Abstract

Dilated cardiomyopathy is the most common type of the heart failure which can be characterized by impaired ventricular contractility. Mechanical circulatory support devices were introduced into practice for the heart failure patients to bridge the time between the decision to transplant and the actual transplantation which is not sufficient due to the state of donor organ supply. In this study, the hemodynamic response of a cardiovascular system that includes a dilated cardiomyopathic heart under support of a newly developed continuous flow left ventricular assist device—Heart Turcica Axial—was evaluated employing computer simulations. For the evaluation, a numerical model which describes the pressure-flow rate relations of Heart Turcica Axial, a cardiovascular system model describing the healthy and pathological hemodynamics, and a baroreflex model regulating the heart rate were used. Heart Turcica Axial was operated between 8000 rpm and 11000 rpm speeds with 1000 rpm increments for assessing the pump performance and response of the cardiovascular system. The results also give an insight about the range of the possible operating speeds of Heart Turcica Axial in a clinical application. Based on the findings, operating speed of Heart Turcica Axial should be between 10000 rpm and 11000 rpm.

Highlights

  • Dilated cardiomyopathy (DCM) is the most common type of nonischemic cardiomyopathy and a major cause of congestive heart failure [1, 2]

  • We aim to evaluate the hemodynamical response of a DCM cardiovascular system model under support of a newly developed CF-LVAD-Heart Turcica Axial (HTA) [17]

  • There is a range for the optimum operating speed for such a device in the clinical applications and the optimal pump speed is determined according to the hemodynamical data monitoring the cardiac index and the left ventricle size in a patient [14]

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Summary

Introduction

Dilated cardiomyopathy (DCM) is the most common type of nonischemic cardiomyopathy and a major cause of congestive heart failure [1, 2]. It leads to the weakening and enlargement of the heart and impairs its function to pump blood. It can be caused by genetic, viral, immune, alcoholic-toxic, or unknown factors. It can be associated with a different cardiovascular disease. With progression of the disease, systemic arterial pressure decreases and this leads to an increased workload on the right ventricle. Right ventricular systolic pressure and pulmonary arterial pressure increase resulting in pulmonary hypertension [4,5,6,7,8,9,10,11,12,13]

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