Systolic blood pressure: arterial compliance and early wave reflection, and their modification by antihypertensive therapy.

Arterial stiffness (the inverse of compliance) is the major determinant of left ventricular and central aortic peak systolic pressure. Recent prospective epidemiological studies (MRFIT, Framingham) have confirmed the importance of systolic (rather than diastolic) pressure in the development of cardiac failure and stroke, and in all-cause mortality. Arteries stiffen in hypertension and with increasing age. Arterial stiffening increases systolic pressure by two mechanisms. The first is by causing a higher pressure to be generated at the peak of ventricular ejection (through increase in aortic characteristic impedance), and the second is by causing a secondary rise attributable to early return of wave reflection from peripheral sites (through an increase in arterial pulse wave velocity). ACE inhibitors, and also nitrates, decrease arterial stiffness. They also dilate peripheral conduit arteries; this reduces wave reflection. These drugs thus reduce systolic pressure in central arteries not only by reducing arterial stiffness but also by reducing inappropriately early wave reflection. Quantitatively, the latter action seems to be more important than the former. Neither action is seen with beta-blocking agents. These beneficial actions on central systolic pressure are not always apparent when pressure is measured in a peripheral artery such as the brachial or radial. This is because the reflected wave constitutes the peak of the pressure wave in central arteries but is usually just an undulation on the downstroke of the wave in peripheral arteries. Hence sphygmomanometric recordings underestimate reduction in central systolic pressure and in left ventricular load brought about by ACE inhibitors and by nitrates.