Arterial stiffening and vascular/ventricular interaction.

Arterial stiffness is the major determinant of systolic pressure and increases with age and hypertension, especially in the thoracic aorta and major central elastic arteries. The effects of arterial stiffening on aortic and left ventricular systolic pressure are underestimated when taken from conventional recordings of systolic pressure in the brachial artery or in other arteries of the upper limb, as a consequence of pressure wave transmission in the upper limb. A method has been devised to synthesise the ascending aortic pressure wave from the radial or brachial artery pressure wave, as measured invasively by arterial cannula or noninvasively by applanation tonometry. Results obtained in this way are similar to, but more consistent than, those obtained through measurement of carotid artery pressure waves by applanation tonometry. The ability to synthesise the ascending aortic waveform enables one to measure augmentation of late systolic pressure caused by arterial stiffening as well as the effects of antihypertensive drug therapies on systolic pressure augmentation. Results have shown that drugs which dilate small peripheral arteries and thereby reduce wave reflection (nitrates, ACE inhibitors, calcium antagonists) reduce ascending aortic pressure augmentation during systole, often without corresponding reduction in brachial or radial artery systolic pressure. These agents are more appropriate therapy for isolated systolic hypertension than beta-blockers and diuretics.