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Updated: Jun 21, 2026
Utilizing Percutaneous Ventricular Assist Devices in Acute Myocardial Infarction Complicated by Cardiogenic Shock
Published on: June 12, 2021
First evaluation of a novel pulsatile LVAD: Feasibility and haemodynamic impact in acute heart failure
Sara Knigge1, Marcelo B Bastos2, Bastian Schmack1
1Department of Cardiac-, Thoracic-, Transplantation and Vascular Surgery, Hannover Medical School, Hannover, Germany.
Aims:
Non-pharmacological therapies for acute decompensated heart failure (HF) and cardiogenic shock have evolved considerably in recent decades. Short-term mechanical circulatory support (MCS) devices can be used as circulatory backup. While nearly all available devices use continuous flow, evidence indicates that pulsatile flow can be more effective. This study presents the first experimental use of a novel counter-pulsatile left ventricular (LV) assist device (LVAD) with a primary focus on assessing its feasibility and effectiveness.
Methods:
The pulsatile ventricular assist platform (pVAP) was applied in six porcine models of acute ischaemic HF with the inlet in the left atrium and the outlet in the aorta. HF was induced through stepwise ligation of the left anterior descending artery and its diagonal branches. The pVAP functioned driven by a conventional IABP console while LV pressure-volume (PV) loops and standard haemodynamics with the device OFF and ON were recorded. Absolute values and percent variations were compared using Mann-Whitney's U test and Wilcoxon's sign-rank test.
Results:
The device's output flow is frequency dependent, with an output flow of 2.64 ± 0.22 L/min at 80 bpm. Activation reduced the EDV [132 (90-145) vs. 118 (83-130) mL, P < 0.05], EDP 9 (6-10) vs. 6 (5-9) mmHg, P < 0.001], native cardiac output [CON, 3.64 (2.88-6.71) vs. 1.67 (1.24-2.48) L/min, P < 0.001] and myocardial oxygen consumption [pressure-volume area * heart rate (PVA*HR), 4592 (2944-9272) vs. 2901 (1915-4437) mJ, P < 0.001]. Contractility decreased, with right-shifting the end-systolic PV relationship (ESPVR) while ESP and forward cardiac output COF were constant. The mean arterial pressure increased [54 (48-60) vs. 49 (42-55) mmHg, P < 0.001] and mPAP decreased [10 (8-11) to 9 (7-10) mmHg, P < 0.01]. The PV loop shifted left and downward. No changes occurred in the passive-elastic properties of the LV in diastole.
Conclusions:
The pVAP reduced the LV mechanical load while increasing systemic pressures and reducing pulmonary pressures. Its functionality as an LVAD is characterised by consistent and predictable performance. Further research is necessary to elucidate the physiological and clinical impact of the device in animals and, subsequently, in humans.
