Arterial Pressure Wave Research Articles

Effects of Sympathetic Activation on Aortic Stiffness in Young Healthy and Hypertensive Adults

Aortic stiffness is a major link between hypertension and cardiovascular risk. Anatomic features of the artery including the smooth muscle regulate aortic stiffness, in part. Importantly, vascular smooth muscle is under sympathetic nervous system control, and thus aortic stiffness may be influenced by the sympathetic nervous system. When exposed to physiological stress, older hypertensive adults demonstrate an exaggerated blood pressure response that may correspond with transient arterial stiffness increases, but this response in young hypertensive adults remains unknown.PURPOSEWe tested the hypothesis that sympathetic activation would increase aortic stiffness in young healthy adults (control, CTL), and that aortic stiffness increases during sympathetic activation would be greater in young hypertensive adults (HTN).METHODSSix healthy controls (males=4, females=2; 28.3±5.5 years; BMI: 23.5 ± 3.5 kg/m2) and three young hypertensive participants (males=2, females=1; 28.3±6.0 years; BMI: 30.3±8.2 kg/m2) were studied. Mean arterial pressure (MAP) and carotid‐femoral pulse wave velocity (PWV) were measured at rest and during 5 min of brachial circulatory occlusion (sympathetic activation condition) that followed isometric handgrip exercise.RESULTSResting MAP was higher in HTN (100±6 mmHg) than CTL (90±5 mmHg; P=.029). Occlusion MAP was also higher in HTN (116±6 mmHg) than CTL (102±7 mmHg; P=.016). Resting PWV was similar between CTL (8.6±1.6 m/s) and HTN (8.1±0.1 m/s; P=.47). The increase in PWV from rest to occlusion (1.2±1.4 m/s) in CTL was not significant (P=.09), whereas the increase in PWV from rest to occlusion (2.0±0.4 m/s) in HTN was significant (P=.01).CONCLUSIONSympathetic activation may significantly increase aortic stiffness in young hypertensive adults, but not young healthy adults.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

A Novel Interpretation for Arterial Pulse Pressure Amplification in Health and Disease.

Arterial pressure waves have been described in one dimension using several approaches, such as lumped (Windkessel) or distributed (using Navier-Stokes equations) models. An alternative approach consists of modeling blood pressure waves using a Korteweg-de Vries (KdV) equation and representing pressure waves as combinations of solitons. This model captures many key features of wave propagation in the systemic network and, in particular, pulse pressure amplification (PPA), which is a mechanical biomarker of cardiovascular risk. The main objective of this work is to compare the propagation dynamics described by a KdV equation in a human-like arterial tree using acquired pressure waves. Furthermore, we analyzed the ability of our model to reproduce induced elastic changes in PPA due to different pathological conditions. To this end, numerical simulations were performed using acquired central pressure signals from different subject groups (young, adults, and hypertensive) as input and then comparing the output of the model with measured radial artery pressure waveforms. Pathological conditions were modeled as changes in arterial elasticity (E). Numerical results showed that the model was able to propagate acquired pressure waveforms and to reproduce PPA variations as a consequence of elastic changes. Calculated elasticity for each group was in accordance with the existing literature.

Method Comparison and Validation of the Determination of Ejection Duration from Oscillometric Measurements

The ejection duration (ED) is an important indicator of ventricular function as well as ventriculo-arterial coupling, especially for heart failure with reduced ejection fraction. Thus, the non-invasive oscillometric determination of ED from arterial pressure waves could enhance methods of pulse wave analysis. The aim of this work was to compare different approaches to calculate the ED from oscillometric measurements and to test and to validate the determination of ED with results from measurements using radial tonometry. Oscillometric and tonometric pulse wave measurements were obtained in direct succession from each patient with the Mobil-O-Graph and with the Sphygmocor device in a comparative study. Also, the results from the internal algorithm of SphygmoCor were obtained. Several methods for the determination of ED were implemented and applied to the given measurements. The results of Mobil-O-Graph were compared with the ejection durations from the internal algorithm of SphygmoCor. Several algorithms had a mean error lower than the step size of the recordings. The algorithm using numerical central differences to find the maximum curvature of the curve was chosen for the determination of ED due to its lowest standard deviation compared with others, its low mean error and its stability. The mean difference between Mobil-O-Graph and SphygmoCor was 7 ms (35 SD). An algorithm for determination of ED was selected and tested successfully on radial and brachial recordings. As the differences between locations as well as between algorithms are sufficiently small, the determination of ejection duration from brachial oscillometric pulse waves seems feasible.

Arterial Flow, Pulse Pressure and Pulse Wave Velocity in Men and Women at Various Ages.

The increase in pulse pressure (PP) that occurs with advancing age is predominantly due to reduced arterial distensibility leading to decreased aortic compliance, particularly in the elderly, in whom high blood pressure mainly manifests as isolated systolic hypertension. Since age-related changes in stroke volume are minimal compared with changes in PP, PP is often considered a surrogate measure of arterial stiffness. However, since PP is determined by both cardiac and arterial function, a more precise and reliable means of assessment of arterial stiffness is arterial pulse wave velocity (PWV), a parameter that is only dependent on arterial properties. Arterial stiffness as measured by PWV has been found to be a powerful pressure-related indicator for cardiovascular morbidity and mortality. We analyzed PP and PWV in men and women of various age groups in healthy volunteers as well as cardiac patients with different types of diseases. The findings identified several striking sex-specific differences which demand consideration in guidelines for diagnostic procedures, for epidemiological analysis, and in evaluation of therapeutic interventions.

Review of emerging methods and techniques for arterial pressure and flow waves acquisition and analyses

Background A brief review of the principles and tools for arterial pressure measurements is presented The methods are based on compression of an artery like brachial radial digital or some other arteries that go back to the pulse diagnostics of oriental medicine decompression Riva Rocci method and the first sphygmograph invented by E Marey Existing tools for the pulse palpation and arterial pressure auscultation are discussed from the point of view of their accuracy and reliability Applanation tonometry and light absorption methods and their implantation into the lightweight wearable devices are discussed Advantages and disadvantages of different methods are formulated It is shown the direct intra arterial pressure measurements via a catheter remains the only reliable for anaesthetized postoperative and patients of the cardiac intensive care unit and persons with cardiovascular diseases obesity faint pulse arrhythmia and some others Despite increased interest in non invasive pressure monitoring many commercially available tools have failed to satisfy the AAMI standards The systems for continuous noninvasive arterial pressure monitoring based on photosensors are reviewed Accuracy and reliability of portable units for pulse oxymetry are discussed The recently developed mobile apps technologies and microchips are promising future technologies for continuous health monitoring based on the multisensory design though nowadays their accuracy is not satisfactory

Mathematical modelling of cardiac pulse wave reflections due to arterial irregularities.

This research aims to model cardiac pulse wave reflections due to the presence of arterial irregularities such as bifurcations, stiff arteries, stenoses or aneurysms. When an arterial pressure wave encounters an irregularity, a backward reflected wave travels upstream in the artery and a forward wave is transmitted downstream. The same process occurs at each subsequent irregularity, leading to the generation of multiple waves. An iterative algorithm is developed and applied to pathological scenarios to predict the pressure waveform of the reflected wave due to the presence of successive arterial irregularities. For an isolated stenosis, analysing the reflected pressure waveform gives information on its severity. The presence of a bifurcation after a stenosis tends do diminish the amplitude of the reflected wave, as bifurcations' reflection coefficients are relatively small compared to the ones of stenoses or aneurysms. In the case of two stenoses in series, local extrema are observed in the reflected pressure waveform which appears to be a characteristic of stenoses in series along an individual artery. Finally, we model a progressive change in stiffness in the vessel's wall and observe that the less the gradient stiffness is important, the weaker is the reflected wave.

Bipolar disorder and related mood states are not associated with endothelial function of small arteries in adults without heart disease.

Individuals with bipolar disorder are at increased risk for adverse cardiovascular disease (CVD) events. This study aimed to assess endothelial function and wave reflection, a risk factor for CVD, as measured by finger plethysmography in bipolar disorder to investigate whether CVD risk was higher in bipolar disorder and altered during acute mood episodes. We hypothesized that EndoPAT would detect a lower reactive hyperemia index (RHI) and higher augmentation index (AIX) in individuals with bipolar disorder compared with controls. Second, we predicted lower RHI and higher AIX during acute mood episodes. Reactive hyperemia index and augmentation index, measures of microvascular endothelial function and arterial pressure wave reflection respectively, were assessed using the EndoPAT 2000 device in a sample of 56 participants with a DSM-IV diagnosis of bipolar I disorder with 82 measures spanning different mood states (mania, depression, euthymia) and cross-sectionally in 26 healthy controls. RHI and AIX were not different between adults with and without bipolar disorder (mean age 40.3 vs. 41.2years; RHI: 2.04±0.67 vs. 2.05±0.51; AIX@75 (AIX adjusted for heart rate of 75): 1.4±19.7 vs. 0.8±22.4). When modeled in linear mixed models with a random intercept (to account for repeated observations of persons with bipolar disorder) and adjusting for age and sex, there were no significant differences between those with bipolar disorder and controls (p=0.89 for RHI; p=0.85 for AIX@75). Microvascular endothelial function and wave reflection estimated by finger plethysmography were unable to detect differences between adults with and without bipolar disorder or changes with mood states. Future research is necessary to identify more proximal and sensitive, yet relevant, biomarkers of abnormal mood-related influences on CVD risk or must target higher risk samples.

Abnormal pressure wave reflection accelerates the development of hypertension via the increase of arterial stiffness

ObjectivesIt is noted that not only arterial stiffness but also abnormal pressure wave reflection are risks for the development of hypertension. However, the association between arterial stiffness and pressure wave reflection in the development of hypertension has not been fully clarified. The present study was conducted to examine whether the abnormal pressure wave reflection accelerates the development of hypertension via the increase of arterial stiffness.MethodsIn 3102 middle-aged healthy Japanese men without hypertension at baseline, systolic/diastolic blood pressures, brachial-ankle pulse wave velocity (baPWV), and radial augmentation index (rAI) were annually measured during a 9-year study period.ResultsIn multivariate linear regression analysis and in mixed model linear regression analysis, baPWV was not longitudinally associated with rAI. Linear regression analysis demonstrated that the higher rAI at the baseline was associated with the larger longitudinal increase of baPWV (beta = 0.17, p < 0.01). At the end of study period, 404 subjects were developed to hypertension. The prevalence rate of the development of hypertension during the study period was higher in subjects with higher baPWV and higher rAI at the baseline (220 in 939 subjects: 23%) than that in other 3 groups classified by the status of baPWV and rAI at the baseline (e.g. 52 in 942 subjects with low baPWV combined with low rAI: 6%, p < 0.01).ConclusionThe abnormal pressure wave reflection, which may be derived from both arterial stiffness and peripheral vascular damages, may be an accelerator for the development of hypertension via the increase of arterial stiffness.

165 - Effect of Nitrite and N-acetylcysteine Treatment on Blood Pressure, Arterial Stiffness and Vascular Function in Spontaneously Hypertensive Rats

Introduction Reduced nitric oxide (NO) bioavailability and increased generation of reactive oxygen species and inflammation with advancing age play a major role in the development of cardiovascular disease (CVD) risk factors of hypertension, endothelial dysfunction and arterial stiffness. Therefore, increase in NO bioavailability by supplementing inorganic nitrite and improve in antioxidant defense system by supplementing N-acetylcysteine (NAC) could protect against the CVD. Hypertension is highly prevalent in a population and cause endothelial dysfunction and arterial stiffness. Hence spontaneously hypertensive rats (SHR) were used in this study as a model for hypertension-mediated endothelial dysfunction and arterial stiffness. Hypothesis Treatment of SHR with nitrite or NAC will reduce blood pressure, arterial stiffness, and endothelial dysfunction. Methods SHR (18 weeks) and normotensive Wistar Kyoto (WKY) rats were divided into 4 groups: 1) WKY, 2) SHR-cont, 3) SHR-nitrite and 4) SHR-NAC. Group 3 rats received nitrite (60 mg/L) in drinking water and group 4 rats received NAC pH 7.2 (1.2 g/L) for 3 months. Mean arterial pressure (MAP; tail-cuff method) and pulse wave velocity (PWV, a measure of arterial stiffness) were measured. Aortic endothelial function was determined with a wire myograph. Results MAP & PWV of SHR-cont were 1.8-fold and 1.6-fold higher compared with WKY respectively. MAP was modestly decreased in nitrite and NAC groups compared with that of SHR-cont. PWV did not decrease significantly with NAC or nitrite treatment. Endothelium dependent vasorelaxation was significantly decreased in SHR-cont compared with WKY. This decreased vasorelaxation was restored to WKY level in both nitrite and NAC groups. Conclusion Nitrite and NAC treatments completely protected against the hypertension induced endothelium dysfunction in SHR. Nitrite and NAC appears to be very promising dietary components to protect against age-associated endothelial dysfunction.

A Detailed Protocol for Physiological Parameters Acquisition and Analysis in Neurosurgical Critical Patients.

Intracranial pressure (ICP) monitoring is now widely used in neurosurgical critical patients. Besides mean ICP value, the ICP derived parameters such as ICP waveform, amplitude of pulse (AMP), the correlation of ICP amplitude and ICP mean (RAP), pressure reactivity index (PRx), ICP and arterial blood pressure (ABP) wave amplitude correlation (IAAC), and so on, can reflect intracranial status, predict prognosis, and can also be used as guidance of proper treatment. However, most of the clinicians focus only on the mean ICP value while ignoring these parameters because of the limitations of the current devices. We have recently developed a multimodality monitoring system to address these drawbacks. This portable, user-friendly system will use a data collecting and storing device to continuously acquire patients' physiological parameters first, i.e., ABP, ICP, and oxygen saturation, and then analyze these physiological parameters. We hope that the multimodality monitoring system will be accepted as a key measure to monitor physiological parameters, to analyze the current clinical status, and to predict the prognosis of the neurosurgical critical patients.

Association of interleukin-6 with aortic stiffness in end-stage renal disease

Cardiovascular disease (CVD) is the leading cause of mortality in patients with chronic kidney disease (CKD). Aortic stiffness, a nontraditional risk factor, is associated with high rate of mortality in CKD. Using a CKD animal model with medial vascular calcification, we previously reported increased mRNA expression of interleukin-6 (IL-6), tumor necrosis factor (TNF), and interleukin-1β (IL-1β) in calcified aorta. The aim of the study was to investigate the association between IL-6, TNF, IL-1β, and aortic stiffness in end-stage renal disease patients. In a cross-sectional study, we enrolled 351 patients on dialysis. Aortic stiffness was assessed by carotid-femoral pulse wave velocity (cf-PWV), while central pulse pressure and augmentation index were assessed using generalized transfer function applied to the radial artery pressure wave form. Plasma IL-6, TNF, and IL-1β were measured by enzyme-linked immunosorbent assay. IL-6 was associated with cf-PWV adjusted for mean blood pressure (MBP) (standardized β = 0.270; P < .001). In a multivariate adjusted model for age, diabetes, hypertension, CVD, and MBP, IL-6 was still associated with cf-PWV (standardized β = 0.096; P = .026). The impact of age, diabetes, and CVD on cf-PWV was partially mediated by IL-6 in a mediation analysis. However, there were no associations between TNF, IL-1β, and aortic stiffness. While IL-6 was associated with augmentation index (standardized β = 0.224; P < .001) and central pulse pressure (standardized β = 0.162; P = .001) when adjusted for MBP and heart rate, this relationship was not significant after adjusting for potential confounders.This study suggests a potential role of IL-6 for CKD-related aortic stiffness.

Multiple coupled resonances in the human vascular tree: refining the Westerhof model of the arterial system.

The human arterial vascular tree can be described by multicompartment models using electrical components. First introduced in the 1960s by Noordergraaf and Westerhof, these hardware-based approaches required several simplifications. We were able to remove the restrictions using modern software simulation tools and improve overall model quality considerably. Whereas the original Westerhof model consisted of 121 Windkessel elements, the refined model has 711 elements and gives realistic pulse waveforms of the aorta and brachial and radial arteries with realistic blood pressures. Moreover, novel insights concerning the formation of the physiological aortic-to-radial transfer function were gained. Its being potentially due to the coupling of many small resonant elements gives new impetus to the discussion of arterial pressure wave reflection. The individualized transfer function derived from our improved model incorporates distinct patient characteristics and can potentially be used for estimation of central blood pressure values. NEW & NOTEWORTHY We were able to find an individualized transfer function giving realistic pulse waveforms and blood pressures using a multicompartment model of the arterial system. Based on the hardware-built Westerhof approach, several simplifications initially introduced in the 1960s could be reversed using software simulation. Overall model quality was improved considerably, and multiple coupled resonances were identified as potential explanation for the formation of the aortic-to-radial transfer function, giving new impetus to the discussion of arterial pressure wave reflection.

Central diastolic pressure exponential decay constant and subendocardial flow supply.

Central diastolic pressure exponential decay constant and subendocardial flow supply.

Evaluation of cardiac function in pediatric intensive care unit

Cardiac is closely related to circulatory function, and both terms can be integrated together as hemodynamics . Thus the author will use the collective term rather than function . There are several ways to evaluate hemodynamic status.Briefly, we can use physical examination as clinical indices of hemodynamics.The physical examination method can detect cardiac impulse position, liver size, peripheral edema, distension of jugular vein to identify circulatory dysfunction.Besides relative simple basic method, there are other means to detect circulatory function.We usually divided them into 2 categories: invasive versus non-invasive means.The non-invasive means include echocardiography and impedance electrocardiography.Echocardiography can provide portable, easily operated platform to evaluate classical cardiac including fractional shortening, cardiac wall thickness, pressure gradient evaluation and ejection fraction(EF). The impedance electrocardiography can provide continuous index for circulatory functional evaluation.The invasive means include arterial pressure wave analysis, central venous pressure monitoring, floating catheter for capillary wedge pressure monitoring and cardiac output.The relatively newer device includes pressure index countour cardiac output(PiCCO) method, using similar but simple not only to derive cardiac output, but also lung water and other complex indices.In summary, hemodynamic evaluation of circulatory functional status is rather complex, a thorough understanding of ongoing pathophysiology is of prime importance.All clinicians working in the intensive card unit should carefully select the most appropriate ones according to the accessibility and familiarity and mechanism of operation. Key words: Cardiac function; Circulatory function; Hemodynamics; Pediatric intensive care unit,

Abstract P518: Abnormal Pressure Wave Reflection Accelerates the Development of Hypertension via the Increase of Arterial Stiffness

Objectives: Arterial stiffness (macrovascular damage) and peripheral vascular damage (microvascular damage) affect pressure wave reflection, and several prospective studies have demonstrated that not only arterial stiffness but also abnormal pressure wave reflection are risks for the development of hypertension. However, the association between arterial stiffness and pressure wave reflection in the development of hypertension has not been fully clarified. The present study was conducted to examine whether the abnormal pressure wave reflection accelerates the development of hypertension via the increase of arterial stiffness. Methods: In 3102 middle-aged healthy Japanese men without hypertension at baseline, systolic/diastolic blood pressures, brachial-ankle pulse wave velocity (baPWV), and radial augmentation index (rAI) were annually measured during a 9-year study period. Results: In multivariate linear regression analysis and in mixed model linear regression analysis, baPWV was not longitudinally associated with rAI. Linear regression analysis demonstrated that the higher rAI at the baseline was associated with the larger longitudinal increase of baPWV (beta = 0.17, p&lt;0.01). At the end of study period, 404 subjects were developed to hypertension. Binary logistic regression analysis demonstrated that baPWV (per SD increase = 1.43; 1.25 – 1.62, p&lt;0.01) and rAI (per SD increase = 1.56; 1.33 – 1.82, p&lt;0.01) at the baseline had significant odds ratio for the prediction of the development of hypertension. The prevalence rate of the development of hypertension during the study period was higher in subjects with higher baPWV and higher rAI at the baseline (220 in 939 subjects: 23 %) than that in other 3 groups classified by the status of baPWV and rAI at the baseline (e.g. 52 in 942 subjects with low baPWV combined with low rAI: 6%, p&lt;0.01). Conclusion: The abnormal pressure wave reflection, which may be derived from both arterial stiffness and peripheral vascular damages, may be an accelerator for the development of hypertension via the increase of arterial stiffness. In there, the combination of macro- and micro-vascular damages may accelerate the development of hypertension.

Cardiac cycle-induced EPI time series fluctuations in the brain: Their temporal shifts, inflow effects and T2∗ fluctuations

The cardiac-induced arterial pressure wave causes changes in cerebral blood flow velocities and volumes that affect the signals in echo-planar imaging (EPI). Using single-echo EPI time series data, acquired fast enough to unalias the cardiac frequency, we found that the cardiac cycle-induced signal fluctuations are delayed differentially in different brain regions. When referenced to the time series in larger arterial structures, the cortical voxels are only minimally shifted but significant shifts are observed in subcortical areas. Using double-echo EPI data we mapped the voxels’ “signal at zero echo time”, S0, and apparent T2∗ over the cardiac cycle. S0 pulsatility was maximised for voxels with a cardiac cycle-induced timing that was close to the arterial structures and is likely explained by enhanced inflow effects in the cortical areas compared to subcortical areas. Interestingly a consistent T2∗ waveform over the cardiac cycle was observed in all voxels with average amplitude ranges between 0.3-0.55% in grey matter and 0.15–0.22% in white matter. The timing of the T2∗ waveforms suggests a partial volume fluctuation where arteriolar blood volume changes are counterbalanced by changes in CSF volumes.

Abstract 216: Hdac2 Modulates Atherosclerosis

Objective: We recently described a novel regulatory role for histone deacetylase 2 (HDAC2) in vascular endothelial cell protection against the known endothelial injury stimulus Oxidize Low Density Lipoprotein (OxLDL). The goal of current study is to determine the effects of endothelial-specific HDAC2 overexpression on endothelial dysfunction and atherogenesis in vivo . Approach and Results: To study the effect of endothelial HDAC2 overexpression on vascular function and atherogenesis, we generated and characterized an endothelial specific human HDAC2 overexpressing transgenic mouse (HDAC2-Tg) under the control of the tie2 promoter. The founder HDAC2-overexpressing mice appear to have a normal phenotype- normal weight, mean arterial blood pressure (MAP) and pulse wave velocity (PWV). Isolated intact aortas from endothelial-specific overexpressing HDAC2 transgenic mice (HDAC2-Tg) exhibited a healthier vascular function profile with higher nitric oxide levels and less OxLDL-mediated vascular dysfunction. Further, we induced atherogenesis in C57BL6 and HDAC2-Tg mice by injecting adeno-associated viruses (AAV) encoding PCSK9 (D377Y) under the control of a liver-specific promoter by tail vein injection followed by high fat diet regimen for 12 weeks and measured endothelium-dependent vasorelaxation in isolated blood vessels, pulse wave velocity, an index of vascular stiffness and mean arterial blood pressure. HDAC2-Tg exhibited protected endothelial dependent vascular relaxation and no significant changes in MAP and PWV as compared to control mice. Conclusion: HDAC2 is a critical regulator of endothelial function. Overexpression or activation of HDAC2 represents a novel therapy for endothelial dysfunction and atherosclerosis.

What is important for aging-induced arterial stiffening, autonomic dysfunction, vascular characteristics or both?

Aging decreases arterial distensibility via changes in arterial impedance, arterial pressure, and flow wave contours; these aging-induced pathological changes in large arterial walls are qualitatively similar to those observed in hypertensive patients.1, 2, 3, 4 Therefore, hypertension is often considered as an accelerated form of aging.5

Altered Blood Flow Response to Small Muscle Mass Exercise in Cancer Survivors Treated With Adjuvant Therapy.

BackgroundAdjuvant cancer treatments have been shown to decrease cardiac function. In addition to changes in cardiovascular risk, there are several additional functional consequences including decreases in exercise capacity and increased incidence of cancer‐related fatigue. However, the effects of adjuvant cancer treatment on peripheral vascular function during exercise in cancer survivors have not been well documented. We investigated the vascular responses to exercise in cancer survivors previously treated with adjuvant cancer therapies.Methods and ResultsPeripheral vascular responses were investigated in 11 cancer survivors previously treated with adjuvant cancer therapies (age 58±6 years, 34±30 months from diagnosis) and 9 healthy controls group matched for age, sex, and maximal voluntary contraction. A dynamic handgrip exercise test at 20% maximal voluntary contraction was performed with simultaneous measurements of forearm blood flow and mean arterial pressure. Forearm vascular conductance was calculated from forearm blood flow and mean arterial pressure. Left ventricular ejection time index (LVETi) was derived from the arterial pressure wave form. Forearm blood flow was attenuated in cancer therapies compared to control at 20% maximal voluntary contraction (189.8±53.8 vs 247.9±80.3 mL·min−1, respectively). Forearm vascular conductance was not different between groups at rest or during exercise. Mean arterial pressure response to exercise was attenuated in cancer therapies compared to controls (107.8±10.8 vs 119.2±16.2 mm Hg). LEVTi was lower in cancer therapies compared to controls.ConclusionsThese data suggest an attenuated exercise blood flow response in cancer survivors ≈34 months following adjuvant cancer therapy that may be attributed to an attenuated increase in mean arterial pressure.

Non-Invasive Assessment of Early Atherosclerosis Based on New Arterial Stiffness Indices Measured with an Upper-Arm Oscillometric Device

The clinical significance of detecting early atherosclerosis is now widely recognized. Measurement methods available at present are usually not suitable for use in primary care where rapid screening for a large population is needed. The Arterial Velocity-pulse Index (AVI) and Arterial Pressure-volume Index (API) are new noninvasive arterial stiffness indices that can be rapidly measured using an oscillometric device. The purpose of this study was to determine whether high AVI and API values are predictive of early atherosclerosis prior to the onset of obstructive coronary artery disease (CAD). A total of 183 patients were enrolled and allocated to the CAD group (n = 109), early atherosclerosis (AS) group (n = 34) or an apparently healthy (non-AS) group (n = 40) based on the results of angiographic examinations. Measurements for arterial blood pressure, AVI, API and brachial-ankle pulse wave velocity (baPWV) were collected. Statistical analyses revealed that AVIs were significantly lower in the non-AS group than in the AS group and the CAD group. The inter-group differences in API were not statistically significant among the 3 patient groups. As a reference, baPWV was found to be statistically higher in the CAD group than in the non-AS group, whereas there was no significant difference between the CAD group and the AS group, or between the AS group and the non-AS group. The AVI and API were both significantly correlated with baPWV. This study demonstrated that AVI was more sensitive than baPWV and API in indicating early atherosclerosis, although elevated AVI and baPWV were both predictive of CAD.