Background: The end-systolic pressure-volume relationship is often considered as\r\na load-independent property of the heart and, for this reason, is widely used as\r\nan index of ventricular contractility. However, many criticisms have been\r\nexpressed against this index and the underlying time-varying elastance theory:\r\nfirst, it does not consider the phenomena underlying contraction and second, the\r\nend-systolic pressure volume relationship has been experimentally shown to be\r\nload-dependent.\r\nMethods: In place of the time-varying elastance theory, a microscopic model of\r\nsarcomere contraction is used to infer the pressure generated by the contraction\r\nof the left ventricle, considered as a spherical assembling of sarcomere units. The\r\nleft ventricle model is inserted into a closed-loop model of the cardiovascular\r\nsystem. Finally, parameters of the modified cardiovascular system model are\r\nidentified to reproduce the hemodynamics of a normal dog.\r\nResults: Experiments that have proven the limitations of the time-varying\r\nelastance theory are reproduced with our model: (1) preload reductions, (2)\r\nafterload increases, (3) the same experiments with increased ventricular\r\ncontractility, (4) isovolumic contractions and (5) flow-clamps. All experiments\r\nsimulated with the model generate different end-systolic pressure-volume\r\nrelationships, showing that this relationship is actually load-dependent.\r\nFurthermore, we show that the results of our simulations are in good agreement\r\nwith experiments.\r\nConclusions: We implemented a multi-scale model of the cardiovascular system,\r\nin which ventricular contraction is described by a detailed sarcomere model.\r\nUsing this model, we successfully reproduced a number of experiments that have\r\nshown the failing points of the time-varying elastance theory. In particular, the\r\ndeveloped multi-scale model of the cardiovascular system can capture the loaddependence\r\nof the end-systolic pressure-volume relationship.
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