Arterial stiffness: reflections on the arterial pulse.

Arteriosclerosis—arterial stiffening—is the basic cause of isolated systolic hypertension (ISH) and the present epidemic of heart failure in the elderly. Arteriosclerosis is equally important for the development of coronary events, stroke, dementia, and renal failure. The underlying pathology was described by Osler as ‘senile arteriosclerosis’ to distinguish it from essential hypertension (Osler’s ‘diffuse arteriosclerosis’) and ‘nodular arteriosclerosis’ that is now described as atherosclerosis. Although we usually identify the precursor as ISH, the measurement of blood pressure by cuff sphygmomanometer is only a surrogate of the underlying disease and an unsatisfactory method for detecting its early presence and progress. Recognizing this, the European Societies of Cardiology and of Hypertension (ESC and ESH, respectively) established guidelines for the management of arterial hypertension, and drew attention to methods for measuring arterial stiffness as pulse wave velocity or analysing the pulse waveform, which may identify the arterial target organ damage at an early stage. An important step in this field is the publication of a consensus document on arterial stiffness from a European group in good standing with professional associations, and led by Stephane Laurent. Specific statements are given on key issues, based on review and mechanism, practicality of measurement, and evidence of value. The document is a logical development from previous statements and publications including the most recent Handbook of Hypertension to which most authors contributed. It is timely, since the ESC and ESH are reviewing guidelines on management of hypertension in the light of new information that has emerged since the last publication. Why is this necessary when ISH can be recognized years before development of cardiac failure, and can be (but often is not) treated effectively? The problem is with cuff blood pressure measurement—its accuracy when measured simultaneously by different methods, its accuracy in comparison to intra-arterial pressure, its variability throughout the day and night, and its distortion and amplification in transmission from aorta to brachial and radial arteries. Sphygmomanometric cuff inaccuracy is sufficient to warrant independent measures of arterial stiffness and its effect on the heart and other blood vessels. This is discussed in the document, and in recent literature. The report by Laurent et al. described a hierarchy of methods that can be utilized in clinical trials for gauging arterial stiffness and its effect on the cardiovascular system. The first two of these, favoured by ESC/ESH were applied to this purpose over a century ago, and before introduction of the cuff sphygmomanometer—the pulse wave velocity by Young in the early nineteenth century, and by Bramwell and Hill in the early twentieth century, whereas pulse waveform analysis was applied by Marey, Mahomed, Mackenzie, and Osler, and even implemented into life insurance examinations 100 years ago. As Laurent et al. point out, arterial stiffness is an easy concept to understand but immediately becomes complex when one wishes to measure, quantify, and compare. Laurent et al. review all methods used to describe arterial stiffness as biomarkers before focusing on three as being the most practical and relevant for clinical use. Such biomarkers include arterial pressure itself, and must conform with criteria set out by Vasan which include theoretic basis, reproducibility, ease of use, incremental value over other indices known to predict outcome, and ability to monitor and guide treatment. Assessment of all is ongoing, and has to date been positive, with even suggestion of superiority over cuff blood pressure itself in patient management. There may be disagreement from enthusiasts of other techniques, but failure to make the grade to date is based on failure on the Vasan score. Techniques of arterial compliance measurement have generally failed, but are based on an unrealistic model which ignores wave reflection, while for one (HDI) cardiac output is estimated indirectly from age, body size, and pressure values. The three methods selected by Laurent et al. are all basically simple—so are inherently suitable for many clinical applications and multicentre trials. They are also old, with experience collected over decades; hence their shortcomings are reasonably well appreciated. One might expect that the simplest and most direct measurement of pressure and diameter would be the most useful. Laurent et al. recommended this for mechanistic analysis in physiology, pharmacology, and therapeutics rather than for epidemiological studies. The main problem may have been with local pressure measurement—and