Abstract
Objective:
Transcarotid artery revascularization (TCAR) is a hybrid technique for carotid artery revascularization that relies on proximal carotid occlusion with flow reversal for distal embolic protection. The hemodynamic response of the intracranial circulation to flow reversal is unknown. In addition, the rate and pattern of cerebral embolization during flow reversal has yet to be investigated. The aim of this study was to characterize cerebral hemodynamic and embolization patterns during TCAR.
Methods:
A single institution retrospective study of patients with carotid artery stenosis undergoing TCAR with intraoperative transcranial Doppler (TCD) monitoring of the middle cerebral artery (MCA) was performed. Primary outcomes included changes in MCA velocity and MCA embolic signals observed throughout TCAR.
Results:
Eleven patients underwent TCAR with TCD monitoring of the ipsilateral MCA. The average MCA velocity at baseline was 50.6 ± 16.4 cm/s. MCA flow decreased significantly upon initiation of flow reversal (50.5±16.4 cm/s vs. 19.1±18.4 cm/s; p = 0.02). Re-initiation of antegrade flow resulted in a significant increase in the number of embolic events compared to baseline (p = 0.003), and embolic events were observed in 2 patients during flow reversal.
Conclusions:
TCD monitoring of patients undergoing TCAR revealed that the initiation of flow reversal results in a decrement in ipsilateral MCA velocity. Furthermore, embolic events can occur during flow reversal and are significantly associated with the re-initiation of antegrade flow in the internal carotid artery. However, both of these hemodynamic events were well tolerated in our cohort. These findings suggest that TCAR remains a safe neuroprotective strategy for carotid revascularization.
Keywords: Transcarotid artery revascularization (TCAR), flow reversal, embolic hits, transcranial Doppler (TCD)
TABLE OF CONTENTS SUMMARY
TCD monitoring of 11 patients undergoing TCAR revealed significant decrease in MCA flow velocity upon flow reversal initiation. Additionally, TCD monitoring demonstrated a significant increase in embolic events with restoration of antegrade flow. Despite these findings, data indicate TCAR is a safe procedure.
Introduction
Transcarotid artery revascularization (TCAR) with the ENROUTE Transcarotid Neuroprotection System (Silk Road Medical, Sunnyvale, Calif.) is an emerging technique for carotid artery revascularization with encouraging early results. The Safety and Efficacy Study for Reverse Flow Used During Carotid Artery Stenting Procedure (ROADSTER) is a multicenter, prospective, single-arm clinical trial of TCAR in patients with anatomic or medical high-risk factors for carotid endarterectomy (CEA).1 The study’s 30-day overall stroke rate of 1.4% is the lowest reported for any prospective, multicenter trial of carotid artery stenting. Furthermore, the 1-year ipsilateral stroke rate was 0.6%.2 These promising results have led to an increased utilization of TCAR. However, little is known about the cerebral hemodynamics and embolization rates during flow reversal.
Neurologic deficits following carotid revascularization are primarily the result of embolization secondary to disruption of atheromatous plaque or cerebral hypoperfusion after clamping the carotid artery. TCAR attempts to mitigate these risk factors with a neuroprotective strategy that involves direct carotid access, thereby eliminating the risk of stroke associated with manipulation of wires and catheters in the aortic arch, and utilization of flow reversal to reduce the risk of embolization during lesion crossing, pre- and post-dilation maneuvers, and stenting.3 This approach to neuroprotection also places the ipsilateral hemisphere in a situation where it is solely dependent on collateral blood supply via the anterior or posterior communicating arteries. Several studies have demonstrated that a significant decrease in ipsilateral middle cerebral artery (MCA) velocity during carotid endarterectomy is predictive of carotid intolerance, need for a shunt, and postoperative ischemic events.2,3 Although the initial results with TCAR have been excellent, the neuroprotective strategy employed during TCAR has not been fully evaluated. As the indications for TCAR broaden and the incidence of TCAR increases, it will be critical to have a thorough understanding of intracranial hemodynamics during flow reversal, particularly in the ipsilateral MCA.
Transcranial Doppler (TCD) is a non-invasive imaging modality with the ability to monitor hemodynamic events, such as cerebral blood flow via velocity. In addition, TCD can accurately detect embolic events during carotid artery revascularization, making it the optimal modality to assess TCAR’s neuroprotective strategy.4–5 In this present study, we utilized TCD to analyze ipsilateral MCA velocity and embolic events during TCAR with the goal of characterizing intraprocedural hemodynamic patterns and embolization rates.
Methods
Patient Population and Operative Techniques
Duke University Institutional Review Board approved this study protocol. A waiver of informed consent was granted because all of the collected data existed previously in the electronic medical record. Additionally, there were no study-related interventions or patient contact. Hence, the rights and welfare of these patients were not adversely affected.
A review of our institutional carotid stenting database from July 2017 to June 2019 was performed to identify patients who underwent TCAR with intraoperative TCD monitoring. We identified 11 such patients. A total of 68 TCARs were performed during the study period. All patients received general anesthesia with standard anesthetic monitoring, including intra-arterial blood pressure monitoring, continuous ECG, end-tidal CO2, pulse oximetry, and cerebral oximetry. Blood pressure and end-tidal CO2 were maintained within a narrow range during the procedure. Four vascular surgeons performed all procedures in this study. At our institution, the TCAR technique has remained constant with two exceptions. First, the decision to pre-dilate or post-dilate was at the discretion of the operating surgeon. Second, the interval between stent deployment and restoration of antegrade flow varied between operators.
Transcranial Doppler Ultrasonography
A CareFusion Sonara TCD ultrasonography machine (Madison, Wis.) was used in all cases. A 2-MHz probe was placed over the transtemporal window on the operative side. The MCA was located and insonated at an approximate depth of 50 mm. A headframe was used to maintain the position of the probe during the procedure.
Computed Tomography Arteriogram
Pre-operative contrast enhanced head and neck computed tomography arteriograms (CTA) were performed on 9 patients. Scanning was performed during the arterial phase from the thoracic inlet to the circle of Willis, and 3D reconstructions were obtained to evaluate the vascular anatomy. All CTAs were reviewed by an attending radiologist. An incomplete circle of Willis was defined as a stenosis > 50% in any artery within the circle of Willis.
Outcomes
The TCD parameters collected included MCA mean velocity, measured in units of centimeters per second, and embolic hits. MCA mean velocity was segregated into four phases: baseline, flow-reversal on, re-initiation of antegrade flow, and post re-initiation of antegrade flow. Post re-initiation of antegrade flow captured events that occurred at least 5 minutes and up to 20 minutes following return to antegrade flow. Ipsilateral MCA embolic signals were segregated into the following phases: baseline, sheath placement, flow-reversal on, pre-dilation, stent placement, post-dilation, re-initiation of antegrade flow, and 5 minutes post re-initiation of antegrade flow. MCA velocity and embolic data was relayed to surgeon at the discretion of the sonographer. The intraoperative TCD results had no impact on the conduct of the operation. Additional outcomes included cranial nerve injury, access site complications, and procedural success rate as well as 30-day ipsilateral stroke, death, and myocardial infarction (MI).
Statistical Analysis
All statistical analysis was performed using GraphPad Prism version 8.2.0 for macOS (GraphPad Software, San Diego, Calif., www.graphpad.com). For univariate analyses of changes in MCA flow velocity and embolic hits throughout the TCAR procedures, a Friedman test was performed, followed by Dunn’s multiple comparisons test. A p value < 0.05 was considered significant. A Mann-Whitney test was used for univariate analyses of change in MCA flow velocity upon initiation of flow reversal in patients with and without circle of Willis disease and for evaluation of total embolic hits in patients who did and did not take pre-operative plavix, aspirin, or high-dose statin.
Results
Patient Characteristics
Patient characteristics are presented in Table I. Eleven patients were included in the study. Only 1 patient (9.1%) had symptomatic carotid artery stenosis; the other 10 patients had asymptomatic disease. All patients had severe carotid artery stenosis defined as > 70% stenosis. Approximately one-third of the patients had a prior ipsilateral carotid intervention. Nearly two-thirds of patients reported pre-operative plavix (defined as 75 mg/day at least 7 days prior to their procedure), aspirin, and high-dose statin use.
Table 1 -.
Patient Characteristics
| Characteristics | % of All Patients (N = 11) |
|---|---|
| Mean Patient Age (yr) | 69.2 ± 6.4 |
| Male Sex (%) | 81.8 |
| White Race (%) | 90.9 |
| Prior Carotid Intervention (%) | |
| Ipsilateral | 27.3 |
| Contralateral | 27.3 |
| Asymptomatic Disease (%) | 90.9 |
| Risk Factor (%) | |
| Current Smoker | 9.1 |
| Former Smoker | 45.5 |
| Diabetes | 27.3 |
| History of TIA | 27.3 |
| History of CVA | 36.4 |
| Cardiovascular Disease | 45.5 |
| Pre-Operative Medication Use (%) | |
| Aspirin | 72.7 |
| Plavix* | 72.7 |
| Statin | 72.7 |
Defined as 75mg/day for at least 7 days prior to surgery
Changes in MCA Flow Velocity During TCAR
Figure 1 shows the mean MCA velocity for the entire cohort over the course of the TCAR procedure, while Table II displays individual patient MCA mean velocities. The average baseline MCA velocity was 50.6 ± 16.4 cm/s. There was a significant decrease in MCA flow upon initiation of flow reversal (50.6 ± 16.4 cm/s vs. 19.1 ± 18.4 cm/s; p = 0.02). This decrease represents a 62.3% decline in MCA velocity with flow reversal. Three patients in the cohort demonstrated a MCA velocity of 0 cm/s immediately upon initiation of flow reversal (Table II; Patients #1, #4, and #11). Furthermore, 2 patients demonstrated no significant change in MCA velocity with flow reversal; these patients exhibited a decline in MCA flow of just 0 and 5 cm/s upon flow reversal initiation. The mean MCA velocity approached baseline values upon immediate cessation of flow reversal (50.6 ± 16.4 cm/s vs. 64.0 ± 29.3 cm/s; p = 0.25) and reached baseline values in all patients within 5 minutes of ending flow reversal (50.6 ± 16.4 cm/s vs 53.5 ± 13.0 cm/s; p > 0.99).
Figure 1 -. Mean MCA Flow Velocity Throughout TCAR Procedure (N=11):
Plot of Mean MCA flow velocity (cm/s) at baseline, upon initiation of flow reversal, upon immediate re-initiation of antegrade flow, and 5 minutes after re-initiation of antegrade flow. There was a significant decrease in mean MCA flow velocity upon initiation of flow reversal (p = 0.02). Error bars indicate SEM at each time point.
Table 2 -.
Patient MCA Flow Velocity Throughout TCAR Procedure
| TCAR Timepoint | MCA Flow Velocity (cm/s) | ||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Patient #1 | Patient #2 | Patient #3 | Patient #4 | Patient #5 | **Patient #6 | Patient #7 | **Patient #8 | Patient #9 | Patient #10 | Patient #11 | Mean | SD | |
| Baseline | 59 | 43 | 47 | 38 | 59 | 29 | 56 | 49 | 49 | 93 | 52 | 50.6 | 16.4 |
| Flow Reversal On | 0 | 10 | 5 | 0 | 32 | 24 | 28 | 49 | 14 | 48 | 0 | 19.1 | 18.4 |
| Re-Initiation Antegrade Flow | 34 | 62 | 61 | 72 | 63 | 38 | 56 | 57 | 72 | 144 | 45 | 64.0 | 29.3 |
| Post Re-Initiation Antegrade Flow | 43 | 58 | 54 | 49 | 57 | 31 | 54 | 60 | 52 | 84 | 47 | 53.5 | 13.0 |
Patient had complete Circle of Willis anatomy; all others had incomplete Circle of Willis anatomy
Preoperative head and neck CTAs were available for 9 of the 11 patients. The circle of Willis anatomy was interrogated on the available CTAs. The change in MCA flow velocity upon initiation of flow reversal in patients with a complete versus incomplete circle of Willis anatomy is shown in Figure 2. While slightly outside the level of statistical significance, we observed a trend in MCA velocity change based on the status of the circle of Willis anatomy (p = 0.056). All 7 patients who experienced a significant decrease in MCA velocity had an incomplete anterior circulation collateral pathway. Furthermore, both patients who displayed no change in MCA velocity with initiation of flow reversal had complete circle of Willis anatomy.
Figure 2 -. Change in MCA Flow Velocity from Baseline After Initiation of Flow Reversal in Patients With Complete and Incomplete Circle of Willis Anatomy (N=9):
Patients with incomplete circle of Willis anatomy, defined as stenosis >50% in any artery within the circle of Willis, experienced greater decrease in MCA flow upon initiation of flow reversal compared to those patients with compete circle of Willis anatomy. While not statistically significant (p = 0.056), this suggests the importance of evaluating patients’ circle of Willis anatomy prior to TCAR in order to prevent periods of hypoperfusion.
Embolic Hits During TCAR
Table III depicts the embolic hits for each individual patient at various times during the procedure. Embolic hits per case ranged from 1 to 322 with a mean of 117 ± 109.8 hits (Figure 3). Re-initiation of antegrade flow resulted in a significant increase in the number of embolic hits compared to baseline (p = 0.003). Furthermore, during flow reversal, 2 patients had embolic hits with either pre-dilation, stent deployment, and/or post-dilation maneuvers. Four patients had a shower of embolic events reported upon re-initiation of antegrade flow, indicating there were too many embolic hits for sonographers to count. For study purposes, these embolic showers were counted as 200 embolic events. Therefore, those patients with values greater than 200 embolic hits (Table III, Patients #4, 8, 9, 10) had additional countable events following the initial embolic shower; for example, Patient #8 has 219 MCA embolic hits recorded at “Re-Initiation of Antegrade Flow,” which corresponds to an embolic shower (200 hits) followed by 19 countable embolic events. Pre-operative aspirin, statin, and plavix use was also assessed in all patients, with pre-operative plavix use defined as 75 mg/day at least 7 days prior to the TCAR procedure. Only 3 patients reported no pre-operative plavix (Table II, Patients #3, 4, 8), aspirin (Table II, Patients #5, 7, 8), or statin (Table II, Patients #4, 7, 8); there was no significant association between the total number of MCA embolic hits and pre-operative plavix (p = 0.085), aspirin (p > 0.999), or statin (p = 0.194) use.
Table 3 -.
Patient MCA Embolic Hits Throughout TCAR Procedure
| TCAR T imepoint | MCA Embolic Hits# | ||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Patient #1 | Patient #2 | *Patient #3 | *Patient #4 | Patient #5 | Patient #6 | Patient #7 | *Patient #8 | Patient #9 | Patient #10 | Patient #11 | Mean | SD | |
| Baseline | 0 | 15 | 0 | 0 | 3 | 0 | 17 | 1 | 0 | 0 | 1 | 0.5 | 0.9 |
| Sheath Placement | 7 | 0 | 22 | 0 | - | 0 | - | 2 | 14 | 22 | 0 | 7.6 | 9.3 |
| Flow Reversal On | 0 | 0 | 0 | 37 | 0 | 0 | 0 | 0 | 0 | 0 | 0 | 3.4 | 11.2 |
| Pre-Dilation | 0 | - | 0 | - | - | 23 | 0 | 0 | 0 | 0 | 0 | 3.7 | 8.4 |
| Stent Placement | 0 | 0 | 0 | 80 | 9 | 0 | 0 | - | 0 | 0 | 8.1 | 24.0 | |
| Post-Dilation | - | 0 | - | - | - | 23 | - | - | - | - | 0 | 2.1 | 6.9 |
| Re-Initiation Antegrade Flow | 15 | 8 | 76 | 204** | 22 | 2 | 30 | 219** | 200** | 247** | 0 | 92.6 | 101.0 |
| 5 Min Post Re-Initiation Antegrade Flow | 0 | 0 | 16 | 1 | - | 0 | 0 | 0 | 0 | 0 | 0 | 1.9 | 4.8 |
| Total | 22 | 24 | 120 | 322 | 30 | 57 | 51 | 222 | 214 | 224 | 1 | 117 | 109.8 |
Missing values indicate that TCD reading of MCA embolic hits was not taken at these timepoints for individual patients.
No pre-operative Plavix use; pre-operative Plavix use is defined as 75 mg/day at least 7 days prior to procedure
Embolic shower indicated on TCD report with “too many hits to count,” interpreted as 200 hits for study purposes. Values >200 eported for patients with an embolic shower followed by countable events.
Figure 3 -. Average Number of MCA Embolic Hits Throughout TCAR Procedure (N=11):
Plot of mean MCA embolic hits at baseline, upon initiation of flow reversal, throughout flow reversal, upon immediate re-initiation of antegrade flow, and 5 minutes after re-initiation of antegrade flow. There was a significant increase in the number of embolic events upon re-initiation of antegrade flow compared to baseline (p = 0.003). Error bars indicate SEM at each time point.
Perioperative TCAR Outcomes
Table IV details the clinical outcomes in this patient cohort. There was 1 ipsilateral stroke at 30 days; this patient underwent an angioplasty for recurrent restenosis. There were no deaths at 30 days. There were no perioperative myocardial infarctions. The procedural success rate was 100%. In terms of local complications, there were no cranial nerve injuries and no arterial access complications.
Table 4 -.
Perioperative TCAR Outcomes
| Perioperative TCAR Outcomes | Total Patients (N = 11) |
|---|---|
| 30-Day Ipsilateral Stroke Rate | 1 (9.1%) |
| 30-Day Myocardial Infarction Rate | 0 (0%) |
| 30-Day Mortality | 0 (0%) |
| Procedural Success Rate | 11 (100%) |
| Cranial Nerve Injury | 0 (0%) |
| Arterial Access Complication | 0 (0%) |
Discussion
Utilization of intraoperative TCD monitoring demonstrates that MCA velocity decreases significantly with active flow reversal during TCAR. The maintenance of MCA flow during flow reversal appears to be heavily dependent on intracranial collateral pathways. In addition, embolic hits during flow reversal suggest incomplete neuroprotection with TCAR in some patients.
Perioperative stroke is a significant and devastating complication of any carotid revascularization. The majority of perioperative strokes are the result of thromboembolic events or cerebral hypoperfusion. The primary limitation of TCAR’s neuroprotective strategy is cerebral hypoperfusion during proximal carotid occlusion and flow reversal. The clinical significance of cerebral hypoperfusion during TCAR remains unknown. Acute carotid artery occlusion with antecedent decline in MCA velocity has been demonstrated to cause clinically significant hemispheric ischemia.7 The decrease in MCA velocity necessary to induce cerebral ischemia is debatable, however; Jorgensen et al have reported a reduction of 40% from baseline as significant, while Giller and colleagues reported that a decline of > 65% in MCA velocity was associated with the development of a transient focal neurological deficit during carotid occlusion.8–9 In our study, the average decline in MCA velocity was 62.5%. Despite this decline, there were no adverse neurologic events in patients with a significant decline in MCA velocity from baseline. The one patient in our study who suffered an ipsilateral stroke within 30-days of TCAR experienced only a 5 cm/s decrease in MCA velocity. The absence of adverse clinical sequelae in the setting of cerebral hypoperfusion supports the safety of TCAR. Additionally, in the PROOF study, a safety and feasibility study for TCAR, there were no residual neurologic deficits or permanent clinical sequelae in the 9% of the patients that did not tolerate flow reversal.
Clinical tolerance of carotid occlusion depends on intact collateral pathways. Cross-filling from the contralateral hemisphere via the anterior communicating artery and flow from the posterior circulation via the posterior communicating artery are two of the primary compensatory collateral pathways. Based on historical literature investigating intracranial blood flow during carotid cross-clamping in the setting of CEA, the anterior communicating artery appears to be the most important collateral pathway. In a retrospective study of 67 patients who underwent cerebral angiography followed by CEA with EEG monitoring, patients with cross-filling of the anterior and middle cerebral arteries from the contralateral carotid artery via the anterior communicating artery demonstrated a significantly decreased incidence of EEG ischemic changes compared to patients who were dependent on collateral flow from the posterior circulation through the posterior communicating artery.10 These studies were corroborated in a study by Doblar et al in which MCA velocity during CEA was correlated with functional collateral pathways determined by preoperative cerebral angiography. Patients dependent on the ipsilateral posterior communicating artery displayed a significantly decreased MCA velocity during carotid cross-clamping compared to patients reliant on the anterior communicating artery.11 While not statistically significant, we observed a trend in MCA velocity change based on the status of patients’ circle of Willis anatomy. Notably, all 7 patients who demonstrated a significant decline in MCA velocity had an incomplete anterior collateral pathway. The lack of statistical significance in our study is likely attributable to our small cohort. The impact of circle of Willis anatomy on the maintenance of cerebral blood flow during flow reversal warrants further investigation with a larger cohort in a prospective manner.
Intraoperative microemboli are a significant risk factor for perioperative strokes.12 Indeed, transcarotid stenting with flow reversal was specifically designed to mitigate embolic events, which significantly hampered the widespread adoption of transfemoral carotid stenting. The initial results of TCAR have shown that it has a robust neuroprotective strategy.1, 13 In fact, cerebral embolic rates as determined by postoperative diffusion-weighted MRI are comparable to CEA and lower than transfemoral carotid stenting.6, 13–14 In our study, TCAR provided complete embolic neuroprotection for 9 patients, as demonstrated by the absence of embolic signals during flow reversal. However, there was a consistent and significant increase in embolic events upon re-initiation of antegrade flow. This suggests that some particulate matter remains within the carotid artery, and the return of antegrade flow results in emboli to the ipsilateral hemisphere.
Furthermore, 2 patients demonstrated embolic events during flow reversal, suggesting that there may be antegrade flow within the internal carotid artery in some patients. The mechanisms for these observed embolic events remain unknown. Disparate plaque morphology and variations in medical therapy and operative technique are possible etiologies. In this cohort, preoperative aspirin, plavix, and statin use did not correlate with embolic hits. Furthermore, there was no association between operative technique and emboli. The significance of the embolic events in this study are unclear. In the one patient who suffered a perioperative ipsilateral stroke, there were 57 MCA embolic hits during flow reversal. However, the stroke occurred on postoperative day 15; therefore, the intraoperative embolic hits are an unlikely source. Further investigation is necessary to elucidate both the mechanisms and clinical significance of these observed embolic events.
This study has several limitations that warrant discussion. First, this was a retrospective study with a small number of patients; a larger cohort of patients with similar results would lend more credence to our findings. Moreover, several patients were excluded secondary to poor TCD acoustic windows. Therefore, there is selection bias in our findings. The association between circle of Willis anatomy and MCA velocity during flow reversal would have been strengthened by an additional imaging modality to assess the intracranial circulation, such as intraoperative arteriogram. Finally, there was a clear embolic signal that occurred with resumption of antegrade flow; yet, our ability to determine the clinical significance of this signal is limited by our methodology. While TCD is an excellent modality for detecting embolization, it does not have the ability to discern between particulate and gaseous emboli. The former has been proven to be more injurious.12 Furthermore, pre- and post-operative diffusion weighted MRI would have been an excellent adjunct to intraoperative TCD monitoring to determine if intraoperative embolic events resulted in subclinical cerebral ischemic events.
Conclusion
MCA velocity decline with initiation of flow reversal and an increase in embolic hits with resumption of antegrade flow were consistent and statistically significant observations in our study. Despite these sonographic findings, there were no adverse neurologic events in all but one patient in our cohort. These data suggest that flow reversal is a robust neuroprotective strategy. Studies with a larger sample size are required to better characterize the hemodynamic and embolic events that occur with flow reversal.
ARTICLE HIGHLIGHTS.
Type of Research:
Single-center retrospective study
Key Findings:
Transcranial doppler (TCD) monitoring of 11 patients undergoing transcarotid artery revascularization (TCAR) with flow reversal revealed a significant decrease in middle cerebral artery (MCA) flow velocity upon flow reversal initiation (p = 0.02) and a significant increase in embolic hits (p = 0.003) upon re-initiation of antegrade flow.
Take Home Message:
Despite a significant decrease in MCA velocity with flow reversal and a consistent increase in embolic events with the re-initiation of antegrade flow, TCAR remains a safe and well tolerated procedure.
Acknowledgements
Research reported in this publication is supported by the National Center for Advancing Translational Sciences of the National Institutes of Health under Award Number 1KL2TR002554 (KWS). The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.
Footnotes
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Presentation Information: This work was presented as an oral podium presentation at the 2019 Eastern Vascular Society Annual Meeting, Pittsburgh, Penn, September 5 – 7, 2019.
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