Dural Arteriovenous Fistulas With Cognitive Impairment: Angiographic Characteristics and Treatment Outcomes.

BACKGROUND AND OBJECTIVES: Anecdotal cases of rapidly progressing dementia in patients with dural arteriovenous fistulas (dAVFs) have been reported in small series. However, large series have not characterized these dAVFs. We conducted an analysis of the largest cohort of dAVFs presenting with cognitive impairment (dAVFs-CI), aiming to provide a detailed characterization of this subset of dAVFs. METHODS: Patients with dAVFs-CI were analyzed from the CONDOR Consortium, a multicenter repository comprising 1077 dAVFs. A propensity score matching analysis was conducted to compare dAVFs-CI with Borden type II and type III dAVFs without cognitive impairment (controls). Logistic regression was used to identify angiographic characteristics specific to dAVFs-CI. Furthermore, post-treatment outcomes were analyzed. RESULTS: A total of 60 patients with dAVFs-CI and 60 control dAVFs were included. Outflow obstruction leading to venous hypertension was observed in all dAVFs-CI. Sinus stenosis was significantly associated with dAVFs-CI (OR 2.85, 95% CI: 1.16-7.55, P = .027). dAVFs-CI were more likely to have a higher number of arterial feeders (OR 1.56, 95% CI 1.22-2.05, P < .001) and draining veins (OR 2.05, 95% CI 1.05-4.46, P = .004). Venous ectasia increased the risk of dAVFs-CI (OR 2.38, 95% CI 1.13-5.11, P = .024). A trend toward achieving asymptomatic status at follow-up was observed in patients with successful closure of dAVFs (OR 2.86, 95% CI 0.85-9.56, P = .09). CONCLUSION: Venous hypertension is a key angiographic feature of dAVFs-CI. Moreover, these fistulas present at a mean age of 58 years-old, and exhibit a complex angioarchitecture characterized by an increased number of arteriovenous connections and stenosed sinuses. The presence of venous ectasia further exacerbates the impaired drainage and contributes to the development of dAVFs-CI. Notably, in certain cases, closure of the dAVF has the potential to reverse symptoms.

Cigarette smoking and outcomes after aneurysmal subarachnoid hemorrhage: a nationwide analysis.

OBJECTIVE Although cigarette smoking is one of the strongest risk factors for cerebral aneurysm development and rupture, there are limited data evaluating the impact of smoking on outcomes after aneurysmal subarachnoid hemorrhage (SAH). Additionally, two recent studies suggested that nicotine replacement therapy was associated with improved neurological outcomes among smokers who had sustained an SAH compared with smokers who did not receive nicotine. METHODS Patients who underwent endovascular or microsurgical repair of a ruptured cerebral aneurysm were extracted from the Nationwide Inpatient Sample (NIS, 2009-2011) and stratified by cigarette smoking. Multivariable logistic regression analyzed in-hospital mortality, complications, tracheostomy or gastrostomy placement, and discharge to institutional care (a nursing or an extended care facility). Additionally, the composite NIS-SAH outcome measure (based on mortality, tracheostomy or gastrostomy, and discharge disposition) was evaluated, which has been shown to have excellent agreement with a modified Rankin Scale score greater than 3. Covariates included in regression constructs were patient age, sex, race/ethnicity, insurance status, socioeconomic status, comorbidities (including hypertension, drug and alcohol abuse), the NIS-SAH severity scale (previously validated against the Hunt and Hess grade), treatment modality used for aneurysm repair, and hospital characteristics. A sensitivity analysis was performed matching smokers to nonsmokers on age, sex, number of comorbidities, and NIS-SAH severity scale score. RESULTS Among the 5784 admissions evaluated, 37.1% (n = 2148) had a diagnosis of tobacco use, of which 31.1% (n = 1800) were current and 6.0% (n = 348) prior tobacco users. Smokers were significantly younger (mean age 51.4 vs 56.2 years) and had more comorbidities compared with nonsmokers (p < 0.001). There were no significant differences in mortality, total complications, or neurological complications by smoking status. However, compared with nonsmokers, smokers had significantly decreased adjusted odds of tracheostomy or gastrostomy placement (11.9% vs 22.7%, odds ratio [OR] 0.63, 95% confidence interval [CI] 0.51-0.78, p < 0.001), discharge to institutional care (OR 0.71, 95% CI 0.57-0.89, p = 0.002), and a poor outcome (OR 0.65, 95% CI 0.55-0.77, p < 0.001). Similar statistical associations were noted in the matched-pairs sensitivity analysis and in a subgroup of poor-grade patients (the upper quartile of the NIS-SAH severity scale). CONCLUSIONS In this nationwide study, smokers experienced SAH at a younger age and had a greater number of comorbidities compared with nonsmokers, highlighting the negative ramifications of cigarette smoking among patients with cerebral aneurysms. However, smoking was also associated with paradoxical superior outcomes on some measures, and future research to confirm and further understand the basis of this relationship is needed.

Role of Genetic Polymorphisms in Predicting Delayed Cerebral Ischemia and Radiographic Vasospasm After Aneurysmal Subarachnoid Hemorrhage: A Meta-Analysis.

OBJECTIVE: The pathophysiology on cerebral vasospasm and delayed cerebral ischemia (DCI) remains poorly understood. Much research has been dedicated to finding genetic loci associated with vasospasm and ischemia. We present a systematic review and meta-analysis to identify genetic polymorphisms associated with delayed ischemic neurologic deficit (DIND), radiographic infarction attributed to ischemia, and radiographic vasospasm. METHODS: PubMed, the Cochrane Library, and Excerpta Medica dataBASE (EMBASE) databases were used to identify relevant studies published up to March 2015 containing the subject terms cerebral or intracranial vasospasm and DCI in combination with genetics, gene, polymorphism or marker. Meta-analyses were performed using a random-effects model to calculate summary odds ratio (ORs) and 95% confidence intervals for each respective gene. RESULTS: Of 269 articles initially identified, 20 studies with 1670 patients were included in our comprehensive review, including 27 polymorphisms in 11 genes. The following 6 polymorphisms in 3 genes were selected for subsequent meta-analyses: apolipoprotein E (ApoE2, E4); endothelial nitric oxide (eNOS T786C, VNTR intron 4 a/b, G894T); and haptoglobin (Hp) 1/2 phenotypes. The eNOS VNTR a allele was associated with DIND (a vs. b allele: OR 1.92 [1.31-2.81], padj = 0.008). The Hp 2-2 allele was associated with radiographic vasospasm (2-2 vs. 2-1 and 1-1: OR 3.86 [1.86-8.03], padj = 0.003) but did not reach significance for DIND. CONCLUSIONS: This is the first systemic review and meta-analysis to study and evaluate the associations between genetic polymorphism with DCI and radiographic vasospasm independently. In our study, eNOS VNTR and Hp polymorphisms appear to have the strongest associations with DIND and radiographic vasospasm, respectively.

Neurogenic Stress Cardiomyopathy After Aneurysmal Subarachnoid Hemorrhage.

BACKGROUND: Neurogenic stress cardiomyopathy (NSC) is a known complication of aneurysmal subarachnoid hemorrhage (SAH). Detailed analyses of risk factors for its occurrence across large cohorts are relatively sparse. METHODS: A consecutive group of 300 patients with aneurysmal SAH was reviewed for the presence of markers of myocardial injury, including electrocardiogram changes (long QT, T-wave inversion), elevated plasma troponin levels (≥0.1), and echocardiogram findings (decreased ejection fraction and wall motion abnormalities). NSC was defined as the presence of at least 1 marker of myocardial injury. Univariate and multivariate analyses were conducted to assess the correlation of NSC and individual markers of myocardial injury with age, gender, medical comorbidities, medications, current smoking status, Hunt-Hess grade, and Fisher grade. Medical comorbidities were assessed based on reported medical history or reported use of comorbidity-specific medications at the time of presentation. RESULTS: Across the cohort, 27% of patients had a plasma troponin elevation of at least 0.1; 13%, a prolonged QT interval; 16%, new T-wave inversions; 18%, a depressed ejection fraction (<55%); and 15%, echocardiographic wall motion abnormalities. After a multivariate analysis, significant risk factors for NSC included higher Hunt-Hess grade on presentation (odds ratio [OR] = 2.33, P = 4.52 × 10(-6)), current smoking status (OR = 2.00, P = 0.030), and older age (OR = 1.03, P = 0.048). Hypertension was protective against NSC (OR = 0.48, P = 0.031). Patient gender, hyperlipidemia, diabetes, coronary artery disease, statin use, beta blocker use, angiotensin-converting enzyme inhibitor use, aspirin use, and thicker SAH (Fisher grade 3) were not significant risk factors for NSC. CONCLUSIONS: Higher Hunt-Hess grade, current smoking status, lack of hypertension, and older age were the strongest predictors of NSC.

Treatment modality and vasospasm after aneurysmal subarachnoid hemorrhage.

OBJECTIVE: Vasospasm is the leading source of neurological morbidity after aneurysmal subarachnoid hemorrhage. Our objective was to evaluate the impact of treatment modality on vasospasm, delayed cerebral infarction, and clinical deterioration caused by delayed cerebral ischemia (CD-DCI). METHODS: We reviewed an institutional cohort, comparing rates of vasospasm, delayed cerebral infarction, and CD-DCI between patients managed with only microsurgical clipping and those treated with only endovascular coiling within 72 hours of rupture. Age, sex, smoking status, Hunt-Hess grade, and Fisher grade were adjusted for in a multivariate regression model. RESULTS: Two hundred three patients were treated with clipping and 52 with coiling. There was no significant difference in patient age, sex, smoking status, aneurysm location, and presenting clinical (Hunt-Hess) and radiographic (Fisher) grade between these two groups. Sixty-percent of patients had moderate or severe vasospasm after clipping compared with 38% after coiling (Multivariate odds ratio [OR] 2.32, 95% confidence interval [95% CI] 1.21-4.47, P = 0.01). Clipping was associated with a greater number of territories with vasospasm (mean of 3.1 vs. 2.3, P = 0.03 after multivariate analysis). Delayed radiographic cerebral infarction was more common in the clipping group (17% vs. 6%, multivariate OR 3.66, 95% CI 1.06-12.71, P = 0.04). For CD-DCI, a trend was seen as 16% of patients treated with clipping had CD-DCI compared with 6% of patients treated with coiling (multivariate OR 3.11, 95% CI 0.89-10.86, P = 0.07). CONCLUSION: We demonstrate significantly lower rates of vasospasm and delayed infarction after endovascular coiling of ruptured aneurysms.

Aspirin and aneurysmal subarachnoid hemorrhage.

OBJECTIVE: Recent evidence has suggested a potential beneficial effect of aspirin on the risk of aneurysm rupture. This benefit must be weighed against its potential adverse effects as an antiplatelet agent in the setting of acute aneurysmal subarachnoid hemorrhage (SAH). METHODS: A total of 747 consecutive patients with cerebral aneurysms were reviewed, comparing demographics, aneurysm features, presenting clinical and radiographic grades, vasospasm, and outcome at 1 year between patients with aneurysmal SAH taking aspirin on presentation and those who were not. RESULTS: The rate of hemorrhagic presentation was significantly greater in patients not taking aspirin (40% vs. 28%; P = 0.016). Among 274 patients presenting with aneurysmal SAH, there was no significant difference in presenting clinical (Hunt and Hess) and radiographic (Fisher) grade between patients taking aspirin and those who were not. There was also no significant difference in the rate of subsequent angiographic and delayed cerebral ischemia. Multivariate analysis of outcome at 1 year found only increasing age (odds ratio [OR] 1.07, 95% confidence interval [CI] 1.04-1.12), Hunt and Hess grade (OR 3.01, 95% CI 1.81-5.03), and associated hypertension (OR 3.30, 95% CI 1.39-7.81) to be statistically significant risk factors for poor outcome (death or dependence), whereas aspirin use was not associated with poor outcome (OR 1.19, 95% CI 0.35-4.09; P = 0.78). CONCLUSIONS: In the present study, patients taking aspirin had a lower rate of hemorrhagic presentation. In addition, taking aspirin did not adversely impact presenting clinical grade or radiographic grade, vasospasm, and outcome in the setting of aneurysmal SAH.