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PubMedDate not supplied

The relationship between intimal necrosis and lipid accumulation during the onset and progression of atherosclerotic lesions.

In human coronary arteries, aorta and intracranial arteries, the first areas of intimal necrosis preceded the onset of the first lipid accumulation related to atherosclerotic involvement. Both intra- and extracellular lipid accumulations developed only in preexisting areas of intimal necrosis. Intimal necrosis not only caused an abnormal intraarterial retention of fat, but also caused fat to be deposited preferentially in specific forms and particular locations. The areas with mucoid necrosis appeared as adequate sites for the onset of fatty streaks; the areas with swelling necrosis appeared as adequate sites for a diffuse extracellular retention of tiny lipid droplets; the areas with dissecting necrosis appeared as adequate sites for large fatty deposits rich in cholesterol clefts. The results of this paper demonstrate that human atherosclerosis has many attributes of a necrotizing arteriopathy and that lipid accumulation is a secondary phenomenon. These results add support to the insudative theory of atherogenesis built up by German pathologists at the middle of this century and disagree with the often repeated view that human atherosclerosis is a reaction of the arterial wall to lipid that invade it.

Adolescent↗
PubMed1977

[Pathogenesis of focal, transitory cerebral ischemic accidents].

Transient ischaemic focal cerebral attacks (TIA's) are due to: 1) atherosclerosis when embolism may take place or perhaps transient occlusion of the internal carotid artery or mural or transiently occlusive thrombus of an intracranial artery stenosis or transient systemic hypotension. In recent years embolism may have been overdiagnosed; 2) cardiac embolism due to dysrythmias, myocardial infarction, endocarditis, valvular prosthesis, etc.; 3) miscellaneous causes, often difficult to demonstrate such as tortuosity of the extracranial cerebral arteries, dissecting aneurysms, changes in cerebrovascular resistance; 4) not unfrequently no cause is found, especially in young patients.

Aortic Dissection↗
PubMed1996

Granule-laden perivascular cells observed in rabbits with experimental cerebral atherosclerosis.

Granule-laden perivascular cells distributed around the fine vessels in brain of hypertensive rabbits fed a cholesterol diet were examined by electron microscopy. Perivenule granule-laden cells contained secondary lysosomes, residual bodies, Golgi vesicles, fusion vesicles, and vacuoles. In periarteriole granule-laden cells, secondary lysosomes and vacuoles were not prominent. Findings indicated that the granule-laden cell may be a histiocyte that appears during the vascular reaction to hypertension and hypercholesterolemia. This vascular reaction may occur more strongly in the veins than the arteries.

Animals↗
PubMed1985

Delayed experimental atherosclerotic involvement of cerebral arteries in monkeys and rabbits (light, sem and tem observations).

In monkeys (Rhesus and Cynomolgus) and in rabbits on atherogenic diets, the experimental atherosclerotic involvement of cerebral arteries is strongly delayed. When extracranial arteries appear already heavily involved, no or minimal involvement of intracranial arteries is found even at scanning and/or transmission EM examination. The Concanavalin A reactivity, which is positive at the endothelial cell surface in other arterial districts, is lacking in the cerebral arteries of monkeys and rabbits. The possible significance of these findings is evaluated.

Animals↗
PubMed1995

Safety and efficacy of percutaneous transluminal angioplasty for intracranial atherosclerotic stenosis.

BACKGROUND AND PURPOSE: Percutaneous transluminal angioplasty (PCTA) is increasingly used to treat extracerebral arterial stenosis. The present study evaluates the safety and efficacy of PCTA treatment of symptomatic intracranial atherosclerotic stenosis. METHODS: A series of 22 vessels in 17 patients were treated with PCTA. All patients had recurrent neurological symptoms referable to the stenotic vessel despite optimal medical therapy. Critical (> 70%) arterial stenosis was confirmed by angiogram, and angioplasty was performed with a 3.0- to 3.5-mm Stealth balloon. RESULTS: The average preangioplasty stenosis (North American Symptomatic Carotid Endarterectomy Trial criteria) was 72 +/- 8% (mean +/- SD), with a significant improvement seen after angioplasty; the best angiographic stenosis (after healing of intimal injury, if any) was 43 +/- 24% (P < .001). Overall PCTA was successful in 82% of the vessels. There were two strokes during angioplasty for a 30-day morbidity rate of 9.1% per treated vessel and 11.7% per case. The other 15 patients were clinically evaluated at 3 and 6 months; all cases were without further events. Restenosis was evaluated in 8 patients (12 vessels) with an angiogram at 6 months showing further improvement compared with the initial post-PCTA stenosis (51 +/- 10% versus 37 +/- 21% [P = .05]). CONCLUSIONS: PCTA may be a beneficial therapy in selected cases of symptomatic intracranial atherosclerotic stenosis. Further study using a randomized trial is needed.

Aged↗