The functions of the left and right ventricles are intimately linked. The right ventricle (RV) has transverse muscle fibres in its free wall and also shares oblique fibres in the interventricular septum with the left ventricle (LV). The latter constitute a link between left and right ventricular contractile function such that LV contraction augments RV contraction – a phenomenon called systolic ventricular interaction. When RV afterload is increased (by raised pulmonary artery pressure) overall contractile performance becomes increasingly dependent on this systolic ventricular interaction because the oblique septal fibres are more mechanically efficient than the free wall transverse fibres in conditions of high RV afterload. When LV end diastolic pressure is increased by heart failure due to LV systolic dysfunction, pulmonary artery pressure becomes raised, imposing an increased afterload on the RV. In such patients global LV performance is reduced, consequently systolic ventricular interaction is reduced resulting in a reduction in RV contractile performance even if the RV is not directly involved in the disease process causing LV systolic dysfunction. Furthermore, as the left ventricle becomes progressively more spherical the septal fibres become less oblique, dramatically reducing their mechanical advantage and further impairing RV contractile function. This ultimately leads to clinical right ventricular failure. This in turn typically results in tricuspid regurgitation and a vicious cycle of right ventricular enlargement with further reduction in the oblique nature of the septal fibres. In addition to the systolic interaction of the LV on the RV, when the RV is enlarged and stretches the pericardium, pericardial and right ventricular diastolic pressures may become markedly increased and this can result in constraint to filling of the LV by the pericardium (pericardial constraint) and by the RV via the interventricular septum (diastolic ventricular interaction).