Key points are not available for this paper at this time.
Answers are grounded in this paper and cite their sources.
These mouse atrial changes should not yet change practice; leaves open dietary effects on human endocardial structure.
Light and electron microscopic studies were made of atria of mice (TS stock) fed either a normal diet or one high in fat (28% lard), low in protein (8% casein) and hypolipotropic. After four weeks on the high fat diet there was a pronounced thickening and splitting of the endocardial basement membrane into several layers. Concurrently the basal surface of atrial endothelium became indented and irregular. By 5–6 weeks numerous villous projections were present on the luminal surface of endothelial cells at sites other than at cell junctions, and vacuolization of endothelial cells had developed. Vacuole formation began on the basal surface of atrial endothelial cells. Closure of the indentations on the basal surface of endothelial cells seemed to produce the vacuoles. At seven weeks there was degeneration of the endothelial cells and atrial myocardium, with severe swelling of the mitochondria adjacent to unorganized thrombi. After 8–9 weeks small organizing atrial mural thrombi were observed attached to the atrial wall. Growth and organization of the lesion eventually filled the entire atrial lumen. After 20 weeks on the fat diet, 92% of the mice had large atrial thrombi. Control mice did not develop the above changes.
No takes yet. Share an insight, caveat, or question.
Lockwood et al. (1969) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: