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Nonstenotic Internal Carotid Arteries: Effects of Age and Blood Pressure at the Time of Scanning on Doppler US Velocity Measurements¹

¹ From the Department of Radiology, Duke University Medical Center, Box 3808, Durham, NC 27710. Received July 24, 2000; revision requested September 12; final revision received January 25, 2001; accepted February 7. Address correspondence to M.A.K. (e-mail: kliew001@mc.duke.edu).

	ABSTRACT

TOP ABSTRACT INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION REFERENCES

 
PURPOSE: To assess the effects of age and blood pressure at the time of scanning on internal carotid artery velocities and cross-sectional diameter at Doppler ultrasonography (US).

MATERIALS AND METHODS: During 12 months, 1,020 consecutive patients underwent internal carotid artery Doppler US. No or minimal arterial disease was found in 142 patients (67 women, 75 men). Blood pressure was recorded prior to examination. The angle-corrected internal carotid artery peak systolic and end-diastolic velocities were obtained. The effects of systolic blood pressure, diastolic blood pressure, pulse pressure, age, chronic hypertension, and medications for hypertension on velocities were evaluated by using linear regression analysis.

RESULTS: Peak systolic velocity was influenced by age (P = .008), systolic blood pressure (P = .009), diastolic blood pressure (P = .003), and pulse pressure (P = .017) but not history of hypertension (P = .53) or antihypertensive medication use (P = .77). Increasing age decreased peak systolic velocity by 0.34 cm/sec/y. End-diastolic velocity was influenced by age (P < .001) but not by systolic, diastolic, or pulse pressure (all P values were > .13).

CONCLUSION: Internal carotid artery peak systolic velocities decrease with advancing age and increase with increasing pulse pressure. The effects of blood pressure at the time of scanning are small, but isolated systolic hypertension could cause increases in spurious velocity.

Index terms: Arteriosclerosis, 172.7211 • Carotid arteries, flow dynamics, 172.12983, 172.12984 • Carotid arteries, US, 172.12983, 172.12984

	INTRODUCTION

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Atherosclerotic disease in the extracranial carotid artery causes nearly one-third of cerebrovascular accidents (1,2). Fortunately, such disease is readily amenable to surgical intervention (2,3). The selection of patients for endarterectomy is largely based on the severity of disease as estimated with imaging. Currently, Doppler ultrasonography (US) is the most widely applied screening examination for carotid artery disease (4,5). The accuracy of Doppler techniques depends partly on measured blood velocities, which can be influenced by physiologic factors such as hypertension and cardiac output (6–8). The potential effects of hypertension are especially important when the prevalence of this disease and the associated cerebrovascular morbidity and mortality are considered.

It has been proposed (1,9,10) that hypertension causes elevations in carotid velocities, but reports (11,12) in the literature are conflicting and sometimes contradictory. Chronic hypertension is known to cause intimal-medial wall thickening, alter vessel compliance, and increase the cross-sectional area of carotid vessels (11,13–15). The consequences of these changes have been variably reported to increase or decrease carotid velocities (12). Moreover, to our knowledge, no effort has been made to distinguish the effects of elevated blood pressure at the time of scanning from the chronic effects of longstanding hypertension.

Prior investigators (11,12,14,16) have often arbitrarily assigned patients into hypertensive and normotensive groups. For example, patients with a systolic blood pressure greater than 140 mm Hg might be considered hypertensive, and those with pressures less than 140 mm Hg, normotensive. Blood pressure, however, is a continuous variable, and the segregation of patients into hypertensive and normotensive groups may obscure the effect of subtle changes in blood pressure. Further, chronic hypertension, instantaneous blood pressure (ie, blood pressure at the time of scanning), and aging are intimately related. Therefore, to obtain an estimate of the independent effect of any one factor, one must necessarily control for the effects of the other important covariants.

The purpose of this study was to determine the effects of age and blood pressure at the time of scanning on peak systolic velocity (PSV), end-diastolic velocity (EDV), and cross-sectional area of normal or minimally diseased internal carotid arteries (ICAs), after accounting for sex, a history of hypertension, and the use of antihypertensive medications.

	MATERIALS AND METHODS

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From November 1996 through November 1997, 1,020 consecutive patients underwent Doppler US examination of the extracranial carotid arteries. Patient demographic information was prospectively recorded by one of several experienced sonographers (E.B.S.) and substantiated by means of inspection of the medical record. Information included patient age, sex, medical and surgical history, clinical history of hypertension, and history of antihypertensive therapy. A clinical diagnosis of hypertension was considered present if it was substantiated by the medical record. (This diagnosis was not based on blood pressure readings at the time of the US examination.) Institutional review board approval and informed consent were not required for a study of this type at the time it was performed, since routine clinical methods were used.

All US examinations were performed by experienced sonographers with standard US machines (XP-128, XP-128/ART; Acuson, Mountain View, Calif, or ATL 3000; Advanced Technologies Laboratories, Bothell, Wash). A high-frequency linear-array transducer (5, 7, or 10 MHz) was used for all examinations. Sonographers recorded angle-corrected PSV and EDV, anterior-to-posterior vessel diameter, and transverse vessel diameter in both proximal ICAs (distal to the carotid bulb). Vessel diameters were measured with electronic calipers from the outer wall to the outer wall. Cross-sectional area was calculated as (D₁)(D₂), where D₁ and D₂ were diameters. All Doppler angles were 20°–60°.

By using the standard reference velocities and ratios adopted by our laboratory, stenosis in the ICAs was prospectively categorized in the 1,020 patients by one of several experienced sonologists. Degree of stenosis was determined by using standard Doppler parameters: PSV, EDV, ratio of ICA velocity–to–common carotid artery velocity, color and power Doppler parameters, and gray-scale images (17). To minimize the potential effects of homolateral or contralateral stenoses on carotid velocity measurements, patients with no or less than 40% stenosis were retrospectively selected from the group of 1,020 patients.

To have less than 40% stenosis, the following velocity criteria were met: Ratio of peak systolic ICA velocity–to–common carotid artery velocity was less than 1.5, ratio of peak end-diastolic ICA-to–common carotid artery velocities was less than 2.6, peak systolic velocity was less than 110 cm/sec, and peak EDV was less than 40 cm/sec. Velocity measurements were supplemented by analysis of gray-scale and color Doppler images. Color Doppler imaging was use to account for the possibility of echolucent plaque.

Of the 1,020 patients, a total of 185 patients had a nonstenotic ICA (no or minimal disease in the right ICA and no or minimal disease in the left ICA). Of these 185 patients, 43 patients were excluded for the following reasons: no blood pressure recorded at the time of study (n = 29), prior endarterectomy (n = 13), or incomplete velocity data (n = 1). The remaining 142 patients constituted our study population. Immediately prior to US evaluation, blood pressures were obtained in the left arm, with the patient in the supine position, by using an automated blood pressure device. All blood pressures were obtained by sonographers trained in the use of the automated blood pressure device.

Three multiple linear regression models were constructed for the evaluation of the independent effects of age, sex, chronic hypertension, use of antihypertensive medications, systolic blood pressure, and diastolic blood pressure on the three outcome variables of PSV, EDV, and mean cross-sectional area of both ICAs. Outcome variables were expressed as a mean of measurements from the right and left ICAs in each patient. To encapsulate the opposing effects of systolic and diastolic blood pressures, a derivative variable, pulse pressure, was generated. Pulse pressure (the difference between systolic and diastolic pressures) was then tested in the regression model in place of systolic and diastolic pressure terms.

All statistical analyses were performed by usingSAS software (SAS Institute, Cary, NC). The multiple regression was performed by using overfitting general linear models with all independent variables and then by systematically reducing the model by means of backward elimination. All interaction terms were tested and discarded if their differences were not statistically significant (P < .05). The dependent (outcome) variables were PSV, EDV, and cross-sectional area. The continuous independent (predictor) variables were age, systolic blood pressure, diastolic blood pressure, and pulse pressure. The categorical independent variables were sex, history of hypertension, and use of antihypertensive medication. P values of .05 or less were considered to indicate statistically significant differences.

All extreme data points (>2 SDs from the mean) were identified and examined for accuracy. Images were reviewed as necessary. The effects of extreme values were further tested by repeating the regression analysis with the log transformation of the outcome variables (ie, log PSV and log EDV). The purpose of the log transformation step was to mitigate the effect of outlying values.

	RESULTS

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Of the 142 patients without carotid stenosis, 75 were men and 67 were women. The mean age was 63 years (age range, 19–89 years) (Fig 1). Systolic and diastolic blood pressures at the time of scanning are presented in Figures 2 and 3. Ninety patients had a clinical diagnosis of hypertension, 50 did not have a clinical diagnosis of hypertension, and the status of two patients could not be ascertained from the medical record (records were missing or incomplete). Note that a clinical diagnosis of hypertension was not based on the blood pressure at the time of scanning.

View larger version (54K): [in this window] [in a new window] [Download PPT slide]   Figure 1. Histogram shows the age distribution of the study population (n = 142). Ages are reported in years.

View larger version (75K): [in this window] [in a new window] [Download PPT slide]   Figure 2. Histogram shows the distribution of systolic blood pressures at time of scanning for the study population (n = 142). Blood pressures are reported in millimeters of mercury.

View larger version (64K): [in this window] [in a new window] [Download PPT slide]   Figure 3. Histogram shows the distribution of diastolic blood pressures at time of scanning for the study population (n = 142). Blood pressures are reported in millimeters of mercury.

Scatterplots of PSV versus systolic blood pressure and PSV versus diastolic blood pressure are presented in Figure 4. The effects of age and blood pressure on PSV are summarized in Table 1. PSV was influenced by age (P = .008), systolic blood pressure (P = .009), and diastolic blood pressure (P = .003). However, PSV was not influenced by a history of hypertension (P = .53), the use of antihypertensive medications (P = .77), or sex (P = .52). The effect of age was to decrease the PSV by 0.34 cm/sec/y, and the effect of systolic blood pressure was to increase the PSV by 0.24 cm/sec/mm Hg. Diastolic blood pressure had the opposite effect, tending to decrease the PSV by 0.41 cm/sec/mm Hg.

View larger version (24K): [in this window] [in a new window] [Download PPT slide]   Figure 4a. Scatterplots of PSV and blood pressures at the time of scanning demonstrate the distribution of the data set. PSVs are reported in centimeters per second. (a) PSV versus systolic blood pressure. (b) PSV versus diastolic blood pressure.

View larger version (23K): [in this window] [in a new window] [Download PPT slide]   Figure 4b. Scatterplots of PSV and blood pressures at the time of scanning demonstrate the distribution of the data set. PSVs are reported in centimeters per second. (a) PSV versus systolic blood pressure. (b) PSV versus diastolic blood pressure.

The effects of age, blood pressure, and pulse pressure on EDV are presented in Table 2. EDV was influenced by age (P < .001), but not by systolic blood pressure (P = .689), diastolic blood pressure (P = .139), pulse pressure (P = .837), diagnosis of hypertension (P = .39), use of antihypertensive medications (P = .63), or sex (P = .44). The effect of age was to decrease the EDV by 0.21 cm/sec/y.

Four extreme data points were identified within the data set. These values were examined for accuracy and corrected. From the regression analysis, the independent variables that achieved statistical significance with the untransformed outcome variables were also significant with the transformed outcome variables, indicating that the analysis was robust to outlying data points.

	DISCUSSION

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The Doppler measurement of blood flow velocities is central to estimates of carotid stenosis with US. These measured velocities, however, can be spuriously altered by a variety of technical and physiologic factors. The effects of hypertension are of particular interest; it has been widely asserted that hypertension causes spurious elevations in carotid velocities (1,9,10). Therefore, hypertension could result in overestimation of the degree of carotid stenosis. There is little basis for these assertions because there are few studies (11,12) of carotid velocities in hypertensive patients. Further, most of these studies (13–15,18–20) focused on changes of wall thickness and luminal diameter. Additionally, it is not clear whether alterations in US velocity are produced by the effect of blood pressure at the time of scanning or by the underlying effect of chronic hypertension.

We found that the blood pressure at the time of US had a statistically significant effect on PSV in the ICAs independent of a clinical history of hypertension or the use of antihypertensive medications. The effects of systolic and diastolic pressure were opposing. Accordingly, pulse pressure can be used to summarize their combined effect; an increase in pulse pressure increases the PSV by 0.21 cm/sec/mm Hg. By distinction, EDV measurements in the ICAs were influenced only by age. Therefore, our findings support those of prior studies (21,22) that have established the use of EDV measurements as an important criterion in the evaluation of carotid disease.

The practical consequences of our findings might be best summarized in the following examples. PSV tends to decrease with age at a rate of 0.34 cm/sec/y. For example, in an 80-year-old patient with sonographically normal or minimally diseased ICAs, the PSV would be 13.6 cm/sec less than that in a 40-year-old patient. Conversely, an increase in the immediate systolic blood pressure of 40 mm Hg at the time of scanning (eg, isolated systolic hypertension) would cause the PSV to increase by 9.6 cm/sec. A similar degree of change would be produced with a decrease in diastolic pressure of 20 mm Hg or an increase in pulse pressure of 40 mm Hg. Though the magnitude of these velocity changes are modest, such elevations could cause PSVs to decrease within a higher category of estimated stenosis. Certainly, the converse is also true; isolated increases in diastolic pressure could artifactually decrease carotid velocities.

It is not entirely clear why carotid velocities tend to increase with increasing systolic pressures and decreasing diastolic pressures (ie, increasing pulse pressures). It is likely that the autoregulatory mechanisms of cerebral blood flow blunt velocity changes in the carotid artery to maintain a constant pressure gradient between the cerebral arteries and the brain. In the face of a high systolic blood pressure and relatively low diastolic pressure, however, cerebral vasoconstriction may be down-regulated to maintain flow during the longer lower-pressure diastolic phase of the cardiac cycle. The net effect of this decrease in downstream resistance would be to enhance flow and increase velocities in the setting of an elevated pulse pressure. Conversely, in the setting of a discordant increase in diastolic pressure (ie, a lower pulse pressure), carotid velocities could decrease.

Advancing age was associated with decreased PSV and EDV and increased cross-sectional area. The reason for these findings is more apparent; increases in carotid diameter result in a decrease in velocity to maintain flow. This age-related enlargement in cross-sectional area likely results from stretching of elastic fibers in the vessel wall or an altered baroreceptor reflex (13,23).

There are limitations to this study. First, because all patients underwent imaging for suspected cerebrovascular disease, the effects of blood pressure on carotid velocities in healthy individuals is not known. Further, because the effects of blood pressure were studied only in nonstenotic carotid arteries, these findings may not hold in setting of luminal compromise. Second, this study was based on measurements (vessel diameters, Doppler velocities, blood pressures) that may be prone to variability. Because blood pressures were obtained only in one arm, unsuspected subclavian artery stenosis could have influenced our results by causing under-representation of the effects of blood pressure on carotid velocities. Finally, blood pressure and carotid velocities are influenced by many factors. While we did attempt to control for potentially confounding variables, including age, sex, clinical diagnosis of hypertension, and use of antihypertensive medications, the cardiovascular status of our patients was not known. While cardiovascular function could have influenced carotid velocity measurements, obtaining objective cardiac data in our entire screening population was not possible.

In conclusion, we found that PSVs in the ICA are influenced by systolic and diastolic blood pressures at the time of scanning and by the patient’s age. While these changes were relatively small, the measured velocities could feasibly be elevated into a higher category of estimated luminal stenosis. In particular, patients with an unusually high pulse pressure, such as those with aortic insufficiency or isolated systolic hypertension, could have spuriously high PSV measurements. Additionally, because PSV decreases with age, a very elderly patient could have spuriously decreased PSVs. In these patient populations, measurement of ICA–to–common carotid artery velocity ratios or the use of EDV might be more reliable than the measurement of absolute velocity for the estimation of stenoses.

	FOOTNOTES

 
Abbreviations: EDV = end-diastolic velocity, ICA = internal carotid artery, PSV = peak systolic velocity

Author contributions: Guarantors of integrity of entire study, E.B.S., D.H.S.; study concepts, all authors; study design, D.H.S., M.A.K.; literature research, E.B.S., D.H.S.; clinical studies, B.S.H., B.A.C., M.A.K., J.D.B., R.C.N.; data acquisition, D.H.S., E.B.S.; data analysis, M.A.K., E.B.S., D.H.S.; statistical analysis, M.A.K.; manuscript preparation, E.B.S., D.H.S.; manuscript definition of intellectual content, editing, revision/review, and final version approval, all authors.

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