European Society of Hypertension guidelines recommend use of carotid– femoral pulse wave velocity (cfPWV) as a favored measure of aortic stiffness. However, there is no consensus on the measurement of distance travelled by the pulse wave along the aorta to the femoral artery. The aim of our study was to compare cfPWV, calculated with commonly used noninvasive methods for travel distance assessment, against aortic PWV measured invasively. One hundred and thirty-five patients had aortic PWV measured invasively during cardiac catheterization, from the delay in wave foot and distance travelled as the catheter was withdrawn from the ascending aorta to the aortic bifurcation. On the following day, noninvasive cfPWV was assessed, using the SphygmoCor system, relating the delay between carotid and femoral wavefoot to travel distance, estimated with five different methods on body surface. Mean travel times were in good agreement [(travel time) TTinvasive was 63 ms, TTnoninvasive was 59.3 ms, Spearman's R: 0.8, P < 0.00001]. Mean PWVinvasive was 8.5 m/s. CfPWV, as assessed noninvasively, depended largely on the method used for travel distance estimation: 11.5, 9.9, 8.7, 11.9, and 9.6 m/s, using direct carotid–femoral distance, carotid–femoral minus carotid–suprasternal notch distances, suprasternal notch–femoral minus carotid–suprasternal notch distances, suprasternal notch–femoral plus carotid–suprasternal notch distances, and suprasternal notch–symphysis distance, respectively. There was acceptable correspondence between PWVinvasive and cfPWVnoninvasive (Spearman's R: 0.73–0.77, P < 0.0001). For noninvasive assessment of cfPWV, estimation of pulse wave travel distance is critical. Best agreement with invasive measurements was found for the method of subtracting carotid–suprasternal notch distance from suprasternal notch–femoral distance.

Central aortic pressure waveforms can be calculated from the radial artery pressure waveform using a generalized transfer function to correct for pressure wave distortion in the upper limb. Although validated to standards conventionally applied, reservations are still expressed on use of this process, because of the relatively small number of patients from whom appropriate invasive data were obtained. The study described here supplemented such data with noninvasive data obtained from carotid and radial artery tonometry in 439 patients and normal subjects. The carotid-radial artery transfer function was similar to the aortic-radial when allowance was made for wave travel from aorta to carotid artery. The carotid-radial transfer function was identical in male and female individuals, was similar at different arterial pressures and in mature adults. Differences are relatively small, are seen at frequencies where central pressure wave components are small and are similar to those seen with vasodilator agents in invasive studies. Findings provide further support for use of a generalized transfer function to calculate aortic from upper limb pressure and conform with previously established views on vascular impedance.

Arterial stiffness has been known as a sign of cardiovascular risk since the 19th century. Despite this, accurate measurement and clinical utility ha

The substantial benefits of ramipril over conventional therapy in high-risk patients are not always associated with clinically significant differences in brachial arterial pressure, and largely remain unexplained. We undertook this acute study to establish the magnitude of and reason for different acute effects of ramipril and atenolol on arterial pressure. We enrolled 30 patients, who took 10 mg ramipril, 100 mg atenolol, and placebo at intervals of > or = 7 days, in a randomized, double-blind, placebo-controlled trial. After baseline, measurements were taken at 30-60 min intervals for 5 h, and comprised cuff brachial pressure, radial artery tonometry with generation of central aortic pressure, and pulse wave velocity for aorta, upper limb and lower limb arteries. Both ramipril and atenolol reduced arterial pressure, and the diastolic pressure fall was similar in the aorta and brachial artery, but the systolic pressure fall for ramipril was greater than for atenolol (by 5.2 mmHg, P < 0.0001) in the aorta compared with the brachial artery. The aortic systolic pressure difference with ramipril in comparison with atenolol was accompanied by an absolute difference of 10.7% (P < 0.0001) in the augmentation index, denoting a reduction in peripheral wave reflection by ramipril. The aortic pulse wave velocity fell to a similar degree with ramipril in comparison with atenolol, but fell to a greater degree (1.35 and 0.44 m/s, respectively, P < 0.0001 for both) in muscular arteries of the lower and upper limbs. A greater (average, 5.2 mmHg) decrease in aortic systolic pressure caused by ramipril may explain the greater benefit of ramipril over atenolol. The difference is attributable to decreased stiffness of peripheral arteries and a reduction in wave reflection.

The use of pulse wave analysis with arterial tonometry has accelerated over the last year. Despite approval from the US Food and Drug Administration in 2001 on the use of generalized transfer function to generate the central (aortic) pressure wave from the radial waveform, this technique is still questioned. This review summarizes major findings on (a) value of arterial tonometry in determining indices of cardiovascular function, (b) use of these indices in outcome and drug studies, (c) relevance to major trials on blood pressure reduction. Pulse pressure has emerged as a better predictor of cardiac ischemic events than systolic, diastolic, and mean brachial pressure. Central systolic and pulse pressure and augmentation index have shown an even better relation with cardiovascular events and with outcomes. The claim by specific angiotensin-converting enzyme inhibitor and angiotensin receptor blocker drugs of their benefits ‘beyond blood pressure lowering’ has been challenged on the basis of greater reduction in central and aortic pressure compared with brachial pressure measured by cuff sphygmomanometer, as shown by the pREterax in regression of Arterial Stiffness in a contrOlled double-bliNd study. Augmentation index is higher in hypertension, is inversely related to body height, and can be reduced by exercise. Augmentation index shows a linear relation with age up to 60 years. Regrettably, recent major trials such as the Comparison of Amlodipine versus Enalapril to Limit Occurrences of Thrombosis, Prevention of Events with Angiotensin Converting Enzyme Inhibition, and Valsartan Antihypertensive Long-term Use Evaluation studies have not included pulse wave analysis to distinguish the relative benefit of different drugs. Pulse wave analysis will assist in a better understanding of hypertension as well as in establishing the extent of cardiovascular disease and for monitoring therapy.

Current guidelines on isolated systolic hypertension (ISH) suggest the same treatment to patients of all ages. Application of these guidelines in youth with ISH may not be appropriate, as presently no data show adverse outcome or benefit of drug therapy in this group. Simple noninvasive tonometric techniques now enable physicians to measure the central aortic pressure waveform and amplification of the pressure pulse. ISH in youth is usually caused by high amplification of the central pressure wave, whereas ISH in the elderly (>age 60) is attributable to aortic stiffening. This is the only group with ISH shown to have an adverse prognosis and to warrant drug therapy.