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Am J Physiol Heart Circ Physiol 276: H1839-H1845, 1999;
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Vol. 276, Issue 6, H1839-H1845, June 1999

Systemic arterial compliance is reduced in young patients with IDDM

Karen L. Berry1, R. Andrew P. Skyrme-Jones1, James D. Cameron2, Richard C. O'Brien3, and Ian T. Meredith1

1 Cardiovascular Centre, Centre for Heart and Chest Research, Monash University and Monash Medical Centre; 3 Diabetes Unit, Monash Medical Centre, Clayton 3168; and 2 Department of Electrical Engineering, Latrobe University, Bundoora, Victoria 3083, Australia


    ABSTRACT
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

Arterial elastic properties are altered with increasing age and in various disease states, including non-insulin-dependent diabetes mellitus (NIDDM). Whether young patients with insulin-dependent diabetes mellitus (IDDM) have reduced arterial compliance before developing endothelial dysfunction or overt micro- and macrovascular disease is unclear. Systemic arterial compliance and endothelium-dependent, flow-mediated vasodilation (FMD) was assessed in 25 individuals with uncomplicated IDDM (23 ± 4 yr, 14 females and 11 males) and compared with 30 age-matched controls (15 females and 15 males). Arterial compliance was determined via simultaneous measurements of aortic blood flow and carotid arterial pressure. The relationship between arterial compliance and endothelial function (assessed by brachial artery FMD) was also examined. Arterial compliance was 29% lower in IDDM subjects compared with control subjects (0.46 ± 0.05 vs. 0.65 ± 0.07 arbitrary compliance units, P < 0.05). Blood pressure, lipid levels, and daily energy expenditure (a measure of physical activity levels) were not different between groups. Compliance in the IDDM group was not related to the integrity of endothelial vasodilator function, disease duration, or degree of glycemic control. Arterial compliance is reduced in young patients with IDDM before the development of overt micro- or macrovascular disease. Early assessment of arterial compliance may be useful in predicting the development of diabetic vascular complications.

arterial stiffness; diabetes; insulin-dependent diabetes mellitus; endothelium


    INTRODUCTION
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

ARTERIAL COMPLIANCE is an important property of the vascular system that provides the smooth, continuous flow of blood to the periphery, while maintaining optimal systolic and diastolic blood pressures. It is therefore an important determinant of left ventricular function and coronary blood flow. Reduced arterial compliance is associated with systolic hypertension (13, 35) and coronary artery disease (33, 41). However, a direct relationship between reduced arterial compliance and myocardial infarction, stroke, or death has not yet been established (4).

Several studies have examined the effect of diabetes mellitus on arterial compliance, but the results are inconsistent (19, 28). This inconsistency may in part be the result of including patients with insulin-dependent diabetes mellitus (IDDM), patients with non-insulin-dependent diabetes mellitus (NIDDM) (42), patients with a broad age range (36, 38), or patients with cardiovascular risk factors (39) in the study. Arterial compliance decreases progressively with age in individuals with (42) and without (26) diabetes. Recent data suggest that compliance can be improved both in healthy individuals (23) and in individuals with NIDDM (32). Therefore, treatment of reduced compliance may be of benefit to the long-term maintenance of vascular and cardiac function.

Endothelial vasodilator function is thought to be impaired in large vessels in diabetes (10), and it is not known if arterial compliance is altered as a direct consequence of this. There are few data on arterial compliance in young patients with IDDM who are free of cardiovascular disease and concomitant risk factors, and similarly, there are few data on the relationship between endothelial function and compliance in this group of young patients. Therefore, this study aims to: 1) assess systemic arterial compliance in young individuals with IDDM who were otherwise free of cardiovascular risk factors and determine whether this vascular property is altered early in the course of the disease before micro- or macrovascular complications are evident, and 2) examine whether reduced compliance is related to endothelial vasodilator function.


    METHODS
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

Subjects. Subjects with IDDM were recruited from the Adolescent Diabetes Clinic at Monash Medical Centre, whereas control subjects were recruited from within the hospital and Monash University. All participants gave their written informed consent to participate in the study, which was carried out with the approval of the Monash Medical Centre Ethics Committee.

The study population consisted of 25 individuals with IDDM (11 males and 14 females) all under 40 yr of age (22 ± 4 yr) and 30 healthy control subjects (15 males and 15 females, ages 23 ± 4 yr). All control subjects were nonsmokers and were free of other cardiovascular risk factors. The two groups were matched for body mass index, lipid (Table 1), and blood pressure variables (Table 2).

                              
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  		Table 1.   General characteristics


                              
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  		Table 2.   Hemodynamics

One subject in the group with diabetes was hypertensive and five subjects were current smokers. None of the participants was taking medication aside from their regular insulin dose, except four females with diabetes who were taking oral contraceptives.

The following clinical variables were assessed in subjects with diabetes on the day of the study: fasting plasma lipid profile and glucose levels, ambient glucose levels, and glycated hemoglobin (HbA1c) levels. A 12-h urine sample was collected for measurement of urinary albumin excretion rates.

Average duration of diabetes was 8 ± 4.6 (SE) yr (range 1-20 yr). Uncomplicated diabetes was defined as the absence of nephropathy [identified by microalbuminuria in the range of 20-200 µg/min (22)], overt vascular disease, retinopathy, and neuropathy on clinical examination. All participants completed a 14-day recall questionnaire regarding their exercise habits to enable the calculation of their average daily energy expenditure.

Protocol. Subjects attended the laboratory in a fasting state for determination of plasma glucose and lipids. Studies were performed in subjects in the nonfasting state after having a light breakfast and after the regular morning insulin dose for those subjects with IDDM. All participants abstained from caffeine and smoking for 12-h before the study. Arterial compliance measurements were performed on subjects while in a quiet environment after 10 min of supine rest and two to four automatic brachial blood pressure measurements. After these measurements were completed, brachial artery ultrasound recordings were made before and after 1) 5 min of forearm ischemia and 2) sublingual nitroglycerin (NTG) administration. On completion of the study, we measured the ambient glucose levels.

Arterial compliance. The assessment of systemic arterial compliance (SAC) was carried out noninvasively using the area method of calculation as described by Liu et al. (30). This relies on the simultaneous measurement of aortic flow volume and associated driving pressure to estimate compliance throughout the whole arterial tree. This noninvasive technique for measuring arterial compliance has been well-described (6, 24) with the value of SAC given as SAC = Ad/[R(Ps - Pd)], where Ad is diastolic area, R is total peripheral resistance, and Ps and Pd are end-systolic and end-diastolic blood pressure, respectively.

As previously described (6, 24), flow velocity of the ascending aorta was measured from the suprasternal notch using a continuous-wave hand-held Doppler flow velocimeter (Multi-Dopplex II, Huntleigh Technology, Cardiff, UK). Aortic root dimensions were assessed by two-dimensional echocardiography [HDI Ultramark 9, Advanced Technology Laboratories (ATL)] with measurements taken from the point of insertion of the aortic valve leaflets. Volume flow was then calculated as the product of average systolic aortic flow velocity and aortic root area.

Aortic root pressure was estimated via noninvasive applanometry of the right carotid artery using a Millar Mikro-Tip pressure transducer (model SSD-713, Millar Instruments, Houston, TX). Brachial pressures measured using a Dinamap XL vital signs monitor (model 9300, Critikon, Tampa, FL) were used to calibrate the carotid pressure waveforms obtained by tonometry.

Flow and pressure signals were recorded for 30 s and digitized at 200 Hz using a PCM-DAS16 analog-to-digital conversion card (Computer Boards, Mansfield, MA). Data acquisition and analysis were carried out using purpose-written software, with an average of 5-10 representative pairs of waveforms analyzed for each subject. This technique is very reproducible and has a coefficient of variation of 9.2% and a repeatability coefficient of 0.31 (29).

Endothelial vasodilator function. Flow-mediated dilation of the right brachial artery was assessed using a well-described and validated technique (7) that has a coefficient of variation of 10.8% and a repeatability coefficient of 5.49 (29). The studies were performed using an ultrasound machine (HDI Ultramark 9, ATL) with a 7- to 10-MHz linear array transducer. Subjects rested supine during the study. Heart rate, using a single-lead electrocardiogram, and blood pressure (Dinamap XL vital signs monitor, model 9300, Critikon) were monitored throughout the study. Longitudinal images of the brachial artery were recorded ~8-cm proximal to the cubital fossa. Transmit focal zones and depth were set to optimize the image of the vessel wall, particularly the media-adventitia interface ("M" line), and then the image was magnified. These operating parameters were kept constant throughout the study.

Recordings were made at baseline (after 10 min of rest), during reactive hyperemia, after 15 min of rest, and then in response to NTG administration. Flow-mediated endothelium-dependent responses were assessed after the induction of reactive hyperemia by the inflation of a pressure cuff on the forearm to 200 mmHg for 5 min. Endothelium-independent responses were assessed after the administration of 600 µg of sublingual NTG.

Image analysis. Brachial artery images were recorded onto a Super-VHS videotape. Two representative frames from each time point (baseline, 45-60 s postcuff deflation, pre-NTG, and 3-5 min post-NTG administration) were later digitized using a frame grabber (Scion LG-3) and saved for subsequent analysis. These frames were selected at the point corresponding to the R wave (end diastole) of the electrocardiogram recording. Vessel diameter measurements were carried out using a modified version of the public domain National Institutes of Health (NIH) Image Program, originally developed at NIH. Two observers blinded to the stage of the study performed the analysis, in which the distance between the anterior (intimal-medial interface) and posterior walls (medial-adventitial interface) were measured automatically. Each frame was measured three times, thus six measurements were obtained for each time point and averaged. The percent change in vessel diameter was then calculated in response to reactive hyperemia and NTG administration.

Physical activity assessment. A 14-day recall questionnaire was used to estimate daily energy expenditure. This questionnaire has previously been shown to be a reproducible and reliable measure of assessing physical activity participation (5). Participants are asked to recall the duration and intensity of any leisure-time physical activities that they would typically participate in over a 2-wk period. Daily energy expenditure (kcal · day-1 · kg-1) was estimated from this information and reported in metabolic equivalents (METS). One MET unit is equivalent to the energy expended at rest or the basal metabolic rate of an adult (1 kcal · kg-1 · h-1). Subjects were then grouped into one of four energy expenditure categories according to their MET score as follows: the vigorous group consisted of having energy expenditure >= 3.8 kcal · day-1 · kg-1 as well as participation in aerobic activity at least six times in 2 wk, for at least 20 min per session at an intensity of very or fairly vigorous; the moderate group consists of having energy expenditure >= 1.8 kcal · day-1 · kg-1 and was not included in the vigorous category; the low group consisted of having energy expenditure 0.12-1.79 kcal · day-1 · kg-1; and the inactive group consisted of having energy expenditure <= 0.12 kcal · day-1 · kg-1.

Biochemical analysis. Total cholesterol, high-density lipoprotein cholesterol (HDL-C), and triglyceride levels were measured using a standard enzymatic method. Low-density lipoprotein cholesterol (LDL-C) was calculated according to the Friedewald formula. HbA1c levels were assessed by HPLC. A Beckman Array 36 system was used to measure urinary albumin levels by nephelometry.

Statistics. Results are means ± SE. Between-group comparisons were made using an unpaired t-test. Univariate and multivariate linear regression analyses were used to determine the best predictors and group of predictors of arterial compliance within and across groups and the relationship between arterial compliance and endothelial function. chi 2-Test for proportions was carried out for assessment of differences in physical activity categories.


    RESULTS
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

Systemic arterial compliance was 29% lower in the group with diabetes compared with the control group (0.46 ± 0.05 vs. 0.65 ± 0.07 arbitrary compliance units, P < 0.05) (Fig. 1). This difference in arterial compliance was not because of differences in systolic, diastolic, or pulse pressure, or mean arterial pressure, which were similar between the two groups (Table 2). Resting heart rate was significantly higher in the group with IDDM (72 ± 2 beats/min) compared with the control group (64 ± 2 beats/min, P = 0.01) but was not related to compliance (r2 = 0.001, P = 0.8).


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  		Fig. 1.   Systemic arterial compliance in arbitrary compliance units (acu) in control and insulin-dependent diabetes mellitus (IDDM) subjects. * P < 0.05.

The difference in arterial compliance was not the result of lipid levels because total cholesterol, HDL-C, LDL-C, and triglyceride levels were similar in both control and IDDM groups (Table 1). Fasting and ambient plasma glucose levels were significantly higher in the IDDM group (11.8 ± 1.1 and 11.7 ± 1.1 mmol/l, respectively) than in the control group (4.8 ± 0.1 mmol/l, P < 0.0001); however, no relationship between glucose and compliance was observed across the two groups. There were no differences in age or body mass index between the two groups as shown in Table 1. These observations were not altered with the exclusion of the five smokers and one hypertensive subject from the IDDM group. There was no difference in compliance between males and females either within or across the two groups.

There was no obvious relationship between compliance and endothelium-dependent [flow-mediated dilation (FMD), Fig. 2] or endothelium-independent (NTG) vasodilator responses either in the group with diabetes or across the entire study cohort.


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  		Fig. 2.   Relationship between endothelium-dependent flow-mediated dilation and arterial compliance. r2 = 0.02, P = not significant (NS).

Daily energy expenditure, as assessed by the questionnaire, was similar between the two groups (2.32 ± 0.53 METS for IDDM subjects compared with 2.66 ± 0.57 METS for control subjects). There was no overt relationship between compliance and METS across the two groups (Fig. 3), and the proportion of subjects in each of the four activity categories was not different. Nineteen percent of controls and 22% of diabetics were vigorously active, 33% of controls and 26% of diabetics were in each of the moderate and low categories, whereas 15% of controls and 26% of diabetics were inactive (chi 2-analysis, P = not significant).


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  		Fig. 3.   Relationship between systemic arterial compliance and daily energy expenditure expressed in metabolic equivalents (METS). r2 = 0.01, P = NS.

In the IDDM group, fasting and ambient glucose, HbA1c, albuminuria, or disease duration (Fig. 4) were not related to arterial compliance. HbA1c levels ranged from 6.1 to 11.3% (mean 8.7 ± 0.3%), albuminuria levels ranged from 1.1 to 19.0 µg/min (mean 5.6 ± 0.9 µg/min), and the duration of disease ranged from 1 to 20 yr (mean 8 ± 4.6 yr).


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  		Fig. 4.   Relationship between systemic arterial compliance and disease duration. r2 = 0.04, P = NS.

Univariate analysis revealed the best predictors of arterial compliance for the whole study population were mean arterial pressure (r2 = 0.14, P < 0.005; Fig. 5), systolic blood pressure (r2 = 0.08, P < 0.05), and the presence of diabetes (r2 = 0.08, P < 0.05). Multivariate analysis revealed that the best group of predictors included the presence of diabetes, mean arterial pressure, and total cholesterol levels. These predictors accounted for 20% of the variance in arterial compliance (r2 = 0.2, P < 0.01).


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  		Fig. 5.   Relationship between systemic arterial compliance and mean arterial pressure (MAP). r2 = 0.14, P < 0.005.


    DISCUSSION
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES

In this study we have shown that arterial compliance is reduced in young, normotensive individuals with uncomplicated IDDM early in their course of disease. This finding of increased arterial stiffness is supported by others who have shown reduced aortic (19, 36) and femoral (9) compliance in young IDDM patients without risk factors. Lehmann et al. (27) observed arterial compliance to be increased in IDDM compared with controls, although compliance was reduced in patients with NIDDM. Kool and colleagues (25) found no difference in aortic stiffness between IDDM and control groups as assessed by pulse-wave velocity.

The observed reduction in arterial compliance in IDDM was not simply because of differences in blood pressure even though blood pressure is an important determinant of arterial compliance. As expected, there was a correlation between compliance and mean arterial pressure across the study population; however, as shown in Fig. 5, IDDM and control subjects are scattered evenly throughout the relationship.

Heart rate was elevated in IDDM subjects compared with control subjects, even though levels of physical activity were similar. It is possible that higher insulin levels in this group may have induced sympathetic drive and increased heart rate, because this mechanism has previously been described (3). Preliminary data in healthy individuals have shown that compliance is reduced with increasing heart rate (17), although the mechanisms remain unclear. Higher heart rate may have contributed to the lower compliance in IDDM subjects; however, no correlation between heart rate and compliance was observed in this study.

Differences in lipid levels have been shown to affect compliance. Experimental evidence in animals suggests that elevated lipid levels contribute to reduced arterial compliance (15) by altering structural components of the vessel wall. However, this does not appear to occur in humans (2, 14, 28). Lowering of elevated lipid levels by 15% or more is associated with reduced pulse-wave velocity, which was thought to be a result of improved peripheral hemodynamics rather than of increased compliance (34). Regardless of the effect of lipids on the vasculature, levels were not different between IDDM subjects and control subjects in this study and did not account for the difference in compliance.

Evidence now indicates that both short- and long-term exercise can increase arterial compliance (6, 23). This may account for at least part of the cardiovascular benefits attributed to exercise. Previous studies investigating compliance in IDDM subjects have not accounted for exercise habits. We endeavored to assess levels of physical activity in our study groups using a validated questionnaire (5) that provided a value of daily energy expenditure in METS. There was no difference in the estimated level of daily energy expenditure between groups or in the proportion of individuals categorized into vigorous, moderate, low, or inactive activity levels.

Other mechanisms that affect arterial compliance include alterations in smooth muscle cell tone and modification of arterial wall structure. Endothelial vasodilator function in IDDM subjects has been shown to be abnormal (10, 18), and this may be associated with modifications in other properties of the vasculature, including arterial compliance. Endothelial vasodilator dysfunction is thought to be the result of diminished bioavailability of vasoactive factors such as nitric oxide. To our knowledge, there has been no investigation of this potential relationship in IDDM. The results of this study suggest that the functional capacity of the endothelium and arterial compliance may not be directly related.

Smooth muscle cell function and wall structure may be affected by glucose and insulin levels. In the IDDM group a number of clinical variables were assessed, including disease duration, glucose levels, glycemic control (plasma HbA1c levels), and albuminuria. We and others (20) assessing young patients with uncomplicated IDDM have found no relation between arterial compliance and disease duration. The relatively short disease duration in this study group (mean 8 yr) may account for the absence of a relationship with compliance, however, had we incorporated individuals with a greater disease duration it would have meant including the confounding effects of age itself. In vitro studies on human aorta from older IDDM patients have also shown an increase in wall stiffness and thickness with the reduction in vessel distensibility related to the disease duration (36).

Fasting glucose levels were elevated in the group with IDDM. Hyperglycemia is associated with increased arterial stiffness in NIDDM (40); however, this was not the case in our cohort of IDDM patients. We also postulated that longer term glycemic control as reflected by HbA1c levels might affect arterial compliance, but no relationship was found. The absence of a relationship between glycemic control and arterial compliance is consistent with other studies (20, 25). HbA1c levels in our study population reflected a fair to poor degree of glycemic control. Long-term intensified insulin treatment, hence better glycemic control, has been shown to be associated with greater arterial compliance when compared with standard insulin treatment (21). A longer duration of good control (a longer period than is reflected by a single HbA1c measurement) may therefore be needed to improve arterial compliance.

Arterial compliance may also be influenced by insulin. In addition to acting as a metabolic hormone, it exerts potent effects on vascular tone (11). Insulin can also increase sympathetic nervous activity, which by virtue of vasoconstriction could reduce compliance. After subcutaneous injection, insulin enters the systemic rather than the portal circulation, thus patients with IDDM are relatively hyperinsulinemic (37). Hyperinsulinemia therefore remains a possible cause for the reduction in arterial compliance in this group. Insulin levels were not assessed in our study population, and thus a relationship between insulin levels and arterial compliance was not determined.

Long-term hyperglycemia results in the production of advanced glycation end products, which are thought to play an important role in the development of vascular disease in patients with diabetes. Advanced glycation end product accumulation on collagen causes stiffening of the collagen fibers thereby affecting arterial mechanical properties (8) and stiffness (1). The accumulation of advanced glycation end products is of course just one contributing factor to increased arterial stiffness and thus probably occurs in conjunction with other functional and structural alterations. These include accumulation of fibronectin and type IV collagen and deposition of calcium in the medial layer (31). Cooper et al. (12) have shown that in diabetes there are changes in gene and protein expression of various components of the extracellular matrix, including the activation of a number of growth factors and matrix proteins. It seems likely that arterial stiffening is caused by a combination of genetic, metabolic, and hormonal alterations (16).

Microvascular complications such as retinopathy, neuropathy, and nephropathy are prevalent in many patients with diabetes. We selected subjects with diabetes who had no clinical evidence of microvascular disease, but our data suggest that macrovascular function is impaired in these individuals. This raises the possibility that microvascular disease may occur in conjunction with, or be accelerated by, the presence of subtle preexisting large vessel abnormalities. At the very least, the development of micro- and macrovascular dysfunction may be simultaneous.

In summary, arterial compliance is reduced in individuals with IDDM at a young age without accompanying risk factors for cardiovascular disease. The reduction in arterial compliance could not be accounted for by differences in blood pressure, lipids, or simple indexes of glycemic control. This important vascular mechanical property may prove to be predictive of future atherosclerotic complications in patients with diabetes; therefore long-term assessment of arterial compliance and its relationship to the progression of cardiovascular risk factors is required. It is possible (but as yet unproven) that interventions targeted to increase arterial compliance may retard the progression of micro- and macrovascular disease processes in people with IDDM.


    ACKNOWLEDGEMENTS

The technical assistance of Rachel Dowling, Michelle Greentree, and Binh Tran is greatly appreciated. Biochemical analyses were performed by the Biochemistry Department, Monash Medical Centre.


    FOOTNOTES

This study was supported by the Cardiovascular Centre and Diabetes Unit, Monash Medical Centre. A. P. Skyrme-Jones is supported by a Postgraduate Research Scholarship from the Cardiac Society of Australia and New Zealand.

These data were presented in part at the 45th Annual Scientific Meeting of the Cardiac Society of Australia and New Zealand in August 1997 and at the 70th Scientific Sessions of the American Heart Association in November 1997.

The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.

Address for reprint requests and other correspondence: I. T. Meredith, Cardiovascular Centre, Centre for Heart and Chest Research, Monash Medical Centre, 246 Clayton Rd., Clayton, Melbourne, Victoria 3168, Australia (E-mail: ian.meredith{at}med.monash.edu.au).

Received 20 July 1998; accepted in final form 28 January 1999.


    REFERENCES
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
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Am J Physiol Heart Circ Physiol 276(6):H1839-H1845
0002-9513/99 $5.00 Copyright © 1999 the American Physiological Society


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