Hypertension-Hamer et al. ME JOURNAL 1964;Hanson et al., 1966; Sannerstedt, 1966) the relative depression of cardiac output was similar in the two groups in spite of the electrocardiographic differences. The peripheral resistance rises on standing and then falls during exercise. In group II the resistance does show a tendency to be higher than in group I, as might be expected from the higher systolic pressures, but the changes were not significant. The finding that the mean heart rates as well as the mean cardiac outputs show no difference in the two groups of patients indicates that there is also no difference in stroke volume.Provided there is no change in ventricular volume, the ejection rate reflects the velocity of shortening of the individual myocardial fibres. Patients in group II tend to have bigger hearts on the chest x-ray examination than those in group I. This finding suggests an increase in left ventricular volume in group II, though we have shown a poor correlation between heart size on chest x-ray examination and direct measurements of left ventricular volume in aortic stenosis (Fleming and Hamer, 1968). The slightly faster ejection rate of group II subjects could be accounted for on this basis, as an identical velocity of contraction in a larger ventricle will result in a faster rate of ejection. The relation of the velocity of fibre contraction to the force generated is a useful way of assessing the contractile state of the myocardium (Sonnenblick, 1962). As the force generated by the myocardium in group II patients is, because of both pressure and volume changes, if anything greater than in group I and the ejection rate is no lower, there is no evidence from our studies of impaired myocardial contractility in the patients with the more severe electrocardiographic changes. The higher systolic blood pressures in our patients in group II suggests that the myocardium has to generate greater force in those with S-T segment and T-wave changes. This finding is consistent with the hypothesis that a greater intraventricular systolic pressure leads to a primary change in the S-T segments and T waves by producing localized subendocardial changes which may alter the direction of repolarization (Goldberger, 1947) or interfere with the spread of the activation process (Lepeschkin, 1951). However, the S-T and T-wave changes must represent more than a simple mechanical effect, as they do not resolve immediately when the left ventricular pressure is reduced.Our finding that severe left ventricular hypertrophy on the electrocardiogram is particularly related to systolic blood pressure is in keeping with the suggestion (Ramirez and Garcia Pont, 1965) that cardiac size in hypertension is more closely related to systolic than to diastolic pressure. The evidence suggests, as did our previous work , that the systolic pressure is an important determinant of the pathological effect of hypertension on the heart.