Ambulatory arterial stiffness index: A systematic review and meta-analysis

Κόλλιας, Αναστάσιος; Stergiou, George S.; Dolan, Eamon; O’Brien, Eoin

doi:10.1016/j.atherosclerosis.2012.03.039

Cited by 87 publications

(86 citation statements)

References 69 publications

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“…Despite its limitations, a number of studies have shown that the AASI is a reliable and independent predictor of adverse cardiovascular events in multiple populations and that it is more sensitive than PP for predicting cardiovascular events 10, 16, 17. However, the association between either the AASI or s‐AASI and the pathophysiology of neurologic outcomes remains to be fully established 18. Our goal in this study was to determine the extent to which the AASI, s‐AASI, or PP are associated with shifts in the LLA in patients undergoing cardiac surgery.…”

Section: Introductionmentioning

confidence: 99%

Relationship Between the Ambulatory Arterial Stiffness Index and the Lower Limit of Cerebral Autoregulation During Cardiac Surgery

Obata

Barodka

Berkowitz

et al. 2018

JAHA

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BackgroundPulse pressure, the ambulatory arterial stiffness index (AASI), and the symmetric AASI are established predictors of adverse cardiovascular outcomes. However, little is known about their relationship to cerebral autoregulation. This study evaluated whether these markers of vascular properties relate to the lower limit of cerebral autoregulation (LLA).Methods and ResultsThe LLA was determined during cardiac surgery with transcranial Doppler ultrasonography in 181 patients. All other variables were calculated from continuous intraoperative readings obtained before cardiopulmonary bypass. The LLA varied directly with the AASI (β=3.12 per 0.1 change in AASI, P<0.001) and to a lesser extent the symmetric AASI (β=2.02 per 0.1 change in symmetric AASI, P≤0.022), while peripheral pulse pressure was not significantly related (β=0.0, P>0.99). Logistic regression revealed that the likelihood of LLA being >65 mm Hg increased by 50% (95% confidence interval, 11%–102%, P=0.008) for every 0.1 increase in the AASI. The AASI was able to predict a LLA above certain thresholds (area under the curve receiver operating characteristic for AASI predicting an LLA >65 mm Hg: 0.60; 95% confidence interval, 0.51%–0.68%, P=0.043). Incorporating additional variables improved the model's predictive ability (area under the curve for AASI predicting a LLA >65 mm Hg: 0.75; 95% confidence interval, 0.68–0.82, P=0.036).ConclusionsThese data indicate that the LLA is related to the mechanical properties of the vasculature as represented by the AASI. The AASI can be used to predict LLA threshold levels during cardiac surgery. It is now possible to link elevations in the LLA with an increased AASI as determined from readily accessible intraoperative variables.

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Section: Introductionmentioning

confidence: 99%

Relationship Between the Ambulatory Arterial Stiffness Index and the Lower Limit of Cerebral Autoregulation During Cardiac Surgery

Obata

Barodka

Berkowitz

et al. 2018

JAHA

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“…Another marker of arterial stiffness is the ambulatory arterial stiffness index [AASI: 1 minus the regression slope of DBP and SBP values derived from 24-h ambulatory BP monitoring (ABPM) [18]]. The AASI represents the dynamic relationship between SBP and DBP, as defined by haemodynamic arterio-ventricular properties, and has been reported to be an independent predictor of CV mortality [19].Mean arterial pressure (MAP) is a measure of central haemodynamics that reflects the cardiac cycle and is determined by cardiac output, systemic vascular resistance and [16] and has been shown to be predictive of CV events in patients with T2DM.DIABETES, OBESITY AND METABOLISM original article central venous pressure. MAP is calculated as 2/3 DBP + 1/3 SBP…”

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confidence: 99%

Effects of empagliflozin on blood pressure and markers of arterial stiffness and vascular resistance in patients with type 2 diabetes

Chilton

Tikkanen

Cannon

et al. 2015

Diabetes Obesity Metabolism

433

283

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Aims:To determine the effects of empagliflozin on blood pressure (BP) and markers of arterial stiffness and vascular resistance in patients with type 2 diabetes mellitus (T2DM). Methods:We conducted a post hoc analysis of data from a phase III trial in patients with T2DM and hypertension receiving 12 weeks' empagliflozin and four phase III trials in patients with T2DM receiving 24 weeks' empagliflozin (cohort 1, n = 823; cohort 2, n = 2477). BP was measured using 24-h BP monitoring (cohort 1) or seated office measurements (cohort 2).Results: Empagliflozin reduced systolic BP (SBP) and diastolic BP in both cohorts (p < 0.001 vs placebo), without increasing heart rate. Empagliflozin reduced pulse pressure (PP; adjusted mean difference vs placebo cohort 1: −2.3 mmHg; cohort 2: −2.3 mmHg), mean arterial pressure (MAP; cohort 1, −2.3 mmHg; cohort 2, −2.1 mmHg) and double product (cohort 1, −385 mmHg × bpm; cohort 2, −369 mmHg × bpm) all p < 0.001 vs placebo. There was a trend towards a reduction in the ambulatory arterial stiffness index (AASI) with empagliflozin in cohort 1 (p = 0.059 vs placebo). AASI was not measured in cohort 2. Subgroup analyses showed that there were greater reductions in PP with increasing baseline SBP in cohort 1 (p = 0.092). In cohort 2, greater reductions in MAP were achieved in patients with higher baseline SBP (p = 0.027) and greater reductions in PP were observed in older patients (p = 0.011). Conclusions IntroductionCardiovascular (CV) disease is the major cause of morbidity and mortality in patients with type 2 diabetes (T2DM) [1]. The risk of CV disease in adults with diabetes is double that in adults without diabetes, and diabetes is estimated to account for 10-12% of all vascular deaths [2]. Patients with T2DM often have numerous CV risk factors and a multifactorial approach to addressing CV risk, including controlling glycaemia, blood pressure (BP) and body weight, is recommended in these patients [1,3].The metabolic abnormalities that are characteristic of diabetes, such as hyperglycaemia, excess free fatty acids and insulin resistance, can lead to suppression of nitric oxide production and activation of the renin-angiotensin system, leading to oxidative stress, endothelial dysfunction and activation of the receptor for advanced glycation end products (RAGE) [4][5][6]. These may contribute to hypertension [7] or to increased arterial stiffness related to vascular calcification or accumulation ofCorrespondence to: Odd Erik Johansen, Boehringer Ingelheim Norway KS, Asker, Norway. E-mail: odd_erik.johansen@boehringer-ingelheim.com This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes.collagen [8,9] that could partly explain the increased risk of vascular complications associated with T2DM [4].Arterial stiffness is a strong predictor of CV events, heart failure and death [10][11][12]...

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“…Arterial stiffness is an early and important risk factor for development of cardiovascular diseases (12). Some studies have investigated the possible effects of thyroid hormone excess on arterial stiffness with different measurement methods (13). However, the association between hyperthyroidism and arterial stiffness is still not clear due to controversial results of the previous studies in the literature.…”

Section: Discussionmentioning

confidence: 99%

Evaluation of ambulatory arterial stiffness index in hyperthyroidism

İyidir¹,

Yalcin²,

Altınova³

et al. 2017

Turk J Med Sci

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Background/aim: Hyperthyroidism causes hemodynamic changes that are associated with adverse cardiovascular outcomes. Twentyfour-hour ambulatory blood pressure monitoring recordings provide us with some essential data: BP variability and ambulatory arterial stiffness index (AASI). In this study, we aimed to investigate AASI and short-term BP variability in both overt and subclinical hyperthyroidism and their relationship with thyroid hormones. Materials and methods:We enrolled 36 patients with subclinical hyperthyroidism, 23 patients with overt hyperthyroidism, and 25 healthy euthyroid controls. ABPM recording was performed for 24 h for all patients.Results: There were no statistically significant differences among the overt hyperthyroidism, subclinical hyperthyroidism, and control groups in terms of AASI (0.43 ± 0.15, 0.38 ± 0.12, 0.42 ± 0.13, respectively; P = 0.315). Variability of diastolic BP was significantly higher in patients with overt hyperthyroidism than in patients with subclinical hyperthyroidism (14.8 ± 2.6 vs. 12.8 ± 2.5%, P = 0.023). There were significant positive correlations between AASI and fT3 (r = 0.246, P = 0.02) and fT4 (r = 0.219, P = 0.04) while TSH was not correlated with AASI (r = 0.023, P = 0.838). After adjusting for confounders, age, 24-h systolic and diastolic BP, variability of systolic and diastolic BP, and fT4 were independent predictors of AASI (r 2 = 0.460, P < 0.001). Conclusion:Although AASI did not differ between overt and subclinical hyperthyroidism, there was a positive relationship between AASI and free thyroid hormone levels. Furthermore, short-term BP variability was higher in overt hyperthyroidism than in subclinical hyperthyroidism.

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Ambulatory arterial stiffness index: A systematic review and meta-analysis

Cited by 87 publications

References 69 publications

Relationship Between the Ambulatory Arterial Stiffness Index and the Lower Limit of Cerebral Autoregulation During Cardiac Surgery

Relationship Between the Ambulatory Arterial Stiffness Index and the Lower Limit of Cerebral Autoregulation During Cardiac Surgery

Effects of empagliflozin on blood pressure and markers of arterial stiffness and vascular resistance in patients with type 2 diabetes

Evaluation of ambulatory arterial stiffness index in hyperthyroidism

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