Clinical measurement of arterial stiffness obtained from noninvasive pressure waveforms
Clinical measurement of arterial stiffness obtained from noninvasive pressure waveforms
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DOI：
10.1016/j.amjhyper.2004.10.009
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发表时间：
2005-01-01
影响因子：
3.2
通讯作者：
Nichols, WW
中科院分区：
文献类型：
--
作者：
Nichols, WW
主动脉脉波速度（PWV）和增强指数是心血管不良事件的独立预测因子，包括死亡率。在高血压和衰老患者中，中央弹性动脉变得僵硬，舒张压降低，中央收缩压和脉压增加，这是由于PWV增加和反射波从外周早期返回心脏所致。从中心动脉（主动脉）和外周动脉（桡动脉）的压力波形中都可以获得动脉硬度等有价值的动脉特性信息，但波反射振幅的绝对值和浪费的左室（LV）压力能量只能从中心动脉压力波形中获得。随着动脉系统变硬，中央收缩压和脉压明显增加，左室能量浪费，脉压放大减小。主动脉收缩压和脉压的升高主要是由于PWV和波反射振幅的增加，而入射波振幅的增加很小。对于弹性动脉非常僵硬的个体（例如，患有孤立性收缩期高血压的老年人），舒张压降低。这些压力成分的变化增加了左室后负荷和心肌需氧量，从而导致心室排空与动脉脉搏波传递不匹配，从而促进心室肥厚。高龄或高血压导致的高收缩压和脉压增加了环动脉壁应力，这可能导致内侧弹性蛋白的破坏，增加局部疲劳、内皮损伤和动脉粥样硬化发展的可能性。血管扩张药物对中央大弹性动脉的直接作用可能不大，但同时对周围肌肉动脉的作用可使波反射幅度减小，并显著降低收缩压、脉压和心室后负荷。这些对中心动脉压的有益作用可以在袖带血压（BP）降低或不降低的情况下发生，这可以解释血管紧张素转换酶抑制剂和血管紧张素受体阻滞剂等药物明显的“压力无关”作用。因此，对高血压及其并发症的最佳治疗应考虑动脉僵硬、主动脉压升高、左室能量浪费等因素，并将其降低到尽可能低的水平。(C) 2005中国高血压杂志
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 after-load 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. (C) 2005 American Journal of Hypertension, Ltd.