Collateral Flow Averts Hemorrhagic Transformation After Endovascular Therapy for Acute Ischemic Stroke

Background and Purpose-Collaterals sustain the ischemic penumbra to limit growth of the infarct core before revascularization, yet the impact of baseline collateral flow on hemorrhagic transformation (HT) after endovascular therapy remains unknown. Methods-A collaborative study from 2 stroke centers in distinct geographic regions included 222 consecutive patients who received endovascular therapy for acute cerebral ischemia. The influence of collaterals on HT was analyzed in distinct case scenarios relative to baseline collateral grade at angiography (0 to 1 versus 2 to 4) and recanalization (Thrombolysis in Myocardial Ischemia scale, 0 to 1 versus 2 to 3): good collaterals and successful recanalization (n = 98), poor collaterals with successful recanalization (n = 43), good collaterals and no recanalization(n = 46), and poor collaterals and no recanalization (n = 35). Results-HT after endovascular therapy occurred in 103 (46.4%) patients; 42 (18.9%) were symptomatic. HT was more frequently observed in patients with poor collaterals and recanalization than in other groups (P = 0.048). When revascularization was achieved, patients with poorer collaterals were more likely to have symptomatic worsening with HT (r = -0.181, P = 0.032). Multiple logistic regression analysis identified aggressive treatment (OR, 2.558 for Merci clot retrieval; 95% CI, 1.153 to 5.678; OR, 3.618 for combined fibrinolytics and mechanical therapy; 95% CI, 1.551 to 8.437; and OR, 2.085 for intravenous thrombolysis before endovascular therapy; 95% CI, 1.096 to 3.969), poor collaterals and recanalization (OR, 2.666; 95% CI, 1.163 to 6.113), and serum glucose levels (OR, 1.007; 95% CI, 1.000 to 1.014) as independent predictors of HT. Conclusions-Angiographic grade of collateral flow strongly influences the rate of HT after therapeutic recanalization for acute ischemic stroke. Collateral status readily available from baseline angiography may therefore refine therapeutic decision-making in acute cerebral ischemia. (Stroke. 2011;42:2235-2239.)