Clinical measurement of arterial stiffness obtained from noninvasive pressure waveforms

Abstract

Aortic pulse wave velocity (PWV) and augmentation index are independent predictors of adverse cardiovascular events, including mortality. In hypertension and aging, central elastic arteries become stiffer, diastolic pressure decreases, and central systolic and pulse pressures are augmented due to increased PWV and early return of reflected waves to the heart from the periphery. Valuable information on arterial properties such as stiffness can be obtained from both central (aortic) and peripheral (radial artery) pressure waveforms, but absolute values of wave reflection amplitude and wasted left ventricular (LV) pressure energy can only be obtained from the central arterial pressure waveform. As the arterial system becomes stiffer, there is a marked increase in central systolic and pulse pressures and wasted LV energy, along with a decrease in pulse pressure amplification. The increase in aortic systolic and pulse pressures are due primarily to increases in PWV and wave reflection amplitude with a small increase in incident wave amplitude. In individuals with very stiff elastic arteries (eg, in older persons with isolated systolic hypertension), there is a decrease in diastolic pressure. These changes in pressure components increase LV afterload and myocardial oxygen demand and therefore cause an undesirable mismatch between ventricle emptying and arterial pulse wave transmission, which promotes ventricular hypertrophy. High systolic and pulse pressures resulting from advanced age or hypertension increase circumferential arterial wall stress, which likely causes breakdown of medial elastin and increases the possibility of local fatigue, endothelial damage and development of atherosclerosis. Vasodilator drugs may have little direct effect on large central elastic arteries, but at the same time, their effects on peripheral muscular arteries reduce wave reflection amplitude and markedly lower systolic and pulse pressures and ventricular afterload. These beneficial effects on central arterial pressure can occur with or without a reduction in cuff blood pressure (BP) and may explain the apparent "pressure-independent" effects of drugs such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers. Therefore, optimal treatment of high BP and its complications should include consideration of arterial stiffness, augmentation of aortic pressure, and LV wasted energy, all of which should be reduced to the lowest possible level.

Relationship between blood pressure parameters and pulse wave velocity in normotensive and hypertensive subjects: invasive study

“…For example, during vasodilation, both pressure and diameter decrease in elastic arteries, causing a passive decrease in wall stiffness and a decrease in PWV. 35 As it was cross-sectional and because there was no BP manipulation, our study reveals chronic changes of elastic arteries well. It was further supported by the fourth module of multiple regression analysis (Table 4).…”

Radial pulse transit time is an index of arterial stiffness

“…[1][2][3] Aging is accompanied by increased arterial stiffness and aortic PWV, 4,5 leading to a decrease in PTT. This suggests that arterial stiffness might be assessed by PTT.…”

Impact of passive vibration on pressure pulse wave characteristics

“…Reduction of the amplitude of the reflected wave causes a decrease in AP and AIx, leading to a reduction in left ventricular afterload. 6,[36][37][38] The principal limitations of the present study are the lack of direct measurement of arterial vasodilation and vasoactive substances. However, AIx and P2 changes after acute exercise and vasoactive drug infusion are due to vasodilation of muscular arteries.…”

“…30,31 The aortic pressure pulse wave is a composite of an early forward wave (P1) and a reflected wave traveling from the periphery back to the aorta (P2). 6 In cardiac patients with increased AIx, aortic SBP is determined by P2 whereas peripheral SBP is more dependent on P1. 31 Thus, the reduction in aortic P2 after administration of a vasodilator drug causes a decrease in aortic SBP.…”

“…[1][2][3][4][5] The AIx, a marker of wave reflection, is influenced by both the magnitude and the timing of the pressure wave reflected from peripheral sites to the aorta. 6 Accordingly, increased AIx has been associated with high rates of cardiovascular morbidity and mortality, 5,7 due to an increased left ventricular afterload. 8 Previous research has demonstrated that the AIx reduces following an acute bout of cycling exercise 9,10 and low-intensity leg resistance exercise in healthy young individuals.…”