Search

As a non-invasive assisted circulation therapy, enhanced external counterpulsation (EECP) has demonstrated potential in treatment of lower-extremity arterial disease (LEAD). However, the underlying hemodynamic mechanism remains unclear. This study aimed to conduct the first prospective investigation of the EECP-induced responses of blood flow behavior and wall shear stress (WSS) metrics in the femoral artery. Twelve healthy male volunteers were enrolled. A Doppler ultrasound-based approach was introduced for the in vivo determination of blood flow in the common femoral artery (CFA) and superficial femoral artery (SFA) during EECP intervention, with incremental treatment pressures ranging from 10 to 40 kPa. Three-dimensional subject-specific numerical models were developed in 6 subjects to quantitatively assess variations in WSS-derived hemodynamic metrics in the femoral bifurcation. A mesh-independence analysis was performed. Our results indicated that, compared to the pre-EECP condition, both the antegrade and retrograde blood flow volumes in the CFA and SFA were significantly augmented during EECP intervention, while the heart rate remained constant. The time average shear stress (TAWSS) over the entire femoral bifurcation increased by 32.41%, 121.30%, 178.24%, and 214.81% during EECP with treatment pressures of 10 kPa, 20 kPa, 30 kPa, and 40 kPa, respectively. The mean relative resident time (RRT) decreased by 24.53%, 61.01%, 69.81%, and 77.99%, respectively. The percentage of area with low TAWSS in the femoral artery dropped to nearly zero during EECP with a treatment pressure greater than or equal to 30 kPa. We suggest that EECP is an effective and non-invasive approach for regulating blood flow and WSS in lower extremity arteries. [ABSTRACT FROM AUTHOR]

Enhanced external counterpulsation (EECP) is a noninvasive treatment method for coronary artery atherosclerosis that acts on the vascular endothelial cells. The intracoronary hemodynamic parameters that influence long-term treatment effect are the fundamental factors for the inhibition of intimal hyperplasia, which cannot be measured in real time. In order to optimize the long-term treatment effect of coronary heart disease, it is necessary to establish a method for quantified calculation of intracoronary hemodynamic parameters during counterpulsation to research the long-term hemodynamic mechanism of EECP. A geometric multiscale model coupled by the zero-dimensional (0D) lumped parameter model and the three-dimensional (3D) model of narrow coronary artery was established for the simulation of intracoronary hemodynamic environment. The 3D model was used to calculate the hemodynamic parameters such as wall shear stress (WSS) and oscillatory shear index (OSI), while the 0D model was used to simulate the blood circulatory system. Sequential pressure was applied to calves, thighs, and buttocks module in 0D model with the consideration of vessel collapse. Hemodynamic performance was compared with clinical reports to verify the effectiveness of the method. There were significant increases of the diastolic blood pressure (DBP), coronary flow, and the area-averaged WSS during application of EECP, while OSI behind stenosis has some decrease. The waveforms of coronary flow has good similarity with the clinical measured waveforms, and the differences between calculated mean arterial pressures (MAPs) and clinical measurements were within 1%. The fundamental factor in the cure of coronary heart disease by EECP is the improvement of WSS and the decrease of OSI. Comparing with the clinical reports, the immediate hemodynamic changes demonstrate the effectiveness of model. Intracoronary hemodynamic parameters during EECP could be acquired and the method could be used to simulate the long-term treatment effect of EECP. Graphical abstract. [ABSTRACT FROM AUTHOR]

Traditional clinical mode of enhanced external counterpulsation is not targeted for different diseases. Specialized strategies in the treatment of enhanced external counterpulsation for coronary heart disease and cerebral ischemic stroke are supposed to be distinguished. The goal of treatment for coronary heart disease is diastolic blood pressure/systolic blood pressure = Q ≥ 1.2 after counterpulsation, while the goal of treatment for cerebral ischemic stroke is the improvement of mean arterial pressure. A computational lumped parameter model was established for the simulation of hemodynamic effect of enhanced external counterpulsation on two diseases. Vessel collapse was considered during the simulation of counterpulsation. Based on different pressurized and decompressed rate, pressurized moment, pressure duration, and pressure amplitude, different counterpulsation modes were applied to the model and the immediate hemodynamic effects were compared. Results showed that the pressure duration and pressure amplitude had most influence on two diseases. For cerebral ischemic stroke, the longer pressure duration and the higher pressure amplitude of thighs, the higher mean arterial pressure; while for coronary heart disease, the value of Q was highest when the pressure end moment was 0.6 s during a 0.88-s cardiac cycle, and Q had a linear increase in the pressure amplitude of buttocks, but little change with the increase of calves and thighs pressure amplitude. For patients with coronary heart disease, the pressure duration was not supposed to be too long to avoid the increase of systolic blood pressure, and the improvement of pressure amplitude of buttocks could promise a positive treatment effect for coronary heart disease. While for patients with cerebral ischemic stroke, both the long pressure duration of each part and the high pressure amplitude of thighs could result in the systolic blood pressure and diastolic blood pressure have a certain increase, thus promoting the maximum mean arterial pressure and a best treatment.The specialized treatment strategies of EECP for cardiovascular and cerebrovascular disease [ABSTRACT FROM AUTHOR]

Lumped parameter model (LPM) is a common numerical model for hemodynamic simulation of human's blood circulatory system. The numerical simulation of enhanced external counterpulsation (EECP) is a typical biomechanical simulation process based on the LPM of blood circulatory system. In order to simulate patient-specific hemodynamic effects of EECP and develop best treatment strategy for each individual, this study developed an optimization algorithm to individualize LPM elements. Physiological data from 30 volunteers including approximate aortic pressure, cardiac output, ankle pressure and carotid artery flow were clinically collected as optimization objectives. A closed-loop LPM was established for the simulation of blood circulatory system. Aiming at clinical data, a sensitivity analysis for each element was conducted to identify the significant ones. We improved the traditional simulated annealing algorithm to iteratively optimize the sensitive elements. To verify the accuracy of the patient-specific model, 30 samples of simulated data were compared with clinical measurements. In addition, an EECP experiment was conducted on a volunteer to verify the applicability of the optimized model for the simulation of EECP. For these 30 samples, the optimization results show a slight difference between clinical data and simulated data. The average relative root mean square error is lower than 5%. For the subject of EECP experiment, the relative error of hemodynamic responses during EECP is lower than 10%. This slight error demonstrated a good state of optimization. The optimized modeling algorithm can effectively individualize the LPM for blood circulatory system, which is significant to the numerical simulation of patient-specific hemodynamics. [ABSTRACT FROM AUTHOR]

Background: Enhanced external counterpulsation (EECP) is an effective method for treating patients with cerebral ischemic stroke, while hemodynamics is the major contributing factor in the treatment of EECP. Different counterpulsation modes have the potential to lead to different acute and long-term hemodynamic changes, resulting in different treatment effects. However, various questions about appropriate counterpulsation modes for optimizing hemodynamic effects remain unanswered in clinical treatment.Methods: A zero-dimensional/three-dimensional (0D/3D) geometric multiscale model of the cerebral artery was established to obtain acute hemodynamic indicators, including mean arterial pressure (MAP) and cerebral blood flow (CBF), as well as localized hemodynamic details for the cerebral artery, which includes wall shear stress (WSS) and oscillatory shear index (OSI). Counterpulsation was achieved by applying pressure on calf, thigh and buttock modules in the 0D model. Different counterpulsation modes including various pressure amplitudes and pressurization durations were applied to investigate hemodynamic responses, which impact acute and long-term treatment effects. Both vascular collapse and cerebral autoregulation were considered during counterpulsation.Results: Variations of pressure amplitude and pressurization duration have different impacts on hemodynamic effects during EECP treatment. There were small differences in the hemodynamics when similar or different pressure amplitudes were applied to calves, thighs and buttocks. When increasing pressure amplitude was applied to the three body parts, MAP and CBF improved slightly. When pressure amplitude exceeded 200 mmHg, hemodynamic indicators almost never changed, demonstrating consistency with clinical data. However, hemodynamic indicators improved significantly with increasing pressurization duration. For pressurization durations of 0.5, 0.6 and 0.7 s, percentage increases for MAP during counterpulsation were 1.5%, 23.5% and 39.0%, for CBF were 1.2%, 23.4% and 41.6% and for time-averaged WSS were 0.2%, 43.5% and 85.0%, respectively.Conclusions: When EECP was applied to patients with cerebral ischemic stroke, pressure amplitude applied to the three parts may remain the same. Patients may not gain much more benefit from EECP treatment by excessively increasing pressure amplitude above 200 mmHg. However, during clinical procedures, pressurization duration could be increased to 0.7 s during the cardiac circle to optimize the hemodynamics for possible superior treatment outcomes. [ABSTRACT FROM AUTHOR]