By Marcel Vastesaeger M.D. (auth.), Stewart Wolf (eds.)
Substantial growth towards reconciling disparate theories of the pathogenesis of arteriosclerosis was once recorded in quantity I of this e-book. the complaints of an interdisciplinary workshop convention held at Lindau. Germany, April 19-25, 1970. powerful proof was once advert duced that the early levels of arteriosclerosis include intimal proliferation just like that linked to the rise in arteri al dimension and quality that characterizes general progress. The findings defined bear in mind a concept proposed through Richard Thoma (Thoma and Kaefer, 1889) of Heidelberg towards the tip of the 19th century. He sug gested that the pathogenesis of arteriosclerosis started with intimal thickening that was once firstly adaptive. prior a definite aspect, how ever, the thickening compromised the meals of the artery wall, top necessarily to degenerative adjustments. In 1944 Hueper (Hueper, 1944), reemphasized the danger to the nu tritional help of the artery and proposed that the various etiologic elements in a position to inducing arterial atheroma did so during the ultimate universal pathway of interfering with oxidative mechanisms within the vessel wall. hence, it truly is proposed that arteriosclerosis is largely a side of the "behavior" of the artery. the character of the lesion, as a result, relies extra at the biochemical and structural reaction functions of the tissue itself than at the features of some of the etiologic brokers. the concept arteriosclerosis starts off as out of control or disturbed adaptive habit was once shared by means of Duff and likewise via Winternitz (Duff, 1954; Winternitz, 1954).
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Great growth towards reconciling disparate theories of the pathogenesis of arteriosclerosis used to be recorded in quantity I of this e-book. the complaints of an interdisciplinary workshop convention held at Lindau. Germany, April 19-25, 1970. powerful facts was once advert duced that the early levels of arteriosclerosis encompass intimal proliferation just like that linked to the rise in arteri al dimension and quality that characterizes basic progress.
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Extra resources for The Artery and the Process of Arteriosclerosis: Measurement and Modification
70 • o 5 20 5 , "l', d,' ~ d '' 10 " I 10 20 :'l II' : :" 50 50 p 100 100 - PER 1,000_FOPULATION "C e ~ H >-'l c::: 0:1 H :::e >-'l tfl H t::j Z o f:3 H t'"' ~ c::: 44 CHAPTER 2 B. SPECIES DIFFERENCES IN ANIMALS DR. FRENCH: Comparative pathology and comparative physiology have contributed a great deal to our understanding of the variable factors that can modify the way in which we develop or progress. We may need to recognize a division in this question of species differences between the incidence or prevalence of spontaneous lesions in animals other than man, and secondly, the susceptibility of different animal species to experimental arteriosclerosis.
SINAPIUS: I think it is general experience that myocardial infarctions are very large if they are in young persons. They are usually caused by thrombi that occlude only a short segment, the site of a stenosing arteriosclerotic plaque, with the remainder of the arterial tree free of lesions. DR. ROBERTSON: I wish to emphasize that our study of isolated segmental coronary stenosis is being carried out with a selected group of patients, since they all must have coronary artery disease of sufficient clinical severity to require evaluation by coronary cineangiography and direct surgical treatment of the segmental coronary lesions.
I think there are. The point here is that it depends on what part of the population we are looking at. Usually the hospital population of myocardial cases is different from the people dying suddenly outside the hospital. MEASUREMENT AND CONSEQUENCES 19 DR. SINAPIUS: I think that there is no complete occlusion by plaques without an associated occluding thrombus. In my experience even extensive hemorrhage into atherosclerotic intima plaques does not cause occlusion, but only marked stenosis. DR. VASTESAEGER: I think we have seen cases in which the occlusion was complete and looked like an old atheroma, but we evoked a few hours ago the thrombogenic theory: how should we distinguish an old thrombus, which could look like an atheroma, from an original thrombus.