BackgroundAtrial fibrillation is associated with higher mortality. Identification of causes of death and contemporary risk factors for all‐cause mortality may guide interventions.Methods and ResultsIn the Rivaroxaban Once Daily Oral Direct Factor Xa Inhibition Compared with Vitamin K Antagonism for Prevention of Stroke and Embolism Trial in Atrial Fibrillation (ROCKET AF) study, patients with nonvalvular atrial fibrillation were randomized to rivaroxaban or dose‐adjusted warfarin. Cox proportional hazards regression with backward elimination identified factors at randomization that were independently associated with all‐cause mortality in the 14 171 participants in the intention‐to‐treat population. The median age was 73 years, and the mean CHADS 2 score was 3.5. Over 1.9 years of median follow‐up, 1214 (8.6%) patients died. Kaplan–Meier mortality rates were 4.2% at 1 year and 8.9% at 2 years. The majority of classified deaths (1081) were cardiovascular (72%), whereas only 6% were nonhemorrhagic stroke or systemic embolism. No significant difference in all‐cause mortality was observed between the rivaroxaban and warfarin arms (P=0.15). Heart failure (hazard ratio 1.51, 95% CI 1.33–1.70, P<0.0001) and age ≥75 years (hazard ratio 1.69, 95% CI 1.51–1.90, P<0.0001) were associated with higher all‐cause mortality. Multiple additional characteristics were independently associated with higher mortality, with decreasing creatinine clearance, chronic obstructive pulmonary disease, male sex, peripheral vascular disease, and diabetes being among the most strongly associated (model C‐index 0.677).ConclusionsIn a large population of patients anticoagulated for nonvalvular atrial fibrillation, ≈7 in 10 deaths were cardiovascular, whereas <1 in 10 deaths were caused by nonhemorrhagic stroke or systemic embolism. Optimal prevention and treatment of heart failure, renal impairment, chronic obstructive pulmonary disease, and diabetes may improve survival.Clinical Trial Registration URL: https://www.clinicaltrials.gov/. Unique identifier: NCT00403767.
Introduction Despite the availability of prevention and therapies of stroke, their implementation in clinical practice, even of low-cost ones, remains poor. In 2015, the European Stroke Organisation (ESO) initiated the ESO Enhancing and Accelerating Stroke Treatment (EAST) program, which aims to improve stroke care quality, primarily in Eastern Europe. Here, we describe its methods and milestones. Patients and methods The ESO EAST program is using an implementation strategy based on a ‘detecting-understanding-reducing disparities’ conceptual framework: stroke care quality is first measured (after developing a platform for data collection), gaps are identified in the current service delivery, and ultimately feedback is provided to participating hospitals, followed by the application of interventions to reduce disparities. The ESO EAST program is carried out by establishing a stroke quality registry, stroke management infrastructure, and creating education and training opportunities for healthcare professionals. Results Program management and leadership infrastructure has been established in 19 countries (Country Representatives in 22 countries, National Steering Committee in 19 countries). A software platform for data collection and analysis: Registry of Stroke Care Quality was developed, and launched in 2016, and has been used to collect data from over 90,000 patients from >750 hospitals and 56 countries between September 2016 and May 2019. Training in thrombolysis, nursing and research skills has been initiated. Discussion ESO EAST is the first pan-Eastern European (and beyond) multifaceted quality improvement intervention putting evidence-informed policies into practice. Continuous monitoring of stroke care quality allows hospital-to-hospital and country-to-country benchmarking and identification of the gaps and needs in health care.
A multicenter clinical trial was performed to compare the efficacy and safety of Ginkgo biloba extract EGb 761 and betahistine at recommended doses in patients with vertigo. One hundred and sixty patients (mean age 58 years) were randomly assigned to double-blind treatment with EGb 761 (240 mg per day) or betahistine (32 mg per day) for 12 weeks. An 11-point numeric analogue scale, the Vertigo Symptom Scale—short form, the Clinical Global Impression Scales and the Sheehan Disability Scale were used as outcome measures. Both treatment groups were comparable at baseline and improved in all outcome measures during the course of treatment. There was no significant intergroup difference with regard to changes in any outcome measure. Numerically, improvements of patients receiving EGb 761 were slightly more pronounced on all scales. Clinical global impression was rated “very much improved” or “much improved” in 79% of patients treated with EGb 761 and in 70% receiving betahistine. With 27 adverse events in 19 patients, EGb 761 showed better tolerability than betahistine with 39 adverse events in 31 patients. In conclusion, the two drugs were similarly effective in the treatment of vertigo, but EGb 761 was better tolerated. This trial is registered with controlled-trials.com ISRCTN02262139.
Резюме. Статтю присвячено дослідженню ймовірності розвитку церебральної атрофії (ЦА) за МРТ Ключові слова: хвороба малих судин мозку; церебральна атрофія; маркери ВступХвороба малих судин (ХМС) мозку є захворюван-ням, що притаманне капілярам і малим перфоруючим артеріолам [1]. Навіть за відсутності судинної пато-логії, що фізично обмежує церебральний кровотік, капілярна дисфункція є джерелом інсультоподібної симптоматики та нейродегенерації [2, 3]. У подальшо-му морфоструктурні зміни мозку у пацієнтів з ХМС мозку призводять до погіршення фізичного стану хворих, зниження когнітивних функцій та якості життя. На думку деяких авторів, найбільш ефективним підходом у встановленні ймовірності церебральної атрофії (ЦА) при ХМС мозку є визначення зв'язку між нею та маркерами ХМС мозку [4][5][6][7][8]. Однак на цей час через розбіжності у дизайні та методах оцінки [4] погляди дослідників на зв'язок ХМС мозку з морфо-структурними змінами дуже різняться. Деякі автори розглядають ХМС мозку як чинник ризику церебраль-ної атрофії, але при цьому не пов'язують атрофічні зміни з тяжкістю ХМС мозку [5], а деякі дослідники, навпаки, вважають, що тяжкість ХМС мозку є тісно пов'язаною з ЦА, і саме патерн ЦА відрізняє тяжкість цієї хвороби від старіння та може бути предиктором кількісної оцінки тяжкості загального бала за ХМС мозку [6,7]. Також існує думка, що ЦА є не лише асоційованою з ХМС мозку, а може розглядатися по-ряд з асимптомними ураженнями мозку як ознака цієї хвороби [8]. Однією з причин розбіжностей у поглядах на зв'язок між ЦА і ХМС мозку та її тяжкістю може бути надання переваги лише або типу маркерів ХМС мозку, або їх кількості [4][5][6][7][8]. Чітке визначення ризику ЦА при ХМС мозку за маркерами останньої потребує комплексного підходу з урахуванням одночасно якіс-них і кількісних ознак хвороби, за допомогою якого було б можливим визначення предикативної цінності як окремих маркерів, так і різних їх комбінацій.
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