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The Gore conformable TAG thoracic endoprosthesis (CTAG) was engineered to enhance conformability in the thoracic aorta and has demonstrated greater deployment accuracy and wall apposition than the original TAG device. The Food and Drug Administration approved the CTAG in 2011 based on the 1-year results of the pivotal trial for the CTAG device. In the present report, we have documented the outcomes for those patients through 5 years. The CTAG aneurysm study was a prospective, multicenter trial that assessed the safety and effectiveness of the CTAG device as treatment of descending thoracic aortic aneurysms. Follow-up imaging assessments consisted of radiographs and computed tomography at annual intervals through 5 years. A core imaging laboratory was used to assess the aneurysm size, device integrity, and endoleaks. A total of 66 patients were enrolled (51 pivotal arm patients and 15 continued access patients) from October 2009 through September 2011. The baseline characteristics, procedural characteristics, and outcomes through 2 years were reported previously. Through 5 years, five patients (7.6%) had required device-related reintervention (one type Ia endoleak or contained rupture of the descending thoracic aorta, one type Ib endoleak, two indeterminate endoleaks, and one thoracic aortic pseudoaneurysm). Four patients (6.1%) had died of aneurysm-related causes, with one death occurring within 30 days of the index procedure. A total of 24 patients (36.3%) had died during the 5-year study period. Seven patients (10.6%) had experienced stroke or transient ischemic attack through 5 years, with one early stroke (postoperative day 28). Prosthesis or intercomponent migration was observed in six patients (9.1%) through 5 years; however, no patient had developed a type III junctional endoleak. No stent-graft fracture or compression was observed through 5 years. At 5 years, 14 patients (50.0%) showed sac regression, 5 (17.9%) showed sac expansion, and 9 (32.1%) showed sac stability using on a 5-mm threshold for change. Thoracic endovascular aortic repair with the CTAG device was associated with low rates of aneurysm-related mortality and reintervention through 5 years. Proximal endoleak was rare, and most patients showed sac regression or stability at 5 years after the initial thoracic endovascular aortic repair. [ABSTRACT FROM AUTHOR]

Abstract: Background: The extent to which low medication adherence in hypertensive individuals contributes to disparities in stroke and transient ischemic attack (TIA) risk is poorly understood. Methods: Investigators examined the relationship between self-reported medication adherence and blood pressure (BP) control (<140/90 mm Hg), Framingham Stroke Risk Score, and physician-adjudicated stroke/TIA incidence in treated hypertensive subjects (n = 15,071; 51% black; 57% in Stroke Belt) over 4.9 years in the national population-based REGARDS cohort study. Results: Mean systolic BP varied from 130.8 ± 16.2 mm Hg in those reporting high adherence to 137.8 ± 19.5 mm Hg in those reporting low adherence (P for trend < .0001). In logistic regression models, each level of worsening medication adherence was associated with significant and increasing odds of inadequately controlled BP (≥140/90 mm Hg; score = 1, odds ratio [95% confidence interval], 1.20 [1.09–1.30]; score = 2, 1.27 [1.08–1.49]; score = 3 or 4, 2.21 [1.75–2.78]). In hazard models using systolic BP as a mediator, those reporting low medication adherence had 1.08 (1.04–1.14) times greater risk of stroke and 1.08 (1.03–1.12) times greater risk of stroke or TIA. Conclusion: Low medication adherence was associated with inadequate BP control and an increased risk of incident stroke or TIA. [Copyright &y& Elsevier]

Background: To determine, among employed persons with low risk for obstructive sleep apnea (OSA), if sleep duration is associated with incident stroke symptoms, independent of body mass index (BMI), and if sleep duration mediates racial differences in stroke symptoms. Methods: In 2008, 5666 employed participants (US blacks and whites, ≥45 years) from the longitudinal and nationally representative Reasons for Geographic And Racial Differences in Stroke study self-reported their average sleep duration. Participants had no history of stroke, transient ischemic attack, or stroke symptoms and were at low risk for OSA. After the sleep assessment, self-reported stroke symptoms were collected at 6-month intervals, up to 3 years (M = 751 days). Interval-censored, parametric survival models were conducted to estimate hazard ratios predicting time from sleep duration measurement (<6, 6-6.9, 7-7.9 [reference], 8-8.9, ≥9 hours) to first stroke symptom. Adjusted models included demographics, stroke risk factors, psychological symptoms, health behaviors, and diet. Results: During follow-up, 224 participants reported 1 or more stroke symptoms. In the unadjusted model, short sleep (<6 hours) significantly predicted increased risk of stroke symptoms but not in adjusted models. Stratification by BMI revealed a significant association between short sleep duration and stroke symptoms only for normal BMI persons in unadjusted (hazard ratio: 2.93, 95% confidence interval: 1.38-6.22) and fully adjusted models (hazard ratio: 4.19, 95% confidence interval: 1.62-10.84). The mediating effect of sleep duration on the relationship between race and stroke symptoms was borderline significant in normal weight participants. Conclusions: Among middle-aged to older employed individuals of normal weight and low risk of OSA, self-reported short sleep duration is prospectively associated with increased risk of stroke symptoms. [Copyright &y& Elsevier]