Late systolic augmentation of the ascending aortic and central arterial pressure wave is a characteristic feature of aging, and is attributable to stiffening of the aorta and major central arteries. It is caused by increased pulse wave velocity in these vessels with early return of wave reflection from peripheral sites, predominantly in the lower part of the body. Augmentation is measurable through identification of the shoulder or early systolic peak of pressure, which corresponds to peak flow in the aorta, and measurement from this point to the second peak, or shoulder of the wave in late systole. Difficulties in measurement of augmentation arise from problems in identification of the initial shoulder, especially when this is close to the foot of the reflected wave, to amplification of the pulse wave between ascending aorta and carotid artery, and to a Venturi effect in the aorta at the peak of aortic flow. Augmentation is systematically higher in the left ventricle than in the aorta, and systematically higher in the aorta than in more peripheral arteries such as the carotid or radial. Since properties of upper limb arteries are relatively constant with age, blood pressure, gender and drug therapy, a generalized transfer function can be used to synthesize the aortic from the radial pressure waveform. Comparison of measured directly and aortic pressure calculated with the SphygmoCor process under control conditions and with nitroglycerine infusion gave values of augmentation with mean difference 0.9, SD 7.7 mmHg, which lie within AAMI criteria for equivalence, as do measures of end systolic pressure (difference 3.8, SD 3.6 mmHg).