Antikoagülan Tedavi Alan Non-valvüler Atriyal Fibrilasyon Hastalarında Nöron Spesifik Enolaz ile Tespit Edilen Sessiz Serebral İnfarkt
Amaç: Atriyal fibrilasyonu (AF) olan hastalarda serebral infarkt, klinik olarak sessiz infarkttan katastrofik sonuçları olan duruma kadar, geniş biryelpazede görülebilir. Klinik olarak belirgin inme veya geçici iskemik atak (GİA) yokluğunda, nöron spesifik enolazın (NSE) yükselmesi, sessiz serebralinfarkt (SSİ) olarak adlandırılır ve nörolojik defisitler, kognitif fonksiyonlarda bozulma ve hatta mortalite artışı ile ilişkili olabilir. Oral antikoagülanalmakta olan non-valvüler AF’li hastalarda SSİ prevalansını değerlendirmeyi amaçladık.Gereç ve Yöntem: Kan örnekleri, polikliniğe başvuran non-valvuler AF’li ardışık 100 hastadan toplandı. NSE seviyesinde 12 ng/mL’den fazla artışolması SSİ olarak kabul edildi.Bulgular: Hastaların yaş ortalaması 70 idi ve çoğunlukla kadındı. Kırk dokuz hasta (%49) warfarin kullanıyordu. Ortalama uluslararası normalleştirilmişoran düzeyi 2,3±1,1 idi. Elli bir hasta (%51) direkt oral antikoagülan (DOAC) tedavisi [dabigatran (n=7), rivaroksaban (n=13) ve apiksaban (n=31)]alıyordu. Çalışma popülasyonunun ortalama CHA2DS2-VASc skoru 3,8±1,5 idi. Kırk üç hastada (%43) NSE yükselmesi saptandı. Bu hastalar dahayaşlıydılar, kronik kalp yetmezliği ve geçirilmiş inme/GİA öyküsü daha yüksekti. Artmış sol atriyum çapı, azalmış glomerüler filtrasyon hızı ve yüksekCHA2DS2-VASc skoru, SSİ ile ilişkili diğer faktörlerdi. DOAC alan hastalar ve oral antikoagülan tedaviye ilave aspirin alan hastalarda SSİ görülmeprevalansı daha düşüktü. Çok değişkenli analiz, yüksek CHA2DS2-VASc skorunu [odds oranı (OR): 2,6; %95 güven aralığı (GA): 1,3-5,1; p=0,007] vewarfarinin kullanımını (OR: 3,8; %95 GA: 1,2-11,9; p=0,02) SSİ’nin bağımsız öngördürücüleri olarak göstermiştir.Sonuç: Sessiz beyin hasarı, oral antikoagülan tedaviye rağmen nonvalvüler atriyal fibrilasyonu olan hastalarda oldukça yaygındır.
Silent Cerebral İnfarction in Anticoagulated Patients with Non-valvular Atrial Fibrillation as Detected with Neuron Specific Enolase
Objectives: Cerebral infarction in patients with atrial fibrillation (AF) may vary from being clinically silent to catastrophic. Elevation of neuronspecific enolase (NSE) in the absence of any clinically apparent stroke or transient ischemic attack (TIA), so-called silent cerebral infarction (SCI), may be associated with neurologic deficits, cognitive decline and even increased mortality. We aim to evaluate the prevalence of SCI in patients with non-valvular AF who are taking oral anticoagulants. Materials and Methods: Blood samples were collected from 100 consecutive patients with non-valvular AF admitted to outpatient clinic. NSE levels of greater than 12 ng/mL was considered as SCI. Results: Patients were mainly female with a mean age of 70 years. Fourty-nine of them (49%) were taking warfarin. Mean international normalized rate level was 2.3±1.1. Fifty-one patients (51%) were on direct oral anticoagulant (DOAC) treatment [dabigatran (n=7), rivaroxaban (n=13) and apixaban (n=31)]. Mean CHA2DS2-VASc score of the study population was 3.8±1.5. Fourty-three patients (43%) were found to have NSE elevation. They were older and more likely to have history of chronic heart failure and previous stroke/TIA. Increased left atrial diameter, reduced glomeruler filtration rate, and higher CHA2DS2-VASc score were other factors associated with SCI. Patients taking DOACs and patients who were taking aspirin on top of oral anticoagulant treatment were less likely to have SCI. Multivariate analysis demonstrated higher CHA2DS2-VASc score [odds ratio (OR): 2.6; 95% confidence interval (CI): 1.3-5.1; p=0.007] and use of warfarin (OR: 3.8; 95% CI: 1.2-11.9; p=0.02) as independent predictors of SCI. Conclusion: Silent brain injury is highly prevalent among patients with non-valvular AF despite the use of oral anticoagulant therapy.
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