BACKGROUND: Anticoagulant-related hemorrhage occurs with an incidence of approximately 1%/patient-year in mechanical heart valve recipients. Intracranial hemorrhage poses a difficult clinical choice; continuing anticoagulation therapy may enlarge the volume of the hemorrhage, early reinstitution of anticoagulation therapy may predispose patients to recurrence, and reversal of anticoagulation therapy may place patients at risk for systemic embolization involving the brain. The risk of embolization may also be greater for patients with atrial fibrillation, cage-ball valves in the mitral position, and reduced ventricular function. This dilemma exists because of a lack of data for a large series of patients. METHODS: We reviewed the medical records and neuroimaging studies for a consecutive group of patients admitted with intracranial hemorrhage and mechanical heart valves. We reviewed neurological presenting data, cardiac risk factors for systemic embolization (atrial fibrillation, enlarged atrial chambers, reduced ventricular function, and the type and location of the metallic valve), and hospital management. RESULTS: We studied 39 patients with intracranial hemorrhage and mechanical heart valves (median age, 69 yr). Four patients had experienced previous transient ischemic attacks or minor strokes. The time from valve replacement to intracranial hemorrhage ranged from 2 months to 19 years (median, 6 yr). The type of intracranial hemorrhage was acute subdural hematoma (n = 20), lobar hematoma (n = 10), subarachnoid hemorrhage (n = 4), cerebellar hematoma (n = 3), or basal ganglionic hematoma (n = 2). Thirteen patients died within 2 days of admission. All 26 surviving patients received fresh frozen plasma and vitamin K. Fifteen patients underwent evacuation of acute subdural hematoma, and in one patient an anterior communicating aneurysm was clipped. The duration of discontinuation of anticoagulation therapy varied from 2 days to 3 months (median, 8 d). None of the patients developed transient ischemic attacks, ischemic strokes, valve thrombosis, or systemic embolization. No recurrence of intracranial hemorrhaging was observed during hospitalization and reinstitution of anticoagulation or antiplatelet agent administration. CONCLUSION: Temporary interruption of anticoagulation therapy seems safe for patients with intracranial hemorrhage and mechanical heart valves but without previous evidence of systemic embolization. For most patients, discontinuation for 1 to 2 weeks should be sufficient to observe the evolution of a parenchymal hematoma, to clip or coil a ruptured aneurysm, or to evacuate an acute subdural hematoma.
BACKGROUND: Anticoagulant-related hemorrhage occurs with an incidence of approximately 1%/patient-year in mechanical heart valve recipients. Intracranial hemorrhage poses a difficult clinical choice; continuing anticoagulation therapy may enlarge the volume of the hemorrhage, early reinstitution of anticoagulation therapy may predispose patients to recurrence, and reversal of anticoagulation therapy may place patients at risk for systemic embolization involving the brain. The risk of embolization may also be greater for patients with atrial fibrillation, cage-ball valves in the mitral position, and reduced ventricular function. This dilemma exists because of a lack of data for a large series of patients. METHODS: We reviewed the medical records and neuroimaging studies for a consecutive group of patients admitted with intracranial hemorrhage and mechanical heart valves. We reviewed neurological presenting data, cardiac risk factors for systemic embolization (atrial fibrillation, enlarged atrial chambers, reduced ventricular function, and the type and location of the metallic valve), and hospital management. RESULTS: We studied 39 patients with intracranial hemorrhage and mechanical heart valves (median age, 69 yr). Four patients had experienced previous transient ischemic attacks or minor strokes. The time from valve replacement to intracranial hemorrhage ranged from 2 months to 19 years (median, 6 yr). The type of intracranial hemorrhage was acute subdural hematoma (n = 20), lobar hematoma (n = 10), subarachnoid hemorrhage (n = 4), cerebellar hematoma (n = 3), or basal ganglionic hematoma (n = 2). Thirteen patients died within 2 days of admission. All 26 surviving patients received fresh frozen plasma and vitamin K. Fifteen patients underwent evacuation of acute subdural hematoma, and in one patient an anterior communicating aneurysm was clipped. The duration of discontinuation of anticoagulation therapy varied from 2 days to 3 months (median, 8 d). None of the patients developed transient ischemic attacks, ischemic strokes, valve thrombosis, or systemic embolization. No recurrence of intracranial hemorrhaging was observed during hospitalization and reinstitution of anticoagulation or antiplatelet agent administration. CONCLUSION: Temporary interruption of anticoagulation therapy seems safe for patients with intracranial hemorrhage and mechanical heart valves but without previous evidence of systemic embolization. For most patients, discontinuation for 1 to 2 weeks should be sufficient to observe the evolution of a parenchymal hematoma, to clip or coil a ruptured aneurysm, or to evacuate an acute subdural hematoma.