Clinical Outcome and Prognostic Factors of Acute Symptomatic Intracranial Vertebrobasilar Artery Dissection

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dc.contributor.advisorSeHyuk Kim-
dc.contributor.authorKim, Byung Moon-
dc.date.accessioned2019-10-21T07:17:29Z-
dc.date.available2019-10-21T07:17:29Z-
dc.date.issued2011-02-
dc.identifier.other11214-
dc.identifier.urihttps://dspace.ajou.ac.kr/handle/2018.oak/17851-
dc.description학위논문(박사)--아주대학교 일반대학원 :의학과,2011. 2-
dc.description.tableofcontentsABSTRACT i TABLE OF CONTENTS iv LIST OF FIGURES vi LIST OF TABLES viii I. INTRODUCTION 1 A. Clinicopathological features of intracranial vertebrobasilar dissection 1 B. Treatment and outcomes of intracranial vertebrobasilar dissection 2 C. Purpose of study 4 II. MATERIALS AND METHODS 5 A. Patients and analysis method 5 1. Patients recruitment 5 2. Radiological evaluation 9 3. Grouping of patients 9 4. Follow up 10 B. Unruptured intracranial vertebrobasilar dissection 10 1. Treatment strategy 10 2. Statistical analysis 14 C. Ruptured intracranial vertebrobasilar dissection 15 1. Treatment strategy and the definition of post-treatment recurrence 15 2. Statistical analysis 16 III. RESULTS 18 A. Unruptured intracranial vertebrobasilar dissection 18 1. Clinical and radiological manifestations 18 2. Treatment and treatment-related complications 21 3. Clinical outcomes and prognostic factors 24 B. Ruptured intracranial vertebrobasilar dissection 28 1. Treatment and treatment-related complications 28 2. Post-treatment rebleeding and recurrence 28 3. Clinical outcomes and prognostic factors 39 IV. DISCUSSION 43 A. Unruptured intracranial vertebrobasilar dissection 43 1. Clinical and radiological manifestations 43 2. Treatment of unruptured VBD 44 3. Clinical outcomes and prognostic factors 46 B. Ruptured intracranial vertebrobasilar dissection 46 1. Endovascular treatment methods 46 2. Clinical outcomes and prognostic factors 48 C. Limitations of the study 49 V. CONCLUSION 49 REFERENCES 51 국문요약 63 LIST OF FIGURES Fig. 1. Various radiological findings of intracranial vertebrobasilar dissections 6 Fig. 2. A patient who underwent proximal occlusion of the parent artery for an unruptured right vertebral artery dissection 12 Fig. 3. A patient who was medically treated for an unruptured left vertebral artery dissection 13 Fig. 4. A patient who underwent two overlapping stents for an enlarged dissecting aneurysm 22 Fig. 5. A patient who underwent emergency stent placement for progression of ischemia due to the unruptured basilar artery dissection 23 Fig. 6. A patient with rebleeding after a single stent insertion for a ruptured basilar artery dissection 31 Fig. 7. A patient with rebleeding after internal coil trapping for a ruptured vertebral artery dissection 32 Fig. 8. A patient with rebleeding after proximal occlusion for a ruptured vertebral artery dissection that involves the posterior inferior cerebellar artery origin 33 Fig. 9. A patients who underwent two overlapping stents insertion for a ruptured left vertebral artery dissection 34 Fig. 10. A patient who underwent double stents with coiling for a ruptured vertebral artery dissection 35 Fig. 11. A patient with recurrence after internal coil trapping for a ruptured vertebral artery dissection that involves the posterior inferior cerebellar artery origin 36 LIST OF TABLES Table 1. Clinical and radiographic characteristics, and clinical outcomes of the patients with intracranial vertebrobasilar dissection 7 Table 2. Clinical and radiographic characteristics, and clinical outcome of unruptured VBD 19 Table 3. Predictors of clinical outcome in acute unruptured intracranial vertebrobasilar dissection presenting with ischemic symptoms 25 Table 4. Risk factors of post-treatment recurrence with or without rebleeding 37 Table 5. Clinical outcomes and prognostic factors of the patients with ruptured VBD who underwent endovascular treatment 40-
dc.language.isoeng-
dc.publisherThe Graduate School, Ajou University-
dc.rights아주대학교 논문은 저작권에 의해 보호받습니다.-
dc.titleClinical Outcome and Prognostic Factors of Acute Symptomatic Intracranial Vertebrobasilar Artery Dissection-
dc.title.alternativeClinical Outcome and Prognostic Factors of Acute Symptomatic Intracranial Vertebrobasilar Artery Dissection-
dc.typeThesis-
dc.contributor.affiliation아주대학교 일반대학원-
dc.contributor.alternativeNameByung Moon Kim-
dc.contributor.department일반대학원 의학과-
dc.date.awarded2011. 2-
dc.description.degreeMaster-
dc.identifier.localId569277-
dc.identifier.urlhttp://dcoll.ajou.ac.kr:9080/dcollection/jsp/common/DcLoOrgPer.jsp?sItemId=000000011214-
dc.subject.keywordDissection-
dc.subject.keywordAneurysm-
dc.subject.keywordstroke-
dc.subject.keywordVertebrobasilar Artery-
dc.subject.keyword척추기저동맥박리-
dc.description.alternativeAbstractAlthough intracranial vertebrobasilar dissection (VBD) has been increasingly recognized as a cause of stroke in East Asian populations, its clinical course and treatment method are not yet established. The purpose of this study was to retrospectively evaluate treatment methods, clinical outcome, and prognostic factors of patients with VBD. Two hundred seventy-two patients (M:F=173:99; Mean age, 45 ? 11 years, range, 21 ? 81 years) with ruptured (n=84) or unruptured VBD (n=191) were recruited between January 2001 and December 2008. The patients were divided into two groups, ruptured or unruptured, for evaluation. The investigations were focused on clinical outcome (favorable vs. unfavorable; mRS, 0 ? 1 vs. 2 ? 5 or death for unruptured VBD and mRS, 0 ? 2 vs. 3 ? 5 or death for ruptured VBD) and prognostic factors. Of the 191 patients with an unruptured VBD, 46 patients (24.1%) underwent endovascular treatment. The remaining 145 patients (75.9%) were medically treated with anticoagulants (n=49), antiplatelets (n=48), or analgesics alone (n=48). Clinical follow-up data were available for 178 patients (102 ischemic and 76 non-ischemic) at 12 to 102 months (median, 46 months). None of the unruptured VBD hemorrhaged. All 76 patients without ischemic presentation had favorable outcomes (mRS, 0 ? 1). Of the 102 patients with ischemic presentation, outcomes were favorable in 92 and unfavorable in 10 patients. Four patients died; three died of causes unrelated to VBD, and one died as a result of basilar artery (BA) dissection. Older age (OR, 1.101; 95% CI, 1.101 ? 1.211; p=0.049) and BA involvement (RR, 14.388; 95% CI, 1.983 ? 104.413; power, 0.97; p=0.008) were independent predictors of unfavorable outcomes in siu-VBD patients with ischemic presentation. Of the 81 patients with a ruptured VBD, 76 patients underwent endovascular treatments for a ruptured VBD and 5 patients were managed conservatively. Forty-six patients received deconstructive method using internal coil trapping or proximal occlusion of parent artery and thirty received reconstructive treatment using one to three overlapping stents alone or with coiling. Reconstructive treatment was more frequently used in VBD that involved BA (8/8) or posterior inferior cerebellar artery (PICA) origin (20/30) than in other cases (p < 0.01). Clinical outcomes were favorable (modified Rankin Scale, 0 ? 2) in 59 (77.6%) and unfavorable in 17 patients (22.4%). Nine patients (11.8%) died, and five deaths were due to rebleeding. There were nine recurrences, wherein six had rebleeding and three no rebleeding. PICA origin involvement was the only independent risk factor for recurrence. Outcomes were favorable (mRS, 0 ? 2) in 59 patients (77.6%) and unfavorable in 17 (22.4%). Rebleeding (RR, 22.717; 95% CI, 1.899 ? 271.767; power, 0.99; p=0.014), pre-treatment Hunt & Hess grade (HHG) 4 or 5 (RR, 11.778; 95% CI, 1.822 ? 76.134; power, 0.97; p=0.01), and PICA origin involvement (RR, 4.362; 95% CI, 1.054 ? 19.431; power, 0.51 p=0.042) were independent predictors of unfavorable outcomes. In conclusion, clinical outcome of unruptured VBD was favorable in all without ischemic symptom and in most patients with ischemic symptom. Older age and BA involvement are independent predictors of unfavorable outcome in sui-VBD with ischemic symptom. Clinical outcome of ruptured VBD was favorable in majority of patients who underwent endovascular treatment. Rebleeding, HH 4-5 and PICA origin involvement were independent predictors of unfavorable outcome.-
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