Jacob R, Gülch R W
Physiologisches Institut II, Universität Tübingen, F.R.G.
Basic Res Cardiol. 1988 Sep-Oct;83(5):461-75. doi: 10.1007/BF01906676.
On the basis of theoretical considerations and experimental data this study deals with the functional consequences of structural dilatation, particularly in view of Linzbach's concept of chronic heart failure (34-38). After a short review of the literature, a theoretical analysis of the relationship between stroke volume and ventricular inner radius is presented assuming a thick-walled sphere. Presupposing constant contractility, end-diastolic sarcomere length, end-diastolic wall thickness and end-systolic pressure, only a considerable increase of ventricular radius could be the direct cause of ventricular pumping failure - despite increasing wall stress and reduced ejection fraction. Impaired contractility, as well as insufficient hypertrophy and increased systemic pressure, would intensify the adverse consequences of ventricular enlargement to a predictable extent. Thus, hemodynamic and energetic consequences of dilation, although mutually interacting, should in principle be distinguished. Despite considerable simplifications involved in model calculations, the relative significance of contractility, ventricular size, wall thickness, and extracardiac factors (mechanical overload; neuroendocrine reactions) can be estimated in various animal models with congestive failure. Hence, this theoretical and experimental approach permits the modification and deepening of previous concepts of structural dilatation and also has implications for interpreting the effects of therapeutical interventions.
