Vascular Responses to Hand Posture are Preserved Despite Acute Endothelial Dysfunction: Insights from Pulse Wave Velocity and Finger-to-Finger Timing

The aim of our study was to investigate the effects of endogenous melatonin on arterial distensibility using measurements of the velocity of the aortic pulse wave between the carotid and femoral arteries in healthy young students assessed in the supine position. We studied 29 healthy young students, aged between 18 and 27 years, with 19 being male. The measured the velocity of the aortic pulse wave between the carotid and femoral arteries, along the blood pressures and heart rate, while the subjects were in the supine position at two time points, namely from 01.30-02.30 and 13:30-14:30 hours, during a day, also taking plasma to measure the concentrations of melatonin. The velocity of the pulse waves was determined using an automatic device, the Complior Colson (France), which allowed on-line recording and automatic calculation of the velocity, the calculations being made by measuring the transit time of the pulse wave as it traversed the distance between two sites of recording according, the velocity of the pulse wave in meter per second being equal to the distance in meters divided by the time of transit in seconds. Although the velocity of the pulse wave, systolic, diastolic, and mean blood pressures, and heart rate were all increased in the morning relative to measurement made later in the day, levels of melatonin in the plasma were increased in the night. There was negative correlation between diurnal levels of melatonin and the velocity of the pulse wave. Our findings indicate that increased levels of melatonin during the night may cause a decreased velocity of the aortic pulse wave, along with blood pressures and heart rate.

Postprandial lipemia has been associated with acute endothelial dysfunction. Endothelial dysfunction, in turn, is associated with increased arterial stiffness. However, the relationship between postprandial lipemia and acute changes in arterial stiffness has not been extensively investigated. Therefore, we conducted a pilot study on the effects of postprandial lipemia on arterial stiffness in 19 healthy young adults before and after consumption of a high-fat mixed meal. Arterial stiffness was assessed locally with echo-tracking carotid arterial strain (CAS) and globally with carotid-femoral pulse wave velocity (PWV). As assessed by these two benchmark parameters, arterial stiffness did not differ significantly postprandially. However, the arterial distension period (ADP) was significantly lower 2 hours after mixed meal ingestion. In addition, slopes of carotid artery area (CAA) curves were significantly steeper postprandially. Therefore, we concluded that ADP may be a more sensitive marker of arterial stiffness in healthy young adults when compared to PWV and CAS.

To evaluate, in a group of nondiabetic essential hypertensive patients with normal renal function, the relationship between albumin excretion rate (AER) and carotid-femoral pulse wave velocity (PWV), as an index of aortic stiffness. Cross-sectional study. Outpatient hypertension clinic. Seventy patients with mild-to-moderate essential hypertension, aged 42 +/- 8 years, never pharmacologically treated. All subjects underwent routine laboratory tests, 24-h ambulatory blood pressure (BP) monitoring, measurement of carotid-femoral PWV, by means of a computerized method, and AER. Microalbuminuric patients (AER > or = 20 microg min(-1); n = 19), when compared with normoalbuminuric subjects, showed more elevated 24-h BP (136/88 +/- 10/10 vs. 128/83 +/- 7/6 mmHg; P < 0.001 and P = 0.013, for systolic and diastolic BP respectively) and higher values of carotid-femoral PWV (10.4 +/- 2 m s(-1) vs. 9.2 +/- 1.3; P = 0.006). This latter difference remained statistically significant, even after correction by ancova for 24-h systolic and diastolic BP, and body mass index (BMI, P = 0.016). Univariate regression analysis disclosed a tight correlation between AER and carotid-femoral PWV (r = 0.42; P = 0.0003). This association was confirmed in a multiple regression model (beta = 0.35; P = 0.009) in which, as independent variables, besides PWV, 24-h BP, age, serum glucose values, smoking status, gender and BMI, were added. Our results seem to confirm that microalbuminuria may represent the early renal manifestation of a widespread vascular dysfunction, and therefore it is an integrated marker of cardiovascular risk.

The pulse wave velocity (PWV) has been shown to be associated with the properties of blood vessel and a cardiovascular risk factor such as aneurysm. The global PWV estimation is applied in conventional clinical diagnosis. However, the geometry of blood vessel changes along the wave traveling path and the global PWV estimation may not always detect regional wall changes resulting from cardiovascular diseases. In this study, a fluid structure interaction (FSI) analysis was applied on arch-shaped aortas with and without aneurysm aimed at determining the effects of the number of aneurysm, aneurysm size and the modulus ratio (aneurysm to wall modulus) on the pulse wave propagation and velocity. The characterization for each stage of aneurysmal aorta was simulated by progressively increasing aortic stiffness and aneurysm size. The pulse wave propagations and velocities were estimated from the two-dimensional spatial-temporal plot of the normalized wall displacement based on elastic deformation. The descending forward and arch reflected PWVs of aneurysmal aortic arch models were found up to 9.7% and 122.8%, respectively, deviate from the PWV of non-aneurysmal aortic arch model. The PWV patterns and magnitudes can be used to distinguish the characterization of the normal and aneurysmal aortic walls and shown to be relevant regional markers utilized in clinical diagnosis.

Pulse wave velocity, a common metric of arterial stiffness, is an established predictor for cardiovascular events and mortality. However, its intrinsic pressure-dependency complicates the discrimination of acute and chronic impacts of increased blood pressure on arterial stiffness. Cardio-ankle vascular index (CAVI) represented a significant step towards the development of a pressure-independent arterial stiffness metric. However, some potential limitations of CAVI might render this arterial stiffness metric less pressure-independent than originally thought. For this reason, we later introduced CAVI0. Nevertheless, advantages of one approach over the other are left debated. This review aims to shed light on the pressure (in)dependency of both CAVI and CAVI0. By critically reviewing results from studies reporting both CAVI and CAVI0 and using simple analytical methods, we show that CAVI0 may enhance the pressure-independent assessment of arterial stiffness, especially in the presence of large inter-individual differences in blood pressure.

Disentangling Arterial Stiffness and Blood Pressure

Objective: Acute smoking causes endothelial dysfunction through impairment of nitric oxide (NO) production, or increased oxidative stress, but the exact mechanism still needs to be elucidated. In healthy non-smokers acute endothelial dysfunction caused by smoking one cigarette was counterbalanced by red wine's antioxidants. The aim of the present study is to investigate whether red wine's antioxidant substances could counteract the acute endothelial dysfunction induced by acute cigarette smoking in healthy smokers as well.Methods: Twenty healthy volunteers (12 males) participated in a double-blind, cross-over study, comprised of three study days. All subjects either smoked one cigarette, or smoked and drank 250 ml of red wine, or smoked and drank 250 ml of dealcoholized red wine in each one of the study days. Flow mediated dilatation (FMD) was measured at fast and 30, 60 and 90 minutes after each trial.Results: Smoking one cigarette induced a significant decrease in FMD (p < 0.001), which remained significant 30 (p < 0.001), and 60 (p = 0.003) minutes after the end of smoking. FMD remained statistically unchanged after consumption of either regular red wine, or dealcoholized red wine together with smoking.Conclusions: The observed endothelial dysfunction following smoking of one cigarette was counterbalanced by consumption of either red wine or dealcoholized red wine in healthy smokers. It is possible that acute endothelial dysfunction caused by smoking could be attributed to increased oxidative stress and red wine's antioxidants counteract these acute effects of smoke on endothelium.

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 …

To the Editor: The concerns raised by Lantelme et al1 about the relationship between heart rate and pulse wave velocity (PWV) properly apply to the method they employed, not to the conventional method, nor to the long-established relationship between PWV and arterial stiffness. Lantelme et al used Complior, as did the 3 other studies (Lantelme references 8, 15, 17), which appeared to show increasing PWV with increasing heart rate. In Complior, the sensor used to detect the pulse produces a signal, which is related to the derivative of the pressure pulse. A proprietary algorithm is then used to identify the waveform in a proximal and in a peripheral artery, to measure the time difference between the 2 sites, and thereby to calculate pulse wave velocity from the distance between the sites. In the conventional method, PWV is measured from the time delay between the foot (sharp initial systolic upstroke) of the wave at the 2 sites. The theoretical and experimental basis for using PWV as a measure of arterial stiffness was established in the nineteenth century, and the earliest clinical studies were conducted in 1922.2 We are unaware of data similar to those presented by Lantelme, showing any significant relationship between heart rate and PWV using the conventional …

Detection of aortic wall inclusions using regional pulse wave propagation and velocity in silico

Endothelial dysfunction in the early postoperative period after major colon cancer surgery

Aortic pulse wave velocity measured by pulse wave imaging (PWI): A comparison with applanation tonometry

Type 5 phosphodiesterase inhibition by sildenafil abrogates acute smoking-induced endothelial dysfunction

The relationship between acute endothelial dysfunction and the extravasation of leukocytes was studied in vivo with intravital microscopy of the rat mesenteric microvasculature. Acute endothelial dysfunction of the rat mesenteric microvasculature was induced in vivo by superfusing the mesentery for 90 min with one of three different stimulating agents: NG-nitro-L-arginine methyl ester (L-NAME, 50 microM), thrombin (0.5 U/mL), or hydrogen peroxide (H2O2, 50 microM). All three agents induced a similar increase in leukocyte rolling and adherence, which was significantly greater than that observed in control rats superfused with Krebs-Henseleit solution (P < 0.01). Transendothelial migration of leukocytes into the perivascular space was also increased by superfusion with L-NAME, thrombin, or H2O2. However, there was a greater increase in the number of migrated leukocytes in the rat mesentery after L-NAME and H2O2 superfusion than that observed during thrombin superfusion. In vivo infusion of a neutralizing antibody against platelet-endothelial cell adhesion molecule-1 (PECAM-1) specifically inhibited L-NAME-induced and H2O2-induced migration of leukocytes but did not prevent extravasation of leukocytes induced by thrombin. In rat mesenteries superfused with the three different stimuli, immunohistochemical analysis of endothelial cell adhesion molecules expressed on the microvascular endothelium revealed a significant increase of ICAM-1, but not PECAM-1, endothelial cell surface expression (P < 0.01 and P > 0.05 vs. control rats, respectively). Our data confirm a key role for PECAM-1 acutely in leukocyte extravasation in vivo and indicate that the involvement of constitutively expressed PECAM-1 in leukocyte transendothelial migration is preferentially correlated to oxidative stress-related stimuli in the microvascular endothelium.

Background Pulse wave velocity (PWV) is a marker of arterial stiffness and local measurements could facilitate its widescale clinical use. However, confluence of incident and early reflected waves leads to biased spatiotemporal PWV estimates. Objective We introduce the Double Gaussian Propagation Model (DGPM) to measure local PWV in consideration of wave confluence (PWV[Formula: see text]) and compare it against conventional spatiotemporal PWV (PWV[Formula: see text]), with Bramwell-Hill PWV (PWV[Formula: see text]) and blood pressure (BP) as reference measures. Methods Ten subjects ranging from normotension to hypertension were repeatedly measured at rest and with induced PWV changes. Carotid distension waveforms over a 19 mm wide segment were acquired from ultrasonography, simultaneously with noninvasive continuous BP. Per cardiac cycle, the 8-parameter DGPM (amplitude, centroid, width, and velocity, respectively of forward and backward propagating wave) was fitted to the distension waveforms' systolic foot and dicrotic notch complexes. Corresponding PWV[Formula: see text] was computed from linear fittings of respective feature timings and distances. Regression analyses were conducted with PWV[Formula: see text] and PWV[Formula: see text] as predictors, and various PWV and BP measures as response variables. Results Whereas PWV[Formula: see text] correlations were insignificant, PWV[Formula: see text] estimated the reference PWV[Formula: see text] with a significant reduction in errors (P < 0.001), explained up to 65% PWV[Formula: see text] variability at rest, demonstrated higher intra-method consistency and correlated significantly with all BP measures (P < 0.001). Conclusion The proposed DGPM measures local carotid PWV in consideration of wave confluence, showing significant correlations with Bramwell-Hill PWV and BP at two distinct waveform complexes. Thereby PWV[Formula: see text] outperforms the conventional PWV[Formula: see text] in all investigated respects, potentially enabling PWV assessment in routine clinical practice.