Left ventricular dynamics, coronary blood flow (Vcor), and myocardial oxygen consumption (MVO2) were determined in normal patients (N), in chronic pressure overload (aortic stenosis, AS), in chronic volume overload (aortic incompetence, AI), and in coronary heart disease (CHD). Peak systolic and enddiastolic wall stress were increased in AS and AI by 26-52 per cent, the systolic stress being preferably increased in AS, whereas enddiastolic stress was markedly greater in AI. Vcor and MVO2 were elevated in both groups by 45-55 per cent (p less than 0.001). Sufficient correlation was present between peak systolic wall stress and the MVO2 (r equal to 0.82). Since at a given wall stress the MVO2 was somewhat increased in AI and AS when compared with N and CHD, the considerable inhancement of the rate of pressure development (AS) was well as of the external cardiac work (AI) may contribute to the increase in overall oxygen consumption. It is concluded that systolic wall stress represents a primary determinant of MVO2 in pressure and volume overload and that the MVO2 increases in these diseases when hypertrophy becomes inappropriate with regard to the pressure and volume demands imposed to the left ventricle.