Audrey Adji

Noninvasive determination of carotid-femoral pulse wave velocity depends critically on assessment of travel distance: a comparison with invasive measurement.

Objectives 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. Methods 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invasively during cardiac catheterization, from the delay in wave foot and distance travelled as the catheter was withdrawn from the ascending aorta to the aortic bifurcation.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. Results Mean travel times were in good agreement [(travel time) TTinvasive was 63 ms, TTnoninvasive was 59.3 ms, Spearmans 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 (Spearmans R: 0.73–0.77, P < 0.0001). Conclusion 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.

Benefits from angiotensin-converting enzyme inhibitor ‘beyond blood pressure lowering’: beyond blood pressure or beyond the brachial artery?

Objective 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. Methods We enrolled 30 patients, who took 10 mg ramipril, 100 mg atenolol, and placebo at intervals of ≥ 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. Results 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. Conclusion 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.

Guidelines on guidelines : focus on isolated systolic hypertension in youth

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.

Brachial artery tonometry and the Popeye phenomenon: explanation of anomalies in generating central from upper limb pressure waveforms.

Background: Noninvasive applanation tonometry studies of the brachial and radial artery pressure waves show that the arterial pulse is substantially amplified between the brachial and radial sites. Brachial tonometry waveforms have also been used to calibrate carotid tonometry waves as a measure of central pressure in major clinical trials. These trials assume identity of mean and of DBP in calculation of central (carotid) SBP. None of these trials showed superiority of central over brachial pressure in predicting outcome, but all showed equivalence of SBP and pulse pressure at brachial and carotid sites! Method: We tested this method by measuring pressure waves at brachial, radial and carotid sites by applanation tonometry in 100 patients, with attention to any subtle difference between brachial and radial waveforms, and with both calibrated to cuff SBP and DBP. Results: The results confirmed no proximal and strong distal amplification in the arm. However, this was accompanied by blunting of the brachial compared with radial waveform with brachial pressure 2.7 mmHg higher during most of the cardiac cycle. Form factor of the ensemble-averaged brachial wave [39.1 standard deviation (SD) 4.9%] was similar to the carotid (40.2 SD 4.1%) but different to the radial wave (34.8 SD 3.7%; P < 0.01). Conclusions: All findings were explained by inability to applanate the brachial artery, and resulting systematic error in generating brachial waveforms. In estimation of central pressure with applanation tonometry, the radial pressure wave, which can be accurately applanated, should be used, and calibrated to the brachial cuff.

Influence of Aortic Pressure Wave Components Determined Noninvasively on Myocardial Oxygen Demand in Men and Women

Myocardial oxygen consumption is increased by arterial stiffening. It is not known precisely how. This study aimed to evaluate the role of the incident and reflected pressure wave in raising myocardial oxygen demand. Central (aortic) pressure waveforms were generated from radial waveforms using a generalized transfer function in 1628 cardiology outpatients (1038 males and 590 females). Aortic waveforms were used to derive measures of incident and reflected waves, as well as to measure mean central systolic pressure (an indicator of systolic ventricular load), left ventricular ejection duration, and tension time index (a surrogate of myocardial oxygen demand) using validated techniques. Incident and reflected waves were measured using the conventional and an alternative method (aortic flow triangulation). Relationships were tested before and after correction for age, height, weight, heart rate, and mean arterial pressure using simple and multivariate linear regression models. Analyses were conducted separately by gender. In both genders (according to conventional or alternative methods of wave measurement), both the incident and reflected wave were strong predictors of tension time index (P<0.001). Both pressure waves raised the mean central systolic pressure (P<0.001). The reflected wave (P<0.001), unlike the incident wave (P>0.05), was also associated with a longer cardiac ejection duration. Tension time index (P<0.0001), mean central systolic pressure (P<0.001), and ejection duration (P<0.0001) were greater in women. Changes in arterial properties alter the nature of pressure wave propagation and predispose to cardiac ischemia (especially in women).

Noninvasive Studies of Central Aortic Pressure

Our purpose is to review noninvasive methods for measuring central arterial pressure. Indices of central arterial pressure measured from central aortic and peripheral arterial waveforms have shown value in predicting cardiovascular events and death, as well as in guiding therapeutic management. This article reviews noninvasive techniques of measuring central arterial pressure that have been validated against intra-arterial pressure. This paper explains methods to derive central (aortic and carotid) pressure from radial and brachial sites. It focuses on specific issues of brachial calibration applied to carotid pressure waveforms, which were regarded as a surrogate of aortic pressures used in three major studies (Framingham, Asklepios, and Australian National Blood Pressure 2 studies). We explain why radial-based methods are superior to carotid-based methods for estimating central pressure. Physiological principles of pressure measurement need be satisfied to ensure accurate recording.

Clinical use of applanation tonometry: hope remains in Pandora's box.

Brachial cuff pressure has been used almost exclusively over the last century for individual assessment, epidemiological studies and clinical trials. The Systolic Hypertension in the Elderly Program study [3], whose primary results were released in 1991, showing greater importance of systolic over diastolic pressure, had been commenced on the basis of Kannel et al.’s publication at Framingham [1] that related arterial rigidity, systolic pressure and finger plethysmographic waveform to the risk of stroke.

Arterial aging : a review of the pathophysiology and potential for pharmacological intervention

This review begins with a perspective on the effects of arterial aging on society and world events over the past century. Until recently, the use of just one technique to measure blood pressure non-invasively limited progress in understanding the mechanisms involved and the potential of antihypertensive drug therapies. New methods for extracting information from the arterial waveform have followed the (re)introduction of arterial tonometry into clinical practice, together with mathematical analysis in the frequency and time domains. These new methods have exposed the phenomenon of aortic stiffening with age, and early wave reflection arising therefrom, and identified it as the major cause of cardiovascular degeneration. Such findings point to arterial aging as a logical target for the treatment and prevention not only of cardiac, aortic and large artery disease, but also of damage to microvessels in the brain and kidney, which in turn leads insidiously to dementia and renal failure, respectively.

Principles of cerebral hemodynamics when intracranial pressure is raised: lessons from the peripheral circulation

Background: The brain is highly vascular and richly perfused, and dependent on continuous flow for normal function. Although confined within the skull, pressure within the brain is usually less than 15 mmHg, and shows small pulsations related to arterial pulse under normal circumstances. Pulsatile arterial hemodynamics in the brain have been studied before, but are still inadequately understood, especially during changes of intracranial pressure (ICP) after head injury. Method: In seeking cohesive explanations, we measured ICP and radial artery pressure (RAP) invasively with high-fidelity manometer systems, together with middle cerebral artery flow velocity (MCAFV) (transcranial Doppler) and central aortic pressure (CAP) generated from RAP, using a generalized transfer function technique, in eight young unconscious, ventilated adults following closed head trauma. We focused on vascular effects of spontaneous rises of ICP (‘plateau waves’). Results: A rise in mean ICP from 29 to 53 mmHg caused no consistent change in pressure outside the cranium, or in heart rate, but ICP pulsations increased in amplitude from 8 to 20 mmHg, and ICP waveform came to resemble that in the aorta. Cerebral perfusion pressure (=central aortic pressure – ICP), which equates with transmural pressure, fell from 61 to 36 mmHg. Mean MCAFV fell from 53 to 40 cm/s, whereas pulsatile MCAFV increased from 77 to 98 cm/s. These significant changes (all P < 0.01) may be explained using the Monro–Kellie doctrine, because of compression of the brain, as occurs in a limb when external pressure is applied. Conclusion: The findings emphasize importance of reducing ICP, when raised, and on the additional benefits of reducing wave reflection from the lower body.

Calibration of Noninvasively Recorded Upper-Limb Pressure Waves

To the Editor: The article by Verbeke et al1 raises an important question: how does one calibrate the radial artery waveform obtained by applanation tonometry? Does one apply systolic and diastolic brachial values from the Korotkov technique, the “gold standard”, or does one use an oscillometric wrist technique, despite lack of confidence in any available method? Alternatively, as implied by Verbeke et al, should one use brachial tonometry instead, calibrated to brachial-cuff values? The study by Verbeke et al1 suggests (from noninvasive methods alone) that the present technique of calibrating radial tonometry to brachial-cuff pressure may have substantial inaccuracy. The method by Verbeke et al1 depends on a technique originally described by Kelly and Fitchett2 where systolic pressure was extrapolated on the assumption that diastolic and mean pressure were identical throughout the arterial tree. The technique currently recommended in the SphygmoCor process is based on invasive studies of arterial pressure waves, which showed that amplification between brachial and radial artery is small in comparison to that between aorta and brachial artery.3,4 We repeated essentials of the Verbeke et al1 study and confirmed estimation of high pressure amplification between …