The myocardium is an integrated functional unit. The separation of the cardiac cycle into three phases on simultaneous ventricular and arterial pressure curves:contraction, relaxation, diastole, is an artificial distinction of interdependent functions which are superimposed in time in the real mechanical and biochemical phenomena. At the level of the sarcomeres and myofilaments, relaxation is the active process of liberation of the bridges formed between actin and myosin during contraction; diastole is the phase during which there is no cyclic renewal of these bridges, it is the passive phase. Myocardial relaxation in mammals is controlled by the rapid recapture of Ca2+ by the sarcoplasmic reticulum. It plays an important mechanical role during the closure of the aortic semilunar valves, the opening of the mitral valve, the rapid filling of the right ventricle and the diastolic perfusion of the coronary arteries. It is dependent on the load and is influenced by myocardial metabolism (hypoxia, acidosis, ischaemia), temperature and a number of pharmacological agents. Amongst the passive properties of the left ventricle, we need to distinguish between the distensibility of the left ventricle as a filling chamber (parietal rigidity) and the rigidity of each of the myocardial fibres which make up the ventricular wall (myocardial rigidity). The passive properties of the left ventricle can be modified by ventricular geometry, passive mechanical properties of the ventricular wall (thickening, myocardial changes, heart rate and filling rate, cellular oedema, hypoxia, ischaemia, coronary artery filling pressure), the interaction between the pericardium, the right ventricle and the left ventricle and intrathoracic pressure. The large number of factors which are capable of modifying left ventricular relaxation and diastole explains the problems associated with in vivo investigations, which depend on a large number of indices of limited value.