Timing of Spontaneous Recanalization and Risk of Hemorrhagic Transformation in Acute Cardioembolic Stroke

Background and Purpose The relationship between reperfusion and hemorrhagic transformation (HT) remains uncertain. Therefore, we aimed to clarify the relationship between the time course of recanalization and the risk of HT in patients with cardioembolic stroke studied within 6 hours of symptom onset. Methods Fifty-three patients with atrial fibrillation and nonlacunar stroke in the middle cerebral artery (MCA) territory admitted within the first 6 hours after symptom onset were prospectively studied. Serial TCD examinations were performed on admission and at 6, 12, 24, and 48 hours. CT was performed within 6 hours after stroke onset and again at 36 to 48 hours. Results Proximal and distal MCA occlusions were detected in 32 patients (60.4%) and 18 patients (34%), respectively. Early spontaneous recanalization occurring within 6 hours was identified in 10 patients (18.8%). Delayed recanalization (>6 hours) occurred in 28 patients (52.8%). HT on CT scan was detected in 17 patients (32%) within the first 48 hours. Only large parenchymal hemorrhage (PH2) was significantly associated with an increase (P =0.038, Kruskal-Wallis test) in the National Institutes of Health Stroke Scale (NIHSS) score compared with the other subtypes of HT. Univariate analysis revealed that an NIHSS score of >14 on baseline (P =0.001), proximal MCA occlusion (P =0.004), hypodensity >33% of the MCA territory (P =0.012), and delayed recanalization occurring >6 hours of stroke onset (P =0.003) were significantly associated with HT. With a multiple logistic regression model, delayed recanalization (OR 8.9; 95% CI 2.1 to 33.3) emerged as independent predictor of HT. Conclusions Delayed recanalization occurring >6 hours after acute cardioembolic stroke is an independent predictor of HT.

[1]  M E Moseley,et al.  Relationship Between Apparent Diffusion Coefficient and Subsequent Hemorrhagic Transformation Following Acute Ischemic Stroke , 2000, Stroke.

[2]  D Schneider,et al.  Reperfusion and metabolic recovery of brain tissue and clinical outcome after ischemic stroke and thrombolytic therapy. , 2000, Stroke.

[3]  S Hamilton,et al.  The rtPA (alteplase) 0- to 6-hour acute stroke trial, part A (A0276g) : results of a double-blind, placebo-controlled, multicenter study. Thromblytic therapy in acute ischemic stroke study investigators. , 2000, Stroke.

[4]  C. Baird,et al.  The pilot study. , 2000, Orthopedic nursing.

[5]  L Bozzao,et al.  Hemorrhagic transformation within 36 hours of a cerebral infarct: relationships with early clinical deterioration and 3-month outcome in the European Cooperative Acute Stroke Study I (ECASS I) cohort. , 1999, Stroke.

[6]  D. Kilpatrick,et al.  Effects of spontaneous recanalization on functional and electrophysiological recovery in acute ischemic stroke. , 1999, Stroke.

[7]  T Moulin,et al.  Hemorrhagic transformation in acute ischemic stroke. The MAST-E study. MAST-E Group. , 1999, Stroke.

[8]  J. Garcìa,et al.  Hemorrhagic Transformation in Focal Cerebral Ischemia: Influence of Time to Artery Reopening and Tissue Plasminogen Activator , 1999, Pharmacotherapy.

[9]  W. Yuh,et al.  Outcome in Acute Stroke with Successful Intra-Arterial Thrombolysis and Predictive Value of Initial Single-Photon Emission-Computed Tomography , 1999, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[10]  A. Demchuk,et al.  Serum glucose level and diabetes predict tissue plasminogen activator-related intracerebral hemorrhage in acute ischemic stroke. , 1999, Stroke.

[11]  M. Kaste,et al.  Randomised double-blind placebo-controlled trial of thrombolytic therapy with intravenous alteplase in acute ischaemic stroke (ECASS II) , 1998, The Lancet.

[12]  Michael Chopp,et al.  Early (1 h) administration of tissue plasminogen activator reduces infarct volume without increasing hemorrhagic transformation after focal cerebral embolization in rats , 1998, Journal of the Neurological Sciences.

[13]  D. Toni,et al.  Early spontaneous improvement and deterioration of ischemic stroke patients. A serial study with transcranial Doppler ultrasonography. , 1998, Stroke.

[14]  J. Bogousslavsky,et al.  Cerebrovascular Disease: Pathophysiology, Diagnosis and Management , 1998 .

[15]  R. Higashida,et al.  PROACT: a phase II randomized trial of recombinant pro-urokinase by direct arterial delivery in acute middle cerebral artery stroke. PROACT Investigators. Prolyse in Acute Cerebral Thromboembolism. , 1998, Stroke.

[16]  L Bozzao,et al.  Acute stroke: usefulness of early CT findings before thrombolytic therapy. , 1997, Radiology.

[17]  A. Alexandrov,et al.  Predictors of hemorrhagic transformation occurring spontaneously and on anticoagulants in patients with acute ischemic stroke. , 1997, Stroke.

[18]  V Larrue,et al.  Hemorrhagic transformation in acute ischemic stroke. Potential contributing factors in the European Cooperative Acute Stroke Study. , 1997, Stroke.

[19]  T. N. t-P. S. S. Group,et al.  Intracerebral hemorrhage after intravenous t-PA therapy for ischemic stroke. The NINDS t-PA Stroke Study Group. , 1997, Stroke.

[20]  G. Hamann,et al.  Hemorrhagic Transformation and Microvascular Integrity during Focal Cerebral Ischemia/Reperfusion , 1996, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.

[21]  G. Sette,et al.  Hemorrhagic transformation of brain infarct , 1996, Neurology.

[22]  Koroshetz Wj,et al.  Tissue plasminogen activator for acute ischemic stroke. , 1996, The New England journal of medicine.

[23]  Joseph P. Broderick,et al.  Tissue plasminogen activator for acute ischemic stroke. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. , 1995 .

[24]  M. Kaste,et al.  Intravenous thrombolysis with recombinant tissue plasminogen activator for acute hemispheric stroke. The European Cooperative Acute Stroke Study (ECASS) , 1995, JAMA.

[25]  W. Hacke,et al.  Does arterial recanalization improve outcome in carotid territory stroke? , 1995, Stroke.

[26]  C. Pozzilli,et al.  Spontaneous middle cerebral artery reperfusion in ischemic stroke. A follow-up study with transcranial Doppler. , 1995, Stroke.

[27]  T. Brott,et al.  Improved Reliability of the NIH Stroke Scale Using Video Training , 1994, Stroke.

[28]  W. Hacke,et al.  Recombinant tissue plasminogen activator in acute thrombotic and embolic stroke , 1992, Annals of neurology.

[29]  C. Weiller,et al.  Type and extent of hemispheric brain infarctions and clinical outcome in early and delayed middle cerebral artery recanalization , 1992, Neurology.

[30]  J. Bamford,et al.  Hemorrhagic infarction , 1992, Neurology.

[31]  L. Bozzao,et al.  Early angiographic and CT findings in patients with hemorrhagic infarction in the distribution of the middle cerebral artery. , 1991, AJNR. American journal of neuroradiology.

[32]  M. Pessin,et al.  Thrombolytic agents in the treatment of stroke. , 1990, Clinical neuropharmacology.

[33]  H. Ishibashi-Ueda,et al.  Hemorrhagic infarct of the brain without a reopening of the occluded arteries in cardioembolic stroke. , 1989, Stroke.

[34]  M. Fujishima,et al.  Hemorrhagic transformation in cerebral embolism. , 1989, Stroke.

[35]  J. Slattery,et al.  Interobserver agreement for the assessment of handicap in stroke patients. , 1989, Stroke.

[36]  A. Yamadori,et al.  Intracarotid urokinase with thromboembolic occlusion of the middle cerebral artery. , 1988, Stroke.

[37]  W. Hacke,et al.  Local intra-arterial fibrinolytic therapy in acute carotid territory stroke. A pilot study. , 1988, Stroke.

[38]  R. Bloch,et al.  Interobserver agreement for the assessment of handicap in stroke patients. , 1988, Stroke.

[39]  J. Lodder,et al.  Cerebral hemorrhagic infarction at autopsy: cardiac embolic cause and the relationship to the cause of death. , 1986, Stroke.

[40]  R. D. Adams Observations on brain embolism with special reference to the mechanism of hemorrhagic infarction. , 1950, The Journal of clinical investigation.