Związek zakrzepicy żył głębokich z epilepsją po udarze mózgu: badanie retrospektywne w wielu ośrodkach
Association of deep vein thrombosis with poststroke epilepsy after acute ischemic stroke: a multicenter retrospective cohort study
W skrócie
Badacze przeanalizowali dane ponad 21 tysięcy pacjentów po udarze mózgu, aby sprawdzić, czy zakrzepica żył głębokich (skrzepy krwi w nogach) zwiększa ryzyko rozwoju epilepsji. Okazało się, że choć na początku wydawało się, że zakrzepica wiąże się z większym ryzykiem, to po uwzględnieniu ciężkości udaru i rozmieszczenia uszkodzenia mózgu ten związek znikał. Wnioski: zakrzepica żył głębokich nie jest niezależnym czynnikiem ryzyka epilepsji, ale raczej wskaźnikiem bardziej poważnego udaru mózgu.
Oryginalny abstract (angielski)
BACKGROUND: Deep vein thrombosis (DVT) and poststroke epilepsy (PSE) are clinically important complications after acute ischemic stroke. DVT commonly occurs in patients with greater neurological impairment, immobility, inflammation, and hypercoagulability, factors that may also be associated with PSE. Whether DVT is independently associated with PSE remains uncertain. METHODS: We conducted a secondary analysis of a multicenter cohort of 21,459 patients with acute ischemic stroke followed for 1 year. The association between recorded DVT and PSE was examined using sequential logistic regression models adjusting for demographic characteristics, vascular comorbidities, stroke severity, and lesion phenotype. Multicollinearity, sensitivity analyses, subgroup analyses, and joint stratification by DVT and National Institutes of Health Stroke Scale (NIHSS) score were performed. The incremental predictive value of DVT was evaluated using the area under the receiver operating characteristic curve (AUC), Brier score, calibration, and decision curve analysis. RESULTS: Among 21,459 patients, 1,324 (6.2%) had DVT and 936 (4.4%) developed PSE. DVT was associated with higher odds of PSE in the unadjusted analysis (OR, 1.93; 95% CI, 1.56-2.39), and the association remained similar after adjustment for demographic and vascular factors. After further adjustment for NIHSS score, cortical lobe involvement, and anterior and posterior circulation involvement, the association was substantially attenuated and no longer statistically significant (OR, 1.10; 95% CI, 0.86-1.39; = 0.45). Results were consistent across sensitivity analyses. Adding DVT to the clinical model did not improve discrimination (AUC, 0.879 vs. 0.879; DeLong = 0.255), Brier score, calibration, or decision-curve net benefit. CONCLUSIONS: The association between DVT and 1-year PSE was largely explained by stroke severity and lesion phenotype. DVT provided little incremental predictive information beyond established clinical characteristics, supporting its interpretation as a marker of a more severe and clinically complex poststroke phenotype rather than an independent PSE risk factor.