Letícia C Rebello1, Diogo C Haussen1, Samir Belagaje1, Aaron Anderson1, Michael Frankel1, Raul G Nogueira2. 1. From the Emory University School of Medicine/Marcus Stroke and Neuroscience Center-Grady Memorial Hospital, Atlanta, GA. 2. From the Emory University School of Medicine/Marcus Stroke and Neuroscience Center-Grady Memorial Hospital, Atlanta, GA. raul.g.nogueira@emory.edu.
Abstract
BACKGROUND AND PURPOSE: Oral anticoagulation (OAC) plays a major role in atrial fibrillation stroke prevention but represents a contraindication to intravenous tissue-type plasminogen activator. Intra-arterial therapy remains a potential reperfusion strategy in these patients; however, supporting data are scarce. METHODS: Retrospective analysis of prospectively collected consecutive intra-arterial therapies from October 2010 to March 2015 comparing OAC (vitamin-K antagonists and novel oral anticoagulants) versus normal hemostasis versus intravenous tissue-type plasminogen activator patients. Primary safety end point is parenchymal hematoma. Secondary safety end point is 90-day mortality. Efficacy end points are successful reperfusion (modified Thrombolysis in Cerebral Infarction, 2b-3) and good outcome (90-day modified Rankin Scale score of 0-2). Logistic regression for predictors of parenchymal hematoma was performed. RESULTS: A total of 604 patients were qualified for the study. Baseline and outcomes variables were overall similar for vitamin-K antagonists (n=29) and novel oral anticoagulants (n=17) patients. When compared with normal hemostasis (n=265) and intravenous tissue-type plasminogen activator (n=297), OAC (n=46) patients were older and had more comorbidities. There were no statistically significant differences in the rates of parenchymal hematoma (8% versus 5%; P=0.42), 90-day modified Rankin Scale score of 0 to 2 (30% versus 40%; P=0.26), and 90-day mortality (32% versus 26%; P=0.46) among OAC and normal hemostasis patients. Similarly, there were no significant differences between OAC and intravenous tissue-type plasminogen activator patients in terms of parenchymal hematoma (8% versus 4%; P=0.16), 90-day modified Rankin Scale score of 0 to 2 (30% versus 43%; P=0.13), and 90-day mortality (32% versus 22%; P=0.18). The use of OAC was not associated with the occurrence of parenchymal hematoma on multivariate logistic regression analysis. CONCLUSIONS: Intra-arterial therapy seems to be safe in patients taking OACs; however, our study showed a nonsignificant increase in hemorrhage and mortality with a nonsignificant decrease in good outcomes in comparison with non-OAC patients. Although these nominal differences may have been related to older age and more comorbidities in the OAC group, larger studies are needed to confirm our findings given our limited sample size.
BACKGROUND AND PURPOSE: Oral anticoagulation (OAC) plays a major role in atrial fibrillation stroke prevention but represents a contraindication to intravenous tissue-type plasminogen activator. Intra-arterial therapy remains a potential reperfusion strategy in these patients; however, supporting data are scarce. METHODS: Retrospective analysis of prospectively collected consecutive intra-arterial therapies from October 2010 to March 2015 comparing OAC (vitamin-K antagonists and novel oral anticoagulants) versus normal hemostasis versus intravenous tissue-type plasminogen activatorpatients. Primary safety end point is parenchymal hematoma. Secondary safety end point is 90-day mortality. Efficacy end points are successful reperfusion (modified Thrombolysis in Cerebral Infarction, 2b-3) and good outcome (90-day modified Rankin Scale score of 0-2). Logistic regression for predictors of parenchymal hematoma was performed. RESULTS: A total of 604 patients were qualified for the study. Baseline and outcomes variables were overall similar for vitamin-K antagonists (n=29) and novel oral anticoagulants (n=17) patients. When compared with normal hemostasis (n=265) and intravenous tissue-type plasminogen activator (n=297), OAC (n=46) patients were older and had more comorbidities. There were no statistically significant differences in the rates of parenchymal hematoma (8% versus 5%; P=0.42), 90-day modified Rankin Scale score of 0 to 2 (30% versus 40%; P=0.26), and 90-day mortality (32% versus 26%; P=0.46) among OAC and normal hemostasis patients. Similarly, there were no significant differences between OAC and intravenous tissue-type plasminogen activatorpatients in terms of parenchymal hematoma (8% versus 4%; P=0.16), 90-day modified Rankin Scale score of 0 to 2 (30% versus 43%; P=0.13), and 90-day mortality (32% versus 22%; P=0.18). The use of OAC was not associated with the occurrence of parenchymal hematoma on multivariate logistic regression analysis. CONCLUSIONS: Intra-arterial therapy seems to be safe in patients taking OACs; however, our study showed a nonsignificant increase in hemorrhage and mortality with a nonsignificant decrease in good outcomes in comparison with non-OACpatients. Although these nominal differences may have been related to older age and more comorbidities in the OAC group, larger studies are needed to confirm our findings given our limited sample size.
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