Central Augmentation Pressure Research Articles

Abstract 9253: A Randomized Controlled Trial of the Effects of Vitamin D Supplementation on Central Blood Pressures and Aortic Stiffness in Native American Women

Background: Low vitamin D status has been linked to increased cardiovascular disease (CVD) risk. Low vitamin D levels, hypertension, and CVD are highly prevalent in Native American populations. However, it is unclear if vitamin D supplementation improves central blood pressure or arterial stiffness in Native American women. Methods: Healthy postmenopausal Native American women without known CVD and with screening serum 25-hydroxyvitamin D (25(OH)D) between 10-60 ng/mL were randomized to receive daily vitamin D3 either 400 IU or 2,500 IU for 6 months. Central systolic blood pressure (cSBP), central pulse pressure (cPP) and aortic augmentation index (AIx) were estimated by tonometry (AtCor Medical, Sydney, Australia) at baseline and after 6 months of vitamin D supplementation. General linear models were used to evaluate cross-sectional and longitudinal associations. Repeated measures models were adjusted for baseline 25(OH)D. Results: At baseline, study volunteers (n=98) were mean (standard deviation) 61 (7.3) years old. Screening 25(OH)D was 26.4 (11.0) ng/mL; 25(OH)D was less than 20 ng/mL in 33 (34%) participants and between 20-30 ng/mL in 29 (29.6%) participants. Screening 25(OH)D was similar between the two treatment groups (p=0.291), as were baseline cSBP, cPP, age, body-mass index, glucose, lipids, and high sensitivity C-reactive protein levels (all p>0.1). Screening 25(OH)D was associated with cSBP (p=0.022) and cPP (p=0.007), but not AIx (p=0.807). Treatment with 2,500 IU of daily vitamin D3 did not affect cSBP (p=0.546), cPP (p=0.614), or AIx (p=0.103) compared to 400 IU daily. Conclusions: Despite relatively low serum 25(OH)D at baseline, 6 months of vitamin D supplementation did not improve central blood pressure parameters or arterial stiffness in Native American women.

Advanced glycation end products, aortic stiffness, and wave reflection in peritoneal dialysis as compared to hemodialysis

Modification of vascular extracellular matrix by advanced glycation end products (AGEs) may result in vascular stiffness. Because of higher exposure to glucose, we hypothesized that patients on peritoneal dialysis (PD) may have higher tissue levels of AGEs, increased vascular stiffness, and enhanced central augmentation pressure as compared to hemodialysis patients (HD). In a cross-sectional study, 43 PD were matched to 43 HD based on age, gender, diabetes, and dialysis vintage. Tissue levels of AGEs were assessed by skin autofluorescence (skin AF). Aortic stiffness was measured by carotid-femoral pulse wave velocity (cf-PWV), and heart rate-adjusted augmentation pressure (AP@75) was performed by arterial tonometry. Baseline characteristics were similar in both groups except for lower prevalence of cardiovascular disease (CVD) and higher exposure to smoking in PD. Skin AF and cf-PWV were not statistically different, but PD patients had a lower AP@75 (P = 0.023). However, after adjustments for prevalence of CVD and smoking status, skin AF was higher in PD by 0.587 AU (95 % CI 0.091-1.215, P = 0.020), and cf-PWV was higher in PD by 2.20 m/s (95 % CI 0.56-3.84, P = 0.009), while AP@75 was not different. Overall, there was a significant association between skin AF and cf-PWV and AP@75. Skin AF and aortic stiffness were higher in PD after adjustments for imbalances in baseline characteristics. Independent of dialysis modality, there was a positive association between skin AF, aortic stiffness, and enhanced wave reflection.

Associations Between Short-term Changes in Air Pollution and Correlates of Arterial Stiffness: The Veterans Affairs Normative Aging Study, 2007–2011

We investigated associations between short-term exposure to air pollution and central augmentation index and augmentation pressure, correlates of arterial stiffness, in a cohort of elderly men in the Boston, Massachusetts, metropolitan area. This longitudinal analysis included 370 participants from the Veterans Affairs Normative Aging Study with up to 2 visits between 2007 and 2011 (n = 445). Augmentation index (as %) and augmentation pressure (in mmHg) were measured at each visit by using radial artery applanation tonometry for pulse wave analysis and modeled in a mixed effects regression model as continuous functions of moving averages of air pollution exposures (over 4 hours and 1, 3, 7, and 14 days). The results suggest that short-term changes in air pollution were associated with augmentation index and augmentation pressure at several moving averages. Interquartile range (IQR) increases in 3-day average exposure to particles with aerodynamic diameter less than 2.5 μm (3.6-μg/m(3) IQR increase) and sulfate (1.4-μg/m(3) IQR increase) and 1-day average exposure to particle number counts (8,741-counts/cm(3) IQR increase) were associated with augmentation index values that were 0.8% (95% confidence interval (CI): 0.2, 1.4), 0.6% (95% CI: 0.1, 1.2), and 1.7% (95% CI: 0.4, 2.9) higher, respectively. Overall, the findings were similar for augmentation pressure. The findings support the hypothesis that exposure to air pollution may affect vascular function.

Aortic Stiffness in Lone Atrial Fibrillation: A Novel Risk Factor for Arrhythmia Recurrence

BackgroundRecent community-based research has linked aortic stiffness to the development of atrial fibrillation. We posit that aortic stiffness contributes to adverse atrial remodeling leading to the persistence of atrial fibrillation following catheter ablation in lone atrial fibrillation patients, despite the absence of apparent structural heart disease. Here, we aim to evaluate aortic stiffness in lone atrial fibrillation patients and determine its association with arrhythmia recurrence following radio-frequency catheter ablation.MethodsWe studied 68 consecutive lone atrial fibrillation patients who underwent catheter ablation procedure for atrial fibrillation and 50 healthy age- and sex-matched community controls. We performed radial artery applanation tonometry to obtain central measures of aortic stiffness: pulse pressure, augmentation pressure and augmentation index. Following ablation, arrhythmia recurrence was monitored at months 3, 6, 9, 12 and 6 monthly thereafter.ResultsCompared to healthy controls, lone atrial fibrillation patients had significantly elevated peripheral pulse pressure, central pulse pressure, augmentation pressure and larger left atrial dimensions (all P<0.05). During a mean follow-up of 2.9±1.4 years, 38 of the 68 lone atrial fibrillation patients had atrial fibrillation recurrence after initial catheter ablation procedure. Neither blood pressure nor aortic stiffness indices differed between patients with and without atrial fibrillation recurrence. However, patients with highest levels (≥75th percentile) of peripheral pulse pressure, central pulse pressure and augmentation pressure had higher atrial fibrillation recurrence rates (all P<0.05). Only central aortic stiffness indices were associated with lower survival free from atrial fibrillation using Kaplan-Meier analysis.ConclusionAortic stiffness is an important risk factor in patients with lone atrial fibrillation and contributes to higher atrial fibrillation recurrence following catheter ablation procedure.

Combining risk markers improves cardiovascular risk prediction in women

Cardiovascular risk stratification could be improved by adding measures of atherosclerosis to current risk scores, especially in intermediate-risk individuals. We prospectively evaluated the additive value of different non-invasive risk markers (both individual and combined) for gender-specific cardiovascular risk stratification on top of traditional risk factors in a middle-aged population-based cohort. Carotid-plaques, IMT (intima-media thickness), ABI (ankle-brachial index), PWV (pulse-wave velocity), AIx (augmentation index), CAP (central augmented pressure) and CSP (central-systolic pressure) were measured in 1367 CVD (cardiovascular disease)-free participants aged 50-70 years old. Cardiovascular events were validated after a mean follow-up of 3.8 years. AUC (area-under-the-curve) and NRI (net reclassification improvement) analyses (total-NRI for all and clinical-NRI for intermediate-risk groups) were used to determine the additive value of individual and combined risk markers. Cardiovascular events occurred in 32 women and 39 men. Traditional cardiovascular risk factors explained 6.2% and 12.5% of the variance in CVD in women and men respectively. AUCs did not substantially increase by adding individual or combined non-invasive risk markers. Individual risk markers only improved reclassification in intermediate-risk women and more than in men; clinical-NRIs ranged between 48.0 and 173.1% in women and 8.9 and 20% in men. Combined non-invasive-risk markers improved reclassification in all women and even more in those at intermediate risk; 'IMT-presence-thickness-of-plaques' showed largest reclassification [total-NRI=33.8%, P=0.012; IDI (integrated-discrimination-improvement)=0.048, P=0.066; clinical-NRI=168.0%]. In men, combined non-invasive risk markers improved reclassification only in those at intermediate risk; 'PWV-AIx-CSP-CAP-IMT' showed the largest reclassification (total-NRI=14.5%, P=0.087; IDI=0.016, P=0.148; clinical-NRI=46.0%). In all women, cardiovascular risk stratification improved by adding combinations and in women at intermediate risk also by adding individual non-invasive risk markers. The additive value of individual and combined non-invasive risk markers in men is limited to men at intermediate risk only, and to a lesser extent than in women.

Associations between Short-term Changes in Air Pollution and Correlates of Arterial Stiffness: the VA Normative Aging Study

Background: Few observational studies have evaluated changes in arterial stiffness after short-term exposure to air pollution. Aims: We investigated associations between short-term changes in air pollution and central augmentation index (AIx) and augmentation pressure (AP), correlates of arterial stiffness, in a cohort of elderly men in the Boston metropolitan area. Methods: This longitudinal analysis included 378 participants from the VA Normative Aging Study with up to two visits between 2007 and 2011. AIx (%) and AP (mmHg) were measured at each visit using radial artery applanation tonometry for pulse wave analysis, and modeled in a mixed effect regression as continuous functions of moving average (4h, 24h, 2 to 14 days) of air pollution exposures. All models were adjusted for age, body mass index, high density lipoprotein cholesterol level, education, race, alcohol consumption, smoking status, cumulative pack-years smoked, diabetes status, seasonality, day of week, and corresponding moving average of absolute temperature and relative humidity. Results: Statistically significant (p&lt;0.05) positive associations were observed between exposure to sulfate (SO42-) and fine particles (PM2.5), and particle number counts (PNC), and AIx for several moving averages. Interquartile range increases in 2-day average SO42- (1.6 ?g/m3 increase) and PM2.5 (3.8 ?g/m3 increase), and 11-day average PNC (7,354 counts/cm3), were associated with 0.7% (95%CI: 0.1-1.2%), 0.9% (95%CI: 0.3-1.5%), and 2.6% (95%CI: 1.2-4.1%) higher AIx, respectively. Overall, the findings were very similar for AP. Conclusions: Short-term changes in air pollution were associated with correlates of arterial stiffness in this study sample of predominantly elderly white men. The findings support the hypothesis for the role of vascular function in the cardiovascular health effects of air pollution.

Effects of the DPP-4 inhibitor saxagliptin on early vascular changes in the retinal and systemic circulation

In type-2 diabetes early vascular changes (among others) are hyperperfusion in the retinal circulation (like in the kidney) and increased pulse wave reflection leading to increased aortic pressure. We analyzed whether the DPP4-inhibitor saxagliptin reverses early vascular and haemodynamic changes in type-2 diabetes. In this double-blind randomized controlled clinical cross-over trial 42 patients with type-2 diabetes (age 60.3, 13 were females, BMI 30.6 kg/m2, mean duration of diabetes 4 years, HbA1c 7.0%, blood pressure 132/79 mmHg) were consecutively [PB1] included and randomized to placebo or saxagliptin 5 mg for 6 weeks each. Retinal capillary flow (RCF) was assessed at baseline and after flickerlight exposure (as a vasodilatory test) by scanning laser Doppler flowmetry. Central (aortic) systolic blood pressure (SBP), central pulse pressure (PP), augmentation index and pulse wave velocity were determined with the SphygmoCor device. Following treatment with saxagliptin (as opposed to placebo) saxagliptin effected a better glycemic control, a reduced retinal capillary flow (p=0.033) and, in parallel, reduced central systolic augmentation and pulse pressure (see table). In accordance, Flicker light induced increment of RCF (indicative of vasodilatory capacity of the retinal circulation) was numerically 2-fold greater, although not significant. View this table: Table 1 Our data suggest that treatment with saxagliptin for 6 weeks normalizes retinal capillary flow and improves central haemodynamics in type 2 diabetes.

Changes of central hemodynamics and pulse wave velocity after isometric handgrip exercise

Purpose: Dynamic changes of central hemodynamic parameters and arterial stiffness indexes after isometric handgrip exercise may be more sensitive indicators of the arterial stiffness. We investigated the changes of them after 3 min-handgrip exercise. Methods: Forty one subjects who underwent coronary angiography (CAG) were enrolled. After CAG, baseline arterial waveforms were traced at the aortic root and external iliac artery using right coronary catheters. Arterial waveforms were recorded at 1, 2 and 3 min in the aortic root and at 3 min in the external iliac artery after the isometric handgrip exercise at 30∼40% of the maximal handgrip power. AP and AI were measured at the central aortic waveforms. PWV was calculated using the ECG-gated time difference of the upstroke of the arterial waveforms and the distance between the aortic root and the common iliac artery measured by a catheter. Results: Central systolic BP (SBP), pulse pressure (PP), augmentation pressure (AP) and augmentation index (AI) increased from 1 min after exercise and reached peak values at 2 min after exercise. Changes of pulse wave velocity (PWV) showed a diverse pattern. PWV of 22 subjects (54%, 63.4±8.6 years) increased ≥0.5 m/sec, but 19 subjects (46%, 63.1±10.2 years) showed a little increase (<0.5 m/sec) or even decrease after exercise. SBP, PP, and forward pressure increased similarly after exercise, but AP and AI increased only in subjects with ΔPWV ≥0.5 m/sec after exercise. View this table: Conclusions: Isometric handgrip exercise was a simple and easy method to evaluate the dynamic changes of arterial stiffness indexes. Changes of central hemodynamic parameters were correlated with a change of PWV after handgrip exercise.

Percutaneous transluminal angioplasty for peripheral artery disease confers cardiorenal protection

The effects of percutaneous transluminal angioplasty (PTA) on hemodynamic parameters are not established. We tested the hypothesis that PTA would achieve reductions in hemodynamic and target organ damage (TOD) measures in patients with peripheral artery disease (PAD). We enrolled 56 consecutive PAD patients who were scheduled to undergo elective PTA procedures. Brachial blood pressure (BP), central BP, left ventricular mass index (LVMI) and urinary microalbumin excretion ratio (UACR) were assessed at baseline and follow-up. The ankle-brachial index in the diseased leg significantly improved after the PTA (P<0.001). Compared with the pretreatment levels, brachial and central BPs, the carotid augmentation index (AI) and central augmentation pressure (AP) were significantly reduced after the PTA, as were LVMI and UACR. The change in AI in the PTA group was significantly associated with the extent of change in LVMI (P=0.002) and marginally associated with the change in UACR (P=0.07), independently of other covariates. In conclusion, in patients with PAD, significant reductions in carotid AI were observed by PTA treatment; these changes may be attributable to improvements in measures of cardiac and renal target organ damage.

135 CLINICAL APPLICATION AND REPRODUCIBILITY OF CENTRAL PRESSURE AUGMENTATION USING RADIAL ARTERY PULSE WAVE ANALYSIS

BackgroundThe use of surrogate measures for central artery blood pressure (BP) is now commonplace, including radial artery pulse wave analysis (PWA). Prior studies have examined central augmentation index (cAI), defined...

134 PERIPHERAL ARTERIAL WAVEFORMS FOR THE PREDICTION OF CARDIOVASCULAR EVENTS: CAROTID VERSUS RADIAL PULSE WAVE ANALYSIS

Purpose Augmentation of central systolic blood pressure identified with pulse wave analysis (PWA) is a marker of arterial stiffness associated with coronary atheroma and cardiovascular events. We sought to determine if waveforms obtained from the carotid artery would be superior to those from the radial artery. Our hypothesis was that due to proximity to the aorta, carotid PWA would better reflect central aortic pressures. Methods Radial and carotid pulse waveforms were available in 201 patients enrolled into the Alternative Risk Markers in Coronary Artery Disease (ARM-CAD) study with follow-up data at a mean of 1.2 years. Patients were recruited prior to elective coronary angiography into a prospective multicentre observational study. Peripheral waveforms were obtained over 12 s using a Millar tonometer. Augmentation pressure (AP), derived from a signal-averaged waveform, was calculated as the difference in pressure between the first and second systolic shoulders. Radial and carotid PWA were compared by assessing intra-operator variability using Bland & Altman plots, and Cox regression analysis for death or myocardial infarction (MI) adjusted for baseline Framingham Score and cardiac medications. Results Mean age was 66 years, 63% were male, 45% had prior angina/MI, 23% a history of diabetes and 17% some impairment of left-ventricular function. As demonstrated in the example waveforms, there was a marked difference in AP from carotid and radial PWA (20 mm Hg mean difference; p Conclusions The utility of carotid PWA for the prediction of cardiovascular events is restricted by lower reproducibility, leading to higher intrasubject variability. Augmentation pressure from the peripheral radial artery waveform, but not carotid, is associated with cardiovascular events in patients referred for diagnostic angiography.

Contribution of arterial excess pressure and arterial stiffness to central augmentation pressure in healthy subjects

Pulse wave analysis has established that central (aortic) pulse pressure can be subdivided into two components which are the height of the first systolic peak and the augmentation pressure (AP) (Fig. 1 part A). Both central pulse pressure and AP are predictors of adverse cardiovascular events [1]. AP seems to be largely affected by the wave reflection in the periphery of the arterial system as well as by arterial stiffness, age, and gender. Recently, Davies et al. [2] showed that the shape of the arterial pressure waveform is determined largely by the aortic reservoir and partly by the wave reflection.

Wave reflection and central pressure augmentation

aHeart Research Group, Murdoch Childrens Research Institute bDepartment of Paediatrics, University of Melbourne, Melbourne, Australia cBiomedical Simulation Laboratory, University of Toronto, Toronto, Canada Correspondence to Jonathan Mynard, B.Sc., B.Eng., M.Res., Ph.D., Murdoch Childrens Research Institute, Flemington Rd., Parkville, Victoria, 3052, Australia. E-mail: [email protected]

Wave reflection and central pressure augmentation

Cameron, James D.; Hope, Sarah A.; Meredith, Ian T.; Mottram, Philip M.; Tung, Matthew; Cheng, Kevin Author Information

Impact of Opioid Pharmacotherapy on Arterial Stiffness and Vascular Ageing: Cross-Sectional and Longitudinal Studies

Whilst there is a small literature on the cardiovascular toxicity of opiates, there is no detailed antemortem data on non-cardiovascular patient populations. A cross-sectional and longitudinal naturalistic observational study was performed comparing methadone (N = 71)-, buprenorphine (N = 593)-, naltrexone (N = 23)-treated patients with controls (N = 576) on indices of arterial stiffness and vascular age by Pulse Wave Analysis in primary care, 2006-2011. Controls were younger 29.96 ± 0.45 (mean ± SEM) vs. 34.00 ± 0.34-39.22 ± 1.11 years (all P < 0.005) and had fewer smokers (15.9 % vs. 86.9 %-92.96 %, all P < 0.0001). The sex ratio was similar (69.6 vs. 67.7 % male, P = 0.46). These baseline differences were controlled for by multiple regression. Linear regression of vascular age, central augmentation pressure, central augmentation index and other measures against chronologic age showed significant protective effects by treatment group against the treatment standard of methadone, in both sexes in additive and interactive models (all P < 0.02). Interactive terms in treatment type remained significant including all conventional risk factors accounting for differing opiate exposures. The principal findings from multiple regression were confirmed in the time series analysis up to 5 years by repeated measures nonlinear regression. These studies show that the deleterious impact of chronic opiate pharmacotherapy on vascular age and arterial stiffness varies significantly by treatment type.

Effects of Low-Dose Atorvastatin on Arterial Stiffness and Central Aortic Pressure Augmentation in Patients With Hypertension and Hypercholesterolemia

Experimental and clinical data suggest that statins exert anti-inflammatory and antiproliferative actions on vasculature beyond their lipid-lowering properties. Whether these pleiotropic effects of statins translate into a beneficial effect on arterial stiffness is not clear. This study aimed to evaluate the potential effects of low-dose atorvastatin treatment on arterial stiffness and central arterial pressure waveforms in patients with mild hypertension and hypercholesterolemia. In a double-blind, randomized, placebo-controlled fashion, 50 hypertensive and hypercholesterolemic patients were allocated to receive 10 mg of atorvastatin or placebo for 26 weeks. Arterial stiffness was assessed by aortic pulse-wave velocity (PWV) using a Sphygmocor device. Central arterial pressure waveform parameters were estimated by radial artery applanation tonometry. Heart rate-adjusted augmentation index (AIx(75)) was used as measure of wave reflections. At study end, aortic PWV (9.0 ± 1.5 vs. 10.9 ± 2.6 m/sec; P < 0.001) and AIx(75) (24.9% ± 9.7% vs 28.8% ± 11.8%; P < 0.001) were significantly lower in the atorvastatin group than that placebo group. Furthermore, decreases in central aortic systolic blood pressure and pulse pressure were evident at study-end with atorvastatin but not with placebo (130 ± 8 vs. 138 ± 6 mm Hg, P < 0.001; 48 ± 7 vs. 53 ± 6 mm Hg, P < 0.05, respectively). Atorvastatin-induced reductions in aortic PWV during follow-up showed significant associations with changes in AIx(75) and central aortic systolic blood pressure and pulse pressure. This study shows that low-dose atorvastatin treatment improves arterial stiffness and exerts a reduction on central aortic pressures. These effects may represent a potential mechanism of cardiovascular risk reduction observed with statin use. ClinicalTrials.gov Database Identifier Number: NCT01126684.

Renal morphology assessed by ultrasound in relation to central haemodynamics and body fat

There is a correlation between renal function and the morphological characteristics of the kidney. However, little is known about the association between renal morphology and other important predictors of the risk of cardiovascular diseases, such as central haemodynamics or body fat. Thus, in the present study we investigated correlations between renal morphology, body fat and central haemodynamics. Renal morphology and intra-abdominal and subcutaneous fat were assessed by ultrasound, whereas central haemodynamics were evaluated by pulse wave analysis, in 93 healthy, non-obese subjects (mean (±SEM) age 52 ± 1 years; 43 men, 50 women). Significant correlations were found for indices of body fat (waist : hip ratio, body mass index and intra-abdominal fat) and renal morphology (kidney length, width and volume). Significant inverse correlations were found between central augmentation pressure (cAP) and kidney length (r = -0.33; P = 0.0009), width (r = -0.24; P = 0.01) and volume (r = -0.27; P = 0.007). In addition, significant negative correlations were found between the central augmentation index (cAIx) and kidney length (r = -0.36; P = 0.0003), width (r = -0.29; P = 0.003) and volume (r = -0.33; P = 0.0008). Multiple linear regression analysis revealed independent associations between kidney length and both cAP and cAIx. In conclusion, common morphometric characteristics of the kidney, as assessed by ultrasound, are associated with measures of body fat and descriptors of central haemodynamics. The relationships demonstrated in the present study indicate that these associations may be a biologically plausible phenomenon.

Plasma concentrations of extracellular matrix protein fibulin-1 are related to cardiovascular risk markers in chronic kidney disease and diabetes

BackgroundFibulin-1 is one of a few extracellular matrix proteins present in blood in high concentrations. We aimed to define the relationship between plasma fibulin-1 levels and risk markers of cardiovascular disease.MethodsPlasma fibulin-1 was determined in subjects with chronic kidney disease (n = 32; median age 62.5, inter-quartile range 51 – 73 years) and 60 age-matched control subjects. Among kidney disease patients serological biomarkers related to cardiovascular disease (fibrinogen, interleukin 6, C-reactive protein) were measured. Arterial applanation tonometry was used to determine central hemodynamic and arterial stiffness indices.ResultsWe observed a positive correlation of fibulin-1 levels with age (r = 0.38; p = 0.033), glycated hemoglobin (r = 0.80; p = 0.003), creatinine (r = 0.35; p = 0.045), and fibrinogen (r = 0.39; p = 0.027). Glomerular filtration rate and fibulin-1 were inversely correlated (r = −0.57; p = 0.022). There was a positive correlation between fibulin-1 and central pulse pressure (r = 0.44; p = 0.011) and central augmentation pressure (r = 0.55; p = 0.001). In a multivariable regression model, diabetes, creatinine, fibrinogen and central augmentation pressure were independent predictors of plasma fibulin-1.ConclusionIncreased plasma fibulin-1 levels were associated with diabetes and impaired kidney function. Furthermore, fibulin-1 levels were associated with hemodynamic cardiovascular risk markers. Fibulin-1 is a candidate in the pathogenesis of cardiovascular disease observed in chronic kidney disease and diabetes.

Relationship Between Central Arterial Pressure, Exercise and Fitness Level in Stable Coronary Artery Disease

Background: Augmentation of central arterial pressure increases cardiovascular risk, and interventions which lower pressure augmentation may reduce risk. It is not known whether greater physical fitness is associated with reduced central pressure augmentation. Methods: In 173 patients (140 males, age 61 ± 9 years) with stable coronary artery disease (CAD), central augmentation pressure (cAP) and augmentation index (cAI) were measured by Pulsecor R6.5 at rest and after treadmill exercise. Aerobic capacity was determined by measuring maximal oxygen consumption (VO2max) using the Moxus metabolic cart (AEI Technologies). Results: Both cAP and cAI at rest were associated with age (+10 years, cAP 3.1, 95%CI, 1.9 to 4.2 mmHg, p < 0.0001) and height (+10 cm, cAP −2.9, CI −4.4 to −1.5 mmHg, p < 0.0001). There was no association between cAI or cAP at rest and VO2max after adjusting for age and height (for VO2max + 1 mL/kg/m2, cAP 0.1, CI −0.08 to 0.28 mmHg, p = 0.26; cAI 0.3%, CI −0.03 to 0.6%, p = 0.08). Mean cAP decreased from 10.2 ± SD 7.7 at rest to 8.4 ± 6.5 immediately after exercise, 6.4 ± 6.0 five minutes, and 5.2 ± 3.7 mmHg ten minutes after exercise (p < 0.0001). Mean cAI decreased from 27 ± 13% at rest to 18 ± 10% immediately after exercise, 20 ± 11% five minutes, and 19 ± 10% after ten minutes (p < 0.0001). Both cAP and cAI decreased more during recovery in patients who exercised to a higher level as indicated by VO2max (p < 0.001). Conclusion: In CAD patients, increased physical fitness was not associated with central pressure augmentation at rest but was associated with a larger reduction in pressure augmentation after exercise.

Changes in Central Aortic Pressure, Endothelial Function and Biomarkers in Hypertensive African-Americans with the Cardiometabolic Syndrome: Comparison of Amlodipine/Olmesartan versus Hydrochlorothiazide/Losartan

Sixty-six self-identified African-American subjects with stage 1 and 2 hypertension and characteristics of the cardiometabolic syndrome were treated with amlodipine/olmesartan (A/O) versus losartan/hydrochlorothiazide (L/H) for 20 weeks in an open-label, active comparator fashion. Subjects not meeting a blood pressure (BP) value of <125/75 mm Hg on either regimen at week 14 were placed on additional or alternative therapy. After 20 weeks of therapy, systolic BP was reduced by 34.6 ± 4.2 mm Hg in the A/O group and by 27.0 ± 4.1 mm Hg in the L/H group (p = 0.012 A/O vs. L/H). Diastolic BP was reduced by 16.9 ± 2.0 mm Hg in the A/O group and by 12.3 ± 2.0 mm Hg in the L/H group (p = 0.022 A/O vs. L/H). There was a substantial increase in endothelial function of 44 and 103% in the L/H and A/O groups, respectively (p < 0.005 A/O vs. L/H). Central aorta augmentation pressure was significantly reduced by 42% with the A/O treatment, and a smaller, significant reduction of 28% was observed with the L/H treatment (p = 0.034 A/O vs. L/H). There was a reduction in sIL-6 levels of 20 and 33%, a reduction in serum leptin levels of 22 and 40%, and an increase in serum adiponectin of 19 and 46% in the L/H and A/O groups, respectively (p < 0.005 A/O vs. L/H for each biomarker). Treatment with A/O after 14 weeks reduced pulse wave velocity by 22% (p = 0.011 time comparison), whereas L/H treatment had no significant effect. Our findings suggest that, in addition to effective BP reduction, A/O differentially regulates markers of inflammation and obesity, thereby potentially providing greater vascular protection.