Key result
In a computational model of heart failure, continuous flow LVAD therapy decreased right ventricular end-systolic pressure by 53% and pulmonary artery pressure by 71%, while increasing right ventricular ejection fraction by 52% compared to heart failure without LVAD.
Why the study?
Does continuous flow LVAD therapy improve right ventricular mechanics and hemodynamics in a computational model of heart failure?
Does continuous flow LVAD therapy improve right ventricular mechanics and hemodynamics in a computational model of heart failure?
In a computational model, LVAD therapy enhances cardiac output and provides mechanical unloading of both the left and right ventricles, potentially preventing HF-induced pulmonary hypertension.
Answers are grounded in this paper and cite their sources.
LVAD may unload both ventricles in computational HF models; leaves open clinical translation to RV protection or PH prevention.
BACKGROUND AND AIMS: Although it is important to analyze the hemodynamic factors related to the right ventricle (RV) after left ventricular assist device (LVAD) implantation, previous studies have focused only on the alteration of the ventricular shape and lack quantitative analysis of the various hemodynamic parameters. Therefore, we quantitatively analyzed various hemodynamic parameters related to the RV under normal, heart failure (HF), and HF incorporated with continuous flow LVAD therapy by using a computational model. METHODS: In this study, we combined a three-dimensional finite element electromechanical model of ventricles, which is based on human ventricular morphology captured by magnetic resonance imaging (MRI) with a lumped model of the circulatory system and continuous flow LVAD function in order to construct an integrated model of an LVAD implanted-cardiovascular system. To induce systolic dysfunction, the magnitude of the calcium transient function under HF condition was reduced to 70% of the normal value, and the time constant was reduced by 30% of the normal value. RESULTS: Under the HF condition, the left ventricular end systolic pressure decreased, the left ventricular end diastolic pressure increased, and the pressure in the right atrium (RA), RV, and pulmonary artery (PA) increased compared with the normal condition. The LVAD therapy decreased the end-systolic pressure of the LV by 41%, RA by 29%, RV by 53%, and PA by 71%, but increased the right ventricular ejection fraction by 52% and cardiac output by 40%, while the stroke work was reduced by 67% compared with the HF condition without LVAD. The end-systolic ventricular tension and strain decreased with the LVAD treatment. CONCLUSION: LVAD enhances CO and mechanical unloading of the LV as well as those of the RV and prevents pulmonary hypertension which can be induced by HF.
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Park et al. (2018) studied Heart Failure. Continuous flow left ventricular assist device (LVAD) vs. Heart failure condition without LVAD was evaluated on Right ventricular end systolic pressure (RVESP) in mmHg. In a computational model of heart failure, continuous flow LVAD therapy decreased right ventricular end-systolic pressure by 53% and pulmonary artery pressure by 71%, while increasing right ventricular ejection fraction by 52% compared to heart failure without LVAD.
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