Conduit Artery Function Evaluation Research Articles

Hydrochlorothiazide--Teaching an Old Drug New Tricks.

Hydrochlorothiazide--Teaching an Old Drug New Tricks.

Beta-Blockers Lose Luster for Hypertension Therapy

Beta-Blockers Lose Luster for Hypertension Therapy

Editorial: Do We Have Effective Means to Treat Arterial Stiffness and High Central Aortic Blood Pressure in Patients with and without Hypertension?

The reduction or loss of arterial elasticity or distensibility leads to arterial stiffness (AS), which has a substantial predictive value for all-cause and cardiovascular disease (CVD) mortality, as well as for non-fatal CVD events [1]. A plethora of evidence consistently showed the prognostic value of aortic stiffness for fatal and nonfatal CVD events in various populations at different levels of CVD risk, including the general population, elderly subjects and patients with hypertension, type 2 diabetes mellitus (T2DM) and end-stage renal disease (ESRD) [2]. It has been reported that 1-SD increase in pulse wave velocity (PWV) is associated with a 47% increase in the risk for total mortality [95% confidence interval (CI), 1.31-1.64] and a similar 47% increase in the risk for CVD mortality (95% CI, 1.29-1.66) [2].

Blood pressure and retinal small arteries

Blood pressure and retinal small arteries

144 THE POTENTIAL OF SUBJECT-ADAPTIVE CENTRAL SYSTOLIC BLOOD PRESSURE ESTIMATION USING A RECURSIVE LOWPASS FILTER AND MULTIPLE LINEAR REGRESSION

Objectives: Central blood pressure(CBP) is strongly related to cardiovascular diseases(1–3). The aim of this study was to develop a novel algorithm that was subject-adaptive for central systolic blood pressure(CSBP) and confirm its potential significance. Design and methods: We analyzed the data from 2,048 subjects (aged 47–17, 1177 males, 871 females) with SphygmoCor(AtCor, AU) measurements from the Cardiovascular hospital at Yonsei University. A recursive lowpass filter(RLPF) was used to estimate the CSBP, and its equation is as follows: eCBP(t)=α×eCBP(t-1)+(1-α)×PBP(t), where eCBP(t) and PBP(t) are the estimated CBP and peripheral blood pressure in time(t); α is the filter-coefficient which affects the filter characteristics. We calculated the optimal α which has a minimum difference between the CSBP in the SphygmoCor(GTF-CSBP) and the eCSBP, and the prediction equation for α was developed through multiple linear regression(forward stepwise regression) with subject and PBP information. The equation is as follows: αest=1.046+0.001×(0.078×Pulse area/HR-33.038×Harmonic ratio-0.936×PP-0.145×Age +0.623×Weight+0.103×pAIx-1.605×BMI-0.423×Height+1.056×PSBP-0.012×Pulse area-0.44×HR+24.452×PP/HR). The parameters were the Harmonic ratio(1st harmonic/(2nd+3rd +4th+5th harmonic), heart-rate(HR), pulse pressure(PP), body mass index(BMI), peripheral AIx(pAIx), and peripheral systolic blood pressure(PSBP). We applied the αest to the RLPF, and the performance of the proposed method was evaluated through the correlation and Bland-Altman plot between GTF-CSBP and eCSBP. Results: The proposed method had a good correlation coefficient of 0.996(p<0.001) with GTF-CSBP and a difference between GTF-CSBP and eCSBP of -0.023±0.874 mmHg. Comparison of GTF-CSBP and eCSBP showed agreement in the Bland-Altman plots. Conclusions: This study shows that the CSBP can be estimated with the proposed subject-adaptive algorithm.References Roman MJ, Devereux RB, Kizer JR, Lee ET, Galloway JM, Ali T, et al. Central pressure more strongly relates to vascular disease and outcome than does brachial pressure: the Strong Heart Study. Hypertension. 2007;50(1):197–203. Epub 2007/05/09. Williams B, Lacy PS, Thom SM, Cruickshank K, Stanton A, Collier D, et al. Differential impact of blood pressure-lowering drugs on central aortic pressure and clinical outcomes: principal results of the Conduit Artery Function Evaluation (CAFE) study. Circulation. 2006;113(9):1213–25. Epub 2006/02/16. Williams B, Lacy PS. Central haemodynamics and clinical outcomes: going beyond brachial blood pressure? Eur Heart J. 2010;31(15):1819–22. Epub 2010/05/18.

Role of Elevated Heart Rate in the Development of Cardiovascular Disease in Hypertension

That elevated heart rate (HR) is a risk factor for cardiovascular morbidity and mortality in healthy people as well as in patients with cardiac diseases is supported by numerous epidemiological association studies.1–4 Increased HR has been recognized as a negative prognostic factor independent of many other clinical parameters that can influence the HR, including physical activity scores, left ventricular function, or use of β-blockers. Thus, HR appears to satisfy all epidemiological criteria for being considered as a true risk factor, and its predictive value for cardiovascular disease appeared to be as strong as that of most important cardiovascular risk factors. This is particularly true for the results obtained in hypertensive patients. Elevated HR is a common feature among hypertensive individuals.1 Among the young hypertensive subjects participating in the HARVEST study, >15% had a baseline resting HR ≥85 bpm and 27% had a HR ≥80 bpm.5 According to the Tensiopulse study, which evaluated 38 145 patients cared for by 2000 general practitioners all across Italy, >30% of the hypertensive patients had a resting HR ≥80 bpm.6 In a large French population, untreated hypertensive subjects had approximately a 6-bpm faster HR than normotensive individuals.7 Elevated HR is frequently associated with high blood pressure (BP) and metabolic disturbances and increases the risk of new onset hypertension and diabetes.1 Many experimental data obtained both in animals and in human beings support the importance of HR as a true risk factor for atherosclerosis and cardiovascular disease, providing convincing evidence for this pathogenetic mechanism.1–3 The pathogenetic connection between HR and cardiovascular disease has been discussed in several reports1–3,8,9 and is beyond the scope of this review. ### High HR as a Precursor of Hypertension, Obesity, and Diabetes Numerous studies have demonstrated that tachycardia is frequently associated with hypertension in …

Keeping Your Arteries Young: Vascular Health

quoted saying ‘‘you’re only as old as your arteries.’’ 4 At a pathobiological level, aortic wall stiffness has been associated with processes involving wall matrix, inflammation, and mechanical stress. Increased collagen content and extracellular matrix (arteriosclerosis) is commonly seen in hypertension and aging. In contrast, atherosclerosis relates to endovascular inflammation, increased cellular oxidative stress, and plaque formation; however, both processes can lead to increased vascular stiffness. 5 Patients with increased aortic stiffness have increased aortic pulse wave velocity and reduced arterial compliance. 6 The clinical implication of increased aortic stiffness results in increased afterload on the left ventricle; alteration in coronary perfusion, which affects cardiac diastolic relaxation; and increased myocardial oxygen consumption. Moreover, these surrogates have been tested in multiple trials with important CV outcomes data. Based on the studies so far, it is evident that increased aortic pulse wave velocity is a strong independent predictor of CV risk, regardless of whether it plays a causative role in CV risk or merely serves as a marker of CV disease already present. One example is found in the Strong Heart Study, 7 which evaluated 2405 patients without CV disease at entry with a 5-year follow-up. During this period, 344 patients had CV events that were significantly associated with high central pulse pressure, thus associating high central pulse pressure with increased arterial stiffness. 1 Another study, the Conduit Artery Function Evaluation (CAFE) trial 8 substudy (on behalf of the Anglo-Scandinavian Cardiac Outcomes Trial [ASCOT] Investigators), evaluated the differential impact of BPlowering drugs on central aortic pressure and clinical outcomes. The study enrolled 2073 patients from 5 ASCOT centers after being on treatment for about 1 year. A total of 19,257 patients were enrolled in the ASCOT trial. All patients had hypertension and 3 additional risk factors. They were randomized in a 2 2 factorial design to receive 1 of 2 antihypertensive regimens: amlodipine (5 ⁄10 mg) with or without perindopril (4 ⁄8 mg) or atenolol (50 ⁄100 mg) with or without a diuretic. Despite similar brachial arm systolic BPs in the two treatment arms, there was a significant decrease in both central aortic pulse pressure and central aortic systolic pressure in the angiotensin-converting enzyme (ACE) inhibitor ⁄calcium channel blocker (CCB) arm vs the b-blocker ⁄diuretic arm. This study suggested that ACE inhibitor ⁄CCB treatment was significantly better. In addition, using the Cox proportional hazards modeling, they determined that central aortic pulse pressure was significantly associated with a post hoc‐defined composite outcome of total CV events (unadjusted P<.0001; P<.05 after adjustment for baseline variables). Based on these data, it can be inferred that arterial stiffness and its components do affect CV outcomes. The vascular etiologies of these vessel wall changes require a closer look.

Efficacy of Sevikar® compared to the combination of perindopril plus amlodipine on central arterial blood pressure in patients with moderate-to-severe hypertension: Rationale and design of the SEVITENSION study

Background and rationale To date, few studies have investigated the effects of combined renin-angiotensin system blockade/calcium channel blockade on central aortic blood pressure. The Conduit Artery Function Evaluation (CAFE) sub-study of the Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT) investigated the effects of amlodipine/perindopril and atenolol/bendroflumethiazide on central aortic blood pressure (CABP). Similar brachial blood pressure levels were achieved; however, there was a significant difference, in favor of the amlodipine/perindopril combination, on the effects of CABP. No study has investigated the effects of a combination of an angiotensin receptor blocker/calcium channel blocker compared to those of a calcium channel blocker/angiotensin-converting enzyme inhibitor combination. To confirm and support previous findings, the SEVITENSION study will assess the effects on CABP of treatment with the high dose combination of perindopril plus amlodipine as used in ASCOT–CAFE compared with the high dose combination of olmesartan/amlodipine in patients with moderate-to-severe hypertension uncontrolled on amlodipine monotherapy. Objective To demonstrate non-inferiority of fixed-dose olmesartan/amlodipine combination therapy compared with the combination of perindopril plus amlodipine on the mean change from baseline in central aortic systolic blood pressure. Design A multicenter, double-blind, parallel-group, non-inferiority study comprising a 2–4-week open-label run-in period with amlodipine and a 24-week active treatment period. CABP will be measured by the SphygmoCor® Vx Pulse Wave Velocity System. Patients 720 moderate-to-severe hypertensive patients aged ≥ 40 to ≤ 80 years and ≥ 3 additional risk factors will be enrolled. Interventions Study treatment will comprise orally-administered combination of olmesartan/amlodipine (40/10 mg) or perindopril (8 mg) plus amlodipine (10 mg), and matching placebos. (EudraCT number: 2009-012966-30; ClinicalTrials.gov identifier: NCT01101009).

Development and Validation of a Novel Method to Derive Central Aortic Systolic Pressure From the Radial Pressure Waveform Using an N-Point Moving Average Method

The purpose of this study was to develop and validate the novel application of a simple n-point moving average (NPMA)--a mathematical low pass filter--to noninvasively derive central aortic systolic pressure (CASP) from the radial artery pressure waveform (RAPWF) in humans. CASP may be an important independent determinant of clinical outcomes. Development of simple, well-validated methods to noninvasively derive CASP is necessary to facilitate the routine clinical measurement of CASP. Three studies in different population cohorts were used to develop and validate the NPMA method to derive CASP in humans: 1) a development study (n = 217), describing the optimal application of the NPMA to derive CASP; 2) a validation study comparing NPMA-CASP with CASP derived using a generalized transfer function (GTF-CASP [SphygmoCor system, AtCor, Sydney, Australia]) using 5,349 RAPWFs from the CAFE (Conduit Artery Function Evaluation) study; and 3) an invasive validation study (n = 20) comparing NPMA-CASP with direct aortic root pressure measurements during cardiac catheterization. In the development study, when using the NPMA, a denominator of n/4 (where n = tonometer sampling frequency) most accurately defined CASP relative to GTF-CASP. Validation of NPMA-CASP using RAPWFs from the CAFE study revealed excellent correlation and agreement (r(2) = 0.993, mean difference 0.3 ± 1.0 mm Hg). The agreement remained robust after stratification by sex, age, treatment, and diabetes status. There was also excellent correlation and agreement (r(2) = 0.98, p < 0.001) between directly measured aortic root systolic pressures (Millar's catheter) at cardiac catheterization versus NPMA-CASP, derived simultaneously from noninvasive RAPWFs. We show that an NPMA with a denominator of one-quarter of the tonometer sampling frequency accurately defines CASP when applied to noninvasively acquired RAPWFs in man. These novel findings have important implications for the simplification of noninvasive CASP measurement and its wider application in clinical trials and clinical practice.

Arterial stiffening in hypertension: beyond blood pressure levels

Uncontrolled hypertension confers a major risk factor of death worldwide with at least 25% of the world's adult population having elevated arterial blood pressure.1 Hypertension is strongly associated with damage of the vasculature and target organs, leading to cardiovascular and renal disease. Progressive remodelling and impairment of elastic properties of conduit arteries represent a characteristic feature of hypertension strongly associated with unfavourable prognosis. Not surprisingly, the results of the Conduit Artery Function Evaluation (CAFE) study suggest that arterial function may be a useful treatment target in hypertension.2

Central Blood Pressure Under Angiotensin and Calcium Channel Blockade

Hemodynamic studies have shown that, in healthy subjects, there is a gradual widening of the height of the pressure waveform as it travels from the central (aortic) elastic arteries to the peripheral muscular arteries (brachial artery)1 (Figure). This disparity, which tends to disappear in the presence of vascular disease/aging, does not require any additional energy input within the arterial system, because the mean arterial pressure (MAP) and even the diastolic blood pressure (BP) remain almost unchanged between the 2 arterial sites. This finding is mainly attributed to the gradual increase (ie, amplification) of systolic BP (SBP) or pulse pressure (PP) along the arterial tree and is conventionally quantified as the ratio of the SBP or PP between the 2 sites (eg, SBP arm:SBP aorta)1 (Figure). Figure. Schematic personal representation of the forward and reflected pressure waves in the aorta and the influence of their timing on local PP. The definition of SBP amplification is indicated. In the present issue of Hypertension , Matsui et al2 have shown the superiority of calcium channel blockers (CCBs) over diuretics using the following protocol: the angiotensin receptor blocker olmesartan was combined with the CCB azelnidipine and compared with the same olmesartan associated with the diuretic hydrochlorothiazide. Central SBP was reduced to a greater degree with the CCB than with the hydrochlorothiazide. This resulted in an increase of SBP and PP amplification with the CCB, despite the lack of a significant difference in the brachial SBP reduction between the 2 …

Impact of Heart Rate on Central Aortic Pressures and Hemodynamics: Analysis From the CAFE (Conduit Artery Function Evaluation) Study: CAFE-Heart Rate

The CAFE (Conduit Artery Function Evaluation) study showed less effective central aortic pressure lowering with atenolol-based therapy versus amlodipine-based therapy in people with hypertension. The present study examined the importance of heart rate (HR) as a determinant of this effect. Recent analyses have suggested that beta-blockers are less effective at reducing cardiovascular events than alternative blood pressure (BP)-lowering therapies. There has been much debate about the mechanism for this shortfall in benefit and specifically the role of HR lowering by beta-blockers. Central pressures were derived from brachial pressure and radial pulse wave analysis in 2,073 patients, and 7,146 measurements were recorded and analyzed over follow-up for up to 4 years. There was no impact of HR on brachial systolic or pulse pressures; however, there was a highly significant inverse relationship between HR and central aortic systolic and pulse pressures (p < 0.001). This was dependent on a strong inverse relationship between HR and augmentation index, indicative of increased wave reflection at lower HRs. Multiple regression, adjusted for brachial BP, showed HR to be the major determinant of central pressures. Moreover, HR and brachial BP accounted for 92% of the variability in central systolic and pulse pressures. Consequently, drug-related differences in central aortic pressures were markedly attenuated after adjustment for HR. When comparing beta-blocker-based treatments with other BP-lowering strategies, HR reduction with beta-blockers is a major mechanism accounting for less effective central aortic pressure reduction per unit change in brachial pressure.

Impact of Statin Therapy on Central Aortic Pressures and Hemodynamics

Statins reduce the risk of cardiovascular events in people with hypertension. This benefit could arise from a beneficial effect of statins on central aortic pressures and hemodynamics. The Conduit Artery Function Evaluation-Lipid-Lowering Arm (CAFE-LLA) study, an Anglo-Scandinavian Cardiac Outcomes Trial (ASCOT) substudy, investigated this hypothesis in a prospective placebo-controlled study of treated patients with hypertension. CAFE-LLA recruited 891 patients randomized to atorvastatin 10 mg/d or placebo from 5 centers in the United Kingdom and Ireland. Radial artery applanation tonometry and pulse-wave analysis were used to derive central aortic pressures and hemodynamic indices at repeated visits over 3.5 years of follow-up. Atorvastatin lowered low-density lipoprotein cholesterol by 32.4 mg/dL (95% confidence interval [CI], 28.6 to 36.3) and total cholesterol by 35.1 mg/dL (95% confidence interval, 30.9 to 39.4) relative to placebo. Time-averaged brachial blood pressure was similar in CAFE-LLA patients randomized to atorvastatin or placebo (change in brachial systolic blood pressure, -0.1 mm Hg [95% CI, -1.8 to 1.6], P=0.9; change in brachial pulse pressure, -0.02 mm Hg [95% CI, -1.6 to 1.6], P=0.9). Atorvastatin did not influence central aortic pressures (change in aortic systolic blood pressure, -0.5 mm Hg [95% CI, -2.3 to 1.2], P=0.5; change in aortic pulse pressure, -0.4 mm Hg [95% CI, -1.9 to 1.0], P=0.6) and had no influence on augmentation index (change in augmentation index, -0.4%; 95% CI, -1.7 to 0.8; P=0.5) or heart rate (change in heart rate, 0.25 bpm; 95% CI, -1.3 to 1.8; P=0.7) compared with placebo. The effect of statin or placebo therapy was not modified by the blood pressure-lowering treatment strategy in the factorial design. Statin therapy sufficient to significantly reduce cardiovascular events in treated hypertensive patients in ASCOT did not influence central aortic blood pressure or hemodynamics in a large representative cohort of ASCOT patients in CAFE-LLA.

Central Blood Pressure and Hypertension

During the 20th century, the brachial artery auscultatory method of blood pressure (BP) measurement has been the major basis for our understanding of clinical hypertension. First, the height of systolic (S) and diastolic (D) BP was used to define cardiovascular (CV) risk. Second, BP reduction by drug treatment was shown to be associated with a substantial decrease of CV risk in several varieties of high BP, including systolic hypertension in the elderly.1,2 However, drug treatment often reduced DBP more than SBP, resulting in increased pulse pressures (PP) and the related arterial stiffness. An associated increase in coronary risk was also observed.1,3 Because PP and arterial stiffness did not respond readily to drug treatment and was made even less responsive by aging, it has been suggested and shown that mechanical factors such as PP, arterial stiffness, and wave reflections, preferably measured by central (aortic or carotid) BP, should be fully investigated. Because the majority of the studies used noninvasive peripheral BPs the need arose for invasive methods to verify and validate central BP measurement in the evaluation of CV risk.4 In the present issue of this journal, Jankowski et al5 established, in a 4.5-year follow-up of 1109 patients undergoing coronary angiography, that central BP was a significant and independent predictor of CV risk, as potent as cardiac ejection fraction and more powerful than brachial sphygmomanometric measurements. For these coronary patients, the pulsatile …

Pathogenesis of Elevated Peripheral Pulse Pressure

“Ashes to ashes, dust to dust, if the cancer don’t get us, the arteriosclerosis must” — —Richard Gordon in The Alarming History of Medicine, 1993 Substantial evidence suggests that arterial remodeling evolves over a life course under the conjoint influence of genes, environmental factors (including vascular risk factors), and lifestyle characteristics (such as diet and physical activity).1 Such arterial remodeling involves multiple vascular territories and is panarterial, ie, it involves all layers of the arterial wall.1 More recently, considerable attention has focused on the physiological aspects of propagation of blood within the aorta, and several important concepts have evolved. First, the aorta is no longer regarded as just a passive conduit that transports blood to the vital organs. Rather, it is a complex organ that remodels in dynamic fashion in response to biomechanical stresses that accumulate over the life course.1 The different segments of the aorta vary in their relations to risk factors, underscoring the heterogeneity in remodeling characteristics across the arterial tree.2 Second, age-associated changes in the aortic wall include fragmentation of the elastin fibers, increased synthesis of collagen, and calcification. The molecular epidemiology of these vascular remodeling changes have been well characterized, and are complex, being mediated via the interaction of vascular smooth muscle cells, integrins, metalloproteinases, endothelial function, and the renin-angiotensin axis, inflammation, and other pathways.1 Third, vascular flow propagation is the combination of steady flow (mean arterial pressure) and pulsatile (pulse pressure) components. The proximal (central) aorta stiffens with age, and these changes are associated with an increase in the pulsatile component (increased central pulse pressure), which in turn places a burden of increased afterload on the left ventricle. There is widespread agreement that elevated pulsatile load is associated with increased risk of cardiovascular disease, including myocardial infarction, stroke, and heart …

Combination Treatment to Prevent Atherosclerosis

To the Editor: Kushiro et al1 demonstrated that, in patients without a history of cardiovascular disease who have hypertension and mildly elevated cholesterol, pravastatin was effective in reducing the incidence of cardiovascular disease. There were no significant differences in mean baseline total cholesterol, blood pressure levels, or variation in blood pressure during the 5-year period between the diet and diet-plus-pravastatin groups. Nonetheless, pravastatin reduced the burden of cardiovascular disease. This finding is consistent with the Conduit Artery Function Evaluation Lipid-Lowering Arm Study,2 demonstrating that atorvastatin therapy sufficient to significantly reduce cardiovascular events …

Introduction to the Sixth International Workshop on Structure and Function of the Vascular System

Introduction to the Sixth International Workshop on Structure and Function of the Vascular System

Pulsology Reloaded

The Losartan Intervention For Endpoint reduction in hypertension (LIFE) Study,1 the Second Australian National Blood Pressure Trial (ANBP2),2 and the Anglo-Scandinavian Cardiovascular Outcome Trials3 have shown that different antihypertensive treatments may have different impacts on the rate of events in hypertension while achieving comparable brachial blood pressure (BP) reduction. Thus, although brachial BP estimation by classic Riva–Rocci cuff sphygmomanometer and the Korotkoff auscultatory technique have provided almost all of our knowledge on epidemiology, prognosis, and treatment of hypertension,4,5 recent trials1–3 are revealing intrinsic limitations of the conventional approach, because the real goal of treatment in hypertension is the reduction in the number and the rate of untoward events. More recently, the Conduit Artery Function Evaluation (CAFE) Study6 described higher central BP as a key factor explaining the greater number and rate of events with atenolol than with amlodipine plus perindopril. Central pressure waveform and BP values can be estimated by applanation tonometry, a method supported by solid theoretical principles and modeling studies in experimental settings.7 Analysis of the systolic portion of the carotid pressure waveform allows for obtaining indices of the arterial viscous-elastic properties that correlate with end-organ damage and clinical outcomes in hypertension.8 Therefore, the indices of arterial waveform reflection and mechanics and central BP assessed by applanation tonometry have the potential to add significant information for risk stratification beyond and above brachial BP. In fact, the conclusions of the CAFE Study were well received.9 In addition, applanation tonometry has also been associated with 2D-guided M-mode vascular ultrasonography to assess simultaneously the viscous-elastic properties of the carotid artery, the intima–media thickness, and quantification of atherosclerosis.8 Assessment of cardiovascular target organ damage is curial for a global risk assessment …

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). …

Differential Impact of Blood Pressure–Lowering Drugs on Central Aortic Pressure and Clinical Outcomes: Principal Results of the Conduit Artery Function Evaluation (CAFE) Study

Differential Impact of Blood Pressure–Lowering Drugs on Central Aortic Pressure and Clinical Outcomes: Principal Results of the Conduit Artery Function Evaluation (CAFE) Study