = 0.068) in the tirofiban group. The frequency of favorable outcomes 3 months after endovascular revascularization therapy (modified Rankin Scale 0–2) was significantly higher in the tirofiban group (52.5% vs. 32.2%, p = 0.025) and tirofiban administration was an independent predictor of favorable outcomes (odds ratio, 4.013; 95% confidence interval, 1.300–12.386; p = 0.016).

Conclusions

Local tirofiban infusion may be an effective and safe adjuvant treatment option for patients with ICAS-LVO.

Neurology

ischemic stroke

intracranial atherosclerosis

thrombectomy

Since randomized controlled trials for mechanical thrombectomy (MT) were successful, endovascular revascularization therapy (ERT) has been established as a standard treatment for acute ischemic stroke (AIS) with large vessel occlusion (LVO) of the intracranial anterior circulation [1–5]. The MT is mostly based on stent retrieval or contact aspiration, which are designed for removing embolic clots in the occlusion vessel. However, if the occlusion is caused by intracranial atherosclerotic stenosis (ICAS), these MT methods may not be sufficient for recanalization and reperfusion, and rescue treatment are frequently required following MT [6–9]. Until now, angiographic and clinical outcomes after ERT for ICAS-LVO have been reported to be challenging [10–12].

ICAS is a common cause of stroke, especially in Asian populations [13, 14]. In situ thrombosis (IST) is a major mechanism involved in emergent ICAS-LVO [15, 16]. In addition, endothelium of the ICAS can be injured by the use of MT [17. 18]. This thrombogenic milieu can cause thrombus propagation or reocclusion even after partial recanalization [6, 9, 19, 20]. Therefore, stabilization of thrombogenic lesions should be considered for ICAS-related LVO.

In the current Tirofiban for Acute Serious Stroke Due to Intracranial in situ Thrombosis (Tirofiban ASSIST) study, we hypothesized that tirofiban, a locally infused antiplatelet agent, would stabilize the thrombogenic lesion in the ICAS-LVO and improve clinical and angiographic outcomes. Therefore, we aimed to evaluate the safety and efficacy of intra-arterial tirofiban administration during ERT and to identify if this treatment is a predictor of favorable clinical outcomes in ICAS-LVO.

Patients

This was a retrospective case-control study. The patients for this study were recruited from the Acute Stroke due to Atherosclerotic occlusion and Neurointervention-Korean Retrospective (ASIAN KR) registry, which included databases from three stroke centers in Korea (from January 2011 to February 2016) [21]. The criteria for inclusion were as follows: (1) patients had acute occlusion of the intracranial internal carotid artery (ICA), middle cerebral artery (MCA) M1, MCA M2, and vertebrobasilar artery; (2) time from symptom onset to groin puncture was within 24 hours; and (3) patients were diagnosed with ICAS-LVO, which was retrospectively evaluated on the cerebral angiography as the etiology of stroke.

Patients were excluded if (1) the extracranial target arterial occlusion and/or tandem intracranial large arterial occlusion was presented; (2) there were undetermined angiographic etiologies because the occlusion was never recanalized during primary MT; or (3) if patients had other etiologies of stroke, including vasculitis, arterial dissection, or Moyamoya disease. The institutional review board approved this study in each center. The requirement for informed consent was waived due to the retrospective nature of this study. Intra-arterial tirofiban in Korea has been used for ERT with approval from the Korean Food and Drug Administration for each institution.

Etiologic classification of target arterial lesion

The etiology of target arterial lesion was classified based on angiographic findings during ERT. If there was no residual stenosis on angiography after reperfusion, the etiology was classified as an embolism [9, 20]. In contrast, ICAS was defined using the following conditions: (1) presence of over 70% residual stenosis and (2) reocclusion tendency or flow impairment with less 70% of the residual stenosis [9, 20]. If recanalization was not achieved throughout the ERT or without angioplasty or stenting, it was classified as intractable. The etiologic classification was performed by two experienced stroke neurologists, and a consensus was reached (Y.H.H. and J.S.L.).

Endovascular procedures

Stent retrieval and contact aspiration were mainly used as primary MT strategies. If successful reperfusion was achieved but remnant ICAS was seen, follow-up angiography was performed 10–30 minutes after reperfusion. If the stenosis was aggravated, distal flow stagnation developed, or reocclusion occurred, repetitive MT or other rescue treatments, including switching MT strategy, intracranial tirofiban infusion, and balloon angioplasty and/or stenting, were applied.

Patients in the Tirofiban group were locally administered 0.5 mg to 2.0 mg of tirofiban as a rescue treatment. Additionally, 0.5 mg (2 ml) of tirofiban was diluted with 8 ml of normal saline or 1 mg (4 ml) of tirofiban with 6 ml of normal saline for intra-arterial local infusion and the 10 ml of diluted tirofiban was manually administered approximately at a rate of 1 ml/min [6].

Clinical and angiographic data

We analyzed the clinical and demographic data of the patients, including National Institute of Health Stroke Scale (NIHSS) scores, Alberta Stroke Program Early CT Scores (ASPECTS), and pre-stroke modified Rankin Scale (mRS) scores at admission. The Arterial Occlusive Lesion (AOL) grade was used for the measurement of recanalization in the target arterial lesion, and the grade 2–3 was considered an indicator of successful recanalization [22]. Successful reperfusion was defined as a modified Treatment In Cerebral Ischemia (mTICI) score of 2b or 3 based on the final angiography [22]. The brain CT was obtained immediately and 12 to 24 hours after ERT to evaluate hemorrhagic complications. Intracranial hemorrhages were classified based on the European Cooperative Acute Stroke Study [23]. Subarachnoid hemorrhage (SAH) severity was graded according to the modified Fisher scale [24]. Serious hemorrhagic complications were defined as parenchymal hematoma type 2 and/or a modified Fisher grade 3 or 4 of SAH. Postprocedural final infarct volume was measured with diffusion-weighted imaging (J.W.C.) using NordicICE semi-automated software (NordicNeuroLab, Bergen, Norway). Clinical outcomes were evaluated with mRS at 3 months after ERT and a favorable clinical outcome was defined as an mRS score of ≤ 2 or no change compared to the premorbid mRS.

Statistics

Chi-square tests or Fisher’s exact tests were used for categorical variables. Mann–Whitney U tests were used for continuous variables. A binary logistic regression analysis was performed to identify whether local tirofiban administration was an independent predictor of favorable clinical outcomes at 3 months and serious hemorrhagic complications. For all analyses, p < 0.05 was considered statistically significant. Statistical analyses were performed using SPSS 22.0 (IBM, Armonk, NY).

Demographics and baseline characteristics

Baseline characteristics and stroke risk factors are compared in Table 1. The median age of the patients was higher in the tirofiban group than in the non-tirofiban group (non-tirofiban group versus tirofiban group; 63 [55–75] versus 71 [61–78], p = 0.015). The median initial NIHSS scores (15 [12–21] versus 14 [10–20], p = 0.322) and the median ASPECTS scores (8 [4.5–9.5] vs. 8 [6–9], p = 0.530) did not significantly differ between the two groups. Further, the intravenous recombinant tissue plasminogen activator (rtPA) did not significantly differ between the two groups (49.2% versus 33.9%, p = 0.093). Although the incidence of dyslipidemia was higher in the non-tirofiban group than in the tirofiban group (42.4% versus 23.7%, p = 0.031), the other risk factors of stroke did not significantly differ between the two groups.

Table 1

Comparison of baseline characteristics between the tirofiban and non-tirofiban groups
	Non-tirofiban Group (n = 59)	Tirofiban Group (n = 59)	P Value
Age, median (IQR)	63 (55–75)	71 (61–78)	0.015
Female	16 (27.1%)	23 (39.0%)	0.171
Prestroke mRS, median (IQR)	0 (0–0)	0 (0–0)	0.438
Initial NIHSS, median (IQR)	15 (12–21)	14 (10–20)	0.322
ASPECTS, median (IQR)	8 (4.5–9.5) (n = 41)	8 (6–9) (n = 46)	0.530
Intravenous rtPA	29 (49.2%)	30 (33.9%)	0.093
Target occlusion location			0.766
Terminal ICA	9 (15.3%)	8 (13.6%)
MCA M1	34 (57.6%)	38 (64.4%)
MCA M2	2 (3.4%)	3 (5.1%)
VBA	14 (23.7%)	10 (16.9%)
Hypertension	38 (64.4%)	38 (64.4%)	> 0.999
Diabetes mellitus	19 (32.2%)	18 (30.5%)	0.843
Dyslipidemia	25 (42.4%)	14 (23.7%)	0.031
Atrial fibrillation	12 (20.3%)	9 (15.3%)	0.470
Coronary disease	3 (5.1%)	4 (6.8%)	> 0.999^*
Smoking	21 (35.6%)	23 (39.0%)	0.703
Prior antiplatelet	6 (10.2%)	13 (22.0%)	0.080
Prior anticoagulant	4 (6.8%)	1 (1.7%)	0.364^*
ASPECTS, Alberta Stroke Program Early CT Score; IQR, interquartile range; ICA, internal carotid artery; MCA, middle cerebral artery; mRS; modified Rankin Scale; NIHSS, National Institute of Health Stroke Scale; rtPA, recombinant tissue plasminogen activator; VBA, vertebro-basilar artery
^*Fisher’s exact T test

Comparisons of angiographic data and outcomes

The procedural, angiographic, and clinical outcomes for each group are summarized in Table 2. The median time from stroke symptom onset to groin puncture was shorter in the non-tirofiban group than in the tirofiban group (275 minutes versus 395 minutes, p = 0.036). The rate of aspiration thrombectomy and stent retriever thrombectomy, which were used as primary MT strategies, was similar in both groups. Additional rescue treatments such as thrombectomy device switching, balloon angioplasty, and/or stenting were used more frequently in the non-tirofiban group. However, there was no significant difference between the two groups in the use of these treatments, with the exception of intracranial balloon angioplasty. There were no differences in the rate of successful recanalization between the two groups (69.5% versus 69.5%, p > 0.999); however, the rate of successful reperfusion was higher in the tirofiban group than in the non-tirofiban group (86.4% versus 42.4%, p = 0.016). Additionally, the incidence of SAH (p = 0.027) and intraventricular hemorrhage (p = 0.032) was higher in the non-tirofiban group than in the tirofiban group, but the occurrence of intracerebral hemorrhage did not differ between the groups (p = 0.311). The final infarct volume after ERT was smaller in the tirofiban group than in the non-tirofiban group (38.8 ml versus 18.5 ml, p = 0.023). Repeat angiographies during admission after ERT were obtained in 32 patients in the non-tirofiban group and in 45 in the tirofiban group. The incidence of postprocedural reocclusion was significantly higher in the non-tirofiban group than in the tirofiban group (37.5% versus 4.4%, p < 0.001). A favorable outcome 3 months after ERT was more frequent in the tirofiban group than in the non-tirofiban group (52.5% vs. 32.2%, p = 0.025).

Table 2

Details of endovascular treatment and clinical outcomes
	Non-tirofiban Group (n = 59)	Tirofiban Group (n = 59)	P Value
Onset to puncture time	275 (210–482)	395 (274–580)	0.036
Puncture to final angiography time	81 (60–101)	65 (42–108)	0.064
Onset to reperfusion time	380 (298–646)	467 (345–675)	0.066
First-line endovascular treatment			0.096
Aspiration Thrombectomy	29 (49.2%)	33 (55.9%)
Stent retriever	23 (39.0%)	25 (42.4%)
Local fibrinolytics	1 (1.7%)	1 (1.7%)
Angioplasty	6 (10.2%)	0
Immediate reocclusion after first endovascular treatment	10 (17.9%)	24 (41.4%)	0.006
Rescue treatments
Local Tirofiban infusion only	0	48 (81.4%)	< 0.001
Stent retriever to aspiration	1 (1.7%)	0	> 0.999^†
Aspiration to stent retriever	8 (13.6%)	3 (5.1%)	0.113
Intracranial balloon angioplasty	9 (15.3%)	2 (3.4%)	0.027
Intracranial stenting	12 (20.3%)	6 (10.2%)	0.124
Final AOL 2–3	41 (69.5%)	41 (69.5%)	> 0.999
Final mTICI 2b–3	25 (42.4%)	51 (86.4%)	0.016
Postprocedural reocclusion	12 (37.5%, n = 32)	2 (4.4%, n = 45)	< 0.001
Intracerebral hemorrhage			0.311
HT type 1	4 (6.8%)	2 (3.4%)
HT type 2	6 (10.2%)	3 (5.1%)
PH type 1	3 (5.1%)	1 (1.7%)
PH type 2	6 (10.2%)	3 (5.1%)
Subarachnoid hemorrhage	6 (10.2%)	0	0.027^*
Intraventricular hemorrhage	8 (13.6%)	1 (1.7%)	0.032^*
Serious hemorrhagic complication^†	9 (15.3%)	3 (5.1%)	0.068
Final infarct volume, ml (median, IQR)	38.8 (14.3–92.7)	18.5 (7.9–37.2)	0.023
mRS 0–2 at 3 months	19 (32.2%)	31 (52.5%)	0.025
Mortality	12 (20.3%)	4 (6.8%)	0.031
AOL, arterial occlusive lesion; ERT, endovascular revascularization therapy; HT, hemorrhagic transformation; mRS, modified Rankin Scale; MT, mechanical thrombectomy; mTICI, modified treatment in cerebral ischemia; PH, parenchymal hematoma
^*Fisher’s exact t-test; ^†Serious hemorrhagic complications consist of parenchymal hematoma type 2 and/or subarachnoid hemorrhage Fisher grade 3–4.

Using a logistic regression model, local tirofiban infusion (p = 0.016) was found to be an independent predictor of favorable clinical outcomes (Table 3). In another regression model, local tirofiban infusion was not associated with serious hemorrhagic complications; however, the final infarct volume was independently associated with serious hemorrhagic complications (Table 4). Additionally, there was a significant interaction between tirofiban infusion and final infarct volume for serious hemorrhagic complications, which were inversely associated (p = 0.043).

Table 3

Binary logistic regression analysis for favorable clinical outcomes
Variables	Odds ratio (95% CI)	p value
Age	0.926 (0.879–0.977)	0.004
Female	0.552 (0.189–1.607)	0.276
Baseline NIHSS	0.857 (0.780–0.942)	0.001
Intravenous rtPA	1.497 (0.516–4.340)	0.458
Occlusion location		0.166
Terminal ICA	Ref.
MCA M1	6.004 (1.065–33.849)	0.042
MCA M2	4.948 (0.382–64.044)	0.221
VBA	2.571 (0.362–18.289)	0.345
Onset to puncture time	1.000 (0.999–1.001)	0.663
Puncture to final reperfusion time	0.988 (0.976–0.999)	0.035
Successful reperfusion	1.852 (0.507–6.763)	0.351
Serious hemorrhagic complication^*	0.549 (0.101–2.993)	0.488
Local tirofiban infusion	4.013 (1.300-12.386)	0.016
ICA, internal carotid artery; MCA, middle cerebral artery; NIHSS, National Institute of Health Stroke Scale; rtPA, recombinant tissue plasminogen activator; VBA, vertebro-basilar artery
^*Serious hemorrhagic complications consist of parenchymal hematoma type 2 and/or subarachnoid hemorrhage Fisher grade 3–4.

Table 4

Binary logistic regression analysis for serious hemorrhagic complications
Variables	Odds ratio (95% CI)	p value
Age	0.963 (0.894–1.037)	0.320
Female	1.380 (0.146–13.017)	0.778
Intravenous rtPA	0.221 (0.014–3.412)	0.280
Prior use of oral antiplatelet or anticoagulant	1.466 (0.103–20.864)	0.778
Number of ERT technique	0.865 (0.145–5.149)	0.874
Successful reperfusion	1.574 (0.068–36.603)	0.778
Local tirofiban	1.451 (0.049–43.017)	0.829
Onset to groin puncture time	0.999 (0.996–1.002)	0.573
Puncture to final angiography time	0.987 (0.957–1.018)	0.398
Final infarct volume	1.013 (1.002–1.024)	0.020
ERT, endovascular revascularization therapy; rtPA, recombinant tissue plasminogen activator

In the current study, we evaluated the safety and efficacy of local tirofiban infusion as a rescue ERT strategy for AIS for patients with ICAS-LVO. The main findings of this study were as follows: (1) the rates of successful reperfusion and favorable outcomes were higher in the tirofiban group than in the non-tirofiban group; and (2) despite its lytic characteristics, the rate of hemorrhagic complications appeared to be the result of an interaction with the final infarct volume and was lower in the tirofiban group than in the non-tirofiban group. Overall, results from this retrospective registry study demonstrated that local tirofiban infusion may be a safe and effective rescue treatment for patients with ICAS-LVO.

ICAS is one major etiology of LVO, especially in Asian populations, and is still challenging to manage during modern MT [10, 15, 20]. ICAS-related LVO may result from IST beyond a preexisting stenosis [6, 19, 20, 25]. In IST, the rupture of preexisting atherosclerotic plaques and the release of tissue factors from the endothelial surface can lead to a thrombogenic and platelet aggravating environment [16]. In addition, usual MT may induce plaque rupture and cause extensive arterial injury from the endothelium to the tunica media [17, 18]. Therefore, local thrombogenic conditions may be exacerbated, and this often causes the vessel to become reoccluded even after successful reperfusion is achieved by usual MT. Based on this data, early stabilization of the endothelium and intracranial atherosclerotic plaque is an important goal, and antiplatelet administration is ideal to stabilize the thrombogenic lesion. Since the underlying ICAS is hidden in LVO, pretreatment with oral antiplatelet agents cannot be applied in most cases; thus, infusible antiplatelet has been anecdotally used in the IST lesion for the rescue treatment for intracranial LVO [6, 26, 27]. To this end, the glycoprotein IIb/IIIa inhibitor may play a crucial role in the prevention of fibrinogen-induced platelet aggregation and local thrombus formation [28].

Tirofiban is an infusible antiplatelet glycoprotein IIb/IIIa inhibitor. It has been indicated for unstable angina and myocardial infarction [28]. Compared to another glycoprotein IIb/IIIa inhibitor, abciximab, which is an irreversible antiplatelet, tirofiban is a reversible antiplatelet [28]. Due to relatively long platelet recovery time of abciximab (up to 48 h), hemorrhagic complications are of greater concern for abciximab than for tirofiban (up to 2–4 h). While another glycoprotein IIB/IIIA inhibitor, eptifibatide, is not available in Korea, the use of tirofiban in ERT has been approved by the Korean Food and Drug Administration for emergency base.

In the current study, we found an important role of tirofiban in reperfusion beyond recanalization. In terms of recanalization, the rate of successful recanalization graded by AOL was the same in both groups (69.5%, respectively). However, the ERT procedure was completed in 81.4% of patients only after local tirofiban injection was administered as a single rescue treatment in the tirofiban group. In addition, the incidence of postprocedural reocclusion on repeat angiographies was much lower in the tirofiban group. These findings suggest that tirofiban may stabilize the thrombogenic environment in the stenotic lesion and reduce the use of additional MT strategies. Subsequently, endothelial damage and endovascular procedure time may also be reduced. Beyond recanalization, the reperfusion status should also be considered. Reperfusion includes restoration of blood flow into distal branches and the deep brain [22, 29]. In the current study, despite the same rate of successful recanalization in both groups, the rate of successful reperfusion was higher in the tirofiban group than in the non-tirofiban group. In most cases, tirofiban infusion was administered immediately after first partial recanalization in cases with a suspicion of underlying stenosis or in cases of reocclusion after recanalization. Early local tirofiban infusion may contribute to the prevention of downstream embolization by local thrombosis, which may result in a better reperfusion status [30].

Multiple studies have reported that the application of glycoprotein IIb/IIIa inhibitors increases the risk of postprocedural hemorrhagic complications. Although glycoprotein IIb/IIIa inhibitors are not fibrinolytic agents, a high rate of fatal intracerebral hemorrhages has been reported [31, 32]. These studies reported that that glycoprotein IIb/IIIa inhibitors were administered intravenously for at least 12 hours. A relatively high dose of glycoprotein IIb/IIIa inhibiters may be needed to elicit the appropriate action when it in administered intravenously. In addition, because patients were enrolled up to 2011 in these studies, new techniques of MT may have not been incorporated. Further, similar to the failed ERT trials in 2013 [33–35], the rate of successful reperfusions in these studies was relatively low (61.6% in the tirofiban study). Lower rates of successful reperfusion may be related to a greater final infarct volume, which may be more vulnerable to antithrombotic therapy. In contrast, results of the current study revealed that tirofiban did not increase intracerebral hemorrhages when it was slowly infused via catheter and administered at a low dose following newer MT treatment. Recent studies have demonstrated that primary stent retrieval effectively removed in situ thrombi in ICAS-LVO [8, 36]. On the other hand, serious hemorrhagic complications were more strongly associated with the final infarction volume than with intravenous thrombolysis or local tirofiban infusion shown in the current study. Our results suggest that the appropriate administration of tirofiban may maintain the reperfusion status and reduce the infarct volume. Therefore, the risk of serious hemorrhagic complications may be reduced following tirofiban administration.

There were several limitations of this study. First, this since this was a retrospective study, the data may be skewed, and hidden confounders may have affected the discretion of the treatment. Additionally, a previous study reported that stenosis length affects treatment outcomes [37]. However, stenosis length could not be measured in the current study because of the interference caused by IST and LVO or vessel injury of primary MT. Nevertheless, our main results are supported by multivariable adjustments, which consisted of well-known predictors. On the other hand, the dose and infusion speed of tirofiban was not prespecified due to the retrospective nature of this study. However, from early experiences and previous anecdotal reports, the dose did not vary extensively. For example, the total amount of tirofiban infusion was low and only varied from 0.5 mg to 2.0 mg at all three stroke centers. Additionally, the infusion speed was between 0.05 and 0.1 mg/min. Further, although patients with LVO and underlying ICAS were included in this study, some patients also had atrial fibrillation. These cases may have contaminated the effectiveness and outcomes of local tirofiban infusion on IST of ICAS-LVO. To overcome this limitation, we conducted further analyses that excluded patients with atrial fibrillation (shown in the Supplemental document); however, the clinical and angiographic outcomes did not differ. Finally, old-generation contact aspiration catheters were used in some portion of the primary MT devices. However, the frequency of the use did not differ between the groups in our post-hoc analysis. Considering that the main goal of the current study was to identify rescue ERT strategies for underlying ICAS after thrombectomy, the impact of MT devices would be minor.

Local tirofiban infusion following MT may be an effective and safe treatment option for patients with ICAS-LVO. The rate of favorable outcomes was higher and the rate of serious hemorrhagic complications were lower in patients who received tirofiban infusion as a rescue treatment than in patients who did not receive infusions of tirofiban as a rescue treatment.

AIS: Acute Ischemic Stroke; AOL: Arterial Occlusive Lesion; ASIAN KR: Atherosclerotic occlusion and Neurointervention-Korean Retrospective; ASPECTS: Alberta Stroke Program Early CT Scores; ERT: Endovascular Revascularization Therapy; ICA: Internal Carotid Artery; ICAS: Intracranial Atherosclerotic Stenosis; IST: In situ thrombosis; LVO: Large Vessel Occlusion; MCA: Middle Cerebral Artery; mRS: modified Rankin Scale; MT: Mechanical Thrombectomy; mTICI: modified Treatment In Cerebral Ischemia; NIHSS: National Institute of Health Stroke Scale; rtPA: recombinant tissue plasminogen activator; SAH: Subarachnoid Hemorrhage; Tirofiban ASSIST: Tirofiban for Acute Serious Stroke Due to Intracranial in situ Thrombosis

Ethics approval and consent to participate

The protocol for data collection was approved by the Institutional Review Board of each hospital (Ajou University Hospital: AJIRB-MED-OBS-15-483, AJIRB-MED-OBS-17-094, Keimyung University Dongsan Hospital: 2016-01-038-009, Kyungpook National University Hospital: 2016-01-020-006). Our study was implemented in accordance with the ethical standards of the 1964 Declaration of Helsinki and its later amendments. The need for written informed consent was waived because of the retrospective nature of this study.

Consent for publication

Not Applicable

Availability of data and materials

The datasets used and/or analysed during the current study available from the corresponding author on reasonable request.

Competing interests

The authors declare that they have no competing interests.

Funding: The current study was supported by a grant from ASPEN GLOBAL INCORPORATED (J.S.L.); however, the funder had no role in the study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Authors' contributions

Study design YWK, YHH, JSL; data collection YWK, SIS, JY, JHH, CHK, DHK, YSK, SJL, JMH, JWC, YHH, JSL; data analysis YWK, JSL; data interpretation YWK, YHH, JSL; preparation of the manuscript YWK, YHH, JSL; review and editing YWK, SIS, JY, JHH, CHK, DHK, YSK, SJL, JMH, JWC, YHH, JSL. All authors have read and approved the final version of manuscript.

Acknowledgements

Not Applicable

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Local Tirofiban Infusion for Remnant Stenosis in Large Vessel Occlusion: Tirofiban ASSIST study

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Abstract

Background

Methods

Results

Conclusions

Background

Methods

Patients

Etiologic classification of target arterial lesion

Endovascular procedures

Clinical and angiographic data

Statistics

Results

Demographics and baseline characteristics

Comparisons of angiographic data and outcomes

Discussion

Conclusions

Abbreviations

Declarations

References

Supplementary Files

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Journal Publication

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