A Novel Interpretation for Arterial Pulse Pressure Amplification in Health and Disease.

Arterial pressure waves have been described in one dimension using several approaches, such as lumped (Windkessel) or distributed (using Navier-Stokes equations) models. An alternative approach consists of modeling blood pressure waves using a Korteweg-de Vries (KdV) equation and representing pressure waves as combinations of solitons. This model captures many key features of wave propagation in the systemic network and, in particular, pulse pressure amplification (PPA), which is a mechanical biomarker of cardiovascular risk. The main objective of this work is to compare the propagation dynamics described by a KdV equation in a human-like arterial tree using acquired pressure waves. Furthermore, we analyzed the ability of our model to reproduce induced elastic changes in PPA due to different pathological conditions. To this end, numerical simulations were performed using acquired central pressure signals from different subject groups (young, adults, and hypertensive) as input and then comparing the output of the model with measured radial artery pressure waveforms. Pathological conditions were modeled as changes in arterial elasticity (E). Numerical results showed that the model was able to propagate acquired pressure waveforms and to reproduce PPA variations as a consequence of elastic changes. Calculated elasticity for each group was in accordance with the existing literature.

Arterial pressure fractality is highly dependent on wave reflection.

UNLABELLED: Wave reflection is an important factor that influences pressure wave morphology and becomes more significant with aging, when cardiovascular risk increases. A pressure wave, measured at any location in the arterial tree, can be decomposed into its forward and backward components and depends on the corresponding amplitude and shifting time delays. Fractal dimension (FD) quantifies the time series complexity defined by its geometrical representation. OBJECTIVE: The aim of this study was to evaluate the arterial pressure and diameter time series in order to assess the relationship between wave reflection and arterial pressure fractal dimension (FD). METHODS: Simultaneous aortic pressure and diameter were measured in 14 conscious dogs. A pair of ultrasonic crystals, a pressure microtransducer and a pneumatic cuff occluder were positioned in the upper third of the descending aorta. RESULTS: Total reflection induced by the occlusion maneuver decreased FD concomitant to the aortic stiffening. CONCLUSION: Arterial pressure fractality is highly dependent on wave reflection.

Coronary arterial stiffness is related with a loss of fractal complexity in the aortic pressure.

UNLABELLED: Arterial stiffening is a common but highly variable disorder. Additionally, excessive arterial pulsatility is associated with various common diseases of aging and hypertension. Fractal dimension (FD) quantifies the time series complexity defined by its geometrical representation. OBJECTIVE: Arterial pressure and diameter time series were evaluated in order to assess the relationship between arterial stiffness and FD. METHODS: Three Corriedale male sheep were operated. Left anterior descending artery (LAD) was dissected and the external arterial diameter was measured trough sonomicrometry. Similarly, a pressure microtransducer was positioned in the upper third of the ascending aorta. Simultaneous pressure and diameter were measured in normal state and under smooth muscle activation. Each time series FD were assessed by the application of Higuchi's method while arterial wall elastic modulus was evaluated by means of the pressure-strain relationship. RESULTS: Coronary stiffness was increased from normal state to phenylephrine state (47.32%, 21.12%, 10.87%) while aortic pressure FD was decreased (2.11%, 2.57%, 6.85%), respectively. CONCLUSION: Acute hypertension induced by phenylephrine produces an increase in the coronary wall elastic modulus with a concomitant decrease in the fractal nature of the aortic pressure, suggesting that coronary stiffening is associated with an unwrinkled aortic pressure.

Changes in vein dynamics ranging from low to high pressure levels as a determinant of the differences in vein adaptation to arterial hemodynamic conditions.

The causes of the regional differences in venous grafts patency rates are partially understood. Differences in vein dynamics during physiological situations could determine differences in veins' capability to face arterial conditions and could contribute to the dissimilar performance of veins as arterial grafts. In vitro pressure and diameter were measured in four different veins during physiological and arterial (graft) pressure conditions. A diameter-pressure transfer function was designed. Compliance, viscous and inertial properties; circumferential stresses and deformation; and buffering function were calculated. Regional differences in veins' dynamics, but not in buffering function were found during physiological and arterial conditions. The back vein (femoral) showed the least changes when submitted to arterial conditions. Arterial conditions represent different changes in vein dynamics depending on the segment considered. The regional differences in vein dynamics, both at physiological and graft conditions, could contribute to explain the dissimilar results of venous grafts.

Smart damping modulation of carotid wall energetics in human hypertension: effects of angiotensin-converting enzyme inhibition.

Damping is the conversion of mechanical energy of a structure into thermal energy, and it is related to the material viscous behavior. To evaluate the role of damping in the common carotid artery (CCA) wall in human hypertension and the possible improvement of angiotensin-converting enzyme (ACE) inhibition, we used noninvasive CCA pressure (tonometry) and diameter (B-mode echography) waveforms in normotensive subjects (NT group; n=12) and in hypertensive patients (HT group; n=22) single-blind randomized into HT-placebo (n=10) or HT-treated (ramipril, 5 to 10 mg/d during 3 months; n=12). Vascular smooth muscle (VSM) null tonus condition was achieved from in vitro pressure and diameter waveforms (Konigsberg microtransducer and sonomicrometry) measured in explanted human CCA (n=14). Arterial wall dynamics was described by viscous (eta), inertial (M), and compliance (C) parameters, mean circumferential wall stress, viscous energy dissipation (WD), peak strain energy (WSt), damping ratio (xi=WD/WSt), and modeling isobaric indexes CIso and WSt(Iso). The lack of VSM tonus isobarically increased wall stress and reduced eta, CIso, and damping (P<0.01). Wall stress, eta, and WD were greater in HT than in NT (P<0.015) and arrived near normal in HT-treated (P<0.032 respect to HT), with no changes in HT-placebo. Whereas CIso increased in HT-treated (P<0.01) approaching the NT level, xi did not vary among groups. During hypertension, because of the WSt increase, the arterial wall reacts increasing WD to maintain xi. ACE inhibition modulates VSM activation and vessel wall remodeling, significantly improving wall energetics and wall stress. This protective vascular action reduces extra load to the heart and maintains enhanced arterial wall damping.

Juxtaaortic counterpulsation: comparison with intraaortic counterpulsation in an animal model of acute heart failure.

This study was designed to compare the effects of juxtaaortic balloon counterpulsation (JABC), performed in ascending aorta and the aortic arch, with those yielded by intraaortic balloon counterpulsation (IABC) in descending aorta, in experimental animals during induced cardiac failure. JABC was achieved with a manufactured Dacron prosthesis and a balloon pump placed between the prosthesis and the wrapped aorta. JABC resulted in a significant increase of cardiac output (from 2.33+/-0.82 to 2.61+/-1.12 L/min, p < 0.05), cardiac index (from 0.071+/-0.025 to 0.080+/-0.033 L/min/kg, p < 0.05) and diastolic pressure augmentation evaluated through diastolic and systolic areas beneath the aortic pressure curve (DABAC/SABAC) index (from 0.94+/-0.21 to 1.10+/-0.33, p < 0.01). End diastolic aortic pressure showed a significant decrease with JABC (from 31.90+/-7.09 to 27.83+/-9.72 mm Hg, p < 0.05). A close association between percentage of DABAC/SABAC increases obtained with IABC and JABC was observed (r2 = 0.67; p < 0.001). Counterpulsation obtained by a juxtaaortic catheter placed in the arch and the ascending wrapped aorta results in an effective hemodynamic improvement comparable with that achieved by an intraaortic catheter in open chest sheep.

A new approach to assist postoperative heart failure in an animal model: juxta-aortic counterpulsation.

Aortic counterpulsation is a useful technique frequently used in postcardiotomy heart failure. An acute heart failure model in open chest sheep was chosen to evaluate hemodynamic improvement with a counterpulsation balloon pump in juxta-aortic position. This was achieved with a manufactured Dacron prosthesis and a balloon pump placed between the prosthesis and the aorta. Juxta-aortic balloon pump counterpulsation in acute experimental heart failure resulted in a significant improvement of hemodynamic parameters: increase of cardiac output (from 0.86 +/- 0.04 to 1.29 +/- 0.09 L/min, p < 0.05) and cardiac index (from 0.03 +/- 0.01 to 0.04 +/- 0.01 L/min per kg, p < 0.05), and decrease of systemic vascular resistance (from 89.76 +/- 6.69 to 66.56 +/- 6.02 mm Hg/L per min, p < 0.05). The extent of aortic diastolic pressure change evaluated through the diastolic and systolic areas beneath the aortic pressure curve (DABAC/SABAC) index before cardiac failure induction showed a significant increase compared with unassisted values (from 0.81 +/- 0.10 to 1.12 +/- 0.09, p < 0.05). Assisted values of DABAC/SABAC index after heart failure induction also showed a significant increase compared with unassisted values (from 0.78 +/- 0.21 to 1.17 +/- 0.38, p < 0.05). Treatment of experimental acute heart failure by juxta-aortic balloon pump counterpulsation allows an effective hemodynamic improvement in open chest sheep.

Endothelium-dependent arterial wall tone elasticity modulated by blood viscosity.

The role of blood viscosity on arterial wall elasticity before and after deendothelization (DE) was studied. Seven ovine brachiocephalic arteries were studied in vitro under physiological pulsatile flow conditions achieved by a mock circulation loop. Instantaneous pressure and diameter signals were assessed in each arterial segment. Incremental elastic modulus (E(inc)) was calculated using the slope of the pure elastic stress-strain relationship. There was no significant difference between E(inc) values before and after DE (3.11 vs. 3.16 10(7) dyn/cm(2)) at a blood viscosity of 2.00 mPa. s. Increases in blood viscosity (2.50, 3.00, 3.50, and 4.00 mPa. s) always resulted in decreases of E(inc) before DE; inversely, increases in blood viscosity resulted in increases of E(inc) after DE. These values of E(inc), for identical levels of blood viscosity, were always significantly lower (P < 0.05) before DE than those obtained after DE. Arterial wall elasticity assessed through E(inc) was strongly influenced by blood viscosity, probably due to presence or absence of endothelium relaxing factors or to direct shear smooth muscle activation when endothelial cells are removed.