Ventricular aneurysms: a geometrical-dynamical model.
A geometrical-dynamical model has been designed with the aim to reproduce the early phases of ventricular aneurysms formation. Possible deleterious forces within a solidary-dynamic structure start when a partial or localized loss of contractility arises. A following important aspect is related to the compressive effects of those altered cells over the normally contracting neighborhood. An abnormal packing of elements within a cyclic-dynamic structure has taken place and consequently new abnormal forces of compression between altered and normal cells will result in a longitudinal course of progression. When this circle crosses itself, a ventricular aneurysm will be completed. The process could be ascribed to an elastic phenomenon activated by a compressive stress. The chain of events included in this model has been matched with usual pathological findings of ventricular aneurysms, i.e. wavy and broken fibres neatness of aneurysmatic borders, and apical outstanding incidence of aneurysms etc. The proposed geometrical-dynamical model admits the possibility of an interruption in the 7 steps process of ventricular aneurysm formation by means of a "barrier effect". This effect has been related to the fibrous extracellular matrix with its differences in amount and quality of scar formation, which is possible to be observed in ischemic heart disease and chronic Chagas' cardiomyopathy and in some other illustrative entities. An analysis of this particular aspect of scar formation on diverse aneurismogenic entities with different reactions of collagen and particularly different figures of incidence of aneurysmatic formation, show a high correlation with possible alternatives disclosed by this geometrical-dynamical model.
Castagnino
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HE
Department of Medicine, Hospital de Clínicas José de San Martín, Facultad de Medicina, Universidad de Buenos Aires, Argentina.
Toranzos
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FA
D003198:Computer Simulation; D004548:Elasticity; D006322:Heart Aneurysm / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D008433:Mathematics; D008954:Models, Biological; D009200:Myocardial Contraction; D009206:Myocardium / Q000473:pathology