Aortic wave reflection what is it

Williams B, Lacy PS. J Am Coll Cardiol ; 54 : — Heart rate and pulse pressure amplification in hypertensive subjects. Am J Hypertens ; 16 : — A critical review of the systolic time intervals. Circulation ; 56 : — Usefulness of systolic time intervals in the identification of abnormal ventriculo-arterial coupling in stable heart failure patients.

Eur J Heart Fail ; 10 : Hashimoto J, Ito S. Some mechanical aspects of arterial aging: physiological overview based on pulse wave analysis. Ther Adv Cardiovasc Dis ; 3 : — Location of a reflection site is elusive: consequences for the calculation of aortic pulse wave velocity. Hypertension ; 52 : — Quantification of glyceryl trinitrate effect through analysis of the synthesised ascending aortic pressure waveform. Heart ; 88 : — Smooth muscle relaxation: effects on arterial compliance, distensibility, elastic modulus, and pulse wave velocity.

Hypertension ; 32 : — Effects of isosorbide mononitrate and AII inhibition on pulse wave reflection in hypertension. Hypertension ; 41 : — Noninvasive input impedance, pulse wave velocity, and wave reflection in healthy middle-aged men and women. Hypertension ; 49 : — Gender-related differences in the central arterial pressure waveform. J Am Coll Cardiol ; 30 : — Laurent S, Boutouyrie P. Recent advances in arterial stiffness and wave reflection in human hypertension. Endothelial function is associated with pulse pressure, pulse wave velocity, and augmentation index in healthy humans.

Download references. You can also search for this author in PubMed Google Scholar. Correspondence to C-H Chen. Supplementary Information accompanies the paper on the Journal of Human Hypertension website. Reprints and Permissions. Liao, CF. Determinants of pressure wave reflection: characterization by the transit time-independent reflected wave amplitude. J Hum Hypertens 25, — Download citation. Received : 30 May Revised : 09 September Accepted : 15 October Published : 09 December Issue Date : November Anyone you share the following link with will be able to read this content:.

Sorry, a shareable link is not currently available for this article. Provided by the Springer Nature SharedIt content-sharing initiative.

Hypertension Research Advanced search. The onset of the later larger rapid phase consistently coincided with an increased rate of deceleration of both axes during late systole. Forward decompression waves are generated by the LV when the long axis shortening velocity falls. Reflected wave arrival has a detrimental effect on LV function, particularly the minor axis. These observations lend support to suggestions that therapies directed toward reducing wave reflection may be of value in hypertension and cardiovascular disease.

Increased wave reflection is an independent predictor of cardiovascular events in hypertension London et al. Reflected waves arrive at the left ventricle LV during systole Baksi et al. LV motion undergoes a complex pattern of change during the cardiac cycle Codreanu et al. Systolic LV function involves shortening of myocardial fibers oriented in circumferential, longitudinal, and oblique directions Greenbaum et al. This arrangement optimizes work Torrent-Guasp et al. Velocity and strain patterns of various myocardial components have provided valuable information on cardiac function Nagueh et al.

Wave intensity analysis WIA has proved a useful method for studying pressure-flow dynamics in conjunction with LV wall motion patterns in health and disease Parker, Rapid shortening of the LV muscle fibers generates a large forward compression wave FCW in early systole, and this has been proposed as an indicator of LV systolic function Parker et al. A backward compression wave BCW occurring after the initial FCW wave is attributed to reflection of the forward wave from distal sites of impedance mismatch Zambanini et al.

The origin of the late systolic proto-diastolic forward decompression wave FDW that decelerates aortic blood flow Parker et al. We hypothesized that wave reflections would influence LV minor M and long L axis function. Further, to establish mechanistic links between waves and LV function, we used aortic occlusion as means of inducing earlier and larger wave reflections and examined their effect on LV function.

The forelegs and left hind leg of the dogs were used for recording the ECG. An ultrasonic flow probe model T, Transonic Systems Inc. The aortic root catheter was placed approximately 1 cm distal to the aortic valve and was introduced into the aorta via the brachial or the carotid arteries.

The LV pressure catheter was also inserted into either a brachial artery or into the LV directly through the myocardium of the LV apex. A mercury manometer was used to calibrate the pressure catheters before every experiment, and all data were digitally recorded at a sampling rate of Hz. Two pairs of ultrasound sonomicrometer crystals 5MH, Sonometrics, Ontario, Canada were implanted in the mid-wall of the LV myocardium to measure the movement of the long base—apex and short septum—free wall axes throughout the cardiac cycle.

The septum and free wall crystals were implanted at the mid-level, between the base and apex of the LV. Total aortic occlusion was achieved by a snare positioned in the proximal descending thoracic aorta at the level of the aortic valve approximately 13 cm from the measurement site. P , U , and axial shortening velocity were measured for 30 s during control and following aortic occlusion, 3 min after the snare was applied. Wave intensity analysis is based on the solution of the one-dimensional conservation equations of mass and momentum.

Knowledge of c allows d I to be separated into its forward and backward components. P and U waveforms were smoothed using a 7-point Savitzky—Golay filter, and the foot of both waveforms was aligned to take account of time lags in data processing. Shifting by no more than three sampling intervals was required to adjust for the lag caused by the filter in the ultrasonic flow meter Hollander, Up to three representative cardiac cycles were selected from a stable sequence of beats during the 30 s recording period.

Each cardiac cycle was analyzed individually and the data were averaged for each dog. LV volume was calculated by considering the LV as an ellipsoid using the following equation.

Time to peak volume decline V max was determined by plotting the first derivative of volume with respect to time. The onset of ejection was identified from the onset of the upstroke of the aortic flow waveform, which also indicated the onset of the FCW.

The onset of each phase was determined from the first derivative of the forward wave intensity. The time of onset of the reflected waves was identified as the moment the separated backward wave intensity curve became negative. Figure 1. A typical forward wave intensity analysis curve calculated from pressure and velocity measured in the ascending aorta.

The rise of the forward decompression wave, FDW, comprises two phases: a slow D1 then a rapid D2 phase whose onset is clearly shown to occur in mid and late systole, respectively. Also shown is the forward compression wave, FCW, in early systole. Velocity of the LV long L and minor M axis shortening was determined by differentiating the axial displacement with respect to time. As reported previously Page et al. Phase I represents acceleration of axis shortening during early systole; phase II is a period of slow deceleration of axial shortening beginning in mid-systole; phase III occurs near end-systole when there is a sudden increase in the rate of deceleration.

Minor and long axes rate of shortening acceleration and deceleration at each phase were also determined. Figure 2. LV minor dashed line and long solid line axes shortening speed during systole. The minor axis reaches its maximum velocity of shortening before the long axis during control conditions. In late systole, both axes exhibit an inflection point after which their velocity of shortening decreases at an increased rate indicated as rate III.

Where V m is mid-wall volume at any distension and V mu , V ou , and V cu are mid-wall, chamber, and cavity volumes at reference distension. Based on the literature, end diastolic posterior wall thickness was assumed to be 7. Measurement of the time intervals from the peak of the R wave of the QRS complex to the peak shortening velocity of both the minor and long axes as well as to the onset of all three WIA waves was repeated on three separate occasions by a single observer.

Timings were compared by calculating the mean difference between timings in each dog and the standard deviation of the difference. Statistical agreement between timings was assessed using concordance correlation coefficients CCC; asymptotic p -value Lin, Therefore, with increased resistance the higher mean pressure causes an increase in stiffness and pressure wave shape is affected.

In the intact arterial system, the increased resistance causes increased pressure and the elevated mean pressure increases arterial stiffness. Changes in stiffness.

At bifurcations the reflection is determined by the load impedance input impedance distal to the measurement point and characteristic impedance of the mother vessel. Thus with increased stiffness characteristic impedance of mother and daughters increase with a similar factor but the input impedance of the daughters is increased above their characteristic impedance and thus reflection is increased.

The myth of wave travel and reflection lies in fact that the information on arterial properties that can be obtained from wave travel and wave reflection, e. The main factors determining arterial function are peripheral resistance, arterial stiffness 12 — 15 and aortic characteristic impedance. Originally all attention was directed to the periphery, later arterial stiffness became —and still is considered— of major importance 12 — 15 and recently changes in aortic characteristic impedance were suggested to play a role.

Wave from analysis. In this analysis only measured pressure is used. Pressure and flow result from the interaction of the cardiac pump and the arterial load. Thus pressure or flow alone cannot be used to quantify the arterial load accurately. This implies that mean pressure as well as systolic, diastolic, pulse pressure and Augmentation Index, alone cannot accurately characterize the arterial system. At least pressure and flow are required.

For instance, peripheral resistance can only be derived when mean pressure and mean flow are measured. Thus pressure wave form analysis cannot be used to determine relevant arterial parameters accurately.

When pressure and flow are used: wave separation. Wave separation, i. Waves do not exist for mean pressure and therefore resistance cannot be derived from them. Characteristic impedance is used in the analysis to derive forward and backward waves and thus cannot be determined from wave separation.

Therefore only arterial stiffness is, in principle, derivable from wave separation. Wave separation produces information on timing and magnitude of the forward and reflected waves. Due to the many reflection sites return time of the reflected wave, and inflection and shoulder time all differ from each other and change in a complex way with arterial stiffness.

The inflection point in the measured pressure wave is not equal to the return time of the reflected wave. Also the timing of the inflection point and the return time of the reflected wave 18 — 20 change much less with stiffness than one would predict on the basis of Pulse Wave Velocity and assuming a uniform tube model. Thus these times cannot be used for calculation of stiffness.

Increased aortic stiffness alone, increases aortic characteristic impedance, but leaves the distal input impedances unchanged, and thus brings characteristic impedance closer to the input impedances of legs, arms and head, and thus decreasing reflection. The parameter most directly related to aortic stiffness is Pulse Wave Velocity. Two pressures or diameters or flows are required with the travel distance.

In practice carotid to distal aorta wave speed is determined, leaving out the important contribution of proximal ascending aorta.

Also in the calculation of stiffness average radius has to be known. We conclude that waves and their reflections form the explanation of the basis of arterial function, but that the importance of wave form analysis and wave separation is overrated with respect to the estimation of arterial stiffness. There are no conflicts of interest.

NW has no disclosures. Artery Research. Abstract Introduction Background knowledge Disclosures References. Download article PDF. Volume 6, Issue 1 , March , Pages 1 - 6. E-mail address: n. These orthostatic challenges were selected to address the primary aim of the study, which was to determine whether the decrease in AIx is a result of venous pooling independent of body posture. Each orthostatic challenge lasted 5 minutes. Brachial BP measurements were performed immediately prior to each tonometry measurement, while finger BP and HR were captured continuously throughout each condition.

Continuous hemodynamics were averaged over the last 30 seconds of each time point to match timing of tonometry data. Following each orthostatic challenge, 20 minutes of supine rest preceded the next orthostatic condition. Baseline characteristics were assessed via analysis of variance. Continuous variables such as aortic wave reflection characteristics, aortic pressures, and hemodynamic variables were analyzed over time and between conditions HUT vs. HUT with cuffs vs. LBNP by 2-way repeated measures analysis of variance.

All statistical analyses were completed using SigmaStat software version Subject characteristics are shown in Table 1. Peripheral and aortic hemodynamics for the group as a whole are shown in Table 2. Aortic systolic and PP decreased similarly between the 3 orthostatic challenges. HUT conditions.

Figure 1 illustrates responses in aortic wave reflection AIx during each of the orthostatic challenges. Indices of aortic wave reflection are shown in Table 3.

Figure 2 illustrates estimates of SVR during each orthostatic challenge. Augmentation index across orthostatic conditions. Systemic vascular resistance across orthostatic conditions. In the current study, we compared peripheral and aortic hemodynamics across various orthostatic stressors in order to investigate i if minimization of blood pooling in the lower limbs attenuated the decrease in AIx that has been previously reported to occur with HUT, 6 , 9 ii the influence of body position on aortic BP and wave reflection during an orthostatic challenge, and iii whether aortic hemodynamic responses to orthostatic stress differ between young men and women.

Our primary findings suggest i in contrast to previous reports, AIx did not decrease during HUT conditions, and when standardized to HR AIx 75bpm , actually increased slightly; ii application of LBNP-elicited robust changes in aortic hemodynamics as compared to HUT conditions; and iii in response to orthostatic challenges, there were no sex-related differences in AIx or aortic BP.

Taken together, these results suggest that the aortic hemodynamic and wave reflection responses are orthostatic challenge specific. Our finding of no change in AIx during HUT conditions is in stark contrast to previous studies that have reported a decrease in aortic wave reflection during passive HUT. Additionally, AIx decreases with active standing, which is paralleled by decreases in both the forward and reflected waves. As TPR was not significantly elevated during HUT conditions, these results remain puzzling in light of previous observations.

Taken together, it appears that any possible change in AIx with passive HUT is likely HR driven, rather than peripheral resistance, per se. Previous studies have postulated that the fall in AIx during a passive HUT is likely due to venous pooling in the lower limbs.

Accordingly, we conducted a passive HUT trial with rhythmically inflating cuffs on the calves to oppose the hydrostatic-induced venous pressure in the calf and effectively examine whether minimizing venous pooling would attenuate the anticipated fall in AIx during HUT. Unfortunately, the lack of change in AIx during a passive HUT without cuffs in the current study did not allow us to test the hypothesis that minimizing venous pooling would attenuate the fall in AIx during an orthostatic challenge.

In fact, the peripheral and aortic hemodynamic responses during a HUT were nearly identical with and without the application of rhythmically inflated cuffs Tables 2 and 3. LBNP elicits venous pooling independent of gravitational and body position changes, with a concomitant decrease in central venous pressure e. Subsequently, unloading the central baroreceptors results in an increase in sympathetic nerve activity in a posture independent manner.

Lydakis et al. However, since AIx 75 also significantly decreased during LBNP, we contend that the fall in AIx is not solely attributed to an increase in HR, but rather a combination of HR as well as a decrease in cardiac output, perhaps signifying greater venous pooling. Our findings suggest that change in body position alone does not explain the decrease in AIx during orthostatic conditions, and in fact, depends on the specific orthostatic challenge.

Sex differences are apparent in the integration of sympathetic nervous system activity, BP regulation, and orthostatic tolerance. Subsequently, we sought to examine sex differences in aortic BP and wave reflection in response to various orthostatic challenges.

Collectively, these results suggest that males and females exhibit similar responses in aortic wave reflection during orthostatic challenges. The lack of sex differences in aortic wave reflection during orthostatic conditions is somewhat surprising, as young males and females appear to differ in the transduction of sympathetic responses to the vasculature.

As orthostatic challenges typically result in an increase in muscle sympathetic nerve activity, which has been shown to have divergent relationships with aortic wave reflection characteristics in men and women we hypothesized that sex differences at rest would persist throughout orthostatic challenges. There are a few experimental considerations that warrant addressing. The primary focus of this study was to examine how aortic BP and wave reflection are altered with an acute sympathetic stimulus.

However, we did not specifically measure the level of sympathetic activation e. The conditions used within this study were based on previous literature that has examined passive HUT and LBNP, showing similar elevations in TPR and comparable sympathetic neural and cardiovascular responses. In this context, repeated exposures to orthostatic challenges alter volume regulating hormone responses, with LBNP resulting in elevated plasma renin activity.

Therefore, we do not feel the repeated challenges played a major role in the present results. Third, as discussed above, the reason for the divergent findings related to change in AIx during a HUT between our current data and those previously reported are not clear, but could be due to a couple of factors. Previous studies have used varying methods to assess wave reflection variables, including applanation tonometry, 7—9 finger arterial pressure waveform decomposition, 6 and oscillometric methods, 5 making direct comparisons difficult.

Furthermore, it is unclear whether the pulse wave data collected in the previous studies were done so at heart level and thus controlled for the possible confounding influence of hydrostatic pressure in the artery of interest as a result of body position changes supine to HUT.

Importantly, the intraclass correlation coefficients for measurements obtained during HUT are nearly identical to the intraclass correlation coefficients obtained during the LBNP trial a condition in which we observed significant changes in AIx.

Lastly, AIx may not necessarily reflect wave reflection per se.