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(Hypertension. 1995;26:984-988.)
© 1995 American Heart Association, Inc.

Articles

Radial Artery Compliance in Young, Obese, Normotensive Subjects

Arduino A. Mangoni; Cristina Giannattasio; Amelia Brunani; Monica Failla; Manuela Colombo; Giovanbattista Bolla; Francesco Cavagnini; Guido Grassi; Giuseppe Mancia

From Cattedra di Medicina Interna, Università di Milano and Ospedale S. Gerardo, Monza (C.G., M.F., M.C., G.M.); Centro di Fisiologia Clinica e Ipertensione, Ospedale Maggiore, Milano (A.A.M., G.B., G.G.); and Centro Auxologico Italiano, Milano (A.B., F.C.), Italy.

Correspondence to Prof Giuseppe Mancia, Cattedra di Medicina Interna I, Ospedale S. Gerardo Dei Tintori, Via Donizetti 106, 20052 Monza (MI), Italy.

	Abstract

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Abstract Obesity is characterized by a number of cardiovascular alterations, and whether these alterations involve arterial compliance is unknown. In 12 young, obese, normotensive subjects (age, 23.9±1.3 years; mean±SEM) and 12 age- and sex-matched lean control subjects we measured blood pressure, radial artery diameter, and radial artery compliance continuously over the systodiastolic pressure range with a Finapres device and recently developed echo-tracking device. Measurements were obtained at baseline and after prolonged ischemia, that is, when diameter and compliance are increased. Blood pressure values were normal in both groups (obese subjects: 109.2±4.9/68.2±2.7 mm Hg; lean control subjects: 108.2±4.1/60.7±3.8 mm Hg), but in addition to a marked increase in body mass index (38.5±0.8 versus 23.1±0.9 kg/m², P<.01), obese subjects showed a slight and nonsignificant increase in heart rate (71.1±3.2 versus 66.7±3.3 beats per minute, P=NS), increases in left ventricular wall thickness and left ventricular mass index (121.5±4.8 versus 103.4±3.3 kg/m², P<.01), no changes in plasma renin activity and plasma norepinephrine (compared with normal values), and a marked reduction in total body glucose uptake (glucose clamp technique). Obese subjects showed radial artery diameter and compliance values that were greater than those seen in control subjects throughout the systodiastolic pressure range. The differences were 13% (P<.05) and 96% (P<.01), respectively, and both diameter and compliance remained higher in obese than lean subjects after forearm ischemia. In obese and lean subjects baseline radial artery diameter values correlated highly with body weight, body surface area, and body mass index. Thus, radial artery compliance is increased in young, obese, normotensive subjects. Whether these changes are related to functional factors or intravascular or extravascular structural changes remains to be determined. The increase, however, is similar to what has been described in mild essential hypertension, emphasizing the similarity of the cardiovascular alterations in these two conditions.

Key Words: compliance • obesity • cardiovascular system • radial artery

	Introduction

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Conclusive evidence is available that the cardiovascular system is profoundly altered in obesity. The alterations consist of increases in blood volume, cardiac output, and systemic blood flows that, together with a reduction in systemic vascular resistance, make the circulation of obese subjects hyperdynamic.^{1 2 3} The alterations also include an increase in left ventricular mass that is not entirely accounted for by the increased body surface and thus represents an actual cardiac hypertrophic state.⁴ Less information exists on the effects of obesity on peripheral vasculature, and little information is available on whether obesity affects arterial compliance.⁵ This may be an issue of pathophysiological relevance because arterial compliance is a major determinant of arterial impedance and cardiac afterload.^{6 7} Thus, a reduction in arterial compliance (possibly caused by vascular wall hypertrophy) might explain why in obesity left ventricular mass and systolic blood pressure (BP) increase. In the present study we have tested this hypothesis using a technique that allows the measurement of radial artery compliance dynamically over the existing BP range.⁷ To avoid the confounding effect of high BP and aging on arterial compliance, we conducted the study in young, obese, normotensive subjects.

	Methods

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Subjects
We studied 24 young male subjects with an age ranging from 17 to 31 years. Twelve subjects (age, 23.9±1.3 years; mean±SEM) were obese, with a fat distribution of a central type, that is, excessive adipose tissue in the abdomen compared with peripheral regions. The other 12 were age-matched lean control subjects (age, 24.2±0.8 years). All subjects had sphygmomanometric BP values less than 140/90 mm Hg at repeated visits performed in outpatient clinics. No subject had a history of cardiovascular disease and clinical or laboratory evidence of cardiovascular, respiratory, or renal damage. At the time of the study obesity had been present for at least 5 years. All subjects volunteered to participate in the study after being informed of its nature and purpose. The protocol of the study was approved by the Ethics Committees of the institutions involved.

Measurement of Arterial Compliance
Compliance describes the elasticity of volumic structures. Compliance of an artery defines the blood volume that is stored or released in the vessel after a given change in arterial BP.^{6 7 8} Because changes in arterial volume are mainly due to changes in arterial cross section, compliance can also be defined as the change in arterial cross section induced by the change in inside arterial BP and expressed in millimeters squared per millimeters of mercury. Since the elastic properties of the arterial wall are a function of distending pressure, compliance has to be determined at different BP values; that is, it has to be expressed by compliance-pressure curves.^{6 7 8} In the present study the time-dependent changes in arterial diameter were obtained by a new A-mode ultrasonic echo-tracking device (NIUS 01 system, Asulab)⁷ that recorded the displacement of the radial artery over the entire cardiac cycle and thus over the entire systodiastolic pressure range. Briefly, the device made use of a highly focalized transducer operating at a frequency of 10 MHz that was stereotaxically positioned over the radial artery 2 to 4 cm above the wrist, direct contact with the skin being prevented by use of a gel medium. With the subject supine and the arm immobile at heart level, the transducer was oriented perpendicularly to the longitudinal axis and the largest cross-sectional dimension of the artery based on the Doppler acoustic quality signal. After a switch to A-mode, the backscattered echoes from the inner anterior and posterior walls were visualized on an oscilloscope, and the related high–radio frequency signals were picked up by an electronic tracer, allowing a digitalized signal of internal diameter variations to be derived. The internal diameter of the pulsating radial artery was measured 300 times per second, and the device resolution allowed the identification of diameter changes larger than 150 µm.⁸

The device also made use of a photoplethysmographic system (Finapres, TNO Biomedical Instrumentation)^{9 10} that allowed BP to be recorded noninvasively from a finger ipsilateral to the radial artery examined and had an accuracy similar to intra-arterial radial artery pressure^{9 10 11} and a resolution greater than or equal to 2 mm Hg.^{9 10}

The BP and arterial diameter signals were directed to a computer programmed to calculate the cross-sectional pressure curve of the vessel. The curve was then analyzed according to its fit with the arc tangent model of Langewouters et al,¹² which is based on the following formula:

where S is the cross-sectional area of the vessel; P is the intravascular pressure; and , ß, and are three optimal parameters describing the spatial position of the diameter-pressure curve. From this formula, compliance (C=S/P¹³) can be calculated as follows:

and expressed as consecutive values for BP ranging from diastole to systole (compliance-pressure curve). The formula was used for calculation of arterial distensibility (compliance divided by diameter) over the BP range from diastole to systole (distensibility-pressure curve).

All measurements were performed by a single operator. The variation coefficient of radial artery diameter measurements obtained by the same operator in two different sessions (the within-operator variability) was 4%. The corresponding variation coefficients of radial artery compliance and systolic BP were 10% and 2.8%, respectively.

Other Measurements
In nine obese and nine lean control subjects left ventricular diameter, septal wall thickness, and left posterior wall thickness were measured by M-mode echocardiography after identification in B-mode of the left ventricular section to be measured. Left ventricular mass index was calculated according to the Penn convention formula.¹⁴ The measurements were made by a single operator, and the variation coefficient of left ventricular mass measurements obtained by the same operator in two different sessions (the within-operator reproducibility) was 4%. Heart rate was derived from the finger pressure signal as the reciprocal of the pulse interval between consecutive systolic peaks. Plasma renin activity was measured by radioimmunoassay,¹⁵ and plasma norepinephrine was measured by high-performance liquid chromatography.¹⁶ The variation coefficients of the assays from the same blood sample were 2% for plasma renin activity and 5.8% for plasma norepinephrine. A euglycemic insulin clamp test was performed in eight obese subjects according to the technique described in previous studies.¹⁷ The amount of glucose required to maintain euglycemia was taken as an index of the whole-body uptake of glucose and thus of insulin sensitivity.^{18 19}

Protocol and Data Analysis
The study was conducted in the morning after subjects had abstained 24 hours from cigarette smoking and alcohol and caffeine consumption. The protocol of the study was as follows: (1) Each subject was placed in the supine position and fitted with the finger pressure and echo-tracking devices. (2) After a 20-minute interval, BP, heart rate, radial artery diameter, and compliance were continuously measured for 15 minutes. To obtain baseline values we averaged each variable first over periods of 4 seconds and then for five 4-second periods taken at intervals of 3 minutes. (3) Forearm ischemia was produced by occlusion of the brachial artery on the side from which radial artery diameter and compliance were measured for 12 minutes by a cuff inflated to suprasystolic pressure. (4) All aforementioned hemodynamic variables were measured in the 5 minutes after the release of brachial artery occlusion. Over this period each variable was averaged over repeated 4-second periods consecutively taken. Maximal increases in diameter and compliance normally occurred in the first minute after release of brachial artery occlusion, and the related 4-second period was used for analysis. Measurements during reactive hyperemia were collected because this condition markedly increases radial artery diameter and compliance, making it possible to evaluate the ability of compliance to increase in response to an appropriate stimulus, that is, the compliance reserve.²⁰ The subjects were called back to the laboratory 2 days later, again after abstaining 24 hours from smoking and alcohol and caffeine consumption. At this second session echocardiographic measurements were obtained and plasma renin activity, plasma norepinephrine (venous blood sample), and insulin sensitivity were determined.

Diameter-, compliance-, and distensibility-pressure curves from individual subjects were summed and expressed as mean±SEM for the group of obese and lean subjects. Average values (±SEM) for lean and obese subjects were also obtained for (1) radial artery diameter at the diastolic BP value, (2) the area under the curve relating compliance to BP normalized for pulse pressure (this was referred to as the compliance index), and (3) the area under the curve relating distensibility to BP normalized for pulse pressure (distensibility index). This allowed us to obtain single values for each subject, thus facilitating between-subject comparisons. The statistical significance of the differences in the mean values of diastolic diameter and compliance index was assessed by two-way ANOVA. Student's two-tailed t test for paired observations was used to locate differences between baseline and postischemic values, and Student's unpaired t test was used to determine differences between the obese and lean groups. A value of P<.05 was taken as the level of statistical significance.

	Results

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Baseline Values
The Table shows that absolute body weight, body mass index, and body surface area of obese subjects were significantly and markedly greater than those of lean subjects. Systolic BP, diastolic BP, and heart rate were similar in the two groups; this was also the case for plasma renin activity and plasma norepinephrine. However, compared with lean subjects, obese subjects showed greater septal wall thickness, posterior wall thickness, left ventricular end-diastolic diameter, and left ventricular mass index. Furthermore, total body glucose uptake of obese subjects was 2.8±0.4 mg glucose/kg per minute, a value markedly lower than that reported in the literature for young, nonobese, healthy subjects (>8 mg glucose/kg per minute).^{17 18 19}

View this table: [in this window] [in a new window]   Table 1. Baseline Data of Obese and Lean Subjects

Radial Artery Diameter, Compliance, and Distensibility
Fig 1 (left) shows that in both obese and lean subjects an increase in BP from diastolic to systolic values was associated with a small progressive increase in radial artery diameter and a marked progressive reduction in radial artery compliance and distensibility (middle and right, respectively). However, over a similar BP range radial artery diameter was markedly higher in obese than lean control subjects. This was also the case for radial artery compliance and distensibility, the diastolic diameter, compliance index, and distensibility index being 13%, 96%, and 68% greater, respectively, in the former compared with the latter group (Fig 2). In obese and control subjects pooled, radial artery diameter values were significantly correlated with body weight (r=.71, P<.01), body mass index (r=.56, P<.01), and body surface area (r=.76, P<.01).

View larger version (20K): [in this window] [in a new window]   Figure 1. Line graphs show baseline and postischemic diameter-, compliance-, and distensibility-pressure curves from the radial artery. Shown are mean±SEM from obese (, n=12) and lean (, n=12) subjects.

View larger version (13K): [in this window] [in a new window]   Figure 2. Bar graphs show baseline (B) and postischemic (PI) diameter, compliance index, and distensibility index values from the radial artery. Shown are mean±SEM from obese (hatched bars, n=12) and lean (open bars, n=12) subjects. *P<.05; **P<.01.

After prolonged local ischemia both groups showed a pronounced increase in radial artery compliance, distensibility, and diameter values (Fig 2). The increases were similar in the two groups, and thus compliance index, distensibility index, and diastolic diameter remained markedly higher in obese than in control subjects during reactive hyperemia (Fig 2).

	Discussion

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In the present study we tested the hypothesis that radial artery compliance is reduced in obesity, possibly because of arterial wall hypertrophy. We found that radial artery diameter and compliance are markedly greater in young, obese, normotensive subjects than age-matched lean, normotensive control subjects. We also found that this difference is evident throughout the systodiastolic pressure range and that it persists even when radial artery diameter and compliance are markedly increased as a result of release from a prolonged period of ischemia. Thus, increased radial artery diameter and compliance are a feature of young, obese, normotensive subjects that persists across the existing BP range and is independent of factors that increase compliance above baseline values.

Our data do not clarify the mechanisms responsible for the increase in radial artery diameter and compliance of obese subjects. Nonetheless, several possibilities can be discussed. The first one relates to whether the increase in radial artery compliance was induced by the increase in radial artery diameter seen in obese subjects. However, obese subjects were characterized also by a marked increase in arterial distensibility, that is, a measure of wall elasticity that is made independent of arterial diameter values. Furthermore, an increase in arterial diameter is more likely to be associated with a reduction in compliance via stretching of stiffer collagen fibers.^{21 22} It is thus likely that in obesity an increase in radial artery compliance does not result from but rather causes an increase in arterial diameter.

Which factors are responsible for the increase in radial artery compliance? We might speculate that this increase is due to an alteration in the concentration of vasomotor substances, leading to a reduction in vascular smooth muscle contraction and thus an increase in arterial distensibility. However, these substances are unlikely to be norepinephrine and angiotensin II because the renin-angiotensin and sympathetic nervous systems are activated in obesity,^{23 24 25 26} and plasma norepinephrine and renin activity were not less in the obese compared with lean subjects of the present study. Thus, other substances should be sought. One of them could be insulin because obesity is characterized by insulin resistance.^{17 18 19} This leads to hyperinsulinemia, which causes skeletal muscle vasodilatation; that is, insulin has a relaxing effect on arteriolar smooth muscle that may extend to smooth muscle in larger arteries.^{27 28} Another substance could be nitric oxide, the secretion of which might be increased in obesity because of the increase in blood volume, cardiac output, and peripheral blood flow, that is, because of a flow-dependent hypersecretion of endothelium-derived relaxing factors.²⁹ In our study endothelial factors were not quantified, but insulin sensitivity was measured in obese subjects and found to be clearly less than the normal values available in the literature.^{18 19} Unfortunately, we did not measure insulin resistance in lean control subjects, so we could not determine whether insulin resistance correlated with compliance values.

Another possibility is that the increase in radial artery compliance associated with obesity may be due to alterations of the arterial wall or perivascular structures that increase the tissue components that offer less resistance to vessel distension than other components. Possible candidates are the intercellular matrix, adipose cells, and smooth muscle cells, all of which are more distensible than collagen. Functional and structural changes of the radial artery wall and perivascular space may of course coexist and be responsible for the increase in arterial compliance that we observed.

A few other points should be mentioned. First, in subjects ranging from normal to increased body weight, radial artery compliance-pressure curves were similar when BP was obtained noninvasively from a finger or invasively through the radial artery itself.¹¹ Thus, it is unlikely that in the present study noninvasive BP measurements from a site slightly different from the one where arterial diameter was measured introduced any substantial error. Second, because compliance-pressure curves could be established only from the radial artery, whether an obesity-related increase in compliance also occurs in larger arteries with a more elastic structure than the radial artery remains to be demonstrated. Third, it should be emphasized that in our obese, normotensive subjects radial artery diameter was closely related to body weight, body mass index, and body surface area. This confirms previous findings of a relationship between aortic diameter and body size³⁰ and shows that body size affects middle-sized– and large-artery diameters in a similar qualitative fashion.

Finally, increased arterial compliance apparently does not have adverse clinical implications; indeed, one would expect that this might oppose rather than facilitate the increase in left ventricular mass occurring in obesity (see above). On the other hand, the increase in radial artery compliance of obese normotensive subjects is similar to the increase in radial artery compliance previously described in subjects with mild essential hypertension.³¹ We thus can speculate that the increased arterial compliance of obesity has a pathogenetic implication, namely, that this alteration precedes the increase in BP and represents another example of the links existing between conditions characterized by metabolic alterations and subsequent BP elevations.

Received January 18, 1995; first decision February 16, 1995; accepted July 11, 1995.

	References

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