Karl Meisel

The Clinical and Radiographic Importance of Distinguishing Partial from Near-Complete Reperfusion Following Intra-Arterial Stroke Therapy

BACKGROUND AND PURPOSE: Reperfusion following intra-arterial stroke therapy is associated with improved clinical outcomes. However, the degree of reperfusion needed to achieve successful outcomes is unknown. The purpose of this analysis was to determine whether the degree of reperfusion has an impact on final infarct volumes and clinical outcomes. MATERIALS AND METHODS: A retrospective analysis identified 88 consecutive patients who underwent intra-arterial therapy for acute anterior circulation stroke. Reperfusion was graded by using the TICI scale into none (TICI 0 or 1), partial (TICI 2a), or near-complete (TICI 2b/3). Baseline characteristics were compared. For each of these groups, we compared discharge disposition and final infarct volumes. RESULTS: Near-complete, partial, and no reperfusion occurred in 44.3%, 26.1%, and 29.6% of patients, respectively. Baseline characteristics were similar across all 3 groups. The median NIHSS score was 15. Significant differences in discharge disposition were seen, with 41.0% of the TICI 2b/3 group discharged home versus 17.4% of TICI 2a and 7.7% of TICI 0/1. In-hospital mortality was 12.8% for TICI 2b/3 compared with 39.1% for TICI 2a and 34.6% for TICI 0/1. Patients with near-complete reperfusion were significantly more likely to have infarct volumes ≤70 mL (OR = 12.1; 95% CI, 2.7–54.2), compared with patients with partial reperfusion (OR = 2.2; 95% CI, 0.5–9.6). CONCLUSIONS: Significant differences exist in outcomes and infarct volumes between partial (TICI 2a) and near-complete (TICI 2b/3) reperfusion following intra-arterial stroke therapy. Further trials should separately report these groups to facilitate comparison among treatment paradigms.

Brain Emboli After Left Ventricular Endocardial Ablation

Background: Catheter ablation for ventricular tachycardia and premature ventricular complexes (PVCs) is common. Catheter ablation of atrial fibrillation is associated with a risk of cerebral emboli attributed to cardioversions and numerous ablation lesions in the low-flow left atrium, but cerebral embolic risk in ventricular ablation has not been evaluated. Methods: We enrolled 18 consecutive patients meeting study criteria scheduled for ventricular tachycardia or PVC ablation over a 9-month period. Patients undergoing left ventricular (LV) ablation were compared with a control group of those undergoing right ventricular ablation only. Patients were excluded if they had implantable cardioverter defibrillators or permanent pacemakers. Radiofrequency energy was used for ablation in all cases and heparin was administered with goal-activated clotting times of 300 to 400 seconds for all LV procedures. Pre- and postprocedural brain MRI was performed on each patient within a week of the ablation procedure. Embolic infarcts were defined as new foci of reduced diffusion and high signal intensity on fluid-attenuated inversion recovery brain MRI within a vascular distribution. Results: The mean age was 58 years, half of the patients were men, half had a history of hypertension, and the majority had no known vascular disease or heart failure. LV ablation was performed in 12 patients (ventricular tachycardia, n=2; PVC, n=10) and right ventricular ablation was performed exclusively in 6 patients (ventricular tachycardia, n=1; PVC, n=5). Seven patients (58%) undergoing LV ablation experienced a total of 16 cerebral emboli, in comparison with zero patients undergoing right ventricular ablation (P=0.04). Seven of 11 patients (63%) undergoing a retrograde approach to the LV developed at least 1 new brain lesion. Conclusions: More than half of patients undergoing routine LV ablation procedures (predominately PVC ablations) experienced new brain emboli after the procedure. Future research is critical to understanding the long-term consequences of these lesions and to determining optimal strategies to avoid them.

Serial angiographic appearance of segmental arterial mediolysis manifesting as vertebral, internal mammary and intra-abdominal visceral artery aneurysms in a patient presenting with subarachnoid hemorrhage and review of the literature

Segmental arterial mediolysis (SAM) is a rare, non-inflammatory, non-atherosclerotic vasculopathy typically affecting the abdominal arteries although it may also affect the great vessels and cerebral vasculature. Diseased vessels manifest with aneurysms and/or dissections, often presenting clinically with catastrophic thromboembolic injury and less frequently with subarachnoid hemorrhage (SAH). The etiology of SAM remains indeterminate although there is evidence it may be an endogenous pathological response to vasospasm. The SAM literature is reviewed and a case of SAH related to a ruptured dissecting-type vertebral artery aneurysm is described. In addition to furthering awareness of SAM, this unique case offers insight into the acute phase of the disease and the potential role of vasospastic induction.

The manifestation of vortical and secondary flow in the cerebral venous outflow tract: An in vivo MR velocimetry study

Aberrations in flow in the cerebral venous outflow tract (CVOT) have been implicated as the cause of several pathologic conditions including idiopathic intracranial hypertension (IIH), multiple sclerosis (MS), and pulsatile tinnitus (PT). The advent of 4D flow magnetic resonance imaging (4D-flow MRI) has recently allowed researchers to evaluate blood flow patterns in the arterial structures with great success. We utilized similar imaging techniques and found several distinct flow characteristics in the CVOT of subjects with and without lumenal irregularities. We present the flow patterns of 8 out of 38 subjects who have varying heights of the internal jugular bulb and varying lumenal irregularities including stenosis and diverticulum. In the internal jugular vein (IJV) with an elevated jugular bulb (JB), 4Dflow MRI revealed a characteristic spiral flow that was dependent on the level of JB elevation. Vortical flow was also observed in the diverticula of the venous sinuses and IJV. The diversity of flow complexity in the CVOT illustrates the potential importance of hemodynamic investigations in elucidating venous pathologies.

How Patient Demographics, Imaging, and Beliefs Influence Tissue-Type Plasminogen Activator Use: A Survey of North American Neurologists.

Background and Purpose— Understanding physician decision making is increasingly recognized as an important topic of study, especially in stroke care. We sought to characterize the process of acute stroke decision making among neurologists in the United States and Canada from clinical and epistemological perspectives. Methods— Using a factorial design online survey, respondents were presented with clinical data to mimic an acute stroke encounter. The history, examination, computed tomographic (CT) scan, CT angiogram, and CT perfusion were presented in sequence, and respondents rated their diagnostic confidence and likelihood of treatment with tissue-type plasminogen activator after each element. Patient age, race, sex, and CT perfusion imaging results were randomized, whereas the rest of the clinical presentation was held constant. Results— We collected 715 responses, of which 473 (66%) were complete. Diagnostic certainty and likelihood of treatment with tissue-type plasminogen activator rose incrementally as additional clinical data were provided. Diagnostic certainty and treatment likelihood were strongly influenced by the clinical history and the CT scan. Other factors such as physicians’ personal beliefs or biases were not influential. Respondents’ accuracy in interpreting CT angiographic and CT perfusion images was variable and generally low. Conclusions— Diagnostic certainty and likelihood of treatment with tissue-type plasminogen activator increase with additional clinical data, with the history being the most important factor for diagnostic and treatment decisions. Respondents had difficulty in interpreting the results of CT perfusion scans although they had little impact on treatment decisions. We did not identify treatment bias based on patient age, race, or sex.

P-029 Turbulent Flow in the Venous Outflow Tract of Pulsatile Tinnitus Patients with Sigmoid Sinus Diverticulum

Introduction/purpose Pulsatile tinnitus (PT) has been linked to multiple anatomical variants of the venous outflow tract including sigmoid sinus diverticulum (SSD). We hypothesize that turbulence generated by the SSD, which is normally preceded by a transverse sinus stenosis (TSS), can explain the source of sound. Turbulent flow has a known association to vasculogenic bruit. Advanced magnetic resonance velocimetry (MRV) was performed in cerebral venous sinuses and internal jugular veins (IJV) to obtain both volumetric velocity and turbulence maps. Materials and methods A series of MRI protocols was performed at 3 T for patients with suspected venous PT including contrast-enhanced MRA (CE-MRA) to delineate the anatomy and identify SSD, 4 D-flow MR to acquire time-resolved phase (velocity) and flow-encoded magnitudes in all three directions, as well as 2 D flow to obtain flow waveforms. Flow turbulence was quantified based on turbulence kinetic energy (TKE). Five SSD patients were evaluated, four of which had an associated TSS upstream from the SSD. Results The TSS resulted in a jet of flow, the direction of which seemed to determine the position of the SSD downstream. The streamline visualization of the flow patterns revealed recirculation in the diverticulum. A helical flow pattern was also found adjacent to the jet flow opposite and downstream of the SSD (Figure 1). TKE mapping revealed a highly localized region of elevated TKE downstream from the stenosis extending to the opening of the diverticulum with a maximum value of 80 J/m3 (Figure 2).Abstract P-029 Figure 1 A tilted anterior-posterior projection of the venous sinuses and IJV in a PT patient with the SSD and upstream TSS.MRV-based streamlines colored by the magnitude of the velocity are overlaid on to the geometry captured by CE-MRA (black)Abstract P-029 Figure 2 MRV-based measurement of the TKE in the same PT patient as shown in Figure 1. The elevated TKE region is highly localized to the downstream of the stenosis and extends into the opening of the diverticulum Discussion and Conclusion The unique flow patterns and the presence of turbulence introduced by the TSS and SSD may help explain PT in these patients. Treatment of TSS with PTA and stent implantation, or treatment of the SSD with coil embolization can potentially alter the TKE level and pattern. Disclosures S. Kefayati: None. E. Kao: None. J. Liu: None. H. Haraldsson: None. F. Faraji: None. M. Ballweber: None. K. Meisel: None. V. Halbach: None. D. Saloner: None. M. Amans: None.

Survival, Functional Status, and Eating Ability After Percutaneous Endoscopic Gastrostomy Tube Placement for Acute Stroke

To determine the long‐term survival and independence of individuals with stroke and percutaneous endoscopic gastrostomy (PEG) tube placement.

Arteriovenous fistula after ventriculostomy in aneurysmal subarachnoid hemorrhage

A 66-year-old woman was found unresponsive after complaining of severe headache several days prior. She was comatose upon initial evaluation and a cranial CT revealed diffuse subarachnoid hemorrhage. A right posterior communicating artery aneurysm (figure, A, arrow) was successfully treated with endovascular embolization. Conventional angiography performed 7 days following ventriculostomy placement for hydrocephalus demonstrated interval development of a traumatic arteriovenous fistula (AVF) filling by the middle meningeal artery (figure, C and D, arrows). The AVF was treated with intra-arterial embolization. Ventriculostomy-associated AVF has rarely been reported.1 Outcomes of untreated iatrogenic AVF are unknown, but could lead to hemorrhagic complications.

O-032 Venous Blood Flow Visualization in Sigmoid Sinus Diverticulum Using MRI

Introduction/purpose Sigmoid sinus diverticulum (SSD) is one of the potentially treatable causes of pulsatile tinnitus (PT). How SSD causes PT is unknown, but it is thought to be secondary to aberrant blood flow in the diverticulum or parent sinus. We performed velocity field mapping using MR 4 D Flow (MRV) and computational fluid dynamics (CFD) in cerebral venous sinuses and internal jugular veins (IJV). We aim to determine if a distinct blood flow pattern may be responsible for PT in SSD. Materials and methods Patients suspected of venous etiology of PT underwent MRI at 3 T, using contrast-enhanced MRA (timed to venous phase), MRV and CFD. SSD was confirmed on MRA. Flow pathlines were evaluated. In patients with confirmed SSD, additional CFD modelling was performed with the SSD excluded from the models. Results Nineteen patients with suspected venous etiology of PT and 10 controls were evaluated. Six (31.5%) had SSD and five of these had transverse sinus stenosis upstream from the SSD. These five patients also demonstrated a unique pattern of flow not seen in the controls characterized by: 1. High velocity flow jet in an up-stream stenosis in the transverse sinus directed at the SSD opening, 2. Flow jet into the SSD along the long axis of the SSD, either anteriorly or laterally directed, 3. Vortex of flow in the SSD, 4. Prominent vortex component of flow in the sigmoid sinus downstream from SSD, 5. Vortex of flow in the jugular bulb Three of the patients had simulated post-coil treatment models developed excluding the SSD from the models. CFD showed no flow in SSD and decreased vortex component of flow in the sigmoid sinus downstream from the SSD. Conclusion PT caused by SSD may be caused by a unique flow pattern in the SSD and sinuses as visualized on both MRV and CFD.Abstract O-032 Figure 1 Townes projection CFD analysis of a patient with a left SSD and an upstream stenosis in the transverse sinus. The pretreatment analysis (A) shows a jet of flow from the stenosis into the SSD (arrow), vortex of flow in the SSD (double arrow), and a vortex component of flow in the sigmoid sinus down-stream from the SSD (arrow head). The post-treatment model (B) shows absence of the flow in the SSD as well as decreased vortex component of flow in down-stream sigmoid sinus Disclosures M. Amans: None. E. Kao: None. S. Kefayati: None. K. Meisel: None. F. Faraji: None. C. Glastonbury: None. M. Ballweber: None. V. Halbach: None. D. Saloner: None.

P-024 Prominent Condylar Veins Causing Pulsatile Tinnitus: Dynamic Angiographic Confirmation

Introduction/purpose Numerous processes can cause pulsatile tinnitus (PT), some of which are potentially life threatening. This case series describes a cause of PT – prominent condylar veins – that has undergone little investigation to date. This report characterizes angiographic findings in patients with prominent condylar veins and means to localize symptoms to these structures using dynamic angiography with head positioning and venous balloon test occlusion. Materials and methods Retrospective analysis was performed under IRB approved protocol for 43 consecutive PT patients referred for diagnostic angiography at a major academic medical center between January 2013 and December 2015. Rates of different etiologies of PT among patients in this group were noted. In addition to standard diagnostic cervicocerebral angiography, dynamic angiography with head turning was conducted. The effects of provocative maneuvers were measured using time-resolved flow analysis known (iFlow, Siemens Healthcare, Erlangen Germany). Results 5 (11.6%) patients were found to have prominent condylar veins. 16 (37.2%) had a dAVF, 4 (9.3%) had a venous diverticulum, and 9 (20.9%) had no angiographic abnormality detected. The findings of the five patients with prominent condylar veins are summarized in the table. Representative images are provided in the figure.Abstract P024 Figure 1Abstract P024 Table 2 Conclusion Prominent flow in condylar veins should be considered among the numerous causes of PT. This may be a frequent cause of these symptoms in patients who previously would have had no identifiable cause Further investigation is warranted with respect to this cause of PT and PT in general. Disclosures M. Alexander: None. K. Meisel: None. V. Halbach: None. R. Darflinger: None. A. Nicholson: None. F. Settecase: None. D. Cooke: None. R. Higashida: None. C. Dowd: None. S. Hetts: None. M. Amans: None.