Reduced Wave Reflection Research Articles

Superior effect of an angiotensin-converting enzyme inhibitor over a diuretic for reducing aortic systolic pressure

In recent studies, benefit has been shown for angiotensin-converting enzyme (ACE) inhibitors and calcium antagonists over a beta-blocker in hypertension, through a greater reduction in aortic than brachial systolic and pulse pressure. No data are available on diuretics, even though these are the preferred initial treatment of patients with mild hypertension. In this study, 101 patients with mild essential hypertension were randomly assigned to an 8-week period of monotherapy with enalapril 10 mg a day or indapamide 2.5 mg a day. Central as well as brachial systolic, augmented, and pulse pressure were determined using SphygmoCor, as in the REASON and CAFE trials. Enalapril and indapamide reduced brachial systolic, diastolic, mean and pulse pressure to the same extent, and the heart rate was unchanged. Although there was no difference in brachial pressure with enalapril and indapamide, enalapril caused a greater fall in estimated aortic systolic, and pulse pressures. The augmentation index, an index of wave reflection, fell from 33.7 to 28.3% with enalapril but was unchanged with indapamide. Results infer a reduction in wave reflection with enalapril, causing a fall in aortic pressure augmentation, and a corresponding fall in aortic systolic and pulse pressure. These were not apparent from brachial cuff measurements. Results show that a diuretic, like a beta-blocker agent, is not as effective a therapy as an ACE inhibitor in reducing aortic systolic and pulse pressure, and that the difference is not attributable to a change in heart rate.

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.

Triangulating the Peaks of Arterial Pressure

Increased arterial stiffness and excessive pressure pulsatility have emerged as important risk factors for a number of common disorders of aging, including cardiovascular disease, stroke, cognitive impairment, and renal disease. The triple-threat combination of robust associations between arterial stiffness and the foregoing disorders, a marked increase in arterial stiffness with advancing age and the graying of our society, has led to intensive efforts to identify mechanisms that contribute to arterial stiffening and widening pulse pressure to define interventions to prevent or reverse stiffness and potentially reduce the substantial burden of related disease. Wave reflections complicate the task of evaluating arterial hemodynamics and play an unclear role in the foregoing diseases. When the heart ejects, ventricular outflow interacts with characteristic impedance of the proximal aorta to produce the forward pressure wave, which travels down the normally compliant aorta at a finite pulse wave velocity (PWV). When the forward wave encounters impedance mismatch, such as a branch point or a change in diameter or wall properties, a partial reflection occurs. Innumerable reflections arising from locations distributed throughout the arterial tree summate into a remarkably discrete reflected pressure wave with amplitude ≈40% of the incident wave. The summated reflected wave returns to the central aorta in midsystole, creating an inflection point and secondary late systolic pressure rise that often augments central aortic systolic and pulse pressure.1 Variable timing of this retrograde-traveling reflected wave creates regional inequalities in systolic and pulse pressure and, therefore, complicates interpretation of single point pressure measurements, such as standard brachial blood pressure, which may differ from central aortic pressure. Augmentation index (AI), which expresses late systolic pressure augmentation as a percentage of pulse pressure, is frequently used to assess wave reflection (Figure). AI, which depends on both timing and amplitude of the reflected wave, has also been widely …

Atenolol and Eprosartan: Differential Effects on Central Blood Pressure and Aortic Pulse Wave Velocity

Recent data suggest that atenolol may be inferior to other antihypertensive drugs in reducing cardiovascular risk in older individuals with hypertension, despite lowering peripheral blood pressure (BP). We hypothesized that that atenolol fails to reduce central BP as much as other agents. The aim of the present study was to compare the hemodynamic effects of atenolol and eprosartan in a double-blind, randomized, cross-over study. After a 2-week placebo run-in, 21 subjects with never-treated hypertension underwent 6 weeks of therapy with atenolol (50 mg) and eprosartan (600 mg). Central BP and augmentation index were assessed using pulse wave analysis, and aortic pulse wave velocity was measured, at baseline and at the end of each treatment. Both drugs reduced peripheral BP to the same degree. However, there was a significantly greater reduction in central systolic BP with eprosartan (means +/- SEM: 16 +/- 3 v 11 +/- 2 mm Hg; P = .03). Despite identical reductions in mean pressure, atenolol reduced aortic pulse wave velocity more than eprosartan (0.8 +/- 0.1 v 0.5 +/- 0.1 m/sec; P = .005). Conversely, augmentation index and N-terminal pro-brain natiuretic peptide levels were reduced significantly after eprosartan (6% +/- 2% and 11 +/- 5 pg/mL, respectively) but were increased after atenolol (7% +/- 2% and 67 +/- 24 pg/mL, respectively). These data indicate that despite similar effects on peripheral BP and a greater effect on aortic stiffness, atenolol had less impact on central systolic BP than eprosartan because it failed to reduce wave reflection. This provides one potential explanation for the failure of atenolol to improve outcome in older patients with essential hypertension.

Effects of Nifedipine on Systemic and Pulmonary Vascular Impedance in Subjects Undergoing Cardiac Catheterization

Nifedipine 10 mg, administered sublingually to 12 patients following diagnostic cardiac catheterization, caused reduction in systemic resistance, and change of impedance together with alteration in contour of the ascending aortic and left ventricular pressure waves. The substantial reduction in ascending aortic and left ventricular systolic pressure with nifedipine occurred despite an increase in stroke volume and cardiac output, and was associated with similar reductions in mean pressure and indices of wave reflection. In the same patients, there were no significant changes in pulmonary vascular resistance or impedance, nor in pulmonary artery or right ventricular pressure pulse contour. For the systemic circulation, as with nitroglycerin and nitroprusside, reduction in wave reflection appears to be an important factor in the drug's action and for its beneficial effects on cardiac load in the treatment of angina pectoris, systemic hypertension and left ventricular failure. Thus the observed effects of nifedipine were attributed to vasodilatation of the systemic arteries and arterioles.

Beyond Blood Pressure

In this issue of Arteriosclerosis, Thrombosis, and Vascular Biology , Schillaci et al1 raise an interesting possibility—that a drug class (protease inhibitors) can have subtle arterial ill effects, which are not apparent from conventional blood pressure recordings. The authors provide evidence of aortic stiffening (measured as carotid–femoral pulse wave velocity [PWV]), increase in wave reflection from peripheral vessels (measured as aortic augmentation index [AIx]), and impairment of left ventricular subendocardial supply/demand ratio (measured as Buckberg index). Studies to date on arterial stiffening and its implications have concentrated on how age, gender, body height, exercise, lifestyle, and disease affects these properties, and how arterial properties, when deranged by disease, can be improved by drug therapy.2 Such adverse arterial hemodynamic changes with drugs have not been sought before. Before approval of a new drug, government regulatory bodies have required only measurements of cuff brachial systolic and diastolic pressures and assurance that these were not significantly altered. The question arises from the study of Schillaci—is this enough? Is it possible that drug classes may have adverse long-term effects that are not exposed by conventional cuff measurements? The question is relevant to the present concerns on long-term ill effects of COX 2 inhibitors (coxibs), with rofecoxib withdrawn from the market and the subject of legal action in US courts.3 See page 2381 The potential importance of the findings of Schillaci et al on protease inhibitors is unquestioned. These drugs have revolutionised the treatment of AIDS and find routine use in persons who are seropositive to the HIV virus. There were no HIV-positive persons in this study who were not treated with protease inhibitors. Studies of the drugs quoted by Schillaci are in recent issues in the world’s highest impact journals. I will not pursue such important implications to HIV and AIDS, …

Benefits from angiotensin-converting enzyme inhibitor ‘beyond blood pressure lowering’: beyond blood pressure or beyond the brachial artery?

The substantial benefits of ramipril over conventional therapy in high-risk patients are not always associated with clinically significant differences in brachial arterial pressure, and largely remain unexplained. We undertook this acute study to establish the magnitude of and reason for different acute effects of ramipril and atenolol on arterial pressure. We enrolled 30 patients, who took 10 mg ramipril, 100 mg atenolol, and placebo at intervals of > or = 7 days, in a randomized, double-blind, placebo-controlled trial. After baseline, measurements were taken at 30-60 min intervals for 5 h, and comprised cuff brachial pressure, radial artery tonometry with generation of central aortic pressure, and pulse wave velocity for aorta, upper limb and lower limb arteries. Both ramipril and atenolol reduced arterial pressure, and the diastolic pressure fall was similar in the aorta and brachial artery, but the systolic pressure fall for ramipril was greater than for atenolol (by 5.2 mmHg, P < 0.0001) in the aorta compared with the brachial artery. The aortic systolic pressure difference with ramipril in comparison with atenolol was accompanied by an absolute difference of 10.7% (P < 0.0001) in the augmentation index, denoting a reduction in peripheral wave reflection by ramipril. The aortic pulse wave velocity fell to a similar degree with ramipril in comparison with atenolol, but fell to a greater degree (1.35 and 0.44 m/s, respectively, P < 0.0001 for both) in muscular arteries of the lower and upper limbs. A greater (average, 5.2 mmHg) decrease in aortic systolic pressure caused by ramipril may explain the greater benefit of ramipril over atenolol. The difference is attributable to decreased stiffness of peripheral arteries and a reduction in wave reflection.

Clinical measurement of arterial stiffness obtained from noninvasive pressure waveforms

Aortic pulse wave velocity (PWV) and augmentation index are independent predictors of adverse cardiovascular events, including mortality. In hypertension and aging, central elastic arteries become stiffer, diastolic pressure decreases, and central systolic and pulse pressures are augmented due to increased PWV and early return of reflected waves to the heart from the periphery. Valuable information on arterial properties such as stiffness can be obtained from both central (aortic) and peripheral (radial artery) pressure waveforms, but absolute values of wave reflection amplitude and wasted left ventricular (LV) pressure energy can only be obtained from the central arterial pressure waveform. As the arterial system becomes stiffer, there is a marked increase in central systolic and pulse pressures and wasted LV energy, along with a decrease in pulse pressure amplification. The increase in aortic systolic and pulse pressures are due primarily to increases in PWV and wave reflection amplitude with a small increase in incident wave amplitude. In individuals with very stiff elastic arteries (eg, in older persons with isolated systolic hypertension), there is a decrease in diastolic pressure. These changes in pressure components increase LV afterload and myocardial oxygen demand and therefore cause an undesirable mismatch between ventricle emptying and arterial pulse wave transmission, which promotes ventricular hypertrophy. High systolic and pulse pressures resulting from advanced age or hypertension increase circumferential arterial wall stress, which likely causes breakdown of medial elastin and increases the possibility of local fatigue, endothelial damage and development of atherosclerosis. Vasodilator drugs may have little direct effect on large central elastic arteries, but at the same time, their effects on peripheral muscular arteries reduce wave reflection amplitude and markedly lower systolic and pulse pressures and ventricular afterload. These beneficial effects on central arterial pressure can occur with or without a reduction in cuff blood pressure (BP) and may explain the apparent "pressure-independent" effects of drugs such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers. Therefore, optimal treatment of high BP and its complications should include consideration of arterial stiffness, augmentation of aortic pressure, and LV wasted energy, all of which should be reduced to the lowest possible level.

Surface roughness effect of vertical and sloped seawalls in incident random wave fields

Experimental investigations on wave reflections, run-up and run-down, and wave pressures on plane, dentated and serrated seawalls were carried out in random wave fields for a wide range of wave heights, wave periods, seawall slopes in a constant water depth of 0.7 m. Based on the measurements, predictive equations are proposed which can be used for practical purposes. A total performance evaluation is carried out on the plane, dentated and serrated seawalls. The improved performance (reduction of wave reflection, run-up and run-down and wave pressures) of the serrated seawall is elucidated. The serrated seawall is about 20–40% better than a plane seawall for reducing wave reflections, run-up and run-down. The results can be used for a better hydrodynamic design of vertical structures (quay walls in harbors, vertical seawalls, caisson type breakwaters) and sloped structures (seawalls, dikes, wave absorbers in the laboratory).

Nitric oxide and the regulation of large artery stiffness: from physiology to pharmacology.

The association between arterial stiffening and aging is well described and can be observed in almost all populations worldwide. A number of other cardiovascular risk factors including diabetes and cigarette smoking are also associated with increased large artery stiffness, often referred to as “premature arterial stiffening.” It is now apparent that the aortic pulse wave velocity (PWV), a measure of arterial distensibility, predicts outcome in a variety of different populations, including hypertensives,1 diabetics,2 individuals with end-stage renal disease (ESRD),3 and even in older adults.4 Indeed, in some populations, aortic PWV is a better predictor of future events than peripheral blood pressure.4 Moreover, arterial stiffening may be more than just a marker of cardiovascular risk; stiffening may also play a more direct role in the development of atherosclerotic plaques. Thus, arterial stiffness would appear to be a novel therapeutic target for the prevention of excess cardiovascular morbidity and mortality. To exploit such an exciting prospect fully, it is necessary to understand the factors regulating arterial stiffness. Traditionally, the stiffness of a vessel was viewed as simply a function of the structural elements of the vessel wall and distending (mean arterial) pressure. However, the large arteries also have a generous coat of smooth muscle, which can alter the distribution of stresses between the elastic and collagenous fibers of the vessel wall and thus alter arterial stiffness. Because smooth muscle tone is influenced by a number of circulating and local vasoactive mediators, arterial stiffness may be actively regulated, and indeed modifiable, at least in the short-term. The muscular arteries have a rich sympathetic innervation, and catecholamines are known to alter smooth muscle tone. Moreover, removal of the vascular endothelium in animals alters large artery stiffness,5,6 suggesting that endothelial-derived substances regulate arterial stiffness in vivo. However, the endothelium …

Arterial stiffness and function in end-stage renal disease

Cardiovascular disease is a major cause of mortality in patients with end-stage renal disease, with damage to arteries as a major contributing factor. Arterial stiffness is a factor associated with high systolic and pulse pressure in these patients and is a strong independent factor associated with morbidity and mortality. Arterial stiffness is one of the principal factors opposing left ventricular ejection. The appropriate term to define the arterial factor(s) opposing left ventricular ejection is aortic input impedance. Aortic input impedance depends on TPR, arterial distensibility, and wave reflections. Distensibility defines the capacitive properties of arterial stiffness, whose role it is to dampen pressure and flow oscillations and to transform pulsatile flow and pressure in arteries into a steady flow and pressure in peripheral tissues. Stiffness is the reciprocal value of distensibility. These parameters are blood pressure dependent; arteries become stiffer at high pressure. While distensibility provides information about the elasticity of the artery as a hollow structure, the elastic incremental modulus characterizes the properties of the arterial wall biomaterials independent of vessel geometry. Alternatively, arterial distensibility can be evaluated by measuring pulse wave velocity, which increases with the stiffening of arteries. Arterial stiffening increases left ventricular afterload and alters the coronary perfusion. With increased pulse wave velocity, the wave reflections affects the aorta during systole, which increases systolic pressures and myocardial oxygen consumption and decreases diastolic blood pressure and coronary flow. The arterial stiffness is altered primarily in association with increased collagen content and alterations of extracellular matrix and calcification of the arterial wall. The arterial stiffening estimated by changes in aortic pulse wave velocity and intensity of wave reflections are independent predictors of survival in end-stage renal disease and in the general population. Improvement of arterial stiffening could be obtained by antihypertensive treatments as observed with calcium-channel blockers and angiotensin-converting enzyme inhibitors. Angiotensin-converting enzymes inhibitors increase AC and reduce wave reflections. It has been shown that reversibility of aortic stiffening and use of angiotensin-converting enzyme inhibitors had a favorable independent effect on survival in hypertensive patients with advanced renal disease.

Numerical Modeling of Wave Absorbers for Physical Wave Tanks

A 3D numerical solution was derived to determine the wave field in a physical wave tank equipped with a porous wave absorber of variable width and draft. The solution was achieved by applying the boundary element method. The model was applied to analyze the effect of the geometry and material of wave absorbers on wave reflection to eventually equip a wave tank with a proper wave absorber. The results show that absorber geometry has a complex, often surprising and nonintuitive effect on wave reflection. A more pronounced effect on wave reflection possesses physical and hydraulic properties of the material used to build a wave absorber. A reduction of wave reflection can usually be achieved by increasing absorber length and simultaneously decreasing its slope, and often a reduction of wave reflection can be achieved by increasing absorber draft or width. Moreover, a reduction of wave reflection, often substantial, can be achieved by increasing porosity and the damping coefficient. The results and additional analysis show that a reasonable wave reflection level can already be achieved for fairly short absorbers, and the model can be applied to select an optimal wave absorber for any prespecified conditions. Theoretical results are in reasonable agreement with experimental data.

Rapid design of SAW oscillator electronics for sensor applications

This paper presents electronic techniques and a general methodology for the rapid design of two-port surface acoustic wave oscillators. By using a methodical approach, the stability problems and much of the time-consuming experimentation common to radio frequency (RF) oscillator design was avoided. Several oscillators in the range of 200 MHz to 1 GHz were designed using variations of the same basic circuit. Circuit designs included both two-port resonator and delay line SAW devices. The electronics were small in size ( 1.75 cm×1.75 cm ) and inexpensive (<US$ 10 in part cost). The active circuit element of the oscillators was a radio frequency integrated circuit (RFIC) wide-band amplifier. The first step of this systematic method was to identify a readily available RFIC amplifier that met the specifications of the oscillator. The specifications included amplifier gain, bandwidth and maximum input power. Choice of the proper amplifier allowed the same circuit to be used for several SAW oscillators spanning a large frequency range. Next a passive LC filter was designed to limit the open loop gain to a small frequency region around the SAW device’s fundamental frequency. This filter eliminates the problems of mode hopping and oscillation at harmonics. The S-parameters of the oscillator were then measured in an open-loop configuration to determine the phase shift requisite for the closed loop oscillation condition of 0° phase shift. To achieve stable oscillation, a passive LC phase-shifting filter was designed. Using the properties of Butterworth filters and a simple computer program, filters of exact phase shift were designed. The last step of design was the use of microstrip layout techniques to reduce wave reflections and susceptibility to electromagnetic interference.

Arterial Elastance and Wave Reflection Augmentation of Systolic Blood Pressure: Deleterious Effects and Implications for Therapy

Systolic and pulse blood pressures are stronger predictors of stroke, coronary heart disease, myocardial infarction, heart failure, end-stage renal disease, and cardiovascular mortality than diastolic pressure. Furthermore, diastolic pressure is inversely related to coronary heart disease and cardiovascular mortality. Increased elastance (or stiffness, inverse of compliance) of the central elastic arteries is the primary cause of increased systolic and pulse pressure with advancing age and in patients with cardiovascular disease, including hypertension, and is due to degeneration and hyperplasia of the arterial wall; diastolic pressure decreases as arterial elastance increases. As elastance increases, transmission velocity of both forward and backward (or reflected) traveling waves increases, which causes the reflected wave to arrive earlier in the central aorta and augments pressure in late systole. These changes in arterial wall properties cause an increase in left ventricular afterload and myocardial oxygen consumption and a decrease in myocardial perfusion pressure, which may induce an imbalance in the supply-demand ratio, especially in hypertrophied hearts with coronary artery disease. Also, an increase in systolic pressure increases arterial wall circumferential stress, which promotes fatigue and development of atherosclerosis. Vasodilator drugs have little direct active effect on large elastic arteries but can markedly reduce wave reflection amplitude and augmentation index by decreasing elastance of the muscular arteries and reducing pulse wave velocity of the reflected wave from the periphery to the heart. This decrease in intensity (or amplitude) and increase in travel time (or delay) of the reflected wave causes a generalized decrease in systolic pressure and arterial wall stress and an increase in ascending aortic flow during the deceleration phase. The decrease in systolic pressure brought about by this mechanism is grossly underestimated when systolic pressure is measured in the brachial artery.

Hypotensive effects of captopril on physical properties of the arterial system in young and adult rats.

We determined the acute effects of the angiotension converting enzyme inhibitor captopril on the arterial mechanics in rats at different ages, based on the exponentially tapered T-tube model. Male Wistar-Kyoto rats aged 4 and 12 months were individually referred to as young (n = 8) and adult rats (n = 8) and were anesthetized and thoractomized. The pulsatile aortic pressure and flow signals before and after the administration of captopril (20 mg/kg, i.p.) were measured by a high-fidelity pressure sensor and an electromagnetic flow probe, respectively. In each age group, captopril showed little change in basal heart rate as well as cardiac output. However, captopril produced a drop of 15% in mean aortic pressure in young and a fall of 12% in adult rats. In addition. captopril reduced total peripheral resistance by 21% in young and by 23% in adult animals. As for the pulsatile nature of the arterial system, captopril had increased wave transit time of the lower body circulation of 10% in young and of 12% in adult rats. By contrast, captopril reduced wave reflection factor by 22% in young and by 25% in adult animals. In conclusion, the converting enzyme inhibitor captopril has a stiffness-decreasing effect on Windkessel vessels and a dilated effect on resistance arterioles in either young or adult rats. No age dependence of vascular response and reflex tachycardia to captopril has been found in rats between 4 and 12 months.

Analysis of the effect of hemodialysis on peripheral and central arterial pressure waveforms

Arterial stiffening is very pronounced in renal patients. Carotid artery stiffening is a powerful predictor of future cardiovascular mortality, and measures of arterial compliance correlate much better with left ventricular mass (LVM) in dialysis patients than does brachial artery blood pressure (BP). The aim of our study was to describe the influence of a hemodialysis (HD) session on arterial cushioning function and to correlate the potential different types of behavior with echocardiographic derived parameters. Radial artery pressure waveforms were measured and recorded noninvasively by applanation tonometry in 51 healthy patients on regular three times weekly HD. The data were then converted into aortic pressure waveforms using a regression equation (SphymoCortrade mark apparatus). Measurements were done pre- and post-HD in order to ascertain the effect of a single HD session on arterial hemodynamics. The augmentation index (AGI; the difference between early and late pressure peaks divided by the pulse pressure amplitude) was used as an index for vascular compliance. Reproducibility was assessed in 20 young healthy subjects by determining the aortic pulse wave augmentation index twice from radial artery BP measurements one minute apart. Intraobserver error was 2.4%. For 10 dialysis patients similarly studied, the intraobserver error was 1.6%. AGI was correlated with subjects' height (r = -0.37, P = 0.009), weight (r = -0.41, P = 0.002), and BP levels: radial systolic BP (r = 0.33, P = 0.018), radial diastolic BP (r = 0.29, P = 0.036), and central systolic BP (r = 0.51, P < 0.001). Comparing the pre- with the post-HD AGI values, four patterns of evolution became apparent: (1) The AGI was negative before the HD session and became even more negative afterward (N = 3 out of 51). (2) The AGI was positive before the HD session but became negative after dialysis (N = 19 out of 51). (3) The AGI was positive before the HD session and, although diminished afterward, remained positive (N = 23 out of 51). (4) The AGI was positive before the HD session and increased afterward (N = 6 out of 51). We also found that in some patients, AGI remained at lower than predialysis levels for at least 24 hours. Significant relationships between echocardiographic parameters and pulse wave contour (PWC) variables included pre-HD AGI and LVM (r = 0.47, P < 0. 001). There was better correlation between LVM and derived predialysis aortic systolic BP (r = 0.56, P < 0.001) than measured brachial (peripheral) systolic BP (r = 0.35, P = 0.04). Patients whose waveform remained abnormal (AGI remained positive) after HD had a more dilated LV (LV-EDD = 52.07 +/- 3.48 mm) than did those patients for whom HD restored "normal" arterial hemodynamics (LV-EDD 46.86 +/- 4.06 mm, P < 0.05). A standard HD session profoundly affected aortic BP waveform characteristics, with a reduction in wave reflection in 88% of patients. However, restoration by HD of a normal aortic waveform was unusual. Patients whose waveform remained abnormal after HD had larger more dilated LV chambers than did those patients for whom HD restored "normal" arterial hemodynamics.

AN EXPERIMENTAL STUDY OF A MULTIPLE-SLIT-WALL CAISSON BREAKWATER FOR ROUGH SEAS

Due to increasing usage of conventional perforated-wall caissons as breakwaters in relatively calm seas around Japan, we conducted a series of model experiments to develop a special perforated caisson that can withstand severe wave attacks in open seas. The caisson consists of multiple slit walls which allow harbor water exchange without increasing wave transmission, while also reducing wave reflection using a small wave chamber width compared to that of a single-slit-wall caisson.

Reduction of wave reflection is the principal beneficial action of felodipine in isolated systolic hypertension

Reduction of wave reflection is the principal beneficial action of felodipine in isolated systolic hypertension

Wave Overtopping and Wave Reflection of Block Mound Seawalls with Slit Walls on Concrete Caisson

In recent years, there has been shortage of sites suitable for construction of thermal power plants. Therefor, the power plants have been occasionally located on the site exposed to large waves in the open sea. The reclaimation land must be protected from wave overtopping. And, at the same time they are required to be in harmoney with the surrounding environment. So, they must been equipped seawalls to reduce wave reflection. Hydraulic model test was made to develop block mound seawalls with slit walls on concrete caisson taking the advantages of both block seawalls and perforated caissons.

Towards optimization of wave reflection: therapeutic goal for tomorrow?

1. The conventional approach to drug therapy of hypertension and heart failure considers only effects of such drugs on peripheral resistance, cardiac output and heart rate. 2. A more complete approach needs to consider the pulsatile nature of cardiac ejection and so the influence of arterial stiffness and wave reflection properties and the effects of drugs on these. 3. Wave reflection normally aids cardiac function when full body height is achieved and arterial distensibility is high. However, with ageing or in hypertension the arteries stiffen and wave reflection returns early, augmenting systolic pressure, increasing pulse pressure and reducing the capacity for coronary perfusion. 4. In mature or older adults, delay of or reduction in wave reflection is an important therapeutic strategy for management of hypertension, angina pectoris and cardiac failure. 5. Beneficial effects of such therapy cannot always be gauged from conventional recordings of blood pressure, but can be inferred from analysis of pulse waveform.