Left ventricular (LV) dilatation is commonly seen with LV failure and is often aggravated during venoarterial extracorporeal membrane oxygenation (VA ECMO). In this context, the intricate interaction between left and right heart function is considered to be of pivotal importance, yet mechanistically not well understood. We hypothesize that a preserved or enhanced right heart contractility causes increased LV loading both with and without VA ECMO. A closed-loop in-silico simulation model containing the cardiac chambers, the pericardium, septal interactions, and the pulmonary and systemic vascular systems with an option to connect a simulated VA ECMO circuit was developed. Right ventricular contractility was modified during simulation of severe LV failure with and without VA ECMO. Left atrial pressures increased from 14.0 to 23.8 mm Hg without VA ECMO and from 18.4 to 27.0 mm Hg under VA ECMO support when right heart contractility was increased between end-systolic elastance 0.1 and 1.0 mm Hg/ml. Left-sided end-diastolic volumes increased from 125 to 169 ml without VA ECMO and from 150 to 180 ml with VA ECMO. Simulations demonstrate that increased diastolic loading of the LV may be driven by increased right ventricular contractility and that left atrial pressures cannot be interpreted as a reflection of the degree of LV dysfunction and overload without considering right ventricular function. Our study illustrates that modelling and computer simulation are important tools to unravel complex cardiovascular mechanisms underlying the right-left heart interdependency both with and without mechanical circulatory support.