Metabolic Syndrome and Age-Related Progression of Aortic Stiffness

Safar, Michel E.; Thomas, Frédérique; Blacher, Jacques; Nzietchueng, Rosine; Bureau, J.-M.; Pannier, Bruno; Bénétos, Athanase

doi:10.1016/j.jacc.2005.08.052

Cited by 198 publications

(174 citation statements)

References 7 publications

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“…An independent association between MS and arterial stiffness as measured by various techniques including pulse-wave velocity and arterial distensibility has already been described in cross-sectional studies, especially in middle-aged and elderly patients. 16,17 More recently, Safar et al 18 demonstrated that the presence of MS entails an increased progression of age-related arterial stiffness, thus fostering an acceleration of the ageing process. The novelty of our findings resides in the fact that this is the first evidence of the association between MS and AASI, a recently proposed index of arterial stiffness.…”

Section: Discussionmentioning

confidence: 99%

Metabolic syndrome and ambulatory arterial stiffness index in non-diabetic patients with primary hypertension

et al. 2007

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Increased arterial stiffness and the presence of metabolic syndrome (MS) have been shown to predict cardiovascular events in patients with primary hypertension. We investigated the relationship between a recently proposed index of arterial stiffness derived from ambulatory blood pressure (BP) monitoring and MS in 156 untreated, non-diabetic patients with primary hypertension. Ambulatory arterial stiffness index (AASI) was defined as 1 minus the regression slope of diastolic over systolic BP readings obtained from 24-h recordings. A modified National Cholesterol Education Program definition for MS was used, with body mass index replacing waist circumference. The prevalence of MS was 23%. Patients with MS were more frequently male (0.0291) and had increased serum uric acid (P ¼ 0.0005), high-sensitivity C-reactive protein (P ¼ 0.0259), as well as total and low-density lipoprotein (LDL)-cholesterol (P ¼ 0.0374 and P ¼ 0.0350, respectively) as compared to those without MS. After adjusting for these confounders, the association between AASI and the presence of MS was statistically significant (P ¼ 0.0257). Moreover, the prevalence of increased AASI (upper tertile, that is X0.550) was greater in patients with MS (P ¼ 0.0156). After adjusting for age and 24-h mean BP, the presence of MS entailed a more than twofold greater risk for increased AASI (0.0280). MS is associated with increased AASI in non-diabetic patients with primary hypertension. These data support the role of this new index of arterial stiffness as a marker of risk and help to explain the high cardiovascular morbidity and mortality that is observed in hypertensive patients with MS.

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Section: Discussionmentioning

confidence: 99%

Metabolic syndrome and ambulatory arterial stiffness index in non-diabetic patients with primary hypertension

et al. 2007

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“…Thus, both small and large arteries contribute to early reflected waves. 3 In addition to advancing age, the combined effects of metabolic factors 41 endothelial dysfunction, 42 enhanced activity of the renin-angiotensin system, 43 increased circulating endothelin levels, low grade inflammation, 14,44 insulin resistance, 45 sodium retention induced by obesity, 36 atherosclerotic changes within the peripheral and coronary vessel wall 46 may all contribute to arterial stiffening and thus to the early arrival and increased amplitude of wave reflections as well as to LV diastolic dysfunction 3,14,16,36 in hypertensive individuals. Thus, increased arterial stiffness may represent an index of the cumulative effects of several other metabolic, neurohumoral, inflammatory factors, apart of aging, on the pathophysiological processes within the vascular and myocardial wall linking increased arterial stiffness and LV diastolic dysfunction.…”

Section: Association Of Cai and Aos With LV Diastolic Dysfunctionmentioning

confidence: 99%

“…Thus, increased arterial stiffness may represent an index of the cumulative effects of several other metabolic, neurohumoral, inflammatory factors, apart of aging, on the pathophysiological processes within the vascular and myocardial wall linking increased arterial stiffness and LV diastolic dysfunction. 3,14,16,36,41 Arterial wave reflections, as expressed by CAI, reflect the structural and functional changes along the entire thoracic-abdominal aorta and small muscular arteries and arterioles, 3 whereas echocardiographically estimated indices of aortic stiffness, as expressed by AoS, reflect the function of a small portion of the aortic root. As previously discussed, wave reflections may cause impaired myocardial relaxation and a mismatch between myocardial oxygen demands and myocardial perfusion resulting in LV diastolic dysfunction.…”

Section: Association Of Cai and Aos With LV Diastolic Dysfunctionmentioning

confidence: 99%

Incremental value of arterial wave reflections in the determination of left ventricular diastolic dysfunction in untreated patients with essential hypertension

et al. 2008

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Systemic arterial stiffness is an indicator of cardiovascular disease and an independent marker of morbidity and cardiovascular mortality. We investigated the association of arterial wave reflections with left ventricular (LV) diastolic dysfunction and their incremental value to other determinants of LV diastolic dysfunction in patients with essential hypertension. In total 143 patients and 20 controls with similar atherosclerotic risk factors were examined by applanation tonometry of the radial artery (Sphygmocor) and echocardiography. Central augmentation index (CAI%) of reflected arterial waves as well as aortic strain (AoS) assessed by echocardiography were estimated. Doppler diastolic abnormalities were defined as proposed by the European Study Group on diastolic heart failure by measurement of E/A ratio (the ratio of the mitral inflow velocities), isovolumic relaxation time, deceleration time and flow propagation velocity. AoS and CAI were impaired in patients compared with controls (4.67 ± 2.94 vs 6.06 ± 4.91% and 145.8 ± 22.7 vs 135.7 ± 20.3%, Po0.01) as well as in patients with LV diastolic dysfunction compared to patients without, (5.52 ± 4.29 vs 10.73 ± 5.77% and 139.5 ± 21.7 vs 124.5 ± 17.0%, Po0.05). The odds ratio (OR) of AoS and CAI for diastolic dysfunction was OR:0.918, 95% confidence interval (CI):0.837-0.99, P ¼ 0.04 and OR:1.023, 95%CI: 1.023-1.040 P ¼ 0.010, respectively. The addition of CAI to the multivariable model including age, LV mass index, AoS and mean arterial pressure increased the power of the model for determination of LV diastolic dysfunction (À2 log likelihood ¼ 139.368, change of v 2 ¼ 4.2, P-value for change ¼ 0.04). In untreated patients with newly diagnosed essential hypertension, wave reflections are independent and additive determinants of LV diastolic dysfunction.

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“…These relationships are reported individually [11][12][13] or as a cumulative effect of the metabolic syndrome. [14][15][16][17][18][19] and do not specifically address the relative independent strengths of FPG and 2-HPG associations with measures of arterial stiffness.…”

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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Metabolic Syndrome and Age-Related Progression of Aortic Stiffness

Abstract: Metabolic syndrome is associated with an increased progression of aortic stiffness with age, supporting premature senescence in these patients.

Cited by 198 publications

References 7 publications

Metabolic syndrome and ambulatory arterial stiffness index in non-diabetic patients with primary hypertension

Metabolic syndrome and ambulatory arterial stiffness index in non-diabetic patients with primary hypertension

Incremental value of arterial wave reflections in the determination of left ventricular diastolic dysfunction in untreated patients with essential hypertension

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

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