TY - JOUR
AU - Cohn, Jay, N.
AB - Abstract Functional and structural changes of the arterial wall appear to serve as early hallmarks of the hypertensive disease process. Structural vascular changes can be studied by the determination of the intima-media wall thickness (IMT) at the carotid artery. The elastic behavior of the proximal and distal parts of the arterial tree can be assessed from noninvasively recorded radial artery waveforms. The aim of the study was to compare large (proximal, C1) and small (distal, C2) artery elasticity indices in two age-matched study groups with high- and low-normal blood pressure (BP) and to assess the relation between elasticity indices and IMT. A total number of 22 subjects with high-normal BP (40 2 years; BP, 147 ± 2.5/84 ± 1.5 mm Hg) and 22 matched controls with low-normal BP (40 ± 2 years; BP, 123 ± 1.9/69 ± 1.5 mm Hg) were enrolled. The IMT was echographically determined at the common carotid artery by the leading-edge technique. Large artery (C1) and small artery (C2) elasticity indices were calculated from a third-order, four-element model of the arterial circulation. In the group with high-normal BP large and small artery elasticity indices were significantly decreased versus controls with low-normal BP (C1: 1.63 0.08 v 1.99 ± 0.09 mL/mm Hg, P< .01; C2: 0.059 ± 0.005 v 0.076 ± 0.007 mL/mm Hg, P< .05) and IMT increased significantly (0.607 ± 0.039 v 0.516 ± 0.027 mm, P< .05). Moreover, there was an inverse relationship between IMT and small artery elasticity index (r =−0.60, P= .004). In subjects with a high-normal BP there is already a change in the IMT of the carotid artery versus normotension. The IMT is related to the small artery elasticity index (C2). Intima-media thickness, arterial blood pressure, carotid artery, elasticity index, arterial compliance Although high blood pressure (BP) is a well-established cardiovascular risk factor, BP levels alone are unable to fully explain the prognosis and response to treatment of the hypertensive patient.1,–3 Functional and structural changes of the arterial wall serve as early hallmarks of the hypertensive disease process, and may be a sensitive guide to prognosis.4,–6 Arterial compliance (C), defined as the change in volume for a given change in pressure, is a property that characterizes the pulsatile behavior of the vasculature. Whether reduced vascular compliance precedes the development of cardiovascular disease (ie, as a risk factor) or as a consequence of established cardiovascular disease (ie, as a marker) is a matter of debate. Considerable controversy exists about whether abnormalities in arterial compliance in hypertensive patients represent intrinsic changes in the arterial wall or are merely a reflection of pressure changes, and whether the changes in compliance are located primarily in the large vessels or in the small vessels.7,–9 Several methodologies are available to assess arterial compliance, such as invasive volume-pressure relationships and noninvasive methods, including pulse wave velocity and mathematical modeling of the diastolic decays curve.10,,,–14 A cornerstone of adaptive or structural changes at the vessel wall in early atherosclerotic or hypertensive disease is the thickening of the intima-media layers. According to Pignoli et al,15 increased intima-media wall thickness (IMT) may even be the earliest noninvasively measurable change that can be observed. There is evidence that an increase in IMT at the carotid artery is linked to risk factors such as age, smoking, diabetes, cholesterol, and BP.16,,,,,,–23 Whether there is a relationship between reduced arterial compliance and high-normal BP levels has not been addressed as yet. Therefore, the aim of our study was to compare arterial compliance in a patient group with high-normal BP versus an age-matched low-normal group and to assess the relation between arterial compliance and IMT. Materials Patients Twenty-two white male nonsmoking subjects with high-normal BP were enrolled in the study (mean age, 40 ± 2 years; range, 20–54 years; body mass index [BMI], 27.0 ± 0.9 kg/m2). The subjects were all recruited from a yearly medical screening for their health insurance. They were considered to have high-normal BP because they had a systolic blood pressure (SBP) in the range of 140 to 159 mm Hg and a diastolic blood pressure (DBP) lower than 90 mm Hg on three consecutive visits in the previous 12 months. Each clinical measurement was the average of three values recorded with the patient in the sitting position using phase I and phase V of the Korotkoff sounds to define systolic and diastolic readings.10 All patients had appropriate clinical and laboratory evaluations to exclude secondary forms of hypertension. All of them were nonsmokers. No antihypertensive drugs had ever been taken. Concomitant cardiovascular diseases other than arterial hypertension and other chronic diseases, such as diabetes mellitus, liver disease, occlusive atherosclerotic vascular disease, and renal disease, were exclusion criteria as well. Control subjects Male nonsmoking control subjects were also recruited from a population that underwent a yearly medical screening for their health insurance. The BP of the control subjects was measured on two occasions a few weeks apart. To participate in the study, a subject's DBP had to be 80 mm Hg or less and SBP less than 135 mm Hg. All BP measurements during the recruitment procedure were performed by the same specially trained nurse. To be considered as controls, subjects had to be age-matched with the high-normal BP group and the risk factors (cholesterol, LDL-cholesterol, triglycerides, glucose, and creatininemia) had to be in the same range as those of the high-normal BP group. Finally, the control group consisted of 22 men (mean age, 40 ± 2 years; range, 20–54 years; BMI 25.0 ± 0.8 kg/m2). Blood pressure and heart rate characteristics for the patients and the control subjects are summarized in Table 1. Table 1. Subject’s characteristics High-Normal . Low-Normal . n (male) 22 22 Age (years) 40 ± 2 40 ± 2 BMI (kg/m2) 27.0 ± 0.9 25.0 ± 0.8 SBP (mm Hg) 147 ± 2.5* 123 ± 1.9 DBP (mm Hg) 84 ± 1.5* 69 ± 1.5 MAP (mm Hg) 105 ± 1.7* 87 ± 1.7 PP (mm Hg) 63 ± 1.7* 54 ± 0.9 HR (beats/min−1) 74 ± 3† 65 ± 3 Cholesterol (mg/dL) 223 ± 14 192 ± 7 LDL-cholesterol (mg/dL) 136 ± 14 112 ± 8 Triglycerides (mg/dL) 150 ± 14 142 ± 26 TPR (dyne.s.cm−5) 1435 ± 52† 1226 ± 47 High-Normal . Low-Normal . n (male) 22 22 Age (years) 40 ± 2 40 ± 2 BMI (kg/m2) 27.0 ± 0.9 25.0 ± 0.8 SBP (mm Hg) 147 ± 2.5* 123 ± 1.9 DBP (mm Hg) 84 ± 1.5* 69 ± 1.5 MAP (mm Hg) 105 ± 1.7* 87 ± 1.7 PP (mm Hg) 63 ± 1.7* 54 ± 0.9 HR (beats/min−1) 74 ± 3† 65 ± 3 Cholesterol (mg/dL) 223 ± 14 192 ± 7 LDL-cholesterol (mg/dL) 136 ± 14 112 ± 8 Triglycerides (mg/dL) 150 ± 14 142 ± 26 TPR (dyne.s.cm−5) 1435 ± 52† 1226 ± 47 BMI = body mass index; SBP = systolic blood pressure; DBP = diastolic blood pressure; MAP = mean arterial pressure; PP = pulse pressure; HR = heart rate; LDL = low-density lipoprotein; TPR = total peripheral resistance. * P < .01; † P < .05. Open in new tab Table 1. Subject’s characteristics High-Normal . Low-Normal . n (male) 22 22 Age (years) 40 ± 2 40 ± 2 BMI (kg/m2) 27.0 ± 0.9 25.0 ± 0.8 SBP (mm Hg) 147 ± 2.5* 123 ± 1.9 DBP (mm Hg) 84 ± 1.5* 69 ± 1.5 MAP (mm Hg) 105 ± 1.7* 87 ± 1.7 PP (mm Hg) 63 ± 1.7* 54 ± 0.9 HR (beats/min−1) 74 ± 3† 65 ± 3 Cholesterol (mg/dL) 223 ± 14 192 ± 7 LDL-cholesterol (mg/dL) 136 ± 14 112 ± 8 Triglycerides (mg/dL) 150 ± 14 142 ± 26 TPR (dyne.s.cm−5) 1435 ± 52† 1226 ± 47 High-Normal . Low-Normal . n (male) 22 22 Age (years) 40 ± 2 40 ± 2 BMI (kg/m2) 27.0 ± 0.9 25.0 ± 0.8 SBP (mm Hg) 147 ± 2.5* 123 ± 1.9 DBP (mm Hg) 84 ± 1.5* 69 ± 1.5 MAP (mm Hg) 105 ± 1.7* 87 ± 1.7 PP (mm Hg) 63 ± 1.7* 54 ± 0.9 HR (beats/min−1) 74 ± 3† 65 ± 3 Cholesterol (mg/dL) 223 ± 14 192 ± 7 LDL-cholesterol (mg/dL) 136 ± 14 112 ± 8 Triglycerides (mg/dL) 150 ± 14 142 ± 26 TPR (dyne.s.cm−5) 1435 ± 52† 1226 ± 47 BMI = body mass index; SBP = systolic blood pressure; DBP = diastolic blood pressure; MAP = mean arterial pressure; PP = pulse pressure; HR = heart rate; LDL = low-density lipoprotein; TPR = total peripheral resistance. * P < .01; † P < .05. Open in new tab All subjects gave informed consent before entering the study and the study protocol was approved by the local Ethical Committee. Intima-media wall thickness The right and left carotid arteries were examined with a duplex scanner (Diasonics System Five, Horten, Norway) using a 10-MHz probe and a transducer capture of 40 mm. The electrocardiographic signal was simultaneously recorded to synchronize the image capture to the top of the R-wave to minimize variability during the cardiac cycle. The subjects were investigated in the supine position with the head slightly turned away from the investigated side. All measurements were performed by one trained sonographer who was unaware of the subject's BP levels and radial pulse wave contour analysis. Subjects with the presence of atherosclerotic lesions were excluded from the study. The carotid arteries were carefully examined with regard to wall changes. The examination was carried out at 3 cm proximal to the bifurcation. On a longitudinal two-dimensional ultrasound image of the carotid artery, the near and far walls of the carotid artery are displayed as two dual white lines separated by a hypoechogenic space. Intima-media thickness was defined as the distance from the leading edge of the first bright line of the far wall (lumen-intima interface) to the leading edge of the second bright line (media-adventitia interface).21 This procedure was repeated three times at both sides. These arterial measurements of IMT were performed off-line. Recordings of the entire scanning procedure performed by the same expert sonographer were independently analyzed by another sonographer using the appropriate morphometric software of the apparatus. A frozen longitudinal image was captured and recorded on videotape and a short sequence of real-time images was recorded on videotape to assist in the interpretation of the frozen images. For each subject a mean IMT ([left + right]/2) was taken as a measure for current wall thickness of the distal common carotid artery. Large and small artery elasticity indices Research was conducted using the HDI/PulseWave Research CardioVascular Profiling System, which uses a noninvasive arterial pulse pressure sensor to obtain waveforms at the radial artery. The tonometer sensor array adjusts itself automatically to obtain the optimal waveform and repeats its calibration until the waveform is stable. The BP waveform used to derive the elasticity indices presented in the study resulted from computer-based averaging of 10 consecutive individual arterial BP waveforms collected noninvasively during a 30-s period (Hypertension Diagnostics Inc., Eagan, MN).7,13,14 This approach was achieved successfully in all subjects in whom a radial pulse was palpable and demonstratable on the display screen of the instrument. Elasticity indices of the large arteries (C1, capacitative arterial compliance, units in mL/mm Hg, representative of the aorta and major branches) and of the small arteries (C2, reflective arterial compliance, units in mL/mm Hg, representative of the distal part of the circulation) are derived from a third-order four-element modified Windkessel model, which can reproduce arterial pressure waveforms including both exponential and oscillatory pressure decays observed during the diastolic decay portion of the cardiac cycle.7,13,14 The calculation of the elasticity indices is based on a Fourier analysis of the diastolic decay curve of the averaged radial artery pressure pulse wave, with C1 and C2 values being derived from successive terms of the Fourier transform. Calculations of C1 and C2 make use of an estimation of stroke volume (SV) (SV = −6.6 + 0.25 [ejection time in ms − 35] − 0.62 [HR in beats/min] + 40.4 [body surface area in m2] − 0.51 [age in yr]) from demographically derived algorithms and validated against direct, dye-dilution determinations of SV.14 Study protocol After overnight fasting, the subjects were examined between 8:00 and 10:00 AM after 30 min of supine rest. The office BP was measured at the brachial artery using a mercury sphygmomanometer in the sitting position. Means of three measurements at 1-min intervals were taken as study parameters SBP and DBP. Mean arterial pressure (MAP) was calculated as DBP + 1 3 (SBP − DBP), whereas pulse pressure (PP) was calculated as SBP − DBP. Heart rate was determined from the beat-to-beat analysis from the ECG. Thereafter at random, ultrasonography of the carotid arteries and noninvasive radial artery pulse contour wave registration were performed for subsequent analysis of, respectively, IMT and large and small artery elasticity indices (C1 and C2). Statistical analysis Data are given as mean ± SEM. Comparison between the two groups was made by Student's t test. Significance was considered at the level of P < .05. Spearman rank correlations were calculated between IMT and, respectively, C1 and C2 in both groups, as well as age correlations. IMT differences according to quartiles of C1 and C2 calculated for the combined study group were analyzed by the MANOVA test. Results The characteristics of both groups are given in Table 1. Age and BMI were comparable, whereas SBP, DBP, MAP, and PP were significantly (P < .01) higher in the high-normal BP group, as was heart rate (P < .05). Both large and small artery elasticity indices and IMT are given in Table 2. Table 2. Large and small artery elasticity indices and intima media thickness High-Normal . Low-Normal . C1 (mL/mm Hg) 1.63 ± 0.08* 1.99 ± 0.09 C2 (mL/mm Hg) 0.059 ± 0.005† 0.076 ± 0.007 IMT (mm) 0.607 ± 0.039† 0.516 ± 0.027 SV/PP (mL/mm Hg) 1.44 ± 0.37† 1.76 ± 0.41 High-Normal . Low-Normal . C1 (mL/mm Hg) 1.63 ± 0.08* 1.99 ± 0.09 C2 (mL/mm Hg) 0.059 ± 0.005† 0.076 ± 0.007 IMT (mm) 0.607 ± 0.039† 0.516 ± 0.027 SV/PP (mL/mm Hg) 1.44 ± 0.37† 1.76 ± 0.41 C1 = large artery elasticity index; C2 = small artery elasticity index; IMT = intima-media wall thickness; SV = stroke volume; other abbreviation as in Table 1. * P < .01; † P < .05. Open in new tab Table 2. Large and small artery elasticity indices and intima media thickness High-Normal . Low-Normal . C1 (mL/mm Hg) 1.63 ± 0.08* 1.99 ± 0.09 C2 (mL/mm Hg) 0.059 ± 0.005† 0.076 ± 0.007 IMT (mm) 0.607 ± 0.039† 0.516 ± 0.027 SV/PP (mL/mm Hg) 1.44 ± 0.37† 1.76 ± 0.41 High-Normal . Low-Normal . C1 (mL/mm Hg) 1.63 ± 0.08* 1.99 ± 0.09 C2 (mL/mm Hg) 0.059 ± 0.005† 0.076 ± 0.007 IMT (mm) 0.607 ± 0.039† 0.516 ± 0.027 SV/PP (mL/mm Hg) 1.44 ± 0.37† 1.76 ± 0.41 C1 = large artery elasticity index; C2 = small artery elasticity index; IMT = intima-media wall thickness; SV = stroke volume; other abbreviation as in Table 1. * P < .01; † P < .05. Open in new tab C1 and C2 were significantly lower (respectively, P < .01 for C1 and P < .05 for C2) in the high-normal BP group compared to the low-normal BP group. On the contrary, IMT was significantly (P < .05) higher in the high-normal BP group. There was a significantly inverse correlation between IMT and C2 in the high-normal BP group (r = −0.60, P = .004), whereas there was no significant correlation between IMT and C1 (Fig. 1). Total peripheral vascular resistance was significantly correlated with both IMT (r = 0.56, P < .05) and C2 (r = −0.48, P < .05), but not with C1 (r = −0.26, P = NS). Correlation between large artery (C1) and small artery (C2) elasticity indices and intima-media wall thickness (IMT) of the common carotid artery in 22 subjects with high-normal blood pressure. Figure 1. Open in new tabDownload slide Figure 1. Open in new tabDownload slide There were no significant correlations between IMT and C1 or C2 in the low-normal BP group. On the contrary, the correlations between total peripheral vascular resistance and C1 (r = −0.32, P < .05) and C2 (r = −0.47, P < .05) were also significant. Correlation between IMT and total peripheral vascular resistance was not-significant. Finally, data of C1, C2, and IMT were pooled (n = 44) and the relationship between C1, C2, and IMT is depicted (Fig. 2) for quartiles of, respectively, C1 (1.087–1.419, 1.430–1.756, 1.775–2.140, and 2.162–3.082 mL/mm Hg) and C2 (0.015–0.042, 0.045–0.067, 0.071–0.091, and 0.093–0.132 mL/mm Hg). Relationship between quartiles of, respectively, large artery (C1) and small artery (C2) elasticity indices and intima-media wall thickness (IMT) in the combined group (n = 44). Data are mean ± SEM. Figure 2. Open in new tabDownload slide Figure 2. Open in new tabDownload slide With increasing quartiles of C2 there was a progressive decrease in IMT (MANOVA, P = .05). There was no significant correlation between C2 and PP (MANOVA, P = .09) and between PP and IMT (MANOVA, P = .48). There was also no significant relationship (MANOVA, P = .136) between quartiles of C1 and IMT. There was an age dependency of IMT (r = 0.55, P < .001) and C2 (r = −0.457, P = .005). On the other hand, SV/PP was not related to age or IMT, but was BP dependent (r = −0.77, P < .0001 for PP). SV/PP correlated statistically with C1 (r = 0.85, P < .0001) but not with C2 (r = 0.23, P = NS). Discussion Our study has shown for the first time that in high-normal BP there is a pronounced decrease in the large (C1) and small artery (C2) elasticity indices, in comparison to low-normal BP, and it is accompanied by an increase in mean carotid artery IMT. Furthermore, there is an inverse relationship between IMT and the small artery elasticity index. Arterial compliance has previously been studied from normotension to established hypertension.24 Surprisingly, in their patient subpopulation with mean BP 134/82 mm Hg the decrease in arterial compliance was disproportionally higher than the increase in BP would suggest. This conclusion was reached using different methodologies, including pulse wave velocity, the ratio of stroke volume to pulse pressure, and by the DBP decay method; it leads to the suggestion that compliance and distensibility of large arteries become impaired early in the evolutionary process of hypertensive cardiovascular disease, at the time when BP is only intermittently elevated.4 Simon et al25 also described that arterial compliance was clearly more reduced than would be expected from the slight increase in arterial pressure alone in borderline hypertension. In their patients with normal cardiac output there was no correlation between arterial compliance and pressure, which suggests that the reduction in arterial compliance is independent of BP. Therefore, it seems likely that factors other than the magnitude of BP elevation contribute to the reduced arterial compliance of borderline hypertensives; these include sympathetic nervous system, early changes of the blood vessel wall, and humoral mechanisms. Weber et al26 addressed arterial compliance in normotensives (mean, 121/79 mm Hg) and in two groups of hypertensives (borderline, 138/94 mm Hg and established, mean 157/104 mm Hg) using pulse wave contour analysis and demonstrated that the major changes in arterial compliance, particularly in the small artery elasticity index (C2), coincide with the time period that BP increases from normal to borderline elevated. From borderline to overt hypertension there were only small nonsignificant further decreases of C2. Thus the authors concluded that their findings were compelling enough to suggest that changes in vascular structure and function precede the changes in BP. This may point to a role of early decrease of C2 in the pathogenesis of high BP.27 On the other hand, there was a continuous decrease of the large artery compliance (C1) with increasing BP. This differential response of C1 and C2 suggests that marked changes in compliance of the peripheral portion of the arterial circulation participate in the initiation of the hypertension process but that thereafter the rise in BP reduces proximal compliance and contributes to the structural changes in the vasculature. In our study the differences in C1, C2, and IMT between the two groups were thought to be related to pulse pressure differences; both SBP and DBP differences might be involved. We observed a 17% increase in IMT in our high-normal BP group versus low-normal BP group. Although most studies regard noninvasively assessed IMT as a measure of atherosclerosis,19 other investigators described that increased IMT is not merely a precursor of atherosclerosis but an adaptive response of the vessel wall to changes in shear stress and tensile stress. Parallel to the development of atherosclerosis, a widening of the artery is seen that compensates for the restriction of vessel wall lumen.28 These observations suggest the presence of more vascular risk markers in high-normal BP subjects with increased IMT and reduced elasticity indices. Thus, the latter can be considered an early marker for vascular disease in these populations. It has been suggested that arterial compliance decreases between the ages of 20 and 50 years, with a more rapid decrease after the age of 50 years in normotensives as well as in hypertensives.29,30 Also Cohn and Finkelstein31 confirmed a striking age relationship for both C1 and C2 using the same methodology applied in this study. Some of these observed changes are almost certainly because of changes in arterial stiffness, the result of structural changes in collagen and elastin, along with the potential for a noncausal association with atherosclerosis. A reduction in endothelial function with impaired nitric oxide release is characteristic of hypertension, aging, and atherosclerosis. The reduction of small artery compliance observed in the borderline hypertension in this study may reflect functional and structural changes accelerated by endothelial dysfunction. Whether the decreased compliance is a natural phenomenon of aging or is from associated atherosclerosis remains incertain. A population-based ultrasonography study from Finland provided evidence that IMT is also related to age.18 In the meantime, this has been confirmed by other general population studies such as the ARIC study20 and the studies mentioned in the review of Kanters et al.32 Carotid indices reflecting cardiovascular risk are themselves related to or a reflection of more general and perhaps even earlier functional changes in the vasculature. Furthermore, the latter functional indices can be assessed in a simple, noninvasive manner using the arterial pressure pulse waveform analysis. As such, use of this noninvasive and relatively simple vascular compliance technique may improve our ability to assess vascular disease in the routine clinical setting in which patients are normally seen. Only preliminary validation studies33 have been conducted for C1 as a measure of large artery compliance, but no direct physiologic measurements of small artery compliances have ever been reported. As such, the interpretation of C2 as reflecting small artery compliance must therefore remain presumptive at this stage and limited by the physiologic appropriateness of the Windkessel model from which it was derived. Because no direct measurement of BP or flow and no indirect measurement of blood flow were obtained, it is necessary to accept the study conclusions with some caution. Further, as there are no direct methods for determining C2, its relationship to TPR is uncertain and its determination has therefore been based solely on the indirect approach described in the Methods section. In conclusion, in high-normal BP subjects there are significant decreases in large artery (C1) as well as small artery (C2) elasticity indices, accompanied by an increase in carotid artery IMT. 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TI - Relationship between arterial elasticity indices and carotid artery intima-media thickness
JF - American Journal of Hypertension
DO - 10.1016/S0895-7061(00)01203-6
DA - 2000-11-01
UR - https://www.deepdyve.com/lp/oxford-university-press/relationship-between-arterial-elasticity-indices-and-carotid-artery-mbEjM1RRwB
SP - 1226
EP - 1232
VL - 13
IS - 11
DP - DeepDyve
ER -