Changes In Brachial Blood Pressure Research Articles

Sex differences in aortic hemodynamics and associations with white matter hyperintensities in middle‐aged and older adults

Elevated blood pressure (BP) in midlife increases the risk of developing white matter hyperintensities (WMH) in the brain. WMH are associated with increased risk of cognitive decline and dementia. Structural changes of the large central arteries occur prior to changes in brachial BP. We have previously reported positive associations between aortic hemodynamics and WMH in normotensive postmenopausal women. The purpose of this study was to evaluate sex differences in aortic hemodynamics and associations with WMH burden in middle‐aged and older adults. Ninety‐nine participants (age = 63 ± 4y), including n = 35 men and n = 64 postmenopausal women participated in this study. Aortic hemodynamics were derived from radial artery pressure waveforms measured using applanation tonometry. Aortic systolic blood pressure (aSBP), aortic diastolic blood pressure (aDBP), augmented pressure (AP), aortic augmentation index (AIx), and aortic transit time were calculated. WMH lesion volume and intracranial volume (ICV) were measured using a FLAIR and T1 scan on a 3T MRI scanner, respectively. WMH fraction was calculated as (WMH lesion volume/ICV)*100 and cubic root transformed to reduce skewness. Age‐adjusted multiple linear regressions were used to determine the influence of aortic hemodynamics on WMH fraction. There were no sex differences in aSBP or aDBP. AP was greater in women compared with men (16 ± 5 mmHg vs. 11 ± 5 mmHg; P < 0.001). AIx was also greater in women compared with men (28 ± 6 % vs. 18 ± 9 %; P < 0.001). Aortic transit time was lower in women compared with men (140 ± 11 ms vs. 151 ± 12 ms; P < 0.001). There were no sex differences in WMH fraction. There was a positive association between aSBP and WMH fraction in both men (r = 0.37, P = 0.015) and women (r = 0.36, P = 0.017). In addition, aDBP was positively associated with WMH fraction in men (r = 0.47, P = 0.003) and women (r = 0.36, P = 0.017). AP was positively associated with WMH fraction in men (r = 0.34, P = 0.027), but not women (r = 0.24, P = 0.296). AIx was positively associated with WMH fraction in men (r = 0.46, P = 0.004), but not women (r = 0.22, P = 0.570). There were no significant associations between aortic transit time and WMH fraction. In conclusion, AP and AIx were greater in women compared with men. The positive associations between AP and WMH fraction and AIx and WMH fraction were only apparent in men. These findings suggest a sex‐specific association between augmented pressure and augmentation index and WMH burden in middle‐aged and older adults.

Do diurnal changes in blood pressure affect myocardial work indices?

Do diurnal changes in blood pressure affect myocardial work indices?

Altered Vascular Reactivity to Circulating Angiotensin II in Familial Hypercholesterolemia.

We have previously shown increased vascular reactivity to angiotensin (Ang) II in familial combined hyperlipidemia. However, this has not been well studied in familial hypercholesterolemia (FH), a condition with incipient endothelial dysfunction. This study aimed to examine microvascular and macrovascular responses to Ang II in FH. Therefore, we investigated the effects of a 3-hour infusion of Ang II on blood pressure and forearm skin microvascular function in 16 otherwise healthy patients with FH and matched healthy controls. Skin microvascular hyperemia was studied by laser Doppler fluxmetry during local heating. Microvascular resistance was determined by the ratio of mean arterial pressure to microvascular hyperemia. Macrovascular reactivity was assessed by changes in brachial blood pressure. Compared with the controls, the FH group had increased baseline systolic blood pressure (127 ± 14 vs. 115 ± 12 mm Hg; P = 0.02), while systolic blood pressure responses were similar (+24 ± 9 vs. +21 ± 7 mm Hg; P = 0.26) after 3 hours of Ang II infusion. At baseline, there were no group differences in microvascular hyperemia or resistance. However, after 3 hours of Ang II infusion, heat-induced microvascular hyperemia was less pronounced in FH (126 ± 95 vs. 184 ± 102 arbitrary units; P = 0.01), while microvascular resistance during heat-induced hyperemia was increased (1.9 ± 0.9 vs. 0.9 ± 0.8, P = 0.01), as compared to controls. Both these responses were further pronounced 1 hour after stopping Ang II. In conclusion, despite similar blood pressure responses to Ang II in the FH group and controls, microvascular dilatation capacity was impaired in the FH group, indicating endothelial dysfunction. These findings and increased microvascular resistance may lead to hypertension and microvascular complications in FH.

FOREARM VASCULAR RESPONSES TO MENTAL STRESS AND DEVICE GUIDED BREATHING ASSOCIATE WITH PLASMA CONCENTRATIONS OF NORMETADRENALINES IN SUBJECTS WITH ESSENTIAL HYPERTENSION

Objective: Forearm vasodilator responses to mental stress (MS) are impaired in hypertensive compared to normotensive individuals by a mechanism that may relate to peripheral alpha-adrenergic activity antagonising that of neuronal nitric oxide. We investigated whether the response to MS may be dependent on the level of basal sympathetic activity as measured by plasma concentrations of normetadrenaline (NM) and how responses to slowing respiratory rate by device guided breathing (DGB, which reduces sympathetic activity) vary according to NM concentrations. Design and method: Subjects with essential hypertension were stratified according to concentrations of plasma NM into those with low NM (< or = 500pmol/L) and high NM (> or = to 750pmol/L). Forearm blood flow (FBF) was measured by venous occlusion plethysmography after 15 minutes of rest, during MS elicited by the Stroop word-colour test and during supervised DGB with breathing rate < 10 breaths/minute. Results: Subjects with high NM (n = 30, 15 men) had greater body mass index than those with low NM (n = 30, 17 men): (mean ± SD) 31 ± 7 vs 27 ± 4 kg/m2 (P < 0.05), but the two groups were similar with respect to age and brachial blood pressure (BP). During MS and DGB, changes in BP were similar in subjects in both low NM and high NM groups. MS increased FBF in both groups but the response in high NM was impaired as compared to subjects with low NM (34 ± 3 vs. 49 ± 3 %, P < 0.05). DGB increased forearm vascular resistance to a lesser extent in subjects with high compared to low NM (1.21 ± 7.95 vs 5.50 ± 6.32 mmHg.100 mL/mL, P < 0.05). Conclusions: These results are consistent with greater sympathetic vascular tone in patients with higher NM that antagonises forearm vascular responses to MS. Circulating concentrations of NM may identify subjects with impaired neuronal nitric oxide signalling.

Would Oscillometry be Able to Solve the Dilemma of Blood Pressure Independent Pulse Wave Velocity - A Novel Approach Based on Long-Term Pulse Wave Analysis?

The utility of pulse wave velocity (PWV) as a surrogate parameter of arterial vessel damage (AVD) beyond the traditional brachial blood pressure (BP) measurement may be questioned as changes in BP are often accompanied by the corresponding changes in PWV. We sought to establish a new way for BP-independent estimation of AVD with PWV. We retrospectively analyzed data from 507 subjects with at least one available 24 h ambulatory BP- and pulse wave analysis, performed with Mobil-O-Graph (I.E.M., Stolberg, Germany). Individual relationship between eaPWV and central systolic BP (cSBP) was analyzed for every 24 h recording. The analysis revealed linear relation between eaPWV and cSBP in all subjects, which is described by equation eaPWV = a∗cSBP + b. We termed “a” as PWVslope and “b” as PWVbaseline. All available demographic parameters and clinical data were correlated with eaPWV, PWVslope and PWVbaseline. 108 subjects had repeated 24 h recordings. Mean age was 60.7 years and 48.7% were female. 92.5% had hypertension, 22.9% were smoker, 20.5% had diabetes mellitus and 29.6% eGFR < 60 ml/min/1,73 m2. Direct correlation was observed between age, SBP and eaPWV, while diastolic BP (DBP) and eGFR correlated inversely with eaPWV. PWVbaseline correlated directly with age and inversely with DBP, while PWVslope didn’t correlate with any inputted parameter. Using simple mathematical approach by plotting eaPWV and cSBP values obtained during ABPM, it is possible to visualize unique course of individual PWV related to BP. Using PWVslope and PWVbaseline as novel parameters could be a feasible way to approach BP-independent PWV, though their clinical relevance should be tested in future studies. Our data underline the importance of BP-independent expression of PWV, when we use it as a clinical surrogate parameter for the vascular damage.

PATTERN OF CHANGES OF CENTRAL BLOOD PRESSURE AND VOLUME DEPENDENT ECHOCARDIOGRAPHIC PARAMETERS IN MONITORING OF NORMOTENSIVE PREGNANCY

Objective: We investigated changes of brachial and central blood pressure (BP) as well as volume dependent echocardiographic parameters in different time points of pregnancy.Design and method: Data from 60 healthy pregnant women (mean age 31.4 ± 4.3 years) were analysed. Hypertensive women were excluded from the study. In all women complete echocardiographic study, brachial and central BP measurements were performed at 11–13, 20–22 and 30–32 weeks of pregnancy. Central and brachial BP was measured by Pulsecor (CardioScope) device. In echocardiography: left ventricle end diastolic volume (LVEDV), early diastolic peak flow velocity (E velocity), late diastolic peak flow velocity (A velocity), left atrium area (LAA) and left atrium volume index (LAVI) were assessed. Also E/A index was calculated. Results: Brachial systolic BP (SBP) was higher and brachial diastolic BP (DBP) was lower as compared to respectively central SBP and central DBP at all three time points (p < 0.0001- for each). Brachial and central SBP and DBP levels were higher at 11–13 as compared to 20–22 weeks, but no difference was found between 20–22 and 30–32 weeks (Table). There was a significant increase of LAVI between all three-time points. LVEDV and LAA increased between 11–13 and 20–22 weeks but not between 20–22 and 30–32 weeks. Significant decrease in E velocity between 20–22 and 30–32 weeks was observed. There were no differences in E/A between subsequent measurements (Table). There were no significant differences in heart rate between time points. Conclusions: Our results indicate that LAVI is the best echocardiographic parameter reflecting physiological changes in blood volume overload in normal uncomplicated pregnancy. We also observed that changes in brachial BP were consistent with changes in central BP. Brachial BP and LAVI are sufficient parameters in monitoring physiological pregnancy.

Post-exercise effects on aortic wave reflection derived from wave separation analysis in young-to middle-aged pre-hypertensives and hypertensives.

Decreases in brachial blood pressure (BP) may occur for several hours following a bout of exercise. Although aortic backward waves predict cardiovascular damage independent of brachial BP, whether decreases in aortic backward waves also occur post-exercise in young-to-middle-aged hypertensives, the extent to which these changes exceed brachial BP changes, and the best method of identifying these changes is uncertain. We examined aortic function at baseline and 15-min post-exercise in 20 pre-hypertensive or hypertensive men and women (age 45±7years). Central aortic pressure, forward (Pf) and backward (Pb) wave pressures, the reflection index (RI) and augmentation pressure (AP) and index (AIx) were determined using applanation tonometry, and SphygmoCor software. Decreases in central aortic (p<0.001) but not brachial systolic BP and pulse pressure (PP) occurred post-exercise. In addition, decreases in post-exercise (baseline versus post-exercise) Pb (19±4 vs 13±3mm Hg p<0.0001), RI (72.9±22.1 vs 47.6±12.8%, p<0.0001), AIx (26.3±10.8 vs 7.8±11.6%, p<0.0001) and AP (9.9±3.9 vs 2.8±3.9mm Hg, p<0.0001), but not Pf, were noted. However, decreases in AIx were not correlated with decreases in Pb, and whilst decreases in aortic PP correlated with decreases in Pb (p<0.0001), no correlations were noted with decreases in AP or AIx. In young-to-middle-aged pre-hypertensive and hypertensive individuals, aortic backward waves decrease post-exercise; this change is not reflected in brachial BP measurements and is poorly indexed by measures of pressure augmentation.

Relation Between Exercise Central Hemodynamic Load and Resting Cardiac Structure and Function in Young Men

Left ventricular (LV) structure and function are predictors of cardiovascular mortality and related to resting peripheral hemodynamic load in older adults. The central hemodynamic response to exercise may reveal associations with LV structure and function not detected by traditional peripheral (brachial) measures in a younger population. PURPOSE: Examine correlations between acute exercise-induced changes in brachial blood pressure (BP), arterial stiffness and wave reflections and measures of resting LV structure and function. METHODS: 16 healthy men (age 26 ± 6 yr; BMI 25.3 ± 2.7 kg·m-2) had measures of central hemodynamic load measured pre/post a 30 second Wingate anaerobic test (WAT). Brachial systolic BP and carotid systolic BP were assessed using an automated cuff and applanation tonometry, respectively. Carotid artery stiffness and reflected wave intensity were assessed as the elastic modulus (Ep) and negative area (NA) from Doppler-ultrasound and wave intensity analysis. Resting LV structure (LV mass) and function (fractional shortening, FS) were assessed using M-mode echocardiography in the parasternal short-axis view. RESULTS: There were significant inverse associations between resting FS and WAT-induced increase in: carotid systolic BP (r = -0.54, p = 0.04), logNA (r = -0.53, p = 0.02) and Ep (r = -0.45, p = 0.04). There were no significant associations between resting FS and increases in brachial systolic BP (r = -0.38, p > 0.05) or between resting LV mass and increases in any hemodynamic variable (p > 0.05). CONCLUSION: Exercise-induced increases in central hemodynamic load reveal associations with resting LV function undetected by traditional peripheral hemodynamics. Changes in LV function may precede changes in LV structure offering insight into lack of associations between central hemodynamic load and LV mass in young healthy men.

Differential responses in brachial and ankle blood pressure during blood pressure reactivity tests

Blood pressure (BP) reactivity has been assessed by a variety of stimuli, including physical, psychological, and physiological perturbations, that can be further classified into cardiac or vascular in regard to the effector organs. In many BP reactivity studies, changes in brachial BP are taken as systemic changes and are combined with leg measurements to assess vasoactive states. Currently, it is unknown if leg BP behaves similarly to arm BP.PurposeWe compared BP changes between the brachial and post‐tibial arteries during acute BP perturbations.MethodsThirty apparently healthy subjects (57% males, 46±4 years) were studied. Both brachial and ankle systolic BP (SBP) were measured simultaneously with the oscillometric technique during resting baseline, head‐up tilt (HUT), head‐down tilt (HDT), mental stress (MS), isometric hand‐grip exercise (HG), and a cold pressor test (CPT).ResultsBrachial (bSBP) and ankle (aSBP) SBP at rest were significantly and highly correlated (r=0.81). Changes in bSBP were significantly and positively associated with changes in aSBP in response to HUT (r=0.46), HDT (r=0.53), MS (r=0.70), HG (r=0.63), and CPT (r=0.75). The magnitudes of bSBP and aSBP changes were not different n response to MS, HG, and CPT since all were within 5 mmHG. There were significant differences in the magnitude of changes in bSBP and aSBP in response to HDT (12±1 mmHg) and HUT (40±2 mmHg).ConclusionBoth brachial and ankle BP respond similarly in many vascular reactivity maneuvers. During head‐down and head‐up tilt, however, differences in their responses may be quite large, presumably due to the hydrostatic pressure gradients created during the maneuvers.Supported by Fukuda Denshi.

Spironolactone to prevent cardiovascular events in early-stage chronic kidney disease (STOP-CKD): study protocol for a randomized controlled pilot trial.

BackgroundChronic kidney disease is associated with increased arterial stiffness even in the early stages and this is thought to be a key mediator in the pathophysiology of the increased cardiovascular risk associated with this condition. The use of low-dose spironolactone has previously been shown to improve arterial stiffness and reduce left ventricular mass safely in early-stage chronic kidney disease in the context of careful monitoring at a university hospital. However, the majority of patients with chronic kidney disease are managed by their general practitioners in the community. It is not known whether similar beneficial effects can be achieved safely using spironolactone in the primary care setting. The aim of this study is to determine whether low-dose spironolactone can safely lower arterial stiffness in patients with stage 3 chronic kidney disease in the primary care setting.Methods/designSTOP-CKD is a multicentre, prospective, randomized, double-blind, placebo-controlled pilot trial of 240 adult patients with stage 3 chronic kidney disease recruited from up to 20 general practices in South Birmingham, England. Participants will be randomly allocated using a secured web-based computer randomization system to receive either spironolactone 25 mg once daily or a matching inactive placebo for 40 weeks, followed by a wash-out period of 6 weeks. Investigators, outcome assessors, data analysts and participants will all be blinded to the treatment allocation. The primary endpoint is improved arterial stiffness, as measured by carotid-femoral pulse wave velocity between baseline and 40 weeks. The secondary endpoints are incidence of hyperkalaemia, change in estimated glomerular filtration rate, change in urine albumin:creatinine ratio, change in brachial blood pressure, change in pulse waveform characteristics and overall tolerability of spironolactone. An additional quality control study, aiming to compare the laboratory serum potassium results of samples processed via two methods (utilizing routine transport or centrifugation on site before rapid transport to the laboratory) for 100 participants and a qualitative research study exploring patients’ and general practitioners’ attitudes to research and the use of spironolactone in chronic kidney disease in the community setting will be embedded in this pilot study.Trial registrationCurrent Controlled Trials ISRCTN80658312.

Effect of whole-body mild-cold exposure on arterial stiffness and central haemodynamics: a randomised, cross-over trial in healthy men and women

Aortic pulse wave velocity (PWV) and augmentation index (AIx) are independent predictors of cardiovascular risk and mortality, but little is known about the effect of air temperature changes on these variables. Our study investigated the effect of exposure to whole-body mild-cold on measures of arterial stiffness (aortic and brachial PWV), and on central haemodynamics [including augmented pressure (AP), AIx], and aortic reservoir components [including reservoir and excess pressures (P ex)]. Sixteen healthy volunteers (10 men, age 43 ± 19 years; mean ± SD) were randomised to be studied under conditions of 12 °C (mild-cold) and 21 °C (control) on separate days. Supine resting measures were taken at baseline (ambient temperature) and after 10, 30, and 60 min exposure to each experimental condition in a climate chamber. There was no significant change in brachial blood pressure between mild-cold and control conditions. However, compared to control, AP [+2 mmHg, 95 % confidence interval (CI) 0.36-4.36; p = 0.01] and AIx (+6 %, 95 % CI 1.24-10.1; p = 0.02) increased, and time to maximum P ex (a component of reservoir function related to timing of peak aortic in-flow) decreased (-7 ms, 95 % CI -15.4 to 2.03; p = 0.01) compared to control. Yet there was no significant change in aortic PWV (+0.04 m/s, 95 % CI -0.47 to 0.55; p = 0.87) or brachial PWV (+0.36 m/s; -0.41 to 1.12; p = 0.35) between conditions. We conclude that mild-cold exposure increases central haemodynamic stress and alters timing of peak aortic in-flow without differentially affecting arterial stiffness.

Effect of beta-1-blocker, nebivolol, on central aortic pressure and arterial stiffness in patients with essential hypertension

Introduction:Blood pressure (BP) reduction is the major determinant of benefit provided by antihypertensive treatment. Although different drugs reduce peripheral BP to some extent, there may be a significant difference in their effect on central BP reduction. It has been shown that beta-blockers are efficient in reducing peripheral, but not central BP. This study was done to assess the effect of beta-1-blocker, nebivolol, in patients with essential hypertension on central aortic pressures and arterial stiffness.Materials and Methods:In this single arm, open-labeled study, 13 patients were given nebivolol, 5 mg orally once daily for 15 days. Primary outcome was change in central aortic pressure, and other measures of efficacy included changes in brachial BP, augmentation index (AIx%), AIx%@75 HR, augmentation pressure (AP), heart rate (HR), and carotid femoral pulse wave velocity (PWVcf).Results:Nebivolol 5 mg significantly reduced central aortic pressures [systolic BP, 131.5–111.6 mmHg; diastolic BP, 96.3–81.7 mmHg; Mean Arterial Pressure (MAP), 111.3–94.0 mmHg (all P<0.0001), and Pulse Pressure (PP), 35.2-29.7 mmHg (P<0.01)]. AIx%@75 HR reduced from 29 to 21.6 (P<0.001) and PWVcf reduced from 8.6 to 7.2 m/s (P<0.001). One subject was lost to followup.Conclusion:Nebivolol 5 mg demonstrated antihypertensive efficacy in patients with essential hypertension by reducing not only peripheral brachial pressures, but also significantly reducing central aortic pressures, augmentation index, and carotid femoral pulse wave velocity, which is the marker of arterial stiffness.

Central and 24-h blood pressure: dwarfs standing upon the shoulders of giants?

Central and 24-h blood pressure: dwarfs standing upon the shoulders of giants?

High dietary salt intake increases carotid blood pressure and wave reflection in normotensive healthy young men

Dietary salt intake is associated with high brachial blood pressure (BP) and increased risk of cardiovascular disease. We investigated whether changes in dietary salt intake are associated with changes in central BP and wave reflection in healthy volunteers. Ten healthy normotensive male volunteers (22-40 yr) participated in a 6-wk double-blind randomized crossover study to compare a low-dietary salt intake (60-80 mmol sodium/day) with a high-salt intake (low salt intake supplemented with 128 mmol sodium/day) on central BP and wave reflection. Brachial and carotid BP, carotid blood flow velocity, forward (P(f)) and backward (P(b)) pressure, wave intensity, body weight, and urinary electrolyte excretion were measured at the end of each crossover period. High salt intake significantly increased carotid systolic BP [98 (SD 11) vs. 91 mmHg (SD 13), P < 0.01] and increased wave reflection [ratio of backward to forward pressure (P(b)/P(f)) 0.13 (SD 0.02) vs. 0.11 (SD 0.03), P = 0.04] despite only small effects on brachial BP [114 (SD 9) vs. 112 mmHg (SD 6), P = 0.1]. Urinary sodium excretion and body weight were also increased following high salt intake. High salt intake disproportionately increases central BP compared with brachial BP as a result of enhanced wave reflection. These effects may contribute to the adverse effect of high dietary salt intake on the risk of cardiovascular disease.

Combination Therapy of Calcium Channel Blocker and Angiotensin II Receptor Blocker Reduces Augmentation Index in Hypertensive Patients

The optimal combination treatment for hypertension has not been established. We investigated the effect of a calcium channel blocker or a diuretic added to angiotensin II receptor blockers (ARBs) on the augmentation index (AI), as a marker of arterial stiffness and wave reflection, in hypertensive patients. Thirty-seven patients treated with ARBs were randomly allocated to either of the 2 groups receiving an ARB plus azelnidipine (AZ group) or trichlormethiazide (TCM group). Changes in brachial blood pressure (BP), AI, high-sensitive C-reactive protein (hsCRP), and serum asymmetric dimethylarginine, as an endogenous nitric oxide synthase inhibitor, were determined. Systolic and diastolic blood pressure after 6 months were significantly reduced in both the groups similarly; however, after adjustment for baseline covariates, the extent of the reduction in AI (%) in the AZ group was significantly greater than in the TCM group (between-group difference was 3.2; 95%CI: 0.2-6.3; P = 0.03). The reduction of high-sensitive C-reactive protein (mg/L) and serum asymmetric dimethylarginine (micromol/L) was significantly greater in the AZ group than in the TCM group (between-group difference was 0.18 and 0.05; 95%CI: -0.01 to 0.36 and -0.01 to 0.11; P = 0.04 and 0.02, respectively). Further, when patients were analyzed according to age younger than 60 years or older than 60 years, the reduction in AI in the AZ group aged older than 60 years was significantly greater than in the TCM group. The results suggest that azelnidipine has a more beneficial effect on vascular properties in combination therapy with ARB than trichlormethiazide.

Mechanism(s) of Systolic Blood Pressure Reduction and Drug Therapy in Hypertension

Antihypertensive drug therapy is a major modality of cardiovascular (CV) disease prevention, especially for stroke, congestive heart failure, and renal insufficiency. Coronary risk is also consistently prevented by antihypertensive treatment, but to a lesser extent.1–4 The Prime Study2 has shown that drug-induced blood pressure (BP) reduction in hypertensive subjects is associated with a significant decrease of coronary risk. However, when treated and untreated subjects are compared, at any given value of systolic BP (SBP), this risk remains higher in treated than in untreated subjects, suggesting the persistence of residual coronary complications. Results of therapeutic trials also indicate that coronary risk is associated with a particular hemodynamic pattern in treated hypertensive subjects.3 Although diastolic BP (DBP) is significantly lowered by drug treatment to <90 mm Hg (80% of the patients), SBP remains above 140 mm Hg in 60%, indicating an increase of pulse pressure (PP), which is the difference between SBP and DBP.4 It is widely accepted that SBP and PP rise sharply with age and that this increase is a major manifestation of vascular aging and stiffening, which are now considered major predictors of CV risk, independent of the mean BP (MBP) level.4 The purpose of this review is to analyze the mechanism(s) of SBP in untreated and chronically treated hypertensive subjects and to determine which pathophysiological factors are susceptible to attenuating consistently coronary and CV complications in hypertensive populations. Ventricular ejection in humans is associated with 2 principal events. First, the coronary circulation is transiently interrupted, as the principal consequence of cardiac contraction, and, second, an acute shock of stroke volume against the aortic wall is observed (Figure 1). Then, the BP curve may be considered as a wave, which travels along the arterial tree at a given speed, the pulse wave velocity (PWV). …

Indices of Pulse Wave Analysis Are Better Predictors of Left Ventricular Mass Reduction Than Cuff Pressure

Studies have required large numbers of patients to associate regression of left ventricular (LV) mass with a decrease in brachial cuff blood pressure (BP) in the treatment of hypertension. Hence, we prospectively examined potential superiority of pulse wave analysis over conventional BP measurement in predicting treatment-induced LV mass reduction. Forty-six untreated patients (mean age, 56 +/- 7 years) with hypertension received standard medical treatment based on international guidelines. Echocardiography and measurements of various LV load indices were made before and after 1 year of treatment. Antihypertensive treatment significantly (P < .05) reduced LV load, manifest by a decrease in measured brachial BP, estimated aortic BP, carotid-femoral pulse wave velocity (PWV(cf)), aortic augmentation index (AI(a)), aortic augmented pressure (AugP), and radial augmentation index (AI(r)). These changes were accompanied by significant reduction in LV mass index (LVMI) and improvements in systolic ejection fraction and diastolic early-to-atrial ratio of transmitral flow velocities. The treatment-induced LVMI change was not correlated with changes in brachial BP or PWV(cf), but was closely correlated with factors influenced by wave reflection - changes in AI(a), AI(r), AugP, and aorta-to-arm pulse pressure amplification. On multivariate analysis, AI(a) change was the strongest determinant of LVMI change, independent of brachial BP and PWV(cf) changes (beta = 0.51, P < .001). Estimated subject numbers required for predicting a significant LVMI reduction were far less when wave reflection-related factors were used rather than conventional bracial BP. These results suggest that reduction in wave reflection is an important therapeutic strategy for reducing LV mass, which can be predicted with modest subject numbers.

Resistance training increases basal limb blood flow and vascular conductance in aging humans

Age-related reductions in basal limb blood flow and vascular conductance are associated with the metabolic syndrome, functional impairments, and osteoporosis. We tested the hypothesis that a strength training program would increase basal femoral blood flow in aging adults. Twenty-six sedentary but healthy middle-aged and older subjects were randomly assigned to either a whole body strength training intervention group (52 +/- 2 yr, 3 men, 10 women) who underwent three supervised resistance training sessions per week for 13 wk or a control group (53 +/- 2 yr, 4 men, 9 women) who participated in a supervised stretching program. At baseline, there were no significant differences in blood pressure, cardiac output, basal femoral blood flow (via Doppler ultrasound), vascular conductance, and vascular resistance between the two groups. The strength training group increased maximal strength in all the major muscle groups tested (P < 0.05). Whole body lean body mass increased (P < 0.05) with strength training, but leg fat-free mass did not. Basal femoral blood flow and vascular conductance increased by 55-60% after strength training (both P < 0.05). No such changes were observed in the control group. In both groups, there were no significant changes in brachial blood pressure, plasma endothelin-1 and angiotensin II concentrations, femoral artery wall thickness, cardiac output, and systemic vascular resistance. Our results indicate that short-term strength training increases basal femoral blood flow and vascular conductance in healthy middle-aged and older adults.

Letter by Cameron et al Regarding Article, “Differential Impact of Blood Pressure-Lowering Drugs on Central Aortic Pressure and Clinical Outcomes: Principal Results of the Conduit Artery Function Evaluation (CAFE) Study”

To the Editor: We read with interest the report of the Conduit Artery Function Evaluation (CAFE) study1 showing a difference in SphygmoCor-derived central systolic blood pressure (SBP) between the 2 arms of an Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT) substudy (despite similar brachial blood pressure changes). We would make 3 points. First, the authors seem to have misinterpreted our work (authors’ Reference 53)2 as showing a “precision” of 1 mm Hg between calculated central aortic and directly measured SBP in the context of noninvasive studies. This figure relates to …

Orthostatic Systolic Hypotension and the Reflection Pressure Wave

Orthostatic hypotension (OH) is a potent predictor of cardiovascular frailty. Although OH is determined by changes in brachial blood pressure (BP), it has been reported that there are significant differences between central BP and peripheral BP. The prevalence of OH has been reported to be higher in subjects with isolated systolic hypertension. Since an early returning of the reflection pressure wave due to advanced arterial stiffness is one of the underlying mechanisms of systolic hypertension, a significant association between alterations of the reflection pressure wave and OH has been hypothesized. To explore this hypothesis, the orthostatic changes in carotid BP and arterial waveform were evaluated. The study subjects were 155 community residents (69 +/- 7 years old). Carotid and brachial BP were measured simultaneously in the supine position and 1 min after standing using a cuff-oscillometric and tonometric method. The carotid augmentation index (AIx) was obtained from the pressure waveform. The orthostatic decline of BP was more prominent in the carotid artery than the brachial artery. Nine subjects were diagnosed with orthostatic systolic hypotension (OSH) from brachial BP, while 21 subjects were diagnosed from carotid BP (p < 0.001). The orthostatic change in carotid systolic BP was significantly associated with that in carotid AIx (r = 0.361, p < 0.001). The decline of the reflection component of carotid pulse pressure (-4.0 +/- 8.4 mmHg) was more prominent than that of the incident component (-1.2 +/- 9.9 mmHg, p = 0.002). These results indicate that evaluation of brachial BP may not represent the orthostatic changes in central BP. Alteration of the reflection pressure wave could be one of the underlying mechanisms of OSH in the central artery.