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Augmentation Index (augmentation + index)
Selected AbstractsAdenosine A1 receptors and vascular reactivityACTA PHYSIOLOGICA, Issue 2 2010Y. Wang Abstract Aim:, Blood pressure is higher in A1 receptor knock-out (A1R,/,) mice than in wild type litter mates (A1R+/+) and we have examined if this could be related to altered vascular functions. Methods:, Contraction of aortic rings and mesenteric arteries were examined. To examine if the adenosine A1 receptor-mediated contraction of aortic muscle was functionally important we examined pulse pressure (PP) and augmentation index (AIX) using a sensor that allows measurements of rapid pressure transients. Results:, Contraction of aortic rings to phenylephrine and relaxation to acetylcholine were similar between genotypes. The non-selective adenosine receptor agonist N -ethyl carboxamido adenosine (NECA) enhanced the contractile response, and this was eliminated in aortas from A1R,/, mice. However, in mesenteric arteries no contractile response was seen and adenosine-mediated relaxation was identical between studied genotypes. A2B adenosine receptors, rather than A2A receptors, may be mainly responsible for the vasorelaxation induced by adenosine analogues in the examined mouse vessels. PP was higher in A1R,/, mice, but variability was unaltered. AIX was not different between genotypes, but the NECA-induced fall was larger in A1R,/, mice. Conclusions:, The role of adenosine A1 receptors in regulating vessel tone differs between blood vessels. Furthermore, contractile effects on isolated vessels cannot explain the blood pressure in A1 knock-out mice. The A1 receptor modulation of blood pressure is therefore mainly related to extravascular factors. [source] Echo-Tracking Assessment of Carotid Artery Stiffness in Patients with Aortic Valve StenosisECHOCARDIOGRAPHY, Issue 7 2009Francesco Antonini-Canterin M.D. Background: There is little information about mechanical properties of large arteries in patients (pts) with aortic stenosis (AS). Methods: Nineteen patients with AS (aortic valve area: 0.88 ± 0.29 cm2) and 24 control subjects without AS but with a similar distribution of risk factors were recruited. , index, pressure-strain elastic modulus (Ep), arterial compliance (AC), augmentation index (AIx), and local pulse-wave velocity (PWV) were obtained at the level of right common carotid artery (CCA) by a real time echo-tracking system. Time to dominant peak of carotid diameter change waveform, corrected for heart rate (tDPc), and maximum rate of rise of carotid diameter (dD/dt) were measured. Systemic arterial compliance (SAC) was also calculated. Parameters of AS severity (mean gradient, valve area, stroke work loss [SWL]) were determined. Results: tDPc was higher in patients with AS than in controls (7.9 ± 0.6 vs. 6.6 ± 0.7, P < 0.0001) while dD/dt was lower (5.3 ± 3.6 mm/s vs. 7.8 ± 2.8 mm/s, P = 0.01). AIx was significantly higher in AS group (32.5 ± 13.6% vs. 20.6 ± 12.2%, P = 0.005) and had a linear correlation both with tDPc (r = 0.63, P < 0.0001) and with dD/dt (r =,0.38, P = 0.01). There was a significant correlation between carotid AC and SAC (r = 0.49, P = 0.03), but only carotid AC was related to SWL (r = 0.51, P = 0.02), while SAC was not (P = 0.26).Conclusions: AIx was the only parameter of arterial rigidity found to be higher in patients with AS than in controls. Carotid AC showed a significant correlation with SAC and it seemed to be more closely related to AS severity than to SAC. [source] Comparison of in vivo effects of nitroglycerin and insulin on the aortic pressure waveformEUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 1 2004J. Westerbacka Abstract Background, Individuals whose platelets are resistant to the antiaggregatory effects of insulin in vitro are also resistant to the antiaggregatory effects of nitroglycerin (GTN). We have previously shown that insulin acutely diminishes central wave reflection in large arteries and that this action of insulin is blunted in insulin-resistant subjects. However, as yet, no studies have compared the haemodynamic effects of insulin and GTN on large arterial function in the same group of subjects. The aim of this study was to determine whether resistance to the haemodynamic effects of insulin is a defect specific to insulin or whether individuals resistant to the vascular actions of insulin are also resistant to GTN. Design and results, Dose,response characteristics of insulin and GTN on the aortic waveform were determined using applanation tonometry and pulse wave analysis (PWA) in seven healthy men (age 26 ± 1 year, BMI 25 ± 2 kg m,2). Three doses of sublingual GTN (500 µg for 1, 3 or 5 min) and insulin (0·5, 1 or 2 mU kg,1 min,1 for 120 min) were administered on three separate occasions. Both agents dose-dependently decreased central pulse pressure and the augmentation index (AIx) without changing brachial artery blood pressure. We next compared responses to insulin (2 mU kg,1 min,1 for 120 min) and sublingual GTN (500 µg for 5 min) in 20 nondiabetic subjects (age 50 ± 2 year, BMI 21·0,36·3 kg m,2). Again, both agents significantly decreased AIx. Although the vascular effects of insulin and GTN vascular were positively correlated [Spearman's r = 0·92 (95% confidence interval 0·81,0·97), P < 0·0001], the time-course for the action GTN was faster than that of insulin. Brachial systolic blood pressure remained unchanged during the insulin infusion (122 ± 3 vs. 121 ± 3 mmHg, 0 vs. 120 min) but aortic systolic blood pressure decreased significantly by 30 min (111 ± 3 vs. 107 ± 3 mmHg, 0 vs. 30 min, P < 0·01). Similarly, GTN decreased aortic systolic blood pressure from 119 ± 4 to maximally 112 ± 3 mmHg (P < 0·001) without significantly decreasing systolic blood pressure in the brachial artery. Conclusions, The effects of insulin and GTN on large arterial haemodynamics are dose-dependent and significantly correlated. The exact mechanisms and sites of action of insulin and GTN in subjects with insulin resistance remain to be established. [source] Interpretation of radial pulse contour during fentanyl/nitrous oxide anesthesia and mechanical ventilationACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 7 2002S. Söderström Background: Peripheral arterial blood pressure is not a reliable substitute for proximal aortic pressure. Recognition of this phenomenon is important for correct appreciation of cardiac afterload. Our aim was to evaluate the utility of the radial pulse wave to better understand ventriculo-vascular coupling during anesthesia. Methods: We observed the differences between aortic systolic pressure (AoSAP, tipmanometry) and radial systolic pressure in 15 patients, (including two women) aged 53,78 years, before coronary artery bypass surgery. We studied the induction of anesthesia with fentanyl (20 µg kg,1), moderate volume loading, and thereafter the addition of 70% nitrous oxide. The circulatory effects of mechanical ventilation were studied by doubling the tidal volumes. Pulse wave contours were assessed by calculation of radical and aortic augmentation indices (AI), which measure the second systolic pressure peak. Results: Radial systolic pressure was higher than AoSAP in the control situation (8±2 mmHg), and this SAP gradient increased further with fentanyl (12±2 mmHg). The gradient persisted throughout the study, but was partially reduced by volume loading and nitrous oxide, respectively. Radial augmentation index was the only parameter remaining in a stepwise multivariate model to explain the variance in the SAP gradient (r2=0.48). Radial augmentation index also correlated with aortic pulse pressure (r2=0.71). Mechanical ventilation had significant and similar effects on pulse wave augmentation both in the aorta and in the radial artery, and did not affect the radial to aortic SAP gradient. Conclusion: These elderly coronary patients had stiff vasculature (high aortic AI) and considerable pulse wave reflection, which was beneficially delayed by fentanyl. Changes in the radial pulse wave augmentation during mechanical ventilation were mainly a result of cyclic changes in the stroke volume, and were seldom associated with an increased systolic pressure gradient from the aorta to the radial artery. [source] ANALYSIS OF SHORT-TERM REPRODUCIBILITY OF ARTERIAL VASOREACTIVITY BY PULSE-WAVE ANALYSIS AFTER PHARMACOLOGICAL CHALLENGECLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 1 2009Biju Paul SUMMARY 1Pulse-wave analysis (PWA) is an established method to assess arterial wave reflections and arterial vasoreactivity in humans. A high short-term reproducibility of baseline augmentation index (AIx) has been reported. However, the short-term reproducibility of AIx changes following pharmacological challenge with either inhaled salbutamol (endothelium-dependent vasodilatation) or sublingual glyceryl trinitrate (GTN; endothelium-independent vasodilatation), using appropriate statistical methods, is largely unknown. 2Baseline AIx and GTN- and salbutamol-mediated changes in AIx (all corrected for a heart rate of 75 b.p.m.) were measured on two separate occasions, 1 h apart, in 22 healthy controls (mean (±SD) age 52.0 ± 13.4 years) and 11 elderly patients with chronic heart failure (CHF; 73.1 ± 8.7 years). Reproducibility was assessed by measuring intraclass correlation coefficients (ICC), coefficients of variation (CV) and Bland,Altman plots. 3Baseline AIx showed good short-term reproducibility with high ICC in both the control and CHF groups (0.90 and 0.87, respectively). In contrast, in the control and CHF groups, the ICC of GTN- (0.58 and 0.17, respectively) and salbutamol-mediated (0.18 and 0.04, respectively) changes in AIx were substantially low. The CV was relatively low for baseline AIx in control and CHF groups (25.0 and 22.5%, respectively), but not for GTN- (22.3 and 59.8%, respectively) or salbutamol-mediated (45.1 and 184.0%, respectively) changes in AIx. Bland,Altman analysis revealed poor reproducibility, with limits of agreement beyond either +15% or ,15% for changes in AIx after GTN and salbutamol for both control and CHF groups. The changes in blood pressure and heart rate following pharmacological challenge were similar between the two measurements. 4The poor reproducibility of changes in AIx following pharmacological challenge questions the use of this method in acute studies. [source] Elevated augmentation index derived from peripheral arterial tonometry is associated with abnormal ventricular,vascular couplingCLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 5 2010Kevin S. Heffernan Summary Background:, Although typically derived from the contour of arterial pressure waveform, augmentation index (AIx) may also be derived from the digital pulse volume waveform using finger plethysmography (peripheral arterial tonometry, PAT). Little is known regarding the physiologic correlates of AIx derived from PAT. In this study, we investigated the relation of PAT-AIx with measures of ventricular,vascular coupling. Methods:, Pulse volume waves were measured via PAT and used to derive AIx. Using 2-dimensional echocardiography, effective arterial elastance index (EaI) was estimated as end-systolic pressure/stroke volume index. Left ventricular (LV) end-systolic elastance index (ELVI) was calculated as end-systolic pressure/end-systolic volume index. Ventricular,vascular coupling ratio was defined as EaI/ELVI. Results:, Given the bi-directional nature of ventricular,vascular uncoupling as measured by echocardiography, patients were separated into three groups: low EaI/ELVI (<0·6, n = 21), optimal EaI/ELVI (mean 0·6,1·2, n = 16) and high EaI/ELVI (>1·2, n = 10). Adjusting for potential confounders (age, mean arterial pressure, height and heart rate), patients with optimal EaI/ELVI had lower AIx (1 ± 4%, P<0·05) compared to those with low EaI/ELVI (13 ± 4%) and high EaI/ELVI (19 ± 5%). Conclusions:, Abnormal ventricular,vascular coupling, arising from either increased effective arterial elastance or increased ventricular elastance, is associated with increased AIx as measured by PAT. Additional research is needed to examine other vascular correlates of PAT-AIx. [source] Interpretation of radial pulse contour during fentanyl/nitrous oxide anesthesia and mechanical ventilationACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 7 2002S. Söderström Background: Peripheral arterial blood pressure is not a reliable substitute for proximal aortic pressure. Recognition of this phenomenon is important for correct appreciation of cardiac afterload. Our aim was to evaluate the utility of the radial pulse wave to better understand ventriculo-vascular coupling during anesthesia. Methods: We observed the differences between aortic systolic pressure (AoSAP, tipmanometry) and radial systolic pressure in 15 patients, (including two women) aged 53,78 years, before coronary artery bypass surgery. We studied the induction of anesthesia with fentanyl (20 µg kg,1), moderate volume loading, and thereafter the addition of 70% nitrous oxide. The circulatory effects of mechanical ventilation were studied by doubling the tidal volumes. Pulse wave contours were assessed by calculation of radical and aortic augmentation indices (AI), which measure the second systolic pressure peak. Results: Radial systolic pressure was higher than AoSAP in the control situation (8±2 mmHg), and this SAP gradient increased further with fentanyl (12±2 mmHg). The gradient persisted throughout the study, but was partially reduced by volume loading and nitrous oxide, respectively. Radial augmentation index was the only parameter remaining in a stepwise multivariate model to explain the variance in the SAP gradient (r2=0.48). Radial augmentation index also correlated with aortic pulse pressure (r2=0.71). Mechanical ventilation had significant and similar effects on pulse wave augmentation both in the aorta and in the radial artery, and did not affect the radial to aortic SAP gradient. Conclusion: These elderly coronary patients had stiff vasculature (high aortic AI) and considerable pulse wave reflection, which was beneficially delayed by fentanyl. Changes in the radial pulse wave augmentation during mechanical ventilation were mainly a result of cyclic changes in the stroke volume, and were seldom associated with an increased systolic pressure gradient from the aorta to the radial artery. [source] |