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Document Details :

Title: Basilar artery steno-occlusive disease is associated with structural changes in the left ventricle
Author(s): K. Kang , S.-H. Lee , B.-W. Yoon
Journal: Acta Cardiologica
Volume: 64    Issue: 4   Date: 2009   
Pages: 493-498
DOI: 10.2143/AC.64.4.2041614

Abstract :
Objectives — Structural changes in the extracranial carotid artery are associated with an increase in left ventricular (LV) mass and relative wall thickness. The present study was performed to determine the relation of LV mass index and relative wall thickness to suspected atherosclerotic steno-occlusive disease of the intracranial arteries on magnetic resonance angiography (MRA) in noncardioembolic ischaemic stroke patients.
Methods — We retrospectively analysed the records of acute ischaemic stroke patients who underwent echocardiography and intracranial MRA. Patients with potential sources of cardioembolism, or known causes of vascular steno-occlusive disease including dissection, vasculitis, and moyamoya disease, were excluded from the study. LV mass indexes and relative wall thicknesses were estimated using echocardiography. Patients were divided into four groups according to their LV mass index and relative wall thickness: concentric LV hypertrophy, eccentric LV hypertrophy, concentric LV remodelling, and normal geometry. MRA was used to evaluate steno-occlusive disease in the basilar artery (BA) and the horizontal portion of the middle cerebral artery.
Results — A total of 212 patients were included, and logistic regression analysis revealed that BA steno-occlusive disease was related to LV relative wall thickness, but not LV mass index. The prevalence of BA disease was significantly higher in the concentric LV hypertrophy group than in the normal geometry group. Steno-occlusive disease of the middle cerebral artery was not closely related to the structural changes in the left ventricle.
Conclusion — Increased LV relative wall thickness may be an independent risk factor for BA stenoocclusive disease or may share pathogenic mechanisms with BA disease.