The acute decrease in LV volume in heart-failure patients following PLV resulted at short-term in unchanged SV, increases in LVEF, and decreases in peak wall stress. The increase in LV synchrony with PLV suggests that the transition to a more uniform LV contraction and relaxation pattern might be a rationale of the working mechanism of PLV.

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Restricted right ventricular filling is the primary cause of the strong decrease in cardiac output during tilting. The Enabler right ventricular support can currently not restore cardiac output to pre-tilting values, mainly caused by its limited output and a decrease in right ventricular output upon Enabler activation. Constant monitoring of cardiac output is crucial during (unsupported or supported) tilting as blood pressure alone may not reflect the extent of the reduction in cardiac function.

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