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(Stroke. 1995;26:418-421.)
© 1995 American Heart Association, Inc.
Articles |
From the Institute of Internal Medicine and Metabolic Diseases, Medical School, Federico II University, Naples, Italy.
Correspondence to L. Aldo Ferrara, MD, Institute of Internal Medicine and Metabolic Diseases, Medical School, Federico II University, Via S Pansini 5, 80131 Naples, Italy.
| Abstract |
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Methods In a sample of 70 hypertensive patients without clinical evidence of target organ damage, we showed a thickening of the intimal plus medial layers compared with age- and sex-matched normotensive control subjects. In this sample we also studied the diameter of the carotid arteries by ultrasound imaging, and we studied flow velocities in common carotid, internal carotid, and middle cerebral arteries by Doppler technique. Pulsatility and resistance indexes were calculated.
Results Absolute values of the carotid diameter were similar in the two groups (6.3±0.7 versus 6.0±0.8 mm); however, the ratio of diameter to blood pressure was significantly reduced in hypertensive compared with normotensive subjects (5.3±0.7 versus 6.5±0.8; P<.001 for mean blood pressure). Parietal stress was increased in the hypertensive subgroup and significantly correlated with arterial diameter in the normotensive group but not in the hypertensive group. No significant differences between the two groups were observed in blood flow velocities, with the exception of a slight significant increase of mean velocity in the internal carotid artery in hypertensive patients (37.5±9.1 versus 32.7±3.0 cm/s; P<.02).
Conclusions These results indicate that in addition to the degenerative changes of the common carotid wall, the diameter of the carotid artery and the relation to parietal stress show an early impairment in patients with uncomplicated hypertension.
Key Words: blood flow velocity cerebral circulation Doppler hypertension
| Introduction |
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Vessels of the cerebral circulation are at present easily studied by recently developed noninvasive techniques. It is therefore possible to evaluate blood flow velocity in extracranial and intracranial arteries by Doppler sonographic instruments,7 8 9 10 11 12 cerebral circulation by radionuclide techniques,13 14 15 and carotid wall thickness, carotid diameter, and progression and/or regression of carotid plaques by ultrasound imaging.16 17 It has been shown that patients with arterial hypertension have a thickening of the carotid wall and increased frequency of carotid plaques.18 19 20 21 These abnormalities of the carotid arteries have also been found in patients with hypercholesterolemia22 and diabetes mellitus.23
The aim of the present study was to investigate whether hypertensive patients without clinically evident end-organ complications also have other abnormalities in the cerebrovascular circulation. For this reason we investigated (1) common carotid artery (CCA) diameter by high-resolution echotomography and (2) blood flow velocity in the CCA, internal carotid artery (ICA), and middle cerebral artery (MCA) by a Doppler sonographic instrument.
| Subjects and Methods |
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Exclusion criteria were the following: (1) duration of known hypertension for more than 10 years; (2) clinical evidence of target organ damage by arterial hypertension (stroke, coronary heart disease, heart failure, renal impairment, third- or fourth-degree retinopathy); (3) evidence of heart disease other than hypertension; (4) presence of liver cirrhosis, chronic lung disease, or renal disease; (5) pregnancy or lactation; (6) use of oral contraceptives; and (7) inability to obtain high-level echography that would produce reproducible measurements.
Sixteen patients had newly discovered hypertension and had never been on antihypertensive treatment; the others were asked to discontinue previous drugs for at least 6 weeks before entering the study. At the end of the washout period, BP and heart rate were measured twice at 9 AM with patients in the supine position by an automatic noninvasive technique (Sentron, Bard Biomedical). Body weight and height were also measured and body mass index (BMI) calculated (BMI=Body Weight/Height2). A questionnaire regarding smoking habits, alcohol intake, and physical activity was completed by each patient. After an overnight fast, a blood sample was taken from a suitable forearm vein to measure hematocrit, serum total cholesterol, triglycerides, and cholesterol content in high-density lipoproteins.
The CCA, carotid bifurcation, and the proximal segment of the ICA were visualized by ultrasound imaging with a Bio-sound echotomographic system (2000 II SA, Bio Dynamics). The instrument generates a wideband ultrasonic pulse with an 8-MHz midfrequency. Real-time images are generated on a television monitor, connected to the instrument, and represent a fourfold magnification of the anatomic structures examined. The carotid bifurcation was recognized by visualizing the tip of the flow divider that identifies the origin of the ICAs and external carotid arteries and provides the best anatomic landmark. The carotid artery has been schematically divided into three parts on the basis of the distance from the tip of the flow divider: the 2-cm segment in the internal branch distal to the flow divider is referred to as the ICA; the 1-cm segment proximal to the flow divider is referred to as the bifurcation; and the segment below the lowest point of the bifurcation is referred to as the CCA. The time-gain compensation curve was calipered to obtain an echo-free lumen limited by two roughly parallel echogenic lines. Measurements of lumen size and intima-media thickness of the CCAs were taken 2 cm below the tip of the flow divider at the level of the far wall of the artery.
In a subgroup of 30 hypertensive patients and 20 normotensive control subjects with a suitable "window" for the evaluation of intracranial arteries, extracranial arteries were also examined with a 5-MHz bidirectional Doppler probe, and the intracranial arteries were investigated by means of a 2-MHz pulsed-wave Doppler instrument (model SD100, Vingmed) with on-line spectrum analysis. Patients were examined in the supine position. The hand-held probe was first positioned over the CCA, just above the clavicle, and angled cephalically until a maximum acoustic signal was obtained. The probe was then advanced sequentially over the bifurcation and the proximal segments of the ICAs and external carotid arteries. Thereafter the probe was placed over a temporal bone window to insonate the MCA. The artery was found at a depth of 45 to 55 mm, and blood flow was shown as upwardly deflected pulse waves. Mean velocity (time-averaged maximum velocity over the cardiac cycle) was expressed in centimeters per second. Pulsatility and resistance indexes24 were calculated from the Doppler spectrum as follows: Pulsatility Index=(Systolic Velocity-Diastolic Velocity)/ Mean Velocity Resistance Index=(Systolic Velocity-Diastolic Velocity)/ Systolic Velocity
All observations were performed by the same investigator under the same standard conditions. In our laboratory the coefficient of variation was less than 1% for carotid echographic measurements and 7% for Doppler examination of extracerebral and intracerebral arteries.
Statistical Analysis
Statistical analysis was performed with use of the
STATISTICAL PACKAGE FOR SOCIAL SCIENCES. Data are given
as mean±SD. Two-tailed statistical tests were performed for all data
analyses, with a value of P<.05 considered significant.
Between-group differences were evaluated by unpaired t test.
The strength of the correlation between carotid diameter and some
demographic and metabolic parameters was assessed by the Pearson linear
correlation and by forward multiple regression analysis.
| Results |
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High-resolution echotomography showed that wall thickness of the CCA
was significantly increased in the hypertensive group, as described
elsewhere.18 With regard to the arterial diameter of the
CCA, no significant difference was detected between the two subgroups
(6.3±0.7 versus 6.0±0.8 mm). However, when the diameter was corrected
by BP values, hypertensive patients had a lower diameter than expected
on the basis of the relation of diameter to BP in normotensive control
subjects. The ratio of diameter · 100 to mean BP was in fact
reduced in hypertensive compared with normotensive control subjects.
Fig 1
shows the difference in the ratio of diameter to
mean BP between hypertensive and normotensive subjects. Similar
differences were observed when we used systolic or diastolic BP.
Significant correlations of the diameter of the CCA with age
(r=.188; P<.05), body weight (r=.234;
P<.02), and mean BP (r=.297; P<.005)
were detected by linear correlation analysis. However, when a
multiple regression analysis was performed to evaluate the
independent influence of these variables on carotid diameter, only BP
was found to predict it, accounting for 14% of the variability of the
parameter (F=11.119; P=.0015). Age, which is significantly
related to carotid wall thickness,18 was inversely related
to the ratio of diameter to wall thickness (r=-.361;
P<.001).
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We also calculated the parietal stress (T) of the carotid artery
according to Lame's approximation for cylindric structures of
Laplace's law, as T=BP · rc/W, where rc is the radius of the
carotid artery and W is the wall thickness of the artery. Parietal
stress was increased in the hypertensive subgroup compared with the
normotensive subgroup, with the difference approaching statistical
significance (77.2±23 versus 68.4±19 N · m-1;
P=.07). We found a significant correlation between parietal
stress and arterial diameter in the normotensive group
(r=.424; P=.03) but not in the hypertensive group
(r=.113; P=.41) (Fig 2
).
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Mean velocity in the CCA and MCA was similar in normotensive and
hypertensive groups, whereas a significant between-group difference
(P=.02) was detected in the ICA (Table 1
).
Pulsatility index (Table 2
) and resistance index (Table 3
) did not show significant between-group differences in
the CCA, ICA, or MCA.
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| Discussion |
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Some data show that arterial flow velocity in the MCA may be used to accurately measure cerebral blood flow9 30 31 32 33 ; therefore, the lack of significant differences of flow velocities compared with control subjects strongly indicates that hypertensive patients without clinically evident signs of cerebrovascular damage have no detectable impairment of cerebral blood flow. Moreover, the lack of difference in pulsatility and resistance indexes compared with normotensive control subjects is apparently in contrast with the observed changes in diameter and wall thickness of the CCA. It is conceivable that in an early stage of hypertensive disease, the impairment in distensibility of the CCA (a medium-sized artery) does not influence the autoregulation of the small arteries of the intracerebral circulation, which remains normal. Pulsatility and resistance indexes, which are within normal limits, confirm that no detectable abnormalities of the hemodynamics of intracerebral vessels have been observed by the noninvasive techniques. On the other hand, the relation of pulsatility and resistance indexes with downstream resistance depends on the viscoelastic properties of the examined arteries. Since it is possible that arterial compliance differs in the two considered populations, similar values of these indexes in the two groups do not necessarily reflect comparable levels of downstream resistance.
Previous reports indicate that hematocrit values might influence transcranial Doppler measurement of the MCA.34 No difference was observed in hematocrit values of hypertensive subjects compared with normotensive control subjects, which is at variance with the findings of other groups.35
In conclusion, the results of this study indicate that in addition to degenerative changes of the common carotid wall, the diameter of the carotid artery and the relation to parietal stress show an early impairment in patients with uncomplicated hypertension. This finding might be related to reduced distensibility of the examined vessels, as suggested by other authors. We cannot confirm this hypothesis on the basis of our data, since the calculation of distensibility would require the measurement of arterial diameter and BP throughout the cardiac cycle. However, this structural damage of the extracranial epiaortic vessels does not seem to alter intracerebral circulation, which remains within normal limits, probably because of the autoregulatory mechanisms of cerebral vessels.
| Acknowledgments |
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Received September 16, 1994; revision received December 13, 1994; accepted December 22, 1994.
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