Background and Purpose— Carotid web (CW) is a rare form of focal fibromuscular dysplasia defined as an abnormal shelf-like projection of intimal fibrous tissue into the carotid bulb. It is theorized that CW leads to ischemic stroke secondary to blood flow stasis and subsequent embolization. The natural history and optimal management of CW are unclear. To address this knowledge gap, we performed a systematic literature review (SLR) of CW. Methods— Our librarians performed a SLR for CW and related terminology. Patient-level demographics, stroke risk factors, neuroimaging findings, stroke recurrence or stroke free-duration, and treatment modality were extracted. We used descriptive statistics to characterize our results. When specific patient-level metrics were not reported, the denominators for reporting percentage calculations were adjusted accordingly. Results— Our literature search produced 1150 articles. Thirty-seven articles including 158 patients (median age 46 years [range 16–85], 68% women, 76% symptomatic) met entry criteria and were included in our SLR. Of the symptomatic CW patients: 57% did not have stroke risk factors, 56% who received medical therapy had recurrent stroke (median 12 months, range 0–97), and 72% were ultimately treated with carotid revascularization (50% carotid stenting, 50% carotid endarterectomy). There were no periprocedural complications or recurrent strokes in carotid revascularization patients. Conclusions— CW leads to ischemic stroke in younger patients without conventional stroke risk factors. We found a high stroke recurrence rate in medically managed symptomatic CW patients, whereas carotid revascularization effectively prevented recurrent stroke. Our findings should be interpreted with caution because of risk of publication and reporting bias.
and the Cochrane Library through Wiley (ending December 15, 2017). Key findings: Of 160 patients with carotid webs, 135 (84%) were symptomatic and 24 (15%) were asymptomatic (1 could not be classified). Twenty-six patients (22%) had bilateral carotid webs. Regarding symptomatic patients, the median age was 46 years, 70% were black, 67% were women, and the majority (84%) had <50% internal carotid artery stenosis. Forty-seven (28%) symptomatic patients were managed medically (91% with antiplatelet agents); more than half of these patients (56%) suffered recurrent strokes distal to the carotid web during follow-up (median, 12 months; range, 0-97 months). Treatment of the other 70 (72%) symptomatic patients was equally divided between carotid endarterectomy and carotid stenting (CAS), and there were no complications.Conclusion: Carotid webs lead to ischemic stroke in younger patients with a high stroke recurrence rate in medically managed symptomatic patients, whereas carotid endarterectomy and CAS effectively prevented recurrent stroke.Commentary: A carotid web is also known as atypical focal carotid bulb fibromuscular dysplasia (FMD). It is defined as an intraluminal filling defect of the posterolateral wall of the most proximal part of the internal carotid artery. This atypical pathologic process is different from the classic "string of beads" seen in medial FMD. The underlying mechanism of stroke in carotid web patients is thought to be due to turbulent flow and stasis just distal to the web, resulting in thrombus and embolus.This study reported that more than half of patients with symptomatic carotid webs who were treated medically (primarily antiplatelet agents) had recurrent strokes. I find three aspects of this report intriguing (or defying belief, in other words). First, the large majority of symptomatic carotid web patients had only mild stenosis, which does not make a lot of sense. Why should lesser degrees of stenosis be associated with more thrombus beyond the web? Second, why did these patients undergo CAS and not plain old carotid balloon angioplasty, which is the recommended treatment for most patients with classic symptomatic FMD despite antiplatelet administration? Third, the authors recommend that patients with carotid web who had a stroke should be treated with CAS because antiplatelet agents did not prevent future strokes in half the patients. However, currently, antiplatelet agents are recommended as first-line treatment of patients with symptomatic carotid FMD, not carotid balloon angioplasty or CAS. Again, it does not make sense why a single web should be treated more aggressively than multiple "webs" or defects found in classic carotid FMD.The law of natural selection: Complex open aortic aneurysm repairs will more commonly be performed at high-volume centersdwithout the need for regulation Hospital Volume Matters: The Volume-Outcome Relationship in Open Juxtarenal AAA Repair O'Donnell TF, Boitano LT, Deery SE, Lancaster RT, Siracuse JJ, Schermerhorn ML, et al. Ann Surg 2018 Nov 29. [Epub ahe...
Ischemic strokes most often occur between 6 AM and 12 AM after awakening from sleep but up to 30% occur during sleep. Wake-up strokes (WUS) are new focal neurological deficit(s) persisting for $ 24 hours attributable to an ischemic event present on patient awakening. Obstructive sleep apnea (OSA) is a major risk factor for WUS because it compounds the instability of the morning environment and increases the likelihood of cardiovascular events, including hypertension, atrial fibrillation, right-to-left shunts, and stroke. Circadian-driven alterations in structural, homeostatic, and serological factors also predispose to WUS. Also, WUS patients are often not considered candidates for time-dependent intravenous thrombolysis therapy because of an uncertain onset time. However, using the tissue clock (positive diffusion weighted imaging-negative fluidattenuated inversion recovery mismatch) dates the WUS as 3 to 4.5 hours old and permits consideration for intravenous thrombolysis and if needed mechanical thrombectomy. Given the high prevalence of moderate/severe OSA in stroke patients and its impact on stroke outcomes, screening with overnight pulse oximetry and home sleep apnea test is needed. Treating OSA poststroke remains challenging. Polysomnographic changes in sleep architecture following acute/subacute stroke may also impact upon stroke outcome.
Introduction: Carotid Web (CW) is a rare form of focal fibromuscular dysplasia that results in an abnormal shelf-like projection of intimal fibrous tissue into the carotid bulb. It is theorized that CW leads to ischemic stroke secondary to blood flow stasis and subsequent embolization. There is uncertainty in diagnosis, prognosis, and optimal management of this uncommon entity. To address this knowledge gap, we performed a systematic literature review (SLR) of CW. Methods: Our literature search for CW and related terms yielded 1017 results. After a preliminary assessment of all 1017 retrieved manuscripts; 72 manuscripts were reviewed in detail. A total of 31 manuscripts met entry criteria and were included in our SLR. We present the demographics, cardiovascular (CV) risk factors, neuroimaging findings, stroke recurrence or stroke free-duration, and treatment modality of CW patients. Results: Our SLR resulted in 104 patients with CW, (median age at presentation: 45.7 [IQR 45-57], 52.3% female). The majority (68.3%) of CW patients did not have CV risk factors, however, 22.2% of patients were smokers. 47.8% of patients suffered recurrent stroke. The majority of patients were ultimately treated with antiplatelet therapy (94.4%) and 21.2% underwent carotid revascularization (4.8% carotid stenting, 16.3% carotid endarterectomy). None of the patients who underwent revascularization had a reported stroke recurrence. See Table. Conclusions: CW is a rare disease leading to ischemic stroke in younger patients without typical CV risk factors. CW patients in our SLR were at extremely high risk for recurrent stroke (47.8%). Aggressive secondary stroke prevention measures are indicated in this patient population, however, the optimal treatment strategies remain unclear. Carotid revascularization may be the definitive treatment for certain patients with CW, but further studies are needed as incomplete reporting and potential publication bias limit our findings.
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