Background and Purpose-To investigate relationships among plaque formation, increasing intima-media thickness, and age, we examined ultrasonographically carotid arteries of subjects who had no major atherosclerotic risk factors and who ranged in age from young adults to centenarians. Methods-We studied 319 healthy subjects (154 men, 165 women; age range, 21 to 105 years) with no history of hypertension, diabetes mellitus, or atherosclerotic disease. Mean intima-media wall thickness (IMT) of common carotid arteries at plaque-free sites and prevalence of plaques were evaluated by B-mode ultrasound. Results-Mean common carotid IMT increased in a linear manner with age for all decades of life, including centenarians [IMTϭ(0.009ϫAge)ϩ0.116] (rϭ0.83). In centenarians (nϭ30), intima-media complexes were diffusely thickened (mean IMT, 1.01 mm). Plaque prevalence increased up to the tenth decade of life (83.3%, nϭ30) but decreased in centenarians (60.0%). IMT and plaque prevalence were closely associated in the seventh and eighth decades of life but not at older ages. Conclusions-The present study indicates that increased IMT is a physiological effect of aging that corresponds to diffuse intimal thickening, especially in very elderly persons, and that IMT is distinct from pathological plaque formation.
Seven cases are reported in which extravasation of contrast medium from the lateral lenticulostriate artery was observed on cerebral angiography performed in the early stage of hypertensive intracerebral hemorrhage.
We advance the theory that continuous bleeding from the ruptured artery with mechanical destruction and displacement of cerebral tissue is the cause of massive hematoma formation, and discuss the possibility of surgical treatment of the acute stage of hypertensive intracerebral hemorrhage.
Fifty patients presenting clinically with TIAs were examined angiographically. Twenty one patients (42%) had no abnormality. Twenty patients (40%) had stenosis or occlusion in the MCA, ACA or intracranial carotid, whereas 11 (22%) had involvement of their extracranial internal carotid artery. Seven of the 28 CTs performed showed basal ganglia infarcts. This suggests that the cause for the TIA was an infarct in the vascular territory of a lenticulostriate artery.
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