Increased Central Artery Stiffness in Impaired Glucose Metabolism and Type 2 Diabetes

Schram, Miranda T.; Henry, Ronald M.A.; Dijk, R A J M van; Kostense, Piet J.; Dekker, Joost; Nijpels, Giel; Heine, Robert J.; Bouter, Lex M.; Westerhof, Nico; Stehouwer, Coen D.A.

doi:10.1161/01.hyp.0000111829.46090.92

Cited by 418 publications

(353 citation statements)

References 39 publications

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“…20) The Hoorn Study revealed that subjects with impaired glucose tolerance and DM had arterial stiffening in both the central and peripheral arterial system using applanation tonometry and that the central arterial stiffness of those with impaired glucose tolerance was intermediate in severity between the group with normal glucose tolerance and DM. 21) In our current study, we also observed that pre-DM patients have statistically significantly higher SI and lower CI than those without DM. SI, derived from the DVP measured by photoplethysmography, is a valid index of wave refl ections and also an acceptable marker for large artery stiffness.…”

Section: Discussionsupporting

confidence: 77%

Effects of Deranged Glucose Homeostasis on Peripheral Arterial Stiffness Index in Patients With Pre-Diabetes Mellitus

et al. 2013

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SummaryPremature arteriosclerosis may be one of the mechanisms linking pre-diabetes mellitus (pre-DM) and cardiovascular disease. We sought to characterize premature arteriosclerosis in pre-DM using different arterial stiffness indices and to fi nd the independent contributors of this process. We recruited 33 patients without DM, 53 patients with pre-DM, and 34 subjects with DM. Both the compliance index (CI) and stiffness index (SI) were measured. Patients with pre-DM and DM had lower CI (3.8 ± 2.1 versus 5.2 ± 3.0 units; P < 0.05 and 3.6 ± 1.8 versus 5.2 ± 3.0 units; P < 0.05, respectively) and higher SI (8.0 ± 2.0 versus 6.7 ± 1.6 m/s; P < 0.01 and 9.4 ± 2.3 versus 6.7 ± 1.6 m/s; P < 0.001, respectively) than patients without DM. Using multivariate linear regression analysis, age, heart rate, and HOMA index were independent determinants for SI (whole model: R 2 = 0.47, P < 0.001), whereas male gender, hsCRP, and HOMA index were independent determinants for CI (whole model: R 2 = 0.34, P < 0.01). The HOMA index was an independent determinant for arterial stiffness. Increased insulin resistance may associate with increased arterial stiffness at peripheral arteries in pre-DM patients. (Int Heart J 2013; 54: 27-32)

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Section: Discussionsupporting

confidence: 77%

Effects of Deranged Glucose Homeostasis on Peripheral Arterial Stiffness Index in Patients With Pre-Diabetes Mellitus

et al. 2013

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“…The study population for this investigation therefore consisted of 466 individuals except for the analyses of the carotidfemoral transit time, which was available in only 193 individuals. 33 …”

Section: Resultsmentioning

confidence: 99%

“…The estimates of artery stiffness were determined as described earlier with the use of arterial ultrasonography, echocardiography and radial applanation tonometry 28,32,33 according to the following: distensibility-an indicator of local arterial elastic properties: ((2DD Â D þ DD 2 )/(DP Â D 2 ) in 10 À3 kPa À1 ; compliance-an indicator of local arterial buffering capacity: p(2D Â DD þ DD 2 )/(4 Â DP) in mm 2 kPa À1 ; Young's elastic modulus-an indicator of local intrinsic elastic wall properties: (D/(IMT) Â distensibility) in kPa (where DP stands for local pulse pressure, 34,35 D for diameter, (DD) for distension and IMT for carotid intima-media thickness); total systemic arterial compliance-an indicator of total arterial buffering capacity-by the exponentialdecay method based on the Windkessel model 36 and the ratio of stroke volume to aortic pulse pressure; 37 aortic augmentation index-an indicator of total stiffness and wave reflection-by the use of a generalized transfer function; 38 and carotid-femoral transit time-an estimate of regional stiffness closely associated with the gold standard estimate of stiffness: pulse wave velocity-by the time delay from the electrocardiograph trigger to 10% of the ascending slope of the distension curve of both arteries subtracted from one another. 39 …”

Section: Arterial Stiffnessmentioning

confidence: 99%

The metabolic syndrome in elderly individuals is associated with greater muscular, but not elastic arterial stiffness, independent of low-grade inflammation, endothelial dysfunction or insulin resistance—The Hoorn Study

et al. 2009

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The metabolic syndrome (MetS) increases cardiovascular disease (CVD) risk. How MetS increases CVD risk is incompletely understood, but increasing arterial stiffness is one candidate link, which in turn could be explained by (low-grade) inflammation, endothelial dysfunction (ED) or insulin resistance (IR). However, MetSrelated increases in stiffness may not be uniformly distributed over muscular and elastic arteries. Therefore, the purpose of this study was to determine: (1) the associations between the MetS, and muscular and elastic arterial stiffness, and (2) whether any such associations could be explained by inflammation, ED or IR. These questions were addressed in the Hoorn Study. MetS was defined according to the NCEP (National Cholesterol Education Program) criteria. Arterial stiffness was determined by ultrasound, tonometry and echocardiography. Inflammation, ED and IR were estimated by C-reactive protein, flow-mediated vasodilation and the homoeostatic model for the assessment of IR, respectively. The results showed that MetS was associated with both femoral and brachial arterial stiffness, significantly so for the distensibility coefficients and for the femoral compliance coefficient. In the carotid artery and aorta, no particular pattern emerged. Additional adjustment for either inflammation, ED or IR did not materially alter the results. The results therefore indicate that muscular arteries may stiffen preferentially over elastic arteries and that distensibility is affected to a greater extent than compliance, thus maintaining volume compliance over vessel wall stiffening. Additionally, the increase in stiffness was not explained by inflammation, ED or IR and suggests that stiffening of the muscular arteries in MetS may not be the consequence of these phenomena.

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“…Premature conduit vessel arteriosclerosis predicts mortality in type 2 diabetes [3] and may be attenuated by therapeutic approaches with potential to lower glucose or blood pressure directly [4][5][6][7]. The independent association of FPG and 2-HPG indices with the haemodynamic consequence of early sclerosis (aortic stiffness) implies that modifiable structural mechanisms connect hyperglycaemia with vascular complications even within prediabetes thresholds of impaired glucose tolerance (IGT) [8][9][10][11] and impaired fasting glycaemia (IFG) [12,13]. These relationships are reported individually [11][12][13] or as a cumulative effect of the metabolic syndrome.…”

Section: Introductionmentioning

confidence: 99%

Impact of metabolic indices on central artery stiffness: independent association of insulin resistance and glucose with aortic pulse wave velocity

et al. 2010

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Aims/hypothesis Non-invasive measures of aortic stiffness reflect vascular senescence and predict outcome in diabetes. Glucose-mediated elastic artery sclerosis may play an integral role in the development of macrovascular complications. We used carotid-femoral pulse wave velocity ( cf PWV) to quantify independent associations of fasting glucose, post-challenge glucose and derived insulin resistance (HOMA-IR) with aortic stiffness. Methods cf PWV was measured using a 4 MHz continuous wave Doppler ultrasound probe within groups with newly identified age-and sex-matched normal glucose metabolism (NGM), impaired glucose regulation (IGR) and diabetes mellitus populations (n=570, mean age 59.1, 56% male). Results After multivariate adjustment, IGR and diabetes were associated with significant aortic stiffening compared with NGM (adjusted cf PWV±SE: NGM, 9.15±0.12 m/s; IGR 9.76±0.11 m/s, p<0.001; diabetes, 9.89±0.12 m/s, p< 0.001). IGR stratification indicated that impaired fasting glucose (IFG; 9.71±0.12 m/s) and post-challenge (impaired glucose tolerance; 9.82±0.24 m/s) categories had similar cf PWV (p=0.83). Modelled predictors of cf PWV were used to assess independent metabolic associations with arterial stiffness. Fasting glucose concentration (β=0.10; 95% CI 0.05, 0.18; p=0.003), 2 h post-challenge glucose (β=0.14; 95% CI 0.02, 0.23; p<0.001) and HOMA-IR (β=0.20, 95% CI 0.05, 0.53; p<0.001) were independently related to cf PWV after adjustment for age, sex, mean arterial pressure, heart rate, body mass index, renal function and antihypertensive medication. Conclusions/interpretation IGR characterised by fasting or post-challenge hyperglycaemia is associated with significant vascular stiffening. Post-challenge glucose and HOMA-IR are the most powerful metabolic predictors of arterial stiffness, implying hyperglycaemic excursion and insulin resistance play important roles in the pathogenesis of arteriosclerosis.

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Increased Central Artery Stiffness in Impaired Glucose Metabolism and Type 2 Diabetes

Cited by 418 publications

References 39 publications

Effects of Deranged Glucose Homeostasis on Peripheral Arterial Stiffness Index in Patients With Pre-Diabetes Mellitus

Effects of Deranged Glucose Homeostasis on Peripheral Arterial Stiffness Index in Patients With Pre-Diabetes Mellitus

The metabolic syndrome in elderly individuals is associated with greater muscular, but not elastic arterial stiffness, independent of low-grade inflammation, endothelial dysfunction or insulin resistance—The Hoorn Study

Impact of metabolic indices on central artery stiffness: independent association of insulin resistance and glucose with aortic pulse wave velocity

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