No 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.

No abstract

Pulse pressure, especially in central arteries, is an independent predictor of adverse cardiovascular events in patients with increased elastic artery stiffness (or elastance). The central arterial pressure wave is composed of a forward traveling wave generated by left ventricular ejection and a later arriving reflected wave from the periphery. Increased stiffness of elastic arteries is the primary cause of increased pulse pressure in subjects with degeneration and hyperplasia of the arterial wall. As stiffness increases, transmission velocity of both forward and reflected waves increase, which causes the reflected wave to arrive earlier in the central aorta and augments pressure in late systole [ie, augmentation index = (augmented pressure/pulse pressure) increases]. These changes in wave reflection properties are associated with vascular disease and aging and cause an increase in left ventricular afterload, myocardial mass, and oxygen consumption. Vasoactive drugs have little direct effect on large elastic arteries but can markedly change wave reflection amplitude and augmentation index by altering stiffness of the muscular arteries and modifying transmission velocity of the reflected wave from the periphery to the heart. This change in amplitude and timing of the reflected wave causes a generalized change in central arterial systolic and pulse pressure that is not detected by cuff pressure measurements in the brachial artery.