Design and Numerical Evaluation of an Axial Partial-assist Blood Pump for Chinese and other Heart Failure Patients

2017 ◽  
Vol 40 (9) ◽  
pp. 489-497 ◽  
Author(s):  
Guang-Mao Liu ◽  
Dong-Hai Jin ◽  
Jian-Ye Zhou ◽  
Xi-Hang Jiang ◽  
Han-Song Sun ◽  
...  
Keyword(s):  
Heart Failure ◽  
Shear Stress ◽  
Flow Rate ◽  
Tangential Velocity ◽  
Pressure Head ◽  
Left Ventricular ◽  
Blood Pump ◽  
Partial Support ◽  
Heart Failure Patients ◽  
Cantilever Structure

A fully implantable axial left ventricular assist device LAP31 was developed for Chinese or other heart failure patients who need partial support. Based on the 5-Lpm total cardiac blood output of Chinese without heart failure disease, the design point of LAP31 was set to a flow rate of 3 Lpm with 100-mmHg pressure head. To achieve the required pressure head and good hemolytic performance, a structure that includes a spindly rotor hub and a diffuser with splitter and cantilevered main blades was developed. Computational fluid dynamics (CFD) was used to analyze the hydraulic and hemodynamic performance of LAP31. Then in vitro hydraulics experiments were conducted. The numerical simulation results show that LAP31 could generate a 1 to 8 Lpm flow rate with a 60.9 to 182.7 mmHg pressure head when the pump was rotating between 9,000 and 12,000 rpm. The average scalar shear stress of the blood pump was 21.7 Pa, and the average exposure time was 71.0 milliseconds. The mean hemolysis index of LAP31 obtained using Heuser's hemolysis model and Giersiepen's model was 0.220% and 3.89 × 105% respectively. After adding the splitter blades, the flow separation at the suction surface of the diffuser was reduced. The cantilever structure reduced the tangential velocity from 6.1 to 4.7–1.4 m/s within the blade gap by changing the blade gap from shroud to hub. Subsequently, the blood damage caused by shear stress was reduced. In conclusion, the hydraulic and hemolytic characteristics of the LAP31 are acceptable for partial support.

Numerical Design of a Partial-Support Axial Blood Pump

2019 ◽  
Author(s):  
Guangmao Liu ◽  
Donghai Jin ◽  
Mengyu Wang ◽  
Xingmin Gui
Keyword(s):  
Heart Failure ◽  
Exposure Time ◽  
Severe Heart Failure ◽  
Pressure Head ◽  
Rotor Blades ◽  
Blood Pump ◽  
Partial Support ◽  
Hydraulic Efficiency ◽  
Heart Failure Patients ◽  
Cfd Method

Abstract Partial-support is the main support mode for “less sick” patients with severe heart failure. But there were fewer partial-support blood pumps for clinical use. An implantable partial-support axial blood pump was developed for heart failure patients. To gain better hemolytic performance and lower pump thrombus risk, the rotor blades were extended to the contractive section of the rotor hub while cone-bearing was adopted. The hydraulic and hemolytic performance of the blood pump was simulated and analyzed by computational fluid dynamics (CFD) method. The flow velocity, hydraulic efficiency, exposure time, scalar shear stress (SSS) and hemolytic performance of the axial blood pump was analyzed. The numerical results showed that the axial blood pump could produce a 1–8 Lpm flow rate with a 54.7–186.7 mmHg pressure head when the pump rotating from 9000 to 13000 rpm. The hydraulic efficiency and SSS distribution corresponded with the typical performance of a blood pump. The mean hemolysis index of the blood pump calculated by the Giersiepen’s model was 5.0 × 10−5%. After extending the rotor blades to the contractive section of the rotor hub, the spiral flow at the inlet of the rotor impeller was reduced. Hemolysis in the blood pump was improved because the exposure time was reduced and the blood damage caused by SSS was reduced.. The designed blood pump satisfies the clinical requirements of partial-assist for less-sick heart failure patients.

Cardiac mitofusin-1 is declined in non-responding patients with idiopathic dilated cardiomyopathy

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
Y Hsiao ◽  
I Shimizu ◽  
T Wakasugi ◽  
S Jiao ◽  
T Watanabe ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Heart Failure ◽  
Ventricular Myocytes ◽  
Severe Heart Failure ◽  
Left Ventricular ◽  
Neonatal Rat ◽  
Heart Failure Patients ◽  
Underlying Mechanisms ◽  
Neonatal Rat Ventricular Myocytes ◽  
Mitofusin 1

Abstract Background/Introduction Mitochondria are dynamic regulators of cellular metabolism and homeostasis. The dysfunction of mitochondria has long been considered a major contributor to aging and age-related diseases. The prognosis of severe heart failure is still unacceptably poor and it is urgent to establish new therapies for this critical condition. Some patients with heart failure do not respond to established multidisciplinary treatment and they are classified as “non-responders”. The outcome is especially poor for non-responders, and underlying mechanisms are largely unknown. Purpose Studies indicate mitochondrial dysfunction has causal roles for metabolic remodeling in the failing heart, but underlying mechanisms remain to be explored. This study tried to elucidate the role of Mitofusin-1 in a failing heart. Methods We examined twenty-two heart failure patients who underwent endomyocardial biopsy of intraventricular septum. Patients were classified as non-responders when their left-ventricular (LV) ejection fraction did not show more than 10% improvement at remote phase after biopsy. Fourteen patients were classified as responders, and eight as non-responders. Electron microscopy, quantitative PCR, and immunofluorescence studies were performed to explore the biological processes or molecules involved in failure to respond. In addition to studies with cardiac tissue specific knockout mice, we also conducted functional in-vitro studies with neonatal rat ventricular myocytes. Results Twenty-two patients with IDCM who underwent endomyocardial biopsy were enrolled in this study, including 14 responders and 8 non-responders. Transmission electron microscopy (EM) showed a significant reduction in mitochondrial size in cardiomyocytes of non-responders compared to responders. Quantitative PCR revealed that transcript of mitochondrial fusion protein, Mitofusin-1, was significantly reduced in non-responders. Studies with neonatal rat ventricular myocytes (NRVMs) indicated that the beta-1 adrenergic receptor-mediated signaling pathway negatively regulates Mitofusin-1 expression. Suppression of Mitofusin-1 resulted in a significant reduction in mitochondrial respiration of NRVMs. We generated left ventricular pressure overload model with thoracic aortic constriction (TAC) in cardiac specific Mitofusin-1 knockout model (c-Mfn1 KO). Systolic function was reduced in c-Mfn1 KO mice, and EM study showed an increase in dysfunctional mitochondria in the KO group subjected to TAC. Conclusions Mitofusin-1 becomes a biomarker for non-responders with heart failure. In addition, our results suggest that therapies targeting mitochondrial dynamics and homeostasis would become next generation therapy for severe heart failure patients. Funding Acknowledgement Type of funding source: None

Sign in / Sign up

Export Citation Format

Share Document