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Arterial stiffening with age is responsible for isolated systolic hypertension, for elevation of systolic pressure with age, and for the majority of cardiovascular events in the elderly, especially left ventricular failure. Change in brachial pulse pressure with age underestimates change in aortic pulse pressure; change with vasodilator agents, especially nitrates, underestimates beneficial effects of these agents on the heart. New methods based on pulse wave analysis complement sphygmomanometry in assessing ill effects of aging and benefits of drug therapy for hypertension.

Objective: Effects of pacing-induced tachycardia on left ventricular function have been studied extensively. However, little attention has been focused on aortic elastic properties during heart rate increments. The aim was to determine the effects of right ventricular pacing on the aortic elastic properties. Methods: We studied 14 normal subjects (baseline blood pressure, 129/84±10/6 mmHg; aortic diameter, 23.5/21.3±2.4/1.9 mm) at rest, during rapid right ventricular pacing (at five stepwise heart rate increases of 20 bpm every 2 min) and after 5 min recovery. Shifts as well as changes in the slope and the stiffness constant of the pressure diameter (p–d) relation, derived from simultaneous tip-micromanometer aortic pressure recordings and high-fidelity ultrasonic intravascular aortic diameter recordings, were used as indices of aortic stiffness. Wave reflection was also studied. Results: Aortic pulse pressure and strain significantly decreased after pacing-induced tachycardia ( p

Since the first report on dual chamber pacing for congestive heart failure (CHF) in 1991, a number of investigators have explored the topic with conflicting results. These conflicts may arise from an incomplete understanding of the mechanisms by which pacing improves cardiac function. Potential mechanisms include: (1) increase in filling time: (2) decrease in mitral regurgitation: (3) optimization of left heart mechanical atrioventricular delay (left heart MAVD); and (4) normalization of ventricular activation. One or more of these mechanisms may be operative in an individual patient, implying that patients may require individuol optimization. Acute pacing studies were conducted on nine CHF patients, NYHA Class II-III to Class IV. Measurements of conduction times in sinus rhythm revealed: (1) normal interatrial conduction times (59 ± 5 ms) in all patients, with wide variations in interventricular conduction times (range, −15–105 ms); and (2) a wide range of left heart MAVD (range, 97–388 ms). While pacing the right, left, or both ventricles, measurement of high fidelity aortic pressure and mitral and aortic velocities revealed the following: (1) 6 of 9 patients increased mean pulse pressure over sinus value during RV orLV pacing at an optimal A V delay: (2) the maximum aortic pulse pressure was achieved when the atrium was not paced: an 8% increase over sinus pulse pressure with paced RV versus a 5% decrease for paced atrium and RV at optimum AV delay (paired Student's t-test, P = 0.01), and a 0% increase over sinus with paced LV versus 7% decrease for paced atrium and LV at optimum AV delay, P < 0.05: (3) significant dependence on pacing site was noted, with 4 patients doing best with RV pacing. 3 patients achieving a maximum with LV pacing, and 2 patients showing no preference; and (4) 2 of 4 patients with restrictive filling patterns were converted to nonrestrictive patterns with optimum pacing. Patient hemodynamics appear to benefit acutely from individually optimized pacing. Increases in filling time, optimization of left heart MAVD, and normalization of intraventricular activation are the most significant mechanisms. Atrial pacing is inferior to atrial sensed modes if the patient has a functional sinus node.

Objectives: Hypertension is associated with increased arterial stiffness, which is an independent predictor of cardiovascular risk. Aortic systolic blood pressure (SBP) and/or pulse pressure (PP) better predicts cardiovascular events than peripheral blood pressure. The present study compared the discriminative ability for increased arterial stiffness of aortic BP with ambulatory peripheral BP, with reference to office brachial SBP or PP in never treated hypertensives. Methods: We enrolled 619 consecutive essential hypertensives (mean age 52.2±12.0 years, 325 men). Arterial stiffness was determined with carotid-femoral pulse wave velocity (PWV) using the Complior® device. Aortic pressures were measured using the Sphygmocor® device and 24h ambulatory SBP and PP were obtained from 24h ambulatory blood pressure monitoring. We employed dichotomous outcome variable (PWV≥75th percentile [8.55 m/s]). Receiver operating characteristic (ROC) curves were generated to evaluate the ability of the pressures to discriminate subjects with and without significant arterial stiffness (PWV ≥75th percentile [8.55 m/s]). Results: All different types of blood pressure significantly discriminated subjects with significant arterial stiffness (all p

Introduction The aim of this study was to investigate the effects of the intra aortic balloon pump (IABP) and of aortic compliance on left ventricular performance, including the effects of baroreflex control. Methods The study was conducted using a hybrid cardiovascular simulator, including a computational cardiovascular sub-model, a hydraulic sub-model of the descending aorta, and a baroreflex computational sub-model. A 40 cc balloon was inserted into a rubber tube component of the hydraulic sub-model. A comparative analysis was conducted for two aortic compliances (C1 = 2.4 and C2 = 1.43 cm3/mmHg, corresponding to an aortic pulse pressure of 23 mmHg and 35 mmHg, respectively), driving the balloon for different trigger timings. Results Under C1 conditions, the IABP induced higher effects on baroreflex activity (decrement of sympathetic efferent activity: 10% for C1 and 14.7% for C2) and ventricular performance (increment of cardiac output (CO): 3.7% for C1 and 5.2% for C2, increment of endocardial viability ratio (EVR): 24.8% for C1 and 55% for C2). The best balloon timing was different for C1 and C2: inflation trigger timing (from the dicrotic notch) -0.09 s for C1 and -0.04 s for C2, inflation duration 0.25 s for C1 and 0.2 s for C2. Conclusions Early inflation ensures better EVR, CO, and an increment of the afferent nerve activity, hence causing peripheral resistance and heart rate to decrease. The best balloon timing depends on aortic compliance, thus suggesting the need for a therapy tailored to the specific conditions of individual patients.

Objective: This study aims to examine the independent and combined impact of hypocaloric diet and lowintensity resistance exercise training (LIRET) on aortic hemodynamics and appendicular skeletal muscle mass (ASM) in obese postmenopausal women. Methods: Forty-one obese postmenopausal women (mean [SD] age, 54 [1] y) were randomly assigned to LIRET (n = 13), diet (n = 14), or diet + LIRET (n = 14). Body weight, waist circumference, aortic systolic blood pressure, aortic pulse pressure, augmentation index, subendocardial viability ratio (SEVR; myocardial perfusion), and heart rate (HR) were measured before and after 12 weeks. ASM was assessed by dual-energy x-ray absorptiometry. Results: Body weight (P G 0.001) and waist circumference (P G 0.01) decreased similarly after diet and diet + LIRET compared with no changes after LIRET. ASM did not change after diet + LIRET, and the decrease observed after diet (P G 0.001) was significant compared with LIRET. Aortic systolic blood pressure decreased similarly after LIRET (P G 0.05), diet (P G 0.01), and diet + LIRET (P G 0.01). Aortic pulse pressure (P G 0.05) decreased similarly after diet and diet + LIRET, but not after LIRET. SEVR (P G 0.01) increased similarly in both diet groups, whereas HR (P G 0.01) decreased only after diet. Changes in SEVR (P G 0.05) and HR (PG 0.01) with diet were different compared with LIRET. The augmentation index did not change in any group. Conclusions: Our findings suggest that diet-induced weight loss may reduce cardiovascular risk by improving SEVR via HR and aortic pulse pressure reductions in obese postmenopausal women. LIRET prevents ASM loss associated with hypocaloric diet but has no additive effects on aortic hemodynamics.

OBJECTIVE: Homocysteine has been shown to be a more accurate predictor of cardiovascular mortality in very old persons than models based on classical risk factors. Arterial stiffening is a structural abnormality involved in the pathway of cardiovascular disease. We expect this underlying pathophysiology to be a possible explanation for the association between homocysteine and cardiovascular risk, particularly in older populations. METHODS: Baseline cross-sectional data of the B-PROOF study were used to determine associations between homocysteine and outcomes of vascular function and structure. The cardiovascular subgroup of the B-PROOF study was included [n = 560, 58% men, age 72.6 ± 5.5 years, median homocysteine level 14.2 μmol/l (IQR 13.0-16.6)]. We assessed carotid distensibility coefficient, carotid compliance coefficient, aortic pulse wave velocity (aPWV), augmentation index (AIx) and aortic pulse pressure (aortic PP). Associations were tested using linear regression analysis and ANCOVA and were adjusted for possible confounders including age, sex, renal function, mean arterial pressure and heart rate. RESULTS: Ln-homocysteine was strongly associated with aPWV [β 0.005 95% confidence interval (0.001-0.009)]. Furthermore, this association was shown to be age-dependent (P = 0.02) and it was most strong in the upper tertile of age (77-98 years). No significant associations with ln-homocysteine were observed for AIx, carotid distensibility coefficient and compliance coefficient and aortic PP. Sex stratification shows the association between ln-homocysteine and aPWV is only significant in men. CONCLUSION: In older persons, homocysteine is associated with aortic stiffness, predominantly in the oldest old. This suggests that the strong association between homocysteine and cardiovascular mortality in the elderly may be mediated by aortic stiffness. © 2013 Wolters Kluwer Health | Lippincott Williams &Wilkins.

A noninvasive ultrasonic technique, based on tracking arterial wall displacements with a vessel wall-tracking device attached to a conventional B-mode imager, to assess end-diastolic aortic diameter (d) and aortic diameter changes during the cardiac cycle (delta d) in anesthetized and awake rats is presented. From these parameters and invasively measured aortic pulse pressure (delta P), aortic distensibility and compliance, the relative and absolute increases in lumen cross-sectional area for a given increase in delta P, respectively, can be calculated. d, delta d, and delta P could be determined with good intra-session (variations per day) and inter-session (variations between days) coefficients of variation (CV). The CVs for delta d were smaller in awake (4.6-6.0%) than in anesthetized rats (7.9-11.0%), probably due to variations in delta P during anesthesia (CV: 9.0-12.3%). The CVs for d in awake (3.3-6.5%) and anesthetized rats (2.6-5.0%) were comparable. In awake rats the CV for delta d, but not for d, increased after implantation of the aortic catheter. It is concluded that d, delta d, and delta P of the aorta can be reliably measured noninvasively in anesthetized and awake rats, allowing the in vivo assessment of aortic distensibility and compliance. The technique is sensitive enough to detect effects of agents on aortic wall properties.

Aging causes progressive changes in the structure and function of the large arteries that adversely impact the heart and vital organs. Vascular aging is a major independent risk factor for the development of cardiovascular diseases and events. Arterial stiffening is the dominant hemodynamic manifestation of vascular aging and a major independent predictor for incident hypertension. Arterial stiffening is therefore responsible for the very high residual lifetime risk for hypertension for middle-aged and elderly individuals. Asian populations may have a predisposition to increased central aortic pulse pressure because of the relatively larger diameter and thinner media at the proximal aorta that affect the interaction between ventricular ejection and arterial load. Increased arterial stiffness with aging was confirmed in several Asian populations, using either carotid-femoral pulse wave velocity (cf-PWV) or brachial-ankle pulse wave velocity (ba-PWV). Both cf-PWV and ba-PWV have been recognized as an independent predictor for cardiovascular events and all-cause mortality in Asian populations. In Asian populations, vascular aging-related medial degeneration but not atherosclerosis is the dominant factor associated with increased arterial stiffness with age. Salt intake has an independent effect on arterial wall properties contributing to increased arterial stiffness with age. Systolic hypertension is a consequence and an accelerator of the vascular aging related arterial stiffness. Asian subjects with systolic hypertension may be more prone to risks of cardiovascular disease, mortality and renal function decline than Western subjects. Strategies to prevent arterial stiffness and control systolic hypertension are urgently needed for the rapidly aging Asian populations.

The aortic pulse pressure (PP), which consists mainly of the incident wave and the reflected wave, has emerged as an important property of systemic blood vessels underlying the pathophysiology of cardiovascular disease. To determine the role of sympathetic nerve activity on the aortic PP response during dynamic exercise, we evaluated aortic hemodynamics during the right-leg knee-extension (40 and 60 % of maximal voluntary contraction) in six young adults with and without the systemic α1-adrenergic receptor blockade using prazosin (1 mg/20 kg body weight). The use of prazosin attenuated the exercise-induced increase in aortic PP (P

Aortic pulse pressure (APP) is related to arterial stiffness and associated with the presence and extent of coronary artery disease (CAD). Besides, the left coronary artery (LCA) has a predominantly diastolic flow while the right coronary artery (RCA) receives systolic and diastolic flow. Thus, we hypothesized that increased systolic-diastolic pressure difference had a greater atherogenic effect on the RCA than on the LCA.A random sample of 433 CAD patients (145 females, 288 males, mean age 65.0 ± 11.1 years) undergoing coronary angiography at Staten Island University Hospital between January 2005 and May 2008 was studied. Coronary lesion was defined as a ≥50% luminal stenosis. Patients were divided into three groups, with isolated LCA lesions (n = 154), isolated RCA lesions (n = 36) or mixed LCA and RCA lesions (n = 243).APP differed significantly between groups, being highest when the RCA alone was affected (67.6 ± 20.3 mm Hg for LCA vs. 78.8 ± 22.0 for RCA vs. 72.7 ± 22.6 for mixed, P = 0.008 for analysis of variance (ANOVA)). Age and gender were not associated with CAD location. Heart rate was associated with CAD location, lowest in RCA group, and negatively correlated with APP. However, left ventricular ejection fraction (LVEF) was lower in the mixed CAD group and positively correlated with APP. The association between APP and right-sided CAD persisted in multivariate logistic regression adjusting for confounders, including heart rate, LVEF and medication use. A similar but less significant pattern was seen with brachial arterial pressures.Aortic pulse pressure may affect CAD along with coronary flow phasic patterns.

The mechanism of the well-documented increase in aortic pulse pressure (PP) with age is disputed. Investigators assuming a classical windkessel model believe that increases in PP arise from decreases in total arterial compliance ( Ctot) and increases in total peripheral resistance ( Rtot) with age. Investigators assuming a more sophisticated pulse transmission model believe PP rises because increases in pulse wave velocity ( cph) make the reflected pressure wave arrive earlier, augmenting systolic pressure. It has recently been shown, however, that increases in cph do not have a commensurate effect on the timing of the reflected wave. We therefore used a validated, large-scale, human arterial system model that includes realistic pulse wave transmission to determine whether increases in cph cause increased PP with age. First, we made the realistic arterial system model age dependent by altering cardiac output (CO), Rtot, Ctot, and cph to mimic the reported changes in these parameters from age 30 to 70. Then, cph was theoretically maintained constant, while Ctot, Rtot, and CO were altered. The predicted increase in PP with age was similar to the observed increase in PP. In a complementary approach, Ctot, Rtot, and CO were theoretically maintained constant, and cph was increased. The predicted increase in PP was negligible. We found that increases in cph have a limited effect on the timing of the reflected wave but cause the system to degenerate into a windkessel. Changes in PP can therefore be attributed to a decrease in Ctot.

OBJECTIVE: To evaluate the impact of body position on the arterial stiffness indices provided by radial applanation tonometry in pregnant and nonpregnant women. METHODS: Twenty-four young women (18-30 years) in the third trimester of a normal pregnancy and 20 healthy nonpregnant women of the same age were enrolled. In each, applanation tonometry was carried out in the sitting and supine position. The following stiffness indices were analyzed: systolic augmentation index (sAix), sAix adjusted for heart rate (sAix@75) and diastolic augmentation index (dAix), all expressed in % of central aortic pulse pressure. RESULTS: The sAix was apparently not influenced by body position, but the transition from seated to supine was associated with a substantial decrease in heart rate. When correcting for this confounder by calculating the sAix@75, systolic augmentation was substantially lower when individuals were supine (mean ± SD: nonpregnant 3.0 ± 14.4%, pregnant 8.8 ± 9.7%) than when they were sitting (nonpregnant 5.7 ± 13.0%, pregnant 11.1 ± 83%, P = 0.005 supine vs. seated in both study groups, P > 0.2 for pregnant vs. nonpregnant). The influence of body position on the dAix went in the opposite direction (supine: nonpregnant 9.7 ± 6.6%, pregnant 4.4 ± 3.5%; seated: nonpregnant 7.7 ± 5.8%, pregnant 3.3 ± 2.4%, P

Decrease in arterial compliance leads to an increased pulse pressure, as explained by the Windkessel effect. Pressure waveform is the sum of a forward running and a backward running or reflected pressure wave. When the arterial system stiffens, as a result of aging or disease, both the forward and reflected waves are altered and contribute to a greater or lesser degree to the increase in aortic pulse pressure. Two mechanisms have been proposed in the literature to explain systolic hypertension upon arterial stiffening. The most popular one is based on the augmentation and earlier arrival of reflected waves. The second mechanism is based on the augmentation of the forward wave, as a result of an increase of the characteristic impedance of the proximal aorta. The aim of this study is to analyze the two aforementioned mechanisms using a 1-D model of the entire systemic arterial tree. A validated 1-D model of the systemic circulation, representative of a young healthy adult was used to simulate arterial pressure and flow under control conditions and in presence of arterial stiffening. To help elucidate the differences in the two mechanisms contributing to systolic hypertension, the arterial tree was stiffened either locally with compliance being reduced only in the region of the aortic arch, or globally, with a uniform decrease in compliance in all arterial segments. The pulse pressure increased by 58% when proximal aorta was stiffened and the compliance decreased by 43%. Same pulse pressure increase was achieved when compliance of the globally stiffened arterial tree decreased by 47%. In presence of local stiffening in the aortic arch, characteristic impedance increased to 0.10 mmHg s/mL vs. 0.034 mmHg s/mL in control and this led to a substantial increase (91%) in the amplitude of the forward wave, which attained 42 mmHg vs. 22 mmHg in control. Under global stiffening, the pulse pressure of the forward wave increased by 41% and the amplitude of the reflected wave by 83%. Reflected waves arrived earlier in systole, enhancing their contribution to systolic pressure. The effects of local vs. global loss of compliance of the arterial tree have been studied with the use of a 1-D model. Local stiffening in the proximal aorta increases systolic pressure mainly through the augmentation of the forward pressure wave, whereas global stiffening augments systolic pressure principally though the increase in wave reflections. The relative contribution of the two mechanisms depends on the topology of arterial stiffening and geometrical alterations taking place in aging or in disease.

A significant link has been reported between aortic stiffening and renal microvascular damage, but the underlying mechanism remains poorly understood. We hypothesized that alterations in central and renal hemodynamics are responsible for this link. In 133 patients with hypertension, pressure waveforms were recorded on the radial, carotid, femoral, and dorsalis pedis arteries with applanation tonometry to estimate the aortic pressures and aortic (carotid-femoral) and peripheral (carotid-radial and femoral-dorsalis pedis) pulse wave velocities. Flow-velocity waveforms were recorded on the renal segmental arteries with duplex ultrasound to calculate the resistive index (RI) as [1 − (end-diastolic velocity/peak systolic velocity)] and on the femoral arteries to calculate the reverse/forward flow index and diastolic/systolic forward-flow ratio. Albuminuria was defined as urinary albumin/creatinine ratio ≥30 mg/g of creatinine. The renal RI (mean: 0.65±0.07) was strongly correlated ( P r =0.62), incident pressure wave ( r =0.55), augmented pressure ( r =0.49), and aortic pulse wave velocity ( r =0.51), although not with the mean arterial pressure or peripheral pulse wave velocities. The correlations remained highly significant after consideration of confounders including age, cholesterol, hemoglobin A 1c , and glomerular filtration rate. The renal RI was inversely correlated with the femoral reverse and diastolic forward flow indices. Both aortic pulse pressure and renal RI correlated with the urinary albumin/creatinine ratio independent of confounders. Each 0.1 increase in renal RI was associated with a 5.4-fold increase in the adjusted relative risk of albuminuria. In conclusion, increased aortic pulse pressure causes renal microvascular damage through altered renal hemodynamics resulting from increased peripheral resistance and/or increased flow pulsation.

The aim of the study was to assess the relationship between non-invasively (NIA) and invasively assessed (IA) aortic pulsatile indices and the presence and severity of coronary artery disease (CAD).The study group consisted of 58 patients who were admitted to our institute for elective coronary angiography (CAG). We measured the aortic systolic, diastolic and mean blood pressure (BP) using non-invasive and invasive techniques. We assessed the pulsatile indices of the aortic pressure waveform (APW) including pulse pressure (PP), fractional PP (FPP, the ratio of PP to mean BP) and pulsatility index (PI, the ratio of PP to diastolic BP). The severity of CAD was assessed by Gensini score.IA aortic PP, FPP and PI were significantly higher in patients with CAD than without CAD, but NIA indices did not show significant differences between two groups. After multivariate stepwise adjustment, the odds ratio (OR) and confidence interval (CI) of having significant CAD was: PP per 10 mmHg, OR = 2.51 (95% CI 1.12-5.63); FPP per 0.1, OR = 3.30 (95% CI 1.25-8.72); and PI per 0.1, OR = 1.88 (95% CI 1.09-3.23). In linear regression analysis, IA aortic systolic BP (SBP), PP, FPP and PI were significantly correlated with Gensini score, but NIA indices were not correlated. The NIA aortic PP was lower than IA aortic PP (mean difference: 6.1 ± 15.8 mmHg).IA aortic PP, FPP and PI were related to the presence and severity of CAD, but NIA assessed indices of APW were not related. NIA aortic PP underestimated IA aortic PP.

OBJECTIVES Arterial hypertension and its complications are associated with an increased morbidity and mortality in patients after aortic coarctation (CoA) repair. It is debatable whether early surgery can prevent it. Residual stenosis of descending aorta (AoD) and stiffness in the precoarctation region supposedly lead to hypertension. The aim of this study was to evaluate aortic pulse-wave parameters in adult patients after CoA repair and to determine the influence of residual stenosis and age at operation on their values. METHODS Eighty-five patients underwent CoA repair (53 males; aged 34.6±10.3 years, age at operation: 10.9±8.2 years). The control group consisted of 30 individuals (18 males; aged 33.6±8.2 years). Augmentation pressure (AP), augmentation index (AI), aortic pulse pressure (APP), and pulse-wave velocity (PWV) were measured with applanation tonometry method. RESULTS Normotensive patients after CoA repair (47/55%) had higher values of AP (7.3±4.6 vs. 4.4±3.6 mmHg; P=0.002), AI (18.6±10.4 vs. 13.5±4.3%; P=0.03), APP (39.6±8.8 vs. 35.1±9.8; P=0.00001), and PWV (6.8±1.2 vs. 5.4±0.9 m/s; P=0.003) than controls. Forty-six patients presented signs of recoarctation. No significant differences in the systolic blood pressure and diastolic blood pressure, AI and PWV were found between AoD(+) and AoD(-) but AoD(+) had significantly higher APP (46.7±13.8 vs. 38.3±6.9; P=0.001) and AP (10.5±6.9 vs. 7.5±4.1; P=0.02). Significant correlations were found between current age and APP, AP, and AI. No significant correlations were found between central parameters and the age at operation. CONCLUSION Normotensive patients after CoA repair have elevated central parameters, related to the residual AoD gradient, regardless of the age at operation. Even early repair cannot prevent progressive vascular impairment in CoA.

The effect of sex on the correlation between oscillometric and central aortic blood pressures (BP) is largely unknown. BP was simultaneously measured in the brachial artery using an oscillometric device and in the aorta using a fluid‐filled catheter in 98 patients undergoing coronary angiography. Mean age (±standard deviation) was 58±12 years, with 55% of the patients being male. Mean BP (MBP) measured by the oscillometric device and in the aorta were similar when the group was examined as a whole, but the oscillometric device overestimated MBP in men and underestimated MBP in women. Oscillometric pressures accurately estimated diastolic BP in women but overestimated diastolic BP in men and underestimated systolic BP in both sexes. The oscillometric device underestimated aortic pulse pressure in both sexes but less in men than in women. The accuracy of oscillometric MBP and diastolic BP varied as a function of aortic MBP, but sex‐related differences in the accuracy of oscillometric pressures remained significant after adjusting for MBP, body mass index, height, age, race, heart rate, diabetes, smoking status, and BP‐lowering therapies using a multivariate logistic regression model. Sex is an important determinant of the accuracy of oscillometric BP. J Clin Hypertens (Greenwich). 2011;13:112–119. © 2010 Wiley Periodicals, Inc.

BACKGROUND In large animals pulse pressure increases from central to peripheral arteries whereas mean arterial pressure decreases slightly. This haemodynamic pattern has not been verified in small animals, particularly in hypertensive rats before and after administration of antihypertensive drugs. DESIGN The intra-arterial blood pressure of normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) was determined along the aorta in anaesthetized and conscious rats. In anaesthetized rats the study was performed before and after acute intravenous nicardipine administration (30 micrograms/kg). RESULTS Mean arterial pressure was significantly higher in untreated SHR than in WKY rats, and within each strain was quite similar along the aortic tree. Pulse pressure increased significantly from the central to the terminal aorta in WKY rats, principally due to an increase in systolic blood pressure. In SHR pulse pressure did not differ along the aortic tree. Compared with in WKY rats, aortic pulse pressure in SHR was significantly elevated whereas femoral pulse pressure was quite similar. Acute nicardipine administration re-established the pulse pressure gradient in SHR, due to a significant decrease in central aortic pulse pressure with no significant change in femoral pulse pressure. CONCLUSIONS These results suggest, first, that since there are large differences in pulse pressure in the proximal aorta of SHR and WKY rats but only small or negligible differences in the distal aorta, the measurement of pulse pressure may be an available index to differentiate normotensive and hypertensive rats, and secondly, that increased aortic pulse pressure in SHR participates in the increase in cardiac afterload independently of mean arterial pressure, and may be a preferential site of action of antihypertensive agents.

A high pulse pressure (PP) is a marker of increased artery stiffness and represents a well-established independent predictor for cardiovascular morbidity and mortality. The objective of the research was to determine whether invasively measured central aortic PP was related to the presence and severity of coronary artery disease. In total 1075 consecutive stable male patients undergoing diagnostic coronary angiography with a preserved left ventricular function were included. Diseased coronary vessel (DCV) was defined by the presence of >50 % stenosis. Men were divided into 3 groups according to the increased value of PP. The average PP in the tertiles was 47.8±7.1 vs. 67.0±4.9 vs. 91.3±12.8 mm Hg (p

Almost the same pathophysiological mechanism has been suggested for both atherosclerosis and calcific aortic stenosis (AS). In this study, we examined any association between ascending aortic pressure-derived indices and hemodynamic characteristics of calcific AS.A total of 90 patients were studied (26 males, 64 females; mean age: 64.4 +/- 11.3 years). The study population consisted of two groups: AS and a control group. Both groups were well matched. Ascending aortic pressure-derived indices were obtained from all patients via catheterization.Two groups were well matched according to demographic characteristics. Aortic pulse/FPPs (fractional pulse pressure = aortic pulse pressure/ aortic mean pressure), and PI (pulsatility index = aortic pulse pressure/aortic diastolic pressure) were significantly higher in patients with AS than in those without. Mean aortic mean gradient had significant positive correlation with aortic diastolic pressure, FPP and PI. The multiple-adjusted odds ratios of the risk of AS was 4.51 (95% CI 1.63-12.48) and 4.34 (95% CI 1.59-11.88) for the higher aortic FPP and PI levels compared with lower levels, respectively.Ascending aortic pressure-derived indices were significantly and independently associated with the presence and severity of calcific AS. This confirms the participation of blood pressure in the pathogenesis of AS.

Peripheral (brachial) pulse pressure normally exceeds central (aortic) pulse pressure but is a less powerful predictor of cardiovascular risk. The difference between the 2 variables, called pulse pressure amplification, has never been specifically studied between the proximal and distal aorta in coronary patients. Our goal was to determine aortic pulse pressure amplification in subjects at high coronary risk, with emphasis on associated renal and inflammatory factors. Blood pressure was measured invasively in the ascending aorta, abdominal aorta (at the level of kidneys), and iliac artery in 101 subjects (mean age, 63±11 years; 61 men) undergoing coronary angiography. Independently of age, sex, and the presence of coronary stenosis, the increase of pulse pressure between the ascending and terminal aorta was over 10 mm Hg ( P P P

The purpose of the present investigation was to study the distensibility of the ascending aorta in patients with arterial hypertension and normal subjects before and after administration of a calcium antagonist, nifedipine.The distensibility of the ascending aorta was measured before and after nifedipine administration in 22 male hypertensive patients and 12 age-matched male normotensive subjects. Aortic distensibility was calculated as a function of changes in aortic diameter and pulse pressure, using the formula: 2 x (pulsatile change in aortic diameter)/[(diastolic aortic diameter) x (aortic pulse pressure)]. Aortic diameters were measured by echocardiography and aortic pressures were obtained by catheterization of the ascending aorta.In the basal state, the distensibility of the ascending aorta and aortic strain were lower in hypertensive patients than in normotensive subjects (p0.001); the lower aortic distensibility, however, was associated with a greater distending pressure. A good inverse correlation (r = -0.81) was found between mean aortic pressure and aortic distensibility. The aortic distensibility was increased after nifedipine administration in both groups; this increase in aortic distensibility, however, was lower in the patients with hypertension compared with normotensive subjects (p0.001).Aortic distensibility is decreased in patients with arterial hypertension. Nifedipine administration increased the distensibility of the ascending aorta both in patients with arterial hypertension and in normotensive subjects. The increase of aortic distensibility after nifedipine administration was lower in hypertensive patients.

There is a substantial incidence and prevalence of chronic kidney disease (CKD) in the United States, with poor outcomes and profound economic implications.1 The burden of morbidity and mortality from CKD derives from the progression to end-stage renal disease, and the disproportionate risk of cardiovascular disease (CVD).2 Carotid intima-media thickness (IMT) has emerged as a noninvasive means to assess cardiovascular (CV) risk. An IMT measurement above the 95th percentile is predictive of coronary heart disease risk.3 Change in IMT in participants with CKD over 2 years has been associated with cardiovascular events.5 Measures of large artery stiffness are increasingly recognized to provide information about CV risk in certain populations. Pulse wave analysis (PWA) is a useful tool to study arterial wave reflection in the central circulation. Augmentation index (AI) measures the magnitude and timing of wave reflection. In very young, healthy individuals, the reflected wave returns to the central circulation after a longer time interval and arrives during diastole that augments coronary perfusion pressure. In health, the amplitude of the returning wave is relatively low because healthy elastic arteries dampen its magnitude. In disease states, such as hypertension, the arteries become stiffer resulting in a large magnitude of the reflected wave and an increased pulse wave velocity. Thus, the reflected wave will return to central circulation earlier during systole hereby increasing the cardiac workload. This contributes to left ventricular hypertrophy and reduces coronary perfusion pressure.6 Central aortic systolic pressure (C_SP) is an estimate of aortic systolic pressure derived from the radial artery waveform. Devices used in PWA often employ applanation tonometry of a peripheral artery and then, by means of a transfer algorithm, estimate C_SP and the aortic pulse pressure (C_PP).7 PWA provides prognostic information above and beyond that from traditional CV risk factors in the general population,8 but its significance in patients with CKD who are not on dialysis is limited.9 PWA measurements are noninvasive, easily made and well-suited to large epidemiological trials. PWA is a highly reproducible measurement in CKD.10 Central pressures are better predictors of atherosclerosis, as measured by carotid IMT and plaque, compared to traditional brachial blood pressures.11 Central pulse pressures (PPs) predict CVD outcomes in normal, hypertensive, and end-stage renal disease populations.12,13 Increased AI is associated with angiographic evidence of coronary artery disease in CKD.14 Although PWA and IMT measurements provide information about CV risk, little is known about their association among CKD patients. The radial artery tonometry procedures used in PWA are more easily and quickly performed, and seem better suited for epidemiology usage compared with carotid ultrasonography. Because carotid IMT and carotid plaque assessments, although technically difficult to obtain, are considered better measures of CV risk compared to PWA, we sought to determine how well common radial PWA parameters, and which ones in particular, correlated best with these more generally accepted parameters. We hypothesized that PWA would correlate with IMT and carotid plaque, which are established predictors of CVD. Further, we anticipated that all PWA-derived measures of large artery stiffness would not be equivalent in their prediction of carotid IMT. Thus, we sought to examine which of the PWA parameters, AI, C_SP or C_PP, best correlates with IMT and carotid plaque among patients with CKD.

Although mildly reduced renal function is associated with increased risk for heart failure in patients with coronary artery disease (CAD), mechanisms underlying the association remain unclear. We tested the hypothesis that abnormal ventricular-arterial interaction may occur in mildly reduced renal function. We examined the relationships of the estimated glomerular filtration rate (eGFR) with various indices reflecting ventricular–arterial coupling [effective arterial elastance (the ratio of left ventricular (LV) end-systolic pressure to stroke volume, E a], LV end-systolic elastance (the ratio of LV end-systolic pressure to end-systolic volume, E es), and the total arterial compliance (the ratio of stroke volume to aortic pulse pressure)] and those of LV systolic and diastolic function [peak systolic and diastolic mitral annular velocities (S′ and E′) and the ratio of peak early diastolic mitral inflow to annular velocity (E/E′)] in 320 consecutive patients who underwent cardiac catheterization for CAD and had normal (≥0.50) ejection fractions (EF). As eGFR decreased, E a and E es increased and total arterial compliance and E′ decreased. eGFR did not correlate with E a/E es, S′, or E/E′. After adjusting for potential confounders, the findings were generally similar, but the correlation of eGFR with E′ did not remain significant. In conclusion, reduced renal function may be associated with combined increases in ventricular-systolic stiffness and arterial load in known or suspected CAD patients with normal EF.

Pulse pressure (PP) is an independent predictor of myocardial infarction, mainly above 50 years of age. In subjects with preserved ejection fraction (EF), aortic PP predicts the severity of coronary atherosclerosis. Comparable findings in subjects with reduced EF have not been evaluated. In 1337 subjects with severe coronary ischaemic disease, intra-aortic and brachial blood pressures were measured together with EF and coronary angiography to evaluate cardiac function, the presence of coronary stenosis and/or occlusions or calcifications. The presence (odds ratio+/-95% CI) of coronary calcification was marginally but not significantly associated (P=0.06) to increased aortic PP (1.32 (0.97-1.80)), whereas that of coronary occlusion was significantly associated (P0.01) with decreased aortic PP (0.62 (0.42-0.91)), even after adjustment to EF and heart rate. Increased aortic PP did not correlate with stenosis number. No comparable predictive value was observed using intra-aortic or non-invasive brachial systolic blood pressure (SBP) or diastolic blood pressure (DBP). In high cardiovascular risk populations, even in the presence of reduced EF and high heart rate, intra-aortic PP, but not SBP or DBP, is a significant predictor of coronary occlusions and possibly calcifications, but not stenosis.

Background Systemic lupus erythematosus (SLE) is associated with premature atherosclerosis and increased arterial stiffness. The QPV interval has been proposed as a measure of arterial stiffness. The QPV interval is based on the premise that transit time from cardiac ejection to brachial artery flow is shortened in patients with increased arterial stiffness. Hypothesis The objective of this study was to determine the significance of the QPV interval as a measure of arterial stiffness in patients with SLE. Methods We prospectively studied 46 female SLE patients. The QPV interval was calculated as the time from onset of the QRS complex to peak flow velocity of the brachial artery during ultrasound examination. Measurements of arterial stiffness: augmentation index (AI) and pulse wave velocity (PWV) were obtained by applanation tonometry while patients were on a stable medical regimen. Results Mean age was 44 ± 14 y and mean QPV interval was 198 ± 18 msec QPV interval correlated inversely with age (r = − 0.39, p = 0.008), AI (r = − 0.41, p = 0.004), PWV (r = − 0.39, p = 0.007), and aortic pulse pressure (PP) (r = − 0.45, p = 0.002). On multivariate regression analysis, QPV interval was found to be an independent predictor of PWV after adjusting for age (R2 = 0.26, p < 0.001). Conclusion In women with SLE, QPV decreases with age and is inversely related with measures of arterial stiffness. QPV may be useful in identifying SLE patients with higher arterial stiffness in the clinical or research setting. Further larger studies are needed to confirm these preliminary results. Copyright © 2009 Wiley Periodicals, Inc.

Background— 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. Methods and Results— 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. Conclusions— 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.

Elevated central arterial (aortic) blood pressure is related to increased risk of cardiovascular disease. Methods of non-invasively estimating this pressure would therefore be helpful in clinical practice. To achieve this goal, a physics-based model is derived to correlate the arterial pressure under a suprasystolic upper-arm cuff to the aortic pressure. The model assumptions are particularly applicable to the measurement method and result in a time-domain relation with two parameters, namely, the wave propagation transit time and the reflection coefficient at the cuff. Central pressures estimated by the model were derived from completely automatic, non-invasive measurement of brachial blood pressure and suprasystolic waveform and were compared to simultaneous invasive catheter measurements in 16 subjects. Systolic blood pressure agreement, mean (standard deviation) of difference was -1 (7)mmHg. Diastolic blood pressure agreement was 4 (4)mmHg. Correlation between estimated and actual central waveforms was greater than 90%. Individualization of model parameters did not significantly improve systolic and diastolic pressure agreement, but increased waveform correlation. Further research is necessary to confirm that more accurate brachial pressure measurement improves central pressure estimation.

Diabetes mellitus and impaired fasting glucose (IFG) are associated with future cardiovascular disorders. Aortic pulse pressure (PP) and fractional pulse pressures (FPPs) are strong and independent indicators of the risk of coronary heart disease. These conditions have been reported to be associated with endothelial dysfunction. In the present study, aortic PP and FPPs of patients with and without impaired fasting glucose were evaluated.Fifty patients with IFG with a mean age of 56.8+/-12.2 years and 47 patients with normal fasting glucose (NFG) with a mean age of 53.1+/-11.2 years were included in the study. All subjects had angiographically proven normal coronary arteries without coronary slow flow. Aortic systolic and diastolic blood pressures were measured invasively. Mean pressure, PP and FPPs (aortic PP/mean pressure) were calculated.All parameters measured were significantly higher in the IFG group than in the control (NFG) group (133+/-21 mmHg and 117+/-12 mmHg, p0.001 for aortic systolic pressure; 79+/-12 mmHg and 74+/-8 mmHg, p = 0.035 for aortic diastolic pressure; 97+/-14 mmHg and 88+/-9 mmHg, p = 0.001 for aortic mean pressure; 54+/-13 mmHg and 43+/-8 mmHg, p0.001 for aortic PP; 0.56+/-0.10 and 0.48+/-0.08, p0.001 for aortic FPP). In addition, in linear regression analysis, a positive correlation was found between fasting plasma glucose and the aortic FPP (p = 0.001, R2 = 0.12).Ascending aorta PP and FPPs are significantly associated with the presence of IFG. These findings suggest that IFG is associated with endothelial dysfunction and so aortic stiffness.

BACKGROUND There is conflicting information with regard to the effect of beta-blockers on arterial stiffness and wave reflection. We compared a vasodilating beta-blocker, nebivolol, with atenolol. METHODS We randomized 40 subjects with untreated hypertension (mean +/- s.e.m. systolic/diastolic blood pressure (BP) of 160 +/- 3/98 +/- 1 mm Hg, age 49 +/- 1 years) 16 of whom were women, to atenolol 50 mg or nebivolol 5 mg daily for 4 weeks. Arterial stiffness was assessed in terms of carotid-femoral pulse wave velocity (PWV, Complior) and arterial wave reflection (augmentation index (AIx) by applanation tonometry, Sphygmocor). RESULTS Both beta-blockers produced an equal reduction in brachial BP but aortic pulse pressure (PP) was reduced to a greater extent by nebivolol (P < 0.05). PWV was decreased significantly by both therapies (nebivolol: from 11.5 +/- 0.5 to 9.9 +/- 0.5 m/s; atenolol: from 11.1 +/- 0.4 to 9.8 +/- 0.4 m/s; P < 0.01) but only nebivolol significantly reduced AIx (from 35 +/- 5 to 28 +/- 2%, P < 0.05). In addition, whereas PP amplification (PP, mm Hg) decreased with atenolol therapy (from 10 +/- 1 to 7 +/- 1, P < 0.01), it increased with nebivolol therapy (from 8 +/- 1 to 14 +/- 3, P < 0.01). Atenolol reduced heart rate to a greater extent than nebivolol did (14 +/- 3/min reduction by atenolol vs. 8 +/- 2/min reduction by nebivolol, P < 0.05). There was no difference between the two treatments in respect of the effect on transit time. CONCLUSION The beta-blockers, atenolol and nebivolol, have a similar effect in reducing arterial stiffness in the large elastic aorta, largely secondary to BP reduction. Nebivolol, in contrast to atenolol, has an effect on small muscular arteries, increasing PP amplification and reducing wave reflection, possibly because of increased levels of nitric oxide (NO). Such ancillary properties may impart important distinct hemodynamic effects, and therefore beta-blockers cannot be regarded as a homogeneous group.

To the Editor: We read with interest the article by Jankowski et al1 about the cardiovascular risk associated with central aortic pulse pressure (aPP). Because the measurement of aPP by invasive methods is impractical for the risk stratification and as a means of monitoring the effectiveness of antihypertensive therapy, the authors highlighted in the discussion to the article that the important value of their findings seems to be “the understanding of the nature of relationship between pressure wave and atherosclerosis complications development.” However, it is a matter of debate whether the current study gives …

1. Obesity appears to influence vascular stiffness, an important cardiovascular risk factor. An accurate picture of arterial stiffness may be obtained when a combination of various techniques is used. 2. The purpose of the present study was to assess whether the body mass index (BMI) and body fat content obtained by bioimpedance were of equal value in estimating the influence of body fatness on various indices of vascular stiffness and wave reflection. 3. A total of 175 healthy subjects was studied. Anthropometric measurements and total body bio-impedance analysis were performed to assess fat mass as a proportion of total body composition. Arterial stiffness and wave reflection were assessed using digital volume pulse analysis and tonometric measurement of the wave reflection indices and central haemodynamics. 4. Significant differences in the stiffness index (SI(DVP); P < 0.0001), peripheral augmentation index (pAI(x); P < 0.0001), central augmentation index (cAI(x); P < 0.0001), peripheral pulse pressure (pPP; P = 0.026) and central pulse pressure (cPP; P < 0.0001) were found when the population examined was divided accordingly to tertile of body fat content. However, subdividing various indices of arterial stiffness according to the tertile of BMI did not reveal any significant differences between groups, except for pPP and cPP. 5. Body fat content was significantly correlated with SI(DVP), pAI(x), cAI(x), pPP and cPP. The BMI correlated weakly with SI(DVP), pPP and cPP. 6. In conclusion, the BMI is not very useful in predicting changes in arterial stiffness and wave reflection due to obesity. However, stiffness and wave reflection indices derived from digital volume pulse analysis, the characteristics of radial and aortic pressure waveforms and peripheral and aortic pulse pressure are all related to body fat content, as estimated by bioimpedance.

Brachial blood pressure is predictive of cardiovascular outcome; however central pressure may better represent the load imposed on the coronary and cerebral arteries and thereby bear a stronger relationship to vascular damage and prognosis. Relations of brachial and central pressures to carotid artery hypertrophy (intimal-medial thickness and vascular mass), extent of atherosclerosis (plaque score), and incident cardiovascular events were examined in the Strong Heart Study. Central pressures were calculated using radial applanation tonometry. Among 3520 participants, central and brachial pulse pressures were more strongly related to vascular hypertrophy and extent of atherosclerosis than were systolic pressures. Central pulse pressure was more strongly related to all 3 arterial measures than was brachial pulse pressure ( r =0.364 versus 0.309 for plaque score; P r =0.293 versus 0.249 for intimal-medial thickness; P r =0.320 versus 0.289 for vascular mass; P 2 =13.4, P 2 =6.9, P =0.008). In conclusion, noninvasively-determined central pulse pressure is more strongly related to vascular hypertrophy, extent of atherosclerosis, and cardiovascular events than is brachial blood pressure. These findings support prospective examination of use of central blood pressure as a treatment target in future trials.

Background: Cardiovascular disease is a primary cause of death worldwide. Low parasympathetic nervous activity (PNA) is associated with negative cardiovascular health (CVH) [1]. Central augmentation pressure (CAP), aortic pulse pressure (APP) and augmentation index (Alx) are all strong indicators of CVH. Heart rate variability (HRV) and recovery heart rate (RHR) are both indices of PNA but they do not correlate [2]. Since these indices do not correlation we hypothesized that there would be a difference in their relationship with CVH as determined by CAP, APP and Alx75. Aim: To determine if there is a difference in the relationships between HRV, RHR and CAP, APP and Alx inmen. Methods: Seventeen healthy college aged men were examined for HRV via power spectral density analysis. Recovery heart rate was examined at minute one (RHR1) and two (RHR 2)) following a VO2max test. Pulse wave analysis via applanation tonometry and a generalized transfer function was used to determine CAP, APP and Alx. Results: There was a significant correlation between HRV and CAP (r = 0.61, P = 0.01) and Alx (r = 0.51, P = 0.05). No correlation was observed between RHR 1, RHR 2 and CAP, Alx and APP. Central augmentation pressure was significantly correlated with APP (r = 0.67, P= 0.01) and Alx r = 0.64, P= 0.01). Conclusions: Findings suggest a difference in the relationship between HRV, RHR and CVH. Here HRV was positively correlated with indices of CVH, while RHR did not correlate with these indices. Indicating that HRV seem to be more indicative of CVH versus RHR.

Systemic lupus erythematosus (SLE) is a connective tissue disease where inflammatory activity affects several organ systems. An increased risk of cardiovascular disease has been identified in these patients, even after correction for traditional risk factors. The aim of the present study was to evaluate arterial stiffness and central hemodynamics in women with SLE in comparison to controls. Arterial tonometry was used to measure aortic (carotid-femoral) and arm (carotid-radial) pulse wave velocity (PWV), reflected pressure waves, and aortic augmentation index (AIx) in 27 women with SLE (52 to 68 years) and 27 controls. Aortic PWV was higher in women with SLE than controls, 9.8 m/s versus 8.2 m/s ( P 0.01), after correction for mean arterial pressure and body mass index, 9.5 m/s versus 8.5 m/s ( P 0.05). Other parameters were similar, arm PWV, 8.4 versus 8.5 m/s, AIx 34 versus 33% and calculated central aortic pulse pressure 48 versus 43 mmHg, in SLE and controls, respectively (NS). Aortic PWV was positively associated to C-reactive protein (CRP) and complement factor 3 (C3). Women with SLE have increased stiffness of their elastic central arteries. This may be one factor contributing to the increased cardiovascular risk seen in this cohort.

Peripheral arterial pulse pressure is increasingly used to assess hemodynamic status. Our aim was to test the respective influence of arterial stiffness, stroke volume, peripheral resistance, and various hemodynamic and demographic variables on peripheral pulse pressure in critically ill patients. Prospective study. Medical intensive care unit of a university hospital. None. 67 sinus rhythm patients (mean age 57 ± 17 years) of whom 17 received vasoactive agents. The stroke volume was calculated by Doppler echocardiography. Radial pressures were calibrated from systolic and diastolic brachial cuff pressures. Central aortic pressure was estimated by radial applanation tonometry. The arterial compliance was estimated from the aortic pressure curve using the area method and the arterial stiffness was calculated as 1/compliance. The influences of age, body surface area, arterial stiffness, stroke volume, peripheral resistance, and time intervals on peripheral pulse pressure were tested using univariate and multivariate analyses. The mean arterial pressure ranged from 42 to 113 mmHg. Peripheral pulse pressure (59 ± 17 mmHg) was higher than aortic pulse pressure (40 ± 14 mmHg, p

Angina with normal coronary arteries, cardiac syndrome X, is a diagnosis of exclusion. The exact mechanism of this clinical syndrome remains unclear. Although the prognosis is as good as equal to that of the normal population, symptoms related to the syndrome largely impair quality of life. Aortic pulse and fractional pulse pressures are strong and independent indicators of the risk of coronary heart disease. An increase in these hemodynamic parameters is significantly associated with the presence of coronary artery disease in men and women.We evaluated aortic pulse and fractional pulse pressures of patients with cardiac syndrome X and control subjects, and investigated the relation between the two groups. One hundred and twenty-six patients with cardiac syndrome X with a mean age of 53.1 +/- 9.5 years and 76 patients without the syndrome with a mean age of 53.1+/-11.2 years were studied consecutively from May 2004 to May 2005. Aortic systolic, diastolic, mean and pulse pressures were measured and the fractional pulse pressure was calculated (aortic pulse pressure/mean pressure). Aortic pulse and fractional pulse pressures were significantly higher in the cardiac syndrome X group than in the control group (51 +/- 13 mmHg and 43+/-9 mmHg, p0.001; 0.54 +/- 0.11 and 0.47 +/- 0.08, p0.001, respectively). All patients were classified into tertiles of aortic pulse pressure level to evaluate whether aortic pulse pressure was associated with the presence of cardiac syndrome X in the study. The multiple-adjusted odds ratio of the risk of cardiac syndrome X was 6.72 (95% CI 2.76-16.37) for tertile 2 and 29.94 (95% CI 5.59-160.44) for tertile 3 of aortic pulse pressure level compared with tertile 1. In addition, all patients were divided into two groups as lower and higher levels of aortic fractional pulse pressure. The multiple-adjusted OR of the risk of cardiac syndrome X was 4.09 (95% CI 2.05-8.15) for the higher group compared with the lower group of aortic fractional pulse pressure level.Ascending aorta pulse and fractional pulse pressures are significantly associated with the presence of cardiac syndrome X and these associations are independent of age and other cardiovascular risk factors.

Background. Studies indicated that both aortic pulse pressure (PP) and aortic pulsatility are independently associated with angiographic coronary artery disease (CAD). However, most of these studies included a majority of male subjects, and women were underrepresented. Objective. We investigated the relation of aortic PP and aortic pulsatility derived from invasively measured ascending aortic pressure waveform and presence of angiographic CAD in women undergoing diagnostic coronary angiography. Methods and results. From September 2003 to April 2004, 262 unselected female subjects undergoing first cardiac catheterization were consecutively included in the study. Systolic, diastolic and mean pressure waveforms of the ascending aorta were measured during cardiac catheterization with a fluid-filled system. Aortic pulsatility was estimated as the ratio of aortic PP to mean pressure. Angiographic CAD was detected in 175 (67%) patients. In multiple-adjusted logistic regression, both aortic PP and aortic pulsatility were significantly associated with the presence of CAD (for a 10-mmHg increase in PP: odds ratio [OR] 51.3, 95% confidence interval [CI] 51.1-1.76; for a 0.1 increase in aortic pulsatility: OR = 1.8, 95% CI = 1.3-2.4). When patients were divided into tertiles according to the level of aortic pulsatility, it was noted that multiple-adjusted OR of presence CAD was 2.2 (95% CI = 1.1-4.4) for the middle tertile of the aortic pulsatility level and 5.9 (95% CI = 2.7-12.8) for the highest tertile of the aortic pulsatility level compared with the lowest tertile. Conclusion. In female subjects referred to coronary angiography, ascending aorta PP and aortic pulsatility are significantly associated with the presence of angiographic CAD and these associations are independent of age and other cardiovascular risk factors.

To optimize cardiac resynchronization therapy (CRT) for chronic heart failure (CHF) patients, acute studies show that left ventricular pacing site and atrio-ventricular (AV) delay can be individualized to maximize aortic pulse pressure (PP) increase. In the normal patient it is known that atrial cycle length (ACL) increases as PP increases via the baroreceptor reflex. Therefore, we evaluated another parameter for optimization of pacing parameters - transient ACL, or inversely, sinus heart rate. In a retrospective study, 29 CHF patients, acutely implanted to measure ACL and aortic PP, each received atrial-triggered ventricular pacing in 15 different randomized combinations of 3 pacing sites and 5 AV delays. Each trial contained 15 intrinsic beats (no pacing) and 5 paced beats; PP and ACL changes with pacing were averaged over. the 5 trials. The pacing combination with maximum ACL increase was hypothesized to be statistically related to maximum PP increase. For patients responding to pacing therapy (N = 20), the ACL algorithm predicted optimal or near-optimal (PP increase > 75% of optimal) pacing combinations for most of these patients (85%) and predicted combinations yielding 50-75% of optimal for the rest (15%). This paper describes an algorithm for optimizing PP response via transient ACL measurements. The ACL algorithm may allow rapid and minimally invasive optimization of pacing site and AV delay for CRT in CHF patients.

Objective: Coronary slow flow (CSF) is an angiographic phenomenon characterized by delayed opacification of coronary arteries in the absence of obstructive coronary disease. Recently, increased aortic pulse pressure (PP) and aortic pulsatility were both linked to the presence of angiographic coronary artery disease. In this study aortic PP and aortic pulsatility, derived from the invasively measured ascending aortic pressure waveform, were analyzed in patients with CSF and otherwise normal epicardial coronary arteries and compared with those with completely normal coronary arteries. Methods: Fifty consecutive patients with CSF (35 men, mean age: 51.7 ± 10 years) and fifty age and gender-matched controls (34 men, 51.1 ± 9 years) were included in the study. For determination of coronary flow, the thrombosis in myocardial infarction (TIMI) frame count method was used. Blood pressure waveforms of the ascending aorta were measured during cardiac catheterization with a fluid-filled system. Aortic pulsatility was estimated as the ratio of aortic PP to mean pressure. Results: Study groups were well matched with respect to age, gender and atherosclerotic risk factors. Although systolic, diastolic and mean pressures of the ascending aorta were similar, aortic PP (60.5 ± 19 vs. 51.7 ± 14 mm Hg, p = 0.01) and aortic pulsatility (0.63 ± 0.1 vs. 0.54 ± 0.1, p = 0.006) were significantly higher in patients with CSF compared with the controls. Besides, in all subjects, corrected TIMI frame counts of all three coronary arteries correlated with both ascending aorta PP and aortic pulsatility values. No association was found between corrected TIMI frame counts of coronary arteries and aortic mean blood pressure or brachial blood pressure parameters. Conclusion: Our findings suggest that CSF is, as with obstructive coronary artery disease, associated with more diffuse vascular disease rather than being an isolated finding.

Background Brachial pulse pressure (BPP) is a predictor of outcome in epidemiologic studies, but brachial and aortic pulse pressure (AoPP) may not correspond and both are influenced by multiple parameters including arterial properties and cardiac output. We sought to what extent pulse pressure (PP) measurements reflected direct measurement of arterial properties, assessed as total arterial compliance (TAC). Methods We studied 123 patients (76 men; age 55 +/- 11); 31 normal controls, 46 patients with coronary artery disease and 46 patients with hypertension. PP was determined from brachial cuff pressure and TAC was measured by simultaneous radial applanation tonometry and pulsed wave Doppler of the LV outflow. AoPP was calculated using a transfer function from the radial waveform. Results There was a significant difference between BPP and AoPP (57 +/- 16 vs. 45 +/- 14; P

Background— Despite successful surgical correction, morbidity of patients with coarctation of the aorta is increased. It is well known that these patients have impaired elastic properties of the prestenotic arteries. To find out whether these abnormalities are primarily present or develop later, we studied 17 newborns before and early after surgical repair. Methods and Results— Aortic wall stiffness index and distensibility were calculated using ascending and abdominal aortic diameters determined by M-mode echocardiography and noninvasive estimation of aortic pulse pressure in the right arm and leg. Seventeen patients with aortic coarctation (mean age, 20±26 days) were compared with 17 normal neonates (mean age, 13±7 days) preoperatively and postoperatively (10±6 days after surgery). Ascending aortic distensibility in patients was significantly reduced preoperatively (79±58 versus 105±36; P =0.03) and postoperatively (65±24 versus 105±36; P P =0.04; postoperative, 4.0±1.6 versus 2.7±0.9; P Conclusions— Elastic properties of the prestenotic aorta of patients with coarctation seem to be impaired primarily, even in neonates, and remain unchanged early after successful operation. Surgical correction does not resolve inborn pathology of the prestenotic aortic vascular bed.

The advocated SphygmoCor procedure uses a radial-to-aorta transfer function with calibration on brachial instead of radial artery pressure to assess the central pulse pressure. We compared these values with carotid artery pulse pressures obtained from a validated calibration method, assuming mean minus diastolic blood pressure constant throughout the large artery tree. From 44 healthy subjects (21 males; 22 to 68 years) pressure waves were obtained at the radial, brachial, and carotid artery with applanation tonometry. Using the calibration method, radial and carotid artery pressures were assessed from brachial artery waves and pressures. The effect of brachial-to-radial pulse pressure amplification, brachial pulse pressure, mean pressure, age, gender, height, body mass index, and smoking on differences between the 2 methods was assessed. Brachial artery pressure was 118±12/72±10 mm Hg. SphygmoCor central pulse pressure was 9.7±4.6 mm Hg lower ( P P P =0.005). After calibration of the radial pressure wave with radial instead of brachial artery pressures, the difference between SphygmoCor central pulse pressure and carotid pulse pressure decreased with 4 mm Hg. The advocated SphygmoCor procedure systematically underestimates the central pulse pressure with brachial-to-radial pulse pressure amplification as important determinant. Therefore, calibration of radial artery pressure waves on brachial artery pressures should be avoided. The underestimation of central aortic pulse pressure caused by the radial-to-aorta transfer function itself is much less than previously reported.

We prospectively followed 324 men, who underwent coronary angiography, for 1,161 +/- 418 days. We analyzed the association between ascending aortic pressures measured during cardiac catheterization and the risk of all-cause mortality and a combined end point of major adverse cardiovascular events (MACEs), including unstable angina pectoris, myocardial infarction, coronary revascularization, stroke, or death. Pulse pressure significantly predicted MACEs (hazard ratio [HR] per 10 mm Hg increase 1.09, 95% confidence interval [CI] 1.002 to 1.17, p = 0.04). Diastolic blood pressure (BP) inversely correlated with the risk of MACEs (HR per 10 mm Hg increase 0.85, 95% CI 0.74 to 0.98, p = 0.02). These correlations remained significant after adjusting for other predictors and potential confounders. The association between lower diastolic BP with the risk of MACEs was more pronounced in patients with triple-vessel coronary artery disease (p for interaction = 0.03). Peripheral diastolic BP (but not pulse pressure) correlated inversely with the risk of MACEs (HR 0.87 per 10 mm Hg increase, 95% CI 0.75 to 0.998, p = 0.047). Aortic pulse pressure significantly predicted death (HR per 10 mm Hg increase 1.18, 95% CI 1.05 to 1.33, p = 0.004), and aortic diastolic BP correlated inversely with the risk of death (HR 0.76, 95% CI 0.62 to 0.94, p = 0.01).

Objective: To investigate the elastic properties of the ascending aorta in untreated patients with giant cell arteritis compared with age and sex matched normal controls. Methods: Distensibility of the ascending aorta and aortic strain were measured in 22 patients with a recent diagnosis of giant cell arteritis (documented by a positive temporal artery biopsy) before initiation corticosteroid treatment, and in 44 age and sex matched healthy subjects. Aortic distensibility was calculated as 2x[pulsatile change in aortic diameter]/[(diastolic aortic diameter)x(aortic pulse pressure)], and aortic strain as [pulsatile change in aortic diameter]/[diastolic aortic diameter]. Aortic diameters were measured by echocardiography. Aortic pressures were obtained by external sphygmomanometry. Results: Distensibility of the ascending aorta and aortic strain were both lower in patients with giant cell arteritis than in the controls (p