Associations DO NOTHING FOR RECOVERY! Because you don't have recovery protocols mapped to the problems found. Can't anyone in stroke think at all?
Oops, I'm not playing by the polite rules of Dale Carnegie, 'How to Win Friends and Influence People'.
Telling stroke medical persons they know nothing about stroke is a no-no even if it is true.
Politeness will never solve anything in stroke. Yes, I'm a bomb thrower and proud of it. Someday a stroke 'leader' will try to ream me out for making them look bad by being truthful, I look forward to that day.
Send me personal hate mail on this: oc1dean@gmail.com. I'll print your complete statement with your name(If you can't stand by your name don't bother replying anonymously) and my response in my blog. Or are you afraid to engage with my stroke-addled mind? No excuses are allowed! You're medically trained; it should be simple to precisely state EXACTLY WHY you aren't working on 100% recovery protocols with NO EXCUSES!
Article Commentary: “Association of Biomarkers With Intracerebral Hematoma Expansion and Arterial Thromboembolic Events in Patients With Acute Intracranial Hemorrhage”
Despite advances in acute hemorrhagic stroke care, hematoma expansion (HE) remains a major contributor to early neurological deterioration and poor outcomes in patients with intracerebral hemorrhage (ICH) associated with the use of anti-Xa inhibitors. The ANNEXA-I trial, initially aimed at assessing andexanet alfa for reversing factor Xa inhibitor–associated bleeding, provided a valuable platform to explore the underlying pathophysiological mechanisms — especially those driving hematoma expansion and thromboembolic events, which remain poorly understood. In this biomarker substudy, researchers explored the association between circulating biomarkers and both hematoma expansion and arterial thromboembolic events, aiming to provide additional insights into the mechanism of action of andexanet alfa.
Patients with ICH during treatment with a Factor Xa inhibitor were eligible for inclusion in the original ANNEXA-I trial if they underwent baseline brain imaging within 12 hours of symptom onset and had a hematoma volume of ≤60 mL with HE defined as increase in volume of ≥12.5 mL or ≥35% within 12 hours. The authors further modified criteria to include hematoma volume of 0.5 to 60 mL and with a maximum National Institutes of Health Stroke Scale score of 35 who underwent brain imaging within 6 hours of symptom onset. Hemorrhages needed to be confirmed on neuroimaging within 2 hours before randomization, and the last dose of Factor Xa inhibitor had to be taken within 15 hours of randomization. Patients with GCS <7, plan for surgery <12 hours and history of thromboembolic events in prior 2 weeks were excluded. Arterial thromboembolic events included ischemic stroke, myocardial infarction and systemic embolism occurring within 30 days. Analysis was restricted to patients taking apixaban or rivaroxaban, and to availability of anti-Factor Xa activity or endogenous thrombin potential (ETP) data.
438 subjects with anti-Xa activity and 328 with ETP levels met criteria. In patients with apixaban- or rivaroxaban-associated ICH, the mean age was 79.1 years. Baseline characteristics were similar in the anti-Factor Xa and ETP populations and were well balanced by randomized treatment group. The results showed large reduction between baseline and 1 hour in anti-Factor Xa activity (median difference at 1 hour being andexanet 98.3 ng/mL and for usual care 10.9 ng/mL (between group difference, P<0.001) and a large increase in ETP (andexanet 753.1 nmol/L-min and for usual care 126.6 nmol/L-min (between group difference, P<0.001), but by 12 hours, the contrast between randomized treatment in ETP was no longer evident. Reduction in anti-Factor Xa activity between baseline and 1 hour independently predicted reduced risk of hematoma expansion (per 100 ng/mL: OR, 0.69 [95% CI, 0.53–0.92]; P=0.010). While increase in ETP between baseline and 1 hour independently predicted reduced risk of hematoma expansion (per 100 nmol/L-min: OR, 0.94 [95% CI, 0.90–0.99]; P=0.019). After adjustment for age, baseline biomarker level, prior MI, and high-dose andexanet eligibility, change in ETP from baseline to 1 hour independently predicted arterial thromboembolic events, whereas neither change in anti-Xa from baseline to 1 hour nor change in ETP from baseline to 12 hours was significantly associated with arterial thromboembolic events during 30 days of follow-up.
These results suggest an immediate treatment effect of anti-Xa agents that is limited to the first few hours of treatment. The authors further demonstrated that that change between baseline and 1 hour in ETP was independently associated with increased arterial thromboembolic events. Given most of the hematoma expansion is expected to occur within the first few hours of onset of symptoms, this is further supported by the biomarker findings of enhanced benefit with early and specific anticoagulant reversal to prevent hematoma expansion. Prothrombin complex concentrates that can enhance hemostatic by increasing ETP are recommended in the absence of specific reversal agents, and given their use in usual care, the finding of only a minimal increase in ETP at 1 hour in the usual care arm and lack of association between the change between baseline and 12 hours in ETP and risk of hematoma expansion further supports use of specific anti-Xa agents. Furthermore, biomarker analyses from the ANNEXA-4 cohort study have demonstrated that andexanet is associated with reduced tissue factor pathway inhibitor activity, which may contribute to the early increase in ETP, which is a well-documented risk factor for thromboembolism which is supported by the current study findings.
Strengths of the study include the analysis performed as part of a randomized control trial allowing for causal association between biomarker change and hematoma expansion. Their limitations include lack of statistical power as reflected by the wide CIs and that not all patients in the usual care arm received a prothrombin complex concentrate. However, changes in anti-FXa and ETP were similar in sensitivity analyses that excluded patients who did not receive a prothrombin complex concentrate. The next step would include integrating biomarker data with imaging and clinical variables, alongside mechanistic studies to uncover causal pathways, which could pave the way for biomarker-guided therapeutic trials. Picture this: A patient with ICH arrives in the ED, gets a CT and a rapid biomarker panel, and within minutes, a combined score predicts high risk for hematoma expansion. The team immediately starts hemostatic therapy and tailors anticoagulation timing, preventing both expansion and clotting complications. This is the promise of integrating biomarkers, imaging, and clinical data — turning ICH care into precise, proactive treatment.
No comments:
Post a Comment