61 research outputs found
Time to treatment with bridging intravenous alteplase before endovascular treatment:subanalysis of the randomized controlled SWIFT-DIRECT trial.
BACKGROUND
We hypothesized that treatment delays might be an effect modifier regarding risks and benefits of intravenous thrombolysis (IVT) before mechanical thrombectomy (MT).
METHODS
We used the dataset of the SWIFT-DIRECT trial, which randomized 408 patients to IVT+MT or MT alone. Potential interactions between assignment to IVT+MT and expected time from onset-to-needle (OTN) as well as expected time from door-to-needle (DTN) were included in regression models. The primary outcome was functional independence (modified Rankin Scale (mRS) 0-2) at 3 months. Secondary outcomes included mRS shift, mortality, recanalization rates, and (symptomatic) intracranial hemorrhage at 24 hours.
RESULTS
We included 408 patients (IVT+MT 207, MT 201, median age 72 years (IQR 64-81), 209 (51.2%) female). The expected median OTN and DTN were 142 min and 54 min in the IVT+MT group and 129 min and 51 min in the MT alone group. Overall, there was no significant interaction between OTN and bridging IVT assignment regarding either the functional (adjusted OR (aOR) 0.76, 95% CI 0.45 to 1.30) and safety outcomes or the recanalization rates. Analysis of in-hospital delays showed no significant interaction between DTN and bridging IVT assignment regarding the dichotomized functional outcome (aOR 0.48, 95% CI 0.14 to 1.62), but the shift and mortality analyses suggested a greater benefit of IVT when in-hospital delays were short.
CONCLUSIONS
We found no evidence that the effect of bridging IVT on functional independence is modified by overall or in-hospital treatment delays. Considering its low power, this subgroup analysis could have missed a clinically important effect, and exploratory analysis of secondary clinical outcomes indicated a potentially favorable effect of IVT with shorter in-hospital delays. Heterogeneity of the IVT effect size before MT should be further analyzed in individual patient meta-analysis of comparable trials.
TRIAL REGISTRATION NUMBER
URL: https://www.
CLINICALTRIALS
gov ; Unique identifier: NCT03192332
Letter by Nighoghossian and Mechtouff Regarding Article, "Collateral Recruitment Is Impaired by Cerebral Small Vessel Disease"
International audienc
Response by Mechtouff and Nighoghossian to Letter Regarding Article "Matrix Metalloproteinase-9 and Monocyte Chemoattractant Protein-1 Are Associated With Collateral Status in Acute Ischemic Stroke With Large Vessel Occlusion"
International audienceNo abstract availabl
Lenin's Stroke
International audienceLenin's stroke remains a matter of debate. Here, we propose to assess the potential mechanisms. Lenin died on January 21, 1924 at the age of 53 years. Although some doctors suggested that the origin of his health problems was neurosyphilis, the autopsy findings were consistent with a severe atherosclerosis. This process might account for his recurrent ischemic strokes. In view of the family vascular history, an early hereditary atherosclerosis may be proposed
Matrix metallopeptidase 9 and placental growth factor may correlate with collateral status based on whole-brain perfusion combined with multiphase computed tomography angiography
Word processing in Parkinson's disease is impaired for action verbs but not for concrete nouns
International audienc
Timely initiation of second prevention treatment after hospital discharge following acute stroke in French patients.
Combined life-threatening thromboses and hemorrhages in a patient with afibrinogenemia and antithrombin deficiency
Abstract Background Patients with congenital afibrinogenemia suffer from spontaneous recurrent severe bleeding. While fibrinogen concentrates are known to effectively treat bleeding episodes, thrombotic complications often occur upon replacement therapy, rendering clinical management highly challenging. Case Presentation We hereby report a case of combined afibrinogenemia and congenital antithrombin deficiency manifested by recurrent life-threatening bleeding, as well as spontaneous severe arterial occlusion, such as acute coronary syndrome and stroke, and venous thromboses like pulmonary embolism. Secondary fibrinogen prophylaxis is recommended following any initial life-threatening bleeding episode in patients with afibrinogenemia, yet the high associated risk of thrombosis illustrates the complexity of choosing the most effective prophylaxis strategy combining fibrinogen concentrate with antithrombotic agent for optimal protection against the risk of both severe bleeding and thrombosis. For our patient, the thrombin generation assay objectively confirmed her prothrombotic tendency. Conclusion This case may help us better understand the pathophysiology of arterial thrombosis in afibrinogenemia, while highlighting the difficulty of managing such complications
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