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(Hypertension. 1996;27:168-175.)
© 1996 American Heart Association, Inc.

Articles

Validation of Carotid Artery Tonometry as a Means of Estimating Augmentation Index of Ascending Aortic Pressure

Chen-Huan Chen; Chih-Tai Ting; Amit Nussbacher; Erez Nevo; David A. Kass; Peter Pak; Shih-Pu Wang; Mau-Song Chang; Frank C.P. Yin

From the Division of Cardiology, Departments of Medicine, Veterans General Hospital–Taipei (C.-H.C., S.-P.W., M.-S.C.), the National Yang Ming University (C.-H.C., S.-P.W., M.-S.C., C.-T.T.) and Veterans General Hospital–Taichung (C.-T.T.), Republic of China; and the Division of Cardiology, Johns Hopkins Hospital, Baltimore, Md (A.N., E.N., D.A.K., P.P., F.C.P.Y.).

	Abstract

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Abstract Our objective was to validate a carotid artery tonometry–derived augmentation index as a means to estimate augmentation index (AI) of ascending aortic pressure under various physiological conditions. A total of 66 patients (50 men, 16 women; mean age, 55 years; range, 21 to 78 years; 44 in Taiwan and 22 in the Unites States) undergoing diagnostic catheterization were studied. Arterial pressure contours were obtained simultaneously from the right common carotid artery by applanation tonometry with an external micromanometer-tipped probe and from the ascending aorta by a micromanometer-tipped catheter at baseline (n=62), after handgrip (n=36), or after sublingual nitroglycerin administration (n=17). The AI (expressed as percentage values) was calculated as the ratio of amplitude of the pressure wave above its systolic shoulder to the total pulse pressure. The carotid AI was consistently lower than the aortic AI, but the two were highly correlated at baseline and after both handgrip and nitroglycerin. Mean±SD and correlation coefficients were baseline (14±16, 28⁺±17, .77), handgrip (18±19, 32⁺±15, .86), and nitroglycerin (7±12, 18⁺±13, .52). In addition, after adjusting for age, sex, height, blood pressure, heart rate, and study site, the changes of both AIs from baseline values with handgrip or nitroglycerin were highly associated such that the aortic AI could be approximated from the carotid AI with appropriate regression equations. The high correlations and predictable changes after interventions between the central AI and those estimated from noninvasive carotid tonometry suggest that this technique may have wide applicability for many cardiovascular studies.

Key Words: tonometry • pulse wave • arteries • augmentation index

	Introduction

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The magnitude and timing of wave reflections are major determinants of the central and peripheral arterial pressure wave contours.^{1 2 3} If the reflected waves in the central aorta are sufficiently large and early to arrive during ventricular ejection, they may augment the pressure during ejection and contribute substantially to the ventricular load.^{4 5 6 7 8 9} The magnitude of wave reflections is related to the geometry of the arterial system, with large reflections occurring at regions of impedance mismatch, eg, at junctions of large vessels and at terminations of the arterial system.^{2 10 11 12} The timing of the wave reflections is determined by the propagation properties of the elastic conduit arteries.^{13 14 15} The magnitude and timing of the reflected waves can be affected by systolic blood pressure,^{8 16} age,¹⁷ and various physiological^{12 18 19} and pharmacological manipulations.^{20 21 22 23} The augmentation index (AI) in the central aorta, a time-domain estimate of the contribution of the reflections relative to the pulse pressure, has been proposed as a simple and easily obtainable indicator of the magnitude of wave reflections.^{1 9 24 25}

Recently, the applanation tonometry technique²⁶ of using an externally applied micromanometer-tipped probe has been shown to accurately register peripheral arterial pressure contours.^{27 28 29} Because the pressure waveform and alterations in wall properties with aging of the carotid artery are similar to those of the ascending aorta,^{25 30 31 32} several recent studies have used carotid tonometry to noninvasively estimate central aortic pressure waveform alterations with aging^{24 33} and vasodilators^{34 35} and to assess aortic impedance.³³ Because carotid tonometry may have wide applicability in clinical and epidemiological applications,^{6 20 36} careful validation of the technique together with delineation of both its utility and limitation are needed. Only a few studies have validated limited aspects of this technique,^{25 27 28 33 35} but these studies were restricted to both small and rather homogeneous populations. The general utility of this technique across a wide age range, under both normal and diseased states, and with interventions that both increase and decrease the amount of wave reflections needs to be established.

The purpose of this study was to validate the carotid artery tonometry–derived AI against that directly measured with a micromanometer-tipped catheter in the ascending aorta in a large, diverse population encompassing normal subjects, those with a variety of diseases, and over a wide range of ages. Invasive and noninvasive measurements were compared at baseline and during maneuvers that increase (handgrip) and decrease (nitroglycerin) wave reflections. In addition, carotid AIs obtained simultaneously from a micromanometer in the carotid artery and externally with a tonometer were compared.

	Methods

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Study Population
Sixty-two adult patients referred for diagnostic cardiac catheterization constituted the main study population (designated as group A). Of these, 44 were studied at the Veterans General Hospital–Taipei, Taiwan, and 18 at the Johns Hopkins Hospital. Unlike previous validation studies that examined relatively homogeneous populations, the present study population encompassed a wide range of ages (22 to 78 years), aortic systolic blood pressures (90 to 210 mm Hg), and diseases, with resting left ventricular ejection fractions varying from 20% to 80%. Patients with atherosclerosis of the carotid artery as manifested by bruits during examination were excluded from the study. Table 1 summarizes the clinical characteristics of the patients from each hospital. Another four patients who had previously undergone internal mammary artery bypass grafting and whose internal mammary graft status was being determined composed a second group (designated as group B) for which simultaneous invasive and tonometer-derived carotid artery tracings were compared. Informed consent was provided by all patients, and the protocols were approved by the Joint Committee on Clinical Investigation of the Johns Hopkins Medical Institution and the Veterans General Hospital–Taipei.

View this table: [in this window] [in a new window]   Table 1. General Characteristics and Baseline Augmentation Indexes in Group A Patients

Data Acquisition
In group A, patients' invasive ascending aortic pressure waveforms were obtained with multisensor catheters (models VPC 673-D or VPC 684D, Millar Instruments Inc) incorporating a micromanometer-tipped catheter and an electromagnetic flow-velocity sensor. The catheter was introduced into the aorta through a femoral artery sheath and advanced until the pressure sensor was in the ascending aorta just distal to the aortic valve.⁸ In group B patients, a 2F micromanometer-tipped catheter (model SPC-320, Millar Instruments Inc) was placed within the lumen of a standard 7F Judkins coronary artery catheter and guided into the proximal left carotid artery. Once the guiding catheter was in place, it was pulled back, leaving the micromanometer tip in the left carotid artery. The invasive and noninvasive left carotid signals were recorded simultaneously. In group A patients, the noninvasive right or left common carotid arterial pressures, respectively, were obtained with a pencil-type tonometer incorporating a high-fidelity strain-gauge transducer in a 7-mm-diameter flat tip (model SPC-350, Millar Instruments Inc).²⁹ To avoid biasing the operator, the invasive aortic or carotid tracings were not displayed on the computer monitor while the tonometer signal was being acquired.

According to the theory of applanation tonometry,²⁶ when an arterial wall is completely flattened (applanated) by the tip of the probe, the contact pressure between the probe and the wall equals the intra-arterial pressure. Although there is no direct guide to indicate optimal applanation, it is felt that this condition occurs when the operator adjusts the hold-down force so that the waveform has a stable baseline, maximum amplitude, and a "reasonable" configuration. For an exposed vessel, this optimal state is easily achieved. Since there is substantial soft tissue between the external probe tip and the carotid artery in situ, however, it is more difficult to ascertain when this optimal state is achieved. Hence, a training period is required before one is able to reproducibly and reliably obtain reasonable carotid waveforms.

The simultaneously obtained invasive ascending aortic or carotid artery pressure and flow velocity signals, along with the noninvasive common carotid tonometer signal, were digitized at a rate of 250, 500, or 1000 Hz on an IBM-compatible personal computer and saved for off-line analysis. Recordings were made in the baseline state for all patients, after which 0.4 mg sublingual nitroglycerin was administered (n=17) or isometric handgrip exercise (n=36) was performed. Recordings were repeated at the peak response of the nitroglycerin or exercise interventions.

Data Analysis
The digitized signals were analyzed using custom software written in our laboratory. Two to 10 consecutive beats of the aortic and carotid arterial pressure waves were signal averaged. Premature beats and beats immediately after premature beats were excluded. Because we were interested in comparing waveforms and not absolute values of pressure, the signal-averaged carotid arterial pressure wave was calibrated by matching the systolic and diastolic pressures to the signal-averaged aortic wave. Because the AI is a dimensionless ratio, its value should not be affected by the method of calibration. The algorithm displayed the signal-averaged waveform and identified the inflection point on the upstroke or downstroke of the pressure wave by finding the first local minimum of the first derivative of the signal. This inflection is presumed to signal the onset of the reflected wave.^{24 25} The AI was calculated as the ratio of amplitude of the pressure wave above its systolic shoulder to the total pulse pressure.^{9 24 27 33 35 37} There was one patient with a clear inflection point on the upstroke of the carotid pressure contour but no identifiable inflection point on the ascending aortic pressure waveform (Fig 1A). Since this patient was middle-aged and should have had a reflected wave appearing in systole,²⁴ the inflection point was presumably buried in the waveform. The AI for this case was calculated by determining the pressure at the peak of the simultaneously recorded aortic flow velocity^{24 38} and taking that value to signal the onset of the reflected wave. For another patient with no inflection point on either the upstroke or downstroke of either wave, the AIs were arbitrarily assigned as 0 (Fig 1B).

View larger version (31K): [in this window] [in a new window]   Figure 1. Summary comparisons of waveforms and augmentation indexes (AIs) at baseline for all group A patients. Solid curves indicate carotid AI (AIt); dotted curves, aortic AI (AIm). A, The carotid waveform has a clear inflection point on the upstroke, but no inflection point could be found on the aortic pressure curve. B, No inflection point could be found on either waveform. C, In the vast majority of cases, inflection points were on the upstrokes of both waveforms. D, Inflection points were on the downstrokes of both waveforms. E, Inflection points were on the downstroke of carotid and on the upstroke of aortic waveforms. F, Inflection points were on the upstrokes of both waveforms, but AIt was greater than AIm.

The time difference between the two feet of the simultaneously recorded aortic and carotid pulse waves and the time intervals from the foot of the pressure wave to the first identifiable inflection point for each waveform were measured. The foot of the pulse wave was identified as the point of commencement of the sharp systolic upstroke. These time differences may indicate the wave transmission time between the aortic and carotid recording sites and the time required for the reflected wave to return from its peripheral site, respectively.^{12 13 24} The slopes of the upstroke of the two pulse waves were compared by calculating the ratio of the maximal dP/dt (carotid divided by aortic) from both sites.

Frequency domain analyses were also performed to further examine the differences between the aortic and carotid waveforms. The discrete Fourier transform of the time-averaged waves was evaluated by a commercial software package (routine fft.m in Matlab, version 4.2, The MathWorks) to yield the modulus and phase angle up to the 20th harmonic. The power spectral densities of the two spectra were calculated as the squared modulus values for each harmonic. The spectrum of the tonometric pressure wave was normalized to that of the aortic pressure wave by equating the total power of the two spectra. The transfer function between the two pressure waves was then evaluated by both the differences and ratios of the moduli and by the differences of the phase angles.

Statistical Analysis
In group A patients, correlations between tonometer and catheter AIs under baseline, handgrip, and nitroglycerin conditions were examined using simple and multiple linear regression methods. Partial and simple correlation coefficients were determined and contrasted for each of these three conditions both with and without controlling for age, sex, systolic blood pressure, heart rate, body height, and study site. In addition, the specific relationships between changes in the tonometer and aortic AIs, measured as differences between baseline and peak intervention values, were compared for the handgrip and nitroglycerin interventions. Directly correlating these changes would in effect amount to assuming that correlations between the two AI signals are identical under both baseline and peak interventions. Rather than restricting ourselves to this assumption, we used a regression adjustment model to account for potential differences in the strength of the correlations between the two AIs under these two conditions. The nonparametric Wilcoxon signed-rank test was applied to evaluate changes of AIs after sublingual nitroglycerin or handgrip maneuver. Values are expressed as mean±SD.

	Results

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Table 1 summarizes the general study population characteristics and some baseline hemodynamic results.

Carotid Versus Aortic AI
Fig 1 summarizes the baseline simultaneous carotid and aortic pressure waveforms of the study patients. During baseline conditions, at least one inflection point could be found in 61 carotid and 60 ascending aortic pulse tracings. In the majority of cases (46 of 62) as illustrated in Fig 1C, the inflection point was on the ascending portion of both waveforms. As is evident from these examples, although the carotid pressure contours were generally similar to those in the ascending aorta, on average the carotid AI was smaller than that from the aorta. This is borne out by a significantly lower averaged baseline AI for the carotid artery compared with the aorta (14±16% versus 28±17%, P<.0001). There were, however, isolated instances that did not follow this overall trend.

Fig 2 illustrates simultaneous carotid and aortic waveforms of selected patients with various cardiovascular conditions. Compared with the waveform in the young woman with no vascular disease (Fig 2B) with small negative aortic and carotid AIs, there are prominent reflections in a young and an elderly woman with vascular disease (Figs 2A and 2C) and in a woman with severe aortic regurgitation (Fig 2D). The similarity between the invasive and noninvasive waveforms, particularly in the bizarre waveform observed with aortic regurgitation, is clear.

View larger version (25K): [in this window] [in a new window]   Figure 2. Examples of the carotid and aortic waveforms and augmentation indexes (AIs; expressed as percent) at baseline. Solid curves indicate carotid AI (AIt); dotted curves, aortic AI (AIm). A, A 21-year-old woman with essential hypertension; B, a 37-year-old woman with congenital atrial septal defect; C, a 77-year-old woman with coronary heart disease; and D, a 59-year-old woman with severe aortic regurgitation. The carotid waveforms were generally similar to those from the ascending aorta, but AIt was smaller than AIm.

The averaged time difference between the feet of the two pressure waves was 0.022±0.008 seconds (P<.001). This time difference is likely due to the time needed for transmission of the forward component of the pressure wave between these two sites. In contrast to the significantly different forward wave arrival time, the time required for the reflected wave to return to the two recording sites (ie, the interval from the foot of the pressure wave to the inflection point) was not significantly different (carotid artery, 0.114±0.029 seconds; aorta, 0.111±0.028 seconds; difference, 0.003±0.025 seconds; P=NS). The slope of the carotid pulse wave (maximal dP/dt=789±299 mm Hg/s) was significantly steeper than that of the aortic pulse wave (maximal dP/dt=600±145 mm Hg/s, P<.001) with a ratio of 1.31±0.34.

A scatterplot of carotid artery versus aortic AIs at baseline, during handgrip, and after sublingual nitroglycerin is shown in Fig 3 with the results of the linear regression analysis. With the invasive (aortic) AI as the dependent variable, the simple linear regression equation and correlation coefficient for the pooled data are y=0.78x+17 and r=.78 (P<.0001).

View larger version (19K): [in this window] [in a new window]   Figure 3. Relationship between carotid (AIt) and aortic (AIm) augmentation indexes at baseline (), during handgrip exercise (), and after sublingual nitroglycerin administration (). The overall regression results for the pooled data are shown. Individual regression results are baseline, AIm=0.83AIt+17, r=.77, P<.0001; handgrip, AIm=0.69AIt+19, r=.86, P<.0001; and nitroglycerin, AIm=0.58AIt+14, r=.52, P=.034.

Effects of Handgrip Exercise and Sublingual Nitroglycerin
Fig 4A illustrates the carotid and aortic waveforms during baseline and after handgrip in a representative patient. The hemodynamic results for all patients are summarized in Table 2. During handgrip, the aortic systolic blood pressure increased significantly. There was a highly significant increase in AI at both sites except for one patient in whom the AI decreased 1 percentage point. As expected, the travel time for the reflected wave shortened significantly for both pulse waves, whereas there was no change in the time difference between the feet of the two waves. The slope of the carotid pulse wave (maximal dP/dt=763±261 mm Hg/s) was significantly steeper than that of the aortic pulse wave (maximal dP/dt=580±149 mm Hg/s, P<.001) with a ratio of 1.33±0.29.

View larger version (16K): [in this window] [in a new window]   Figure 4. Representative examples of the effects of handgrip exercise and sublingual nitroglycerin administration on the carotid and aortic pressure contours. Pressure contours derived by invasive Millar catheter or noninvasive tonometer are displayed in left or right, respectively. The pressure contours at baseline (dotted curves) are overlapped with those after intervention (solid curves) for comparison. A, During handgrip exercise, the secondary late systolic wave became larger or more prominent. B, After sublingual nitroglycerin administration, the secondary late systolic wave at baseline became smaller or inconspicuous.

View this table: [in this window] [in a new window]   Table 2. Changes of Blood Pressures, Augmentation Indexes, and Time Intervals After Intervention With Handgrip Exercise or Sublingual Nitroglycerin in Group A Patients

Fig 4B illustrates the carotid and aortic waveforms from the two sites during baseline and after nitroglycerin in a representative patient. The hemodynamic results for all patients are also summarized in Table 2. After sublingual nitroglycerin, the aortic systolic blood pressure decreased significantly. There was a substantial and highly significant decrease in AI at both sites during nitroglycerin. The travel time for the reflected wave increased significantly at both sites, and there was a small but significant increase in the time difference between the feet of the pulse waves. The slope of the carotid pulse wave (maximal dP/dt=829±390 mm Hg/s) was significantly steeper than that of the aortic pulse wave (maximal dP/dt=702±167 mm Hg/s, P=.004), with a ratio of 1.17±0.33.

Fig 5 illustrates the relationships between changes of these two AIs from their respective baseline values after handgrip or nitroglycerin. These relationships were significant both with and without adjusting for age, sex, height, systolic blood pressure, heart rate, or study site. The highly significant adjusted associations demonstrate that the magnitude of the change in AI in the ascending aorta for each individual intervention can be approximated from the change measured at the carotid artery with use of the appropriate equation.

View larger version (15K): [in this window] [in a new window]   Figure 5. Relationships between changes of the carotid (AIt) and aortic (AIm) augmentation indexes (expressed as percent) after interventions with handgrip exercise or sublingual nitroglycerin administration. The magnitude of change of the aortic AI (AIm) could be approximated from AIt at baseline and after interventions by the regression equations.

Invasive Versus Noninvasive Carotid Artery AI
Fig 6 shows tracings of simultaneously recorded invasive and noninvasive signal-averaged carotid pressure waveforms from all four of the group B patients. There is little difference between the invasively and noninvasively obtained carotid AIs.

View larger version (26K): [in this window] [in a new window]   Figure 6. Tracings from all four group B patients illustrate simultaneously recorded invasively (micromanometer) and noninvasively (tonometer) obtained carotid artery waveforms as well as the invasive (AIm) and noninvasive (AIt) augmentation indexes (expressed as percent).

Spectral Analyses
Fig 7 shows the results of the spectral analysis from all group A patients at baseline. The carotid pulse wave appeared to have a slightly larger modulus, a higher percentage of power, and a greater modulus ratio beginning with the second harmonic. Phase differences between the two pulse waves were small. Similarly, differences between invasive and noninvasive spectra were observed during handgrip and nitroglycerin (data not shown). In contrast, for the group B patients, there were essentially no differences of either the moduli or percentage power content between the invasively and noninvasively derived carotid pulse waves (Fig 8).

View larger version (22K): [in this window] [in a new window]   Figure 7. Spectral analysis of the simultaneously recorded carotid and aortic pulse waves. Error bars represent 95% confidence intervals. There were slight differences in moduli (A) and percentage of power (B). No significant phase difference was noted (C). The moduli ratio (carotid/aorta) was greater than 1 from the second harmonic on (D).

View larger version (23K): [in this window] [in a new window]   Figure 8. Spectral analysis of the simultaneously recorded invasive (micromanometer) and noninvasive (tonometer) carotid waveforms. Error bars represent 95% confidence intervals. There were essentially no differences in moduli (A), percentage of power (B), or phase angle (C) or modulus ratio (carotid/aorta, D).

	Discussion

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The present study indicates that, across a wide age spectrum in those with and without hypertension and other cardiovascular diseases, the noninvasive AI derived from carotid tonometry is consistently smaller in magnitude than that directly recorded from the ascending aorta. This difference between invasive and noninvasive estimations of AI holds true not only during baseline conditions but also during handgrip exercise and after sublingual nitroglycerin administration. Moreover, the change in absolute value of carotid AI after both interventions reflects the change in value of aortic AI in a predictable way. Hence, it appears that the carotid AI can be used to noninvasively estimate the changes in aortic AI induced by interventions that either increase or decrease wave reflections. Although both tonometry-derived and directly measured aortic AIs were noted to fall after nitroglycerin in an earlier study,¹ the details of the responses were not examined. Our results not only corroborate these and other previously reported results^{25 29 33} but also extend those findings to a larger population with a variety of cardiovascular diseases. More importantly, these results should now enable one to perform large epidemiological studies with more confidence. This may be especially important in clinical trials using antihypertensive drugs, for example, in which a reduction in wave reflection could be of major concern.^{34 36}

In exposed vessels and very superficial ones like the radial artery, AIs recorded from a tonometer and an indwelling catheter have been shown to be close.²⁹ Our group B data extend these findings to the in situ carotid artery. The similarity between the invasively and noninvasively obtained carotid AIs both in the time and frequency domains strongly suggests therefore that the effects of the tissues in the neck are not likely to be the cause of the different magnitudes of AI at the aorta and carotid artery observed in the group A patients. Rather, those differences must be attributable to intrinsic differences in waveforms at those two sites. Theoretically, for two pulse waves with the same pulse pressure (the carotid pulse waves were calibrated against the aortic systolic and diastolic blood pressures), a difference in AI can result from a difference of the upstroke velocity and/or the timing of the reflected wave. The steeper the upstroke, the smaller the AI, and the earlier the reflected wave, the greater the AI. Our results showed that there was no difference in the time intervals from the foot of the pressure wave to the inflection point for the two recording sites, suggesting that there were no large differences in timing of reflection at these sites. On the other hand, our results clearly demonstrated that the carotid artery pulse wave had greater upstroke slope than that of the ascending aorta. To produce the two different AIs that we observed at baseline (average, 14% versus 28%), there should be a slope ratio of 1.19 ([100-14]/[100-28]), which is close to the calculated maximal dP/dt ratio of 1.31. Likewise, to produce the two different AIs during handgrip exercise (average, 18% versus 32%; Table 2), there should be a slope ratio of 1.21 ([100-18]/[100-32]), which is close to the calculated maximal dP/dt ratio of 1.33. To produce the two different AIs after sublingual nitroglycerin administration (average, 7% versus 18%; Table 2), there should be a slope ratio of 1.13, which is also close to the calculated maximal dP/dt ratio of 1.17. Hence, the difference in magnitude of AI at the carotid artery and the ascending aorta can be explained in large part by the difference in the upstroke slopes of the pulse waves, which is also evidenced by the augmentation of the higher frequencies of the transfer function between the aortic and carotid pressure waves (Fig 7). The difference in the upstroke slopes (even with equalized pulse pressure) may indicate a greater distensibility of the aorta compared with the carotid artery.³⁹

Alterations in wave reflection in aging,²⁴ hypertension,⁸ and congestive heart failure^{5 40} have been clearly demonstrated. Because both pressure and flow waveforms are affected by wave reflections, quantifying the amount of wave reflection requires the measurement of both pressure and flow. Nevertheless, since AI is caused by wave reflections, being able to noninvasively index their effects should provide a means for better assessing the clinical implications of alterations in wave reflections. Although the currently configured tonometer containing a high-fidelity Millar micromanometer is useful in obtaining reasonably accurate arterial pressure waveforms—comparable to those obtained invasively—and is subject to less artifact than other noninvasive methods, the registered pressure waves may still be influenced by the hold-down force. This force is in turn directly influenced by the thickness of the intervening tissue, position and angulation of the probe, the presence of atheromatous plaques in the vessel, and head movement and respirations. Given all these possibilities for artifact, there is clearly a period of learning required to obtain reliable carotid artery recordings with the tonometer. Without direct observation of the wall of the artery, however, even well-trained and experienced operators cannot be certain under any particular set of conditions that they are perfectly applanating the wall so that it is flat under the probe. Disregarding the possible effects of the intervening tissue, if the wall of the artery is not flat, the recorded pressure will be an overestimation or underestimation of the true intra-arterial pressure. This uncertainty suggests that absolute measurements of carotid arterial pressure with a tonometer are likely to be unreliable. Nevertheless, as originally described and as confirmed here, this technique may be a valuable tool not only for waveform analysis in the carotid artery but also as a surrogate for central aortic waveform analysis.

	Footnotes

 
Reprint requests to Frank C.P. Yin, MD, PhD, Cardiology Division, Johns Hopkins Hospital, 530 Carnegie Bldg, Baltimore, MD 21287.

Received August 4, 1995; first decision September 21, 1995; accepted November 14, 1995.

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