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The authors described the pathophysiology of left ventricle (LV) overload and correctly underlined the role of the preload in this complex mechanism. LV preload has been often underestimated as an important determinant of LV distension during venoarterial (VA) extracorporeal life support (ECLS). Indeed, the patient's venous return usually exceeds the ECLS drainage and subsequently passes through the pulmonary circulation. As a consequence, the residual transpulmonary blood flow and bronchial venous return may not be counterbalanced by the reduced LV ejection due to impaired contractility and retrograde ECLS-generated blood flow toward the aortic valve, leading to LV dilation and pulmonary congestion.