Effects of arterial stiffness, pulse wave velocity, and wave reflections on the central aortic pressure waveform

Abstract

Brachial systolic and pulse blood pressures (BPs) are better predictors of adverse cardiovascular (CV) events than diastolic BP in individuals older than 50 years. The principal cause of increased systolic and pulse BP is increased stiffness of the elastic arteries as a result of degeneration and hyperplasia of the arterial wall. Recent studies have shown that central BP, the pressure exerted on the heart, brain, and kidneys, is a better predictor of CV risk than brachial BP. As stiffness increases, reflected wave amplitude increases and augments pressure in late systole, producing an increase in left ventricular afterload and myocardial oxygen demand. Vasoactive drugs have little direct effect on large human elastic arteries but can markedly modify wave reflection by altering stiffness of the muscular arteries and changing pulse wave velocity of the reflected wave from the periphery to the heart. Vasodilators decrease the amplitude and increase the travel time (or delay) of the reflected wave, causing a generalized decrease in systolic BP. The decrease in systolic BP brought about by this mechanism is grossly underestimated when systolic BP is measured in the brachial artery.

Figure 1

Age‐related changes in aortic (PWV_e) and brachial artery (PWV_m) transmission velocity in healthy human patients. Data are from the Anglo‐Cardiff Collaborative Trial (ACCT) study population. ⁸ Note the relatively linear relationship for PWV_m (dotted line and open squares), compared with the curved relationship for PWV_e (solid line and closed squares), which changes much more, ³² especially in patients 50 years and older. The broken vertical line represents the age at which the arterial stiffness gradient reverses.

Figure 2

High‐fidelity recordings of ascending aortic pressure and flow waves in 2 middle‐aged men of similar height using a multisensor catheter; 1 patient (56 years of age) was normotensive (left) and the other (61 years of age) had isolated systolic hypertension (ISH)(right). Ascending aortic PWV_e was 466 cm/s in the normotensive patient and 583 cm/s in the ISH patient. A distinct inflection point (P_i) can be identified in the normotensive patient but, in the ISH patient, the reflected pressure wave arrives early and merges with the incident wave so that P_i cannot be identified. Therefore, P_i is measured at the point on the pressure wave where peak flow occurs. These morphologic changes in pressure and flow waves are associated with a decrease in travel time (Tr) of the waves to the periphery and back to the heart and an increase in AI_a from 32% to 40%. The different components of the ascending aortic pressure wave are shown at the left. P_s indicates peak systolic blood pressure; P_d, minimum diastolic blood pressure; Tr, the round‐trip travel time of the forward wave from the ascending aorta to the major reflecting site and back; ED, ejection duration (ED ‐ Tr is reflected wave systolic duration); P_s ‐ P_i, reflected wave amplitude; P_i ‐ P_d, forward wave amplitude; P_s ‐ P_d, pulse pressure; augmentation index, (P_s ‐ P_i)/(P_s ‐ P_d).

Figure 3

Measured radial artery (left) and synthesized aortic pressure (right) waves recorded in a heart failure patient (53 years of age) before (top) and after heart transplant (bottom). The failing left ventricle could not generate enough force to overcome the late systolic pressure boost usually seen at this age. This reduced contractile force resulted in an abbreviated ejection duration (ED) (240 ms) and a low augmentation index (AI_a). After heart transplant, the left ventricle could again generate the necessary force to overcome the late systolic pressure boost, which caused an increase in ED (309 ms) and AI_a. Heart rate was similar before and after transplant (75 b/m). Sp, indicates systolic pressure; Dp, diastolic pressure; MP, mean pressure; PP, pulse pressure; HR, heart rate.

Figure 4

Measured radial artery (left) and synthesized aortic pressure (right) waves recorded in a hypertensive patient at baseline (top) and after treatment with the angiotensin‐converting enzyme inhibitor lisinopril (bottom). The vasodilator caused a delay in transmission velocity of the reflected wave from the periphery to the heart that resulted in a decline of augmented pressure (from 18 mm Hg to 8.0 mm Hg), augmentation index (AI_a) (from 33% to 20%), and AI_a@75 (from 25% to 16%). Reflected wave systolic duration decreased from 158 ms to 139 ms. Aortic systolic blood pressure decreased 25 mm Hg, while brachial systolic blood pressure was less sensitive, decreasing 18 mm Hg.