Two-dimensional FSI simulation of closing dynamics of a tilting disc mechanical heart valve.

The fluid dynamics during valve closure resulting in high shear flows and large residence times of particles has been implicated in platelet activation and thrombus formation in mechanical heart valves. Our previous studies with bi-leaflet valves have shown that large shear stresses induced in the gap between the leaflet edge and the valve housing results in relatively high platelet activation levels whereas flow between the leaflets results in shed vortices not conducive to platelet damage. In this study we compare the result of closing dynamics of a tilting disc valve with that of a bi-leaflet valve. The two-dimensional fluid-structure interaction analysis of a tilting disc valve closure mechanics is performed with a fixed grid Cartesian mesh flow solver with local mesh refinement, and a Lagrangian particle dynamic analysis for computation of potential for platelet activation. Throughout the simulation the flow remains in the laminar regime and the flow through the gap width is marked by the development of a shear layer which separates from the leaflet downstream of the valve. Zones of re-circulation are observed in the gap between the leaflet edge and the valve housing on the major orifice region of the tilting disc valve and are seen to be migrating towards the minor orifice region. Jet flow is observed at the minor orifice region and a vortex is formed which sheds in the direction of fluid motion as observed in experiments using PIV measurements. The activation parameter computed for the tilting disc valve, at the time of closure was found to be 2.7 times greater than that of the bi-leaflet mechanical valve and was found to be in the vicinity of the minor orifice region mainly due to the migration of vortical structures from the major to the minor orifice region during the leaflet rebound of the closing phase.

Towards non-thrombogenic performance of blood recirculating devices.

Implantable blood recirculating devices have provided life saving solutions to patients with severe cardiovascular diseases. However, common problems of hemolysis and thromboembolism remain an impediment to these devices. In this article, we present a brief review of the work by several groups in the field that has led to the development of new methodologies that may facilitate achieving the daunting goal of optimizing the thrombogenic performance of blood recirculating devices. The aim is to describe work which pertains to the interaction between flow-induced stresses and the blood constituents, and that supports the hypothesis that thromboembolism in prosthetic blood recirculating devices is initiated and maintained primarily by the non-physiological flow patterns and stresses that activate and enhance the aggregation of blood platelets, increasing the risk of thromboembolism and cardioembolic stroke. Such work includes state-of-the-art numerical and experimental tools used to elucidate flow-induced mechanisms leading to thromboembolism in prosthetic devices. Following the review, the paper describes several efforts conducted by some of the groups active in the field, and points to several directions that should be pursued in the future in order to achieve the goal for blood recirculating prosthetic devices becoming more effective as destination therapy in the future.

FLOW DYNAMIC COMPARISON BETWEEN RECESSED HINGE AND OPEN PIVOT BI-LEAFLET HEART VALVE DESIGNS.

The flow dynamics through the peripheral and hinge regions of a bi-leaflet mechanical heart valve are complex and result in abnormally high shear stresses particularly during the closing phase of the valve function. It has been observed that, the late stages of closure is more significant in the dynamics of platelet activation; therefore, the later stages of closure is simulated by solving the two-dimensional Navier-Stokes equations using an Eulerian Levelset based sharp interface Cartesian grid method. Using a fixed Cartesian mesh incorporating local mesh refinement for solution accuracy and efficiency, the flow through and within a recessed hinge design and an open pivot hinge design is compared. Platelets are modelled as point particles by Lagrangian particle tracking algorithm with one way coupling. A dilute particle flow is assumed and particle-particle interactions are neglected. It was observed that the hinge region of the open pivot valve indicated a lower potential for activation of platelets compared to that in valves with a recessed hinge design.

Two-dimensional simulation of flow and platelet dynamics in the hinge region of a mechanical heart valve.

The hinge region of a mechanical bileaflet valve is implicated in blood damage and initiation of thrombus formation. Detailed fluid dynamic analysis in the complex geometry of the hinge region during the closing phase of the bileaflet valve is the focus of this study to understand the effect of fluid-induced stresses on the activation of platelets. A fixed-grid Cartesian mesh flow solver is used to simulate the blood flow through a two-dimensional geometry of the hinge region of a bileaflet mechanical valve. Use of local mesh refinement algorithm provides mesh adaptation based on the gradients of flow in the constricted geometry of the hinge. Leaflet motion is specified from the fluid-structure interaction analysis of the leaflet dynamics during the closing phase from a previous study, which focused on the fluid mechanics at the gap between the leaflet edges and the valve housing. A Lagrangian particle tracking method is used to model and track the platelets and to compute the magnitude of the shear stress on the platelets as they pass through the hinge region. Results show that there is a boundary layer separation in the gaps between the leaflet ear and the constricted hinge geometry. Separated shear layers roll up into vortical structures that lead to high residence times combined with exposure to high-shear stresses for particles in the hinge region. Particles are preferentially entrained into this recirculation zone, presenting the possibility of platelet activation, aggregation, and initiation of thrombi.

Micro-scale dynamic simulation of erythrocyte-platelet interaction in blood flow.

Platelet activation, adhesion, and aggregation on the blood vessel and implants result in the formation of mural thrombi. Platelet dynamics in blood flow is influenced by the far more numerous erythrocytes (RBCs). This is particularly the case in the smaller blood vessels (arterioles) and in constricted regions of blood flow (such as in valve leakage and hinge regions) where the dimensions of formed elements of blood become comparable with that of the flow geometry. In such regions, models to predict platelet motion, activation, aggregation and adhesion must account for platelet-RBC interactions. This paper studies platelet-RBC interactions in shear flows by performing simulations of micro-scale dynamics using a computational fluid dynamics (CFD) model. A level-set sharp-interface immersed boundary method is employed in the computations in which RBC and platelet boundaries are tracked on a two-dimensional Cartesian grid. The RBCs are assumed to have an elliptical shape and to deform elastically under fluid forces while the platelets are assumed to behave as rigid particles of circular shape. Forces and torques between colliding blood cells are modeled using an extension of the soft-sphere model for elliptical particles. RBCs and platelets are transported under the forces and torques induced by fluid flow and cell-cell and cell-platelet collisions. The simulations show that platelet migration toward the wall is enhanced with increasing hematocrit, in agreement with past experimental observations. This margination is seen to occur due to hydrodynamic forces rather than collisional forces or volumetric exclusion effects. The effect of fluid shear forces on the platelets increases exponentially as a function of hematocrit for the range of parameters covered in this study. The micro-scale analysis can be potentially employed to obtain a deterministic relationship between fluid forces and platelet activation and aggregation in blood flow past cardiovascular implants.

Two-dimensional dynamic simulation of platelet activation during mechanical heart valve closure.

A major drawback in the operation of mechanical heart valve prostheses is thrombus formation in the near valve region. Detailed flow analysis in this region during the valve closure phase is of interest in understanding the relationship between shear stress and platelet activation. A fixed-grid Cartesian mesh flow solver is used to simulate the blood flow through a bi-leaflet mechanical valve employing a two-dimensional geometry of the leaflet with a pivot point representing the hinge region. A local mesh refinement algorithm allows efficient and fast flow computations with mesh adaptation based on the gradients of the flow field in the leaflet-housing gap at the instant of valve closure. Leaflet motion is calculated dynamically based on the fluid forces acting on it employing a fluid-structure interaction algorithm. Platelets are modeled and tracked as point particles by a Lagrangian particle tracking method which incorporates the hemodynamic forces on the particles. A platelet activation model is included to predict regions which are prone to platelet activation. Closure time of the leaflet is validated against experimental studies. Results show that the orientation of the jet flow through the gap between the housing and the leaflet causes the boundary layer from the valve housing to be drawn in by the shear layer separating from the leaflet. The interaction between the separating shear layers is seen to cause a region of intensely rotating flow with high shear stress and high residence time of particles leading to high likelihood of platelet activation in that region.

Comparison of left anterior descending coronary artery hemodynamics before and after angioplasty.

Coronary artery disease (CAD) is characterized by the progression of atherosclerosis, a complex pathological process involving the initiation, deposition, development, and breakdown of the plaque. The blood flow mechanics in arteries play a critical role in the targeted locations and progression of atherosclerotic plaque. In coronary arteries with motion during the cardiac contraction and relaxation, the hemodynamic flow field is substantially different from the other arterial sites with predilection of atherosclerosis. In this study, our efforts focused on the effects of arterial motion and local geometry on the hemodynamics of a left anterior descending (LAD) coronary artery before and after clinical intervention to treat the disease. Three-dimensional (3D) arterial segments were reconstructed at 10 phases of the cardiac cycle for both pre- and postintervention based on the fusion of intravascular ultrasound (IVUS) and biplane angiographic images. An arbitrary Lagrangian-Eulerian formulation was used for the computational fluid dynamic analysis. The measured arterial translation was observed to be larger during systole after intervention and more out-of-plane motion was observed before intervention, indicating substantial alterations in the cardiac contraction after angioplasty. The time averaged axial wall shear stress ranged from -0.2 to 9.5 Pa before intervention compared to -0.02 to 3.53 Pa after intervention. Substantial oscillatory shear stress was present in the preintervention flow dynamics compared to that in the postintervention case.

Flow in prosthetic heart valves: state-of-the-art and future directions.

Since the first successful implantation of a prosthetic heart valve four decades ago, over 50 different designs have been developed including both mechanical and bioprosthetic valves. Today, the most widely implanted design is the mechanical bileaflet, with over 170,000 implants worldwide each year. Several different mechanical valves are currently available and many of them have good bulk forward flow hemodynamics, with lower transvalvular pressure drops, larger effective orifice areas, and fewer regions of forward flow stasis than their earlier-generation counterparts such as the ball-and-cage and tilting-disc valves. However, mechanical valve implants suffer from complications resulting from thrombus deposition and patients implanted with these valves need to be under long-term anti-coagulant therapy. In general, blood thinners are not needed with bioprosthetic implants, but tissue valves suffer from structural failure with, an average life-time of 10-12 years, before replacement is needed. Flow-induced stresses on the formed elements in blood have been implicated in thrombus initiation within the mechanical valve prostheses. Regions of stress concentration on the leaflets during the complex motion of the leaflets have been implicated with structural failure of the leaflets with bioprosthetic valves. In vivo and in vitro experimental studies have yielded valuable information on the relationship between hemodynamic stresses and the problems associated with the implants. More recently, Computational Fluid Dynamics (CFD) has emerged as a promising tool, which, alongside experimentation, can yield insights of unprecedented detail into the hemodynamics of prosthetic heart valves. For CFD to realize its full potential, however, it must rely on numerical techniques that can handle the enormous geometrical complexities of prosthetic devices with spatial and temporal resolution sufficiently high to accurately capture all hemodynamically relevant scales of motion. Such algorithms do not exist today and their development should be a major research priority. For CFD to further gain the confidence of valve designers and medical practitioners it must also undergo comprehensive validation with experimental data. Such validation requires the use of high-resolution flow measuring tools and techniques and the integration of experimental studies with CFD modeling.

Three-dimensional finite element analysis of residual stress in arteries.

Calculation of residual stress in arteries, using the analytical approach has been quite valuable in our understanding of its critical role in vascular mechanics. Stresses are calculated at the central section of an infinitely long tube by imposing a constant axial stretch while deforming the artery from the stress-free state to its unloaded state. However, segments used to perform opening-angle measurements have finite lengths. Further, the stress-free artery configuration is assumed to be circular. Experiments show that they are slightly noncircular. The numerical approach to residual stress calculation can allow us to study both these issues. Using 3D cylindrical geometries and an isotropic material model, we investigated how segment length can affect residual stress calculations and identified the appropriate segment length for experiments. Further, we recorded and used the true noncircular stress-free state of an artery segment, computed the residual stress distribution, and compared it to that from a similar, but circular segment. Our findings suggest that segment length must be ten times the wall thickness for it to be "long" enough. We also found that the circularity assumption may be a reasonable approximation for typical arteries.

Fluid dynamic analysis in a human left anterior descending coronary artery with arterial motion.

A computational fluid dynamic (CFD) analysis is pre sented to describe local flow dynamics in both 3-D spatial and 4-D spatial and temporal domains from reconstructions of intravascular ultrasound (IVUS) and bi-plane angiographic fusion images. A left anterior descending (LAD) coronary artery segment geometry was accurately reconstructed and subsequently its motion was incorporated into the CFD model. The results indicate that the incorporation of motion had appreciable effects on blood flow patterns. The velocity profiles in the region of a stenosis and the circumferential distribution of the axial wall shear stress (WSS) patterns in the vessel are altered with the wall motion introduced in the simulation. The time-averaged axial WSS between simulations of steady flow and unsteady flow without arterial motion were comparable (-0.3 to 13.7 Pa in unsteady flow versus -0.2 to 10.1 Pa in steady flow) while the magnitudes decreased when motion was introduced (0.3-4.5 Pa). The arterial wall motion affects the time-mean WSS and the oscillatory shear index in the coronary vessel fluid dynamics and may provide more realistic predictions on the progression of atherosclerotic disease.

A method for in-vivo analysis for regional arterial wall material property alterations with atherosclerosis: preliminary results.

Atherosclerosis is a diffuse arterial disease developing over many years and resulting in a complicated three-dimensional arterial morphology. The arterial wall material properties have been demonstrated to show regional alterations with atheroma development and growth. We present a mechanical analysis of diseased arterial segments reconstructed from intravascular ultrasound images in order to quantitatively identify regional alterations in the elastic constants with atherosclerotic lesions. We employ a finite element and a displacement sensitivity analysis to divide the arterial segment into regions with different material properties and use an optimization algorithm to identify the elastic constants in these regions. The results with regional variations identified with this method correlated qualitatively with the extent and location of atherosclerotic lesions identified by visual inspection of the affected arteries. The optimized elastic modulus in regions affected by early atherosclerotic lesions ranged from 90.9 to 93.0 kPa where as the corresponding magnitudes in normal arterial segments ranged from 97.9 to 101.0 kPa. This method can be potentially employed to identify the extent and location of atherosclerotic lesions in a systematic analysis and may potentially be used for the early detection of lesion growth.

Pulsatile flow simulation in arterial vascular segments with intravascular ultrasound images.

Previous studies have indicated a correlation between local variation in wall shear stress in arterial blood flow and atheroma development. The purpose of this study was to analyze the hemodynamics in vascular segments from morphologically realistic three-dimensional (3D) reconstruction, and to compare the computed wall shear stress in a compliant vascular segment model and the corresponding rigid walled model. Cross-sectional images of the segments of femoral and carotid arteries in five Yucatan miniswine were obtained using intravascular ultrasound (IVUS) imaging and the segment geometry was reconstructed at different times in the cardiac cycle. The actual measured wall motion from the reconstruction was employed to specify the moving boundaries for simulation of physiological distensibility. Velocity profiles and wall shear stress were computed using unsteady computational fluid dynamics analysis. The computed results revealed that the maximum wall shear stress in the compliant model was approximately 4-17 percent less than that in the rigid model if the wall motion is larger than 10 percent. Our analysis demonstrates that inaccuracies due to inflow velocity profile can be minimized by the extension of the model upstream. The phase angle between the diameter change and wall shear is affected by the local changes in geometry of the arteries. These simulations can be potentially used to analyze the effect of regional wall motion changes in the presence of atherosclerotic lesions on the local fluid dynamics and to correlate the same with subsequent growth of the lesions.

Numerical simulation of mechanical mitral heart valve closure.

A computational fluid dynamic simulation of a mechanical heart valve closing dynamics in the mitral position was performed in order to delineate the fluid induced stresses in the closing phase. The pressure and shear stress fields in the clearance region and near the inflow (atrial) side of the valve were computed during the mitral heart valve closure. Three separate numerical simulations were performed. The atrial chamber pressure was assumed to be zero in all the simulations. The first simulation was steady flow through a closed mitral valve with a ventricular pressure of 100 mm Hg (1.3 kPa). In the second simulation, the leaflet remained in the closed position while the ventricular pressure increased from 0 to 100 mm Hg at a rate of 2000 mm Hg/s (simulating leaflet closure by gravity before the ventricular pressure rise - gravity closure). In the third case, the leaflet motion from the fully open position to the fully closed position was simulated for the same ventricular pressure rise (simulating the normal closure of the mechanical valve). Normal closure (including leaflet motion towards closure, and sudden stop in the closed position) resulted in a relatively large negative pressure transient which was not present in the gravity closure simulation. The wall shear stresses near the housing and the leaflet edge close to the inflow side were around 4000 Pa with normal closure compared to about 725 Pa with gravity closure. The large negative pressure transients and significant increase in wall shear stresses due to the simulation of normal closure of the mechanical valve is consistent with the previously reported increased blood damage during the closing phase.

Numerical study on the effect of secondary flow in the human aorta on local shear stresses in abdominal aortic branches.

Flow in the aortic arch is characterized primarily by the presence of a strong secondary flow superimposed over the axial flow, skewed axial velocity profiles and diastolic flow reversals. A significant amount of helical flow has also been observed in the descending aorta of humans and in models. In this study a computational model of the abdominal aorta complete with two sets of outflow arteries was adapted for three-dimensional steady flow simulations. The flow through the model was predicted using the Navier-Stokes equations to study the effect that a rotational component of flow has on the general flow dynamics in this vascular segment. The helical velocity profile introduced at the inlet was developed from magnetic resonance velocity mappings taken from a plane transaxial to the aortic arch. Results showed that flow division ratios increased in the first set of branches and decreased in the second set with the addition of rotational flow. Shear stress varied in magnitude with the addition of rotational flow, but the shear stress distribution did not change. No regions of flow separation were observed in the iliac arteries for either case. Helical flow may have a stabilizing effect on the flow patterns in branches in general, as evidenced by the decreased difference in shear stress between the inner and outer walls in the iliac arteries.

In vivo demonstration of cavitation potential of a mechanical heart valve.

Cavitation is implicated as the cause of pitting and erosion of explanted mechanical heart valves that failed. Previous in vitro studies demonstrated transient negative pressure spikes upstream of mechanical heart valves at the instant of leaflet closure. When the magnitude of the transient negative pressure spike is below the vapor pressure of the fluid flowing across the mechanical valve, cavitation bubbles have been documented near the valve housing or occluder disc. To test for the presence of transient negative pressure spikes that are conducive to cavitation in vivo, we measured left atrial pressure at the valve orifice after mitral valve replacement. Mitral valves were replaced with 27 mm prostheses in 10 goats (50-60 kg). Control animals (Group 1, n = 5) received pericardial valves. Study animals (Group 2, n = 5) received bileaflet pyrolytic carbon valves. Pressure was recorded from a high frequency atrial transducer at hyperdynamic and hypodynamic states. Transient negative pressure spikes did not occur in any Group 1 animal. Transient negative pressure spikes below the vapor pressure of blood (-713 mm Hg) were recorded in four of five Group 2 animals at the hyperdynamic state: -900, -950, -800, -400, and -1,400 mm Hg (p = 0.048 Group 1 versus Group 2, Fisher's exact test). No cavitation potential exists in vivo after bioprosthetic valve implantation. Transient negative pressure spikes below the vapor pressure of blood occur in vivo at hyperdynamic physiologic states when this bileaflet pyrolytic carbon valve is implanted in the mitral position. These studies demonstrate the potential for cavitation with implanted mechanical valves in vivo.

Negative pressure transients with mechanical heart-valve closure: correlation between in vitro and in vivo results.

Negative pressure transients (NPT) recorded in a single closing event of mechanical valves in the mitral position in an in vitro setup are compared with data recorded in the left atrium in vivo with the valves implanted in the mitral position in an animal model. The loading at valve closure (dP/dtCL) computed from the in vivo ventricular pressure recording (ranging from 700 to 2300 mm Hg/s) agreed with the magnitudes predicted in our earlier in vitro experiments (750-3000 mm Hg/s). The NPT signals and the corresponding power spectral density plots from the in vivo data were in qualitative agreement with those recorded in vitro. The NPT magnitudes were found to be below the vapor pressure for blood in mechanical valves with rigid occluders suggesting a potential for the valve to cavitate in vivo. Our in vivo results also suggest that the valves with flexible occluders are less likely to cavitate. The correlation of the in vitro and in vivo data also suggests that the flexibility of valve housing used in the in vitro studies is not an important factor in the dynamics of mechanical valve closure in vivo.

Numerical study on the effect of steady axial flow development in the human aorta on local shear stresses in abdominal aortic branches.

The three-dimensional flow through a rigid model of the human abdominal aorta complete with iliac and renal arteries was predicted numerically using the steady-state Navier Stokes equations for an incompressible. Newtonian fluid. The model adapted for our purposes was determined from data obtained from cine-CT images taken of a glass chamber that was constructed based on anatomical averages. The iliac arteries had a bifurcation angle of approximately 35 and a branch-to-trunk area ratio of 1.27. whereas the renal arteries had left and right branch angles of 40 and an area ratio of 0.73. The numerical tool FLOW3D (AEA Industrial Technology, Oxfordshire, UK) utilized body-fitted coordinates and a finite volume discretization procedure. Purely axial velocity profiles were introduced at the entrance of the model for a range of cardiac outputs. The four-branch numerical model developed for this investigation produced flow and shear conditions comparable to those found in other reported works. The total wall shear stress distribution in the iliac and renal arteries followed standard trends. with maximum shear stresses occurring in the apex region and lower shear stresses occurring along the lateral walls. Shear stresses and flow rate ratios in the downstream arteries were more effected by inlet Re than the upstream arteries. These results will be used to compare further simulations which take into effect the rotational component of flow which is present in the aortic arch.

Mechanical valve closing dynamics: relationship between velocity of closing, pressure transients, and cavitation initiation.

In this study, the closing dynamics of mechanical heart valves was experimentally analyzed with the valves mounted in the mitral position of an in vitro flow chamber simulating a single closing event. The average linear velocity of the edge of the leaflet during the final 2.065 degrees of the traverse before closing was measured using a laser sweeping technique, and the negative pressure transients at 2 mm from the leaflet inflow surface in the fully closed position was recorded at the instant of valve closure. The cavitation number was computed for the various mechanical valves at a range of load at valve closure. The data were correlated with cavitation bubble visualization previously obtained with the same experimental set up. Cavitation incipience with mechanical valves was found to be independent of the flexibility of the valve holder. For the same loading rate at valve closure, valves with flexible (polyethylene) leaflets were found to close with comparable velocity to those with rigid (pyrolytic carbon) leaflets, but the negative pressure transients did not reach magnitudes close to the vapor pressure for the fluid with flexible leaflets. For the same leaflet closing velocity (and hence the cavitation number), valves with a seat stop or a seating lip in the region of maximum leaflet velocity were observed to cavitate earlier, suggesting that the effect of "squeeze flow" may be an important factor in cavitation incipience.

A hypothesis regarding vascular acoustic emission accompanying arterial injury induced by balloon angioplasty.

Stress-induced structural damage is often accompanied by sound release. This behavior is known as acoustic emission (AE). We hypothesize that vascular injury such as that produced by balloon angioplasty is associated with AE. Postmortem human peripheral arterial specimens were randomly partitioned into test (n = 10) and control segments (n = 10). Test segments were inserted into a pressurization circuit and subjected to two consecutive hydrostatic pressurizations. Amplitude, frequency, and energy content of the AE signals released during pressurization were quantified. Test and matched control segments subsequently underwent identical histological processing. Pressure-induced tissue trauma was estimated via computerized histomorphometric analysis of the resulting slides (n = 100). Vascular acoustic emission (VAE) signals exhibited an amplitude range of +/- 5.0 mu bars and were observed to occur during periods of increasing intraluminal pressure. The VAE signal power within the monitored bandwidth was concentrated below 350 Hz. More than 25 times as much VAE energy was released during the first pressurization as during the second: 1,855 +/- 513.8 mJ vs. 73 +/- 44.9 mJ (mean +/- SEM, p < 0.006). Estimates of circumferential intimal wall stress at AE onset averaged 170 kPa, slightly below reported values of arterial tissue rupture strength. Histomorphometric estimates of tissue trauma was greater for the test than their matched control segments (p < 0.0001). These preliminary data suggest that detectable acoustic energy is released by vascular tissue subjected to therapeutic stress levels. Histological analysis suggest that the underlying source of sound energy may be related to tissue trauma, independent of histological preparation artifacts. From this preliminary work, we conclude that VAE may be a fundamental property accompanying vascular tissue trauma, which may have applications to improving balloon angioplasty outcomes.

In vitro identification of angioplasty-induced injury by use of vascular acoustic emissions.

BACKGROUND: We have developed a novel method of diagnosing stress-induced vascular injury. This approach uses the sound energy released from atherosclerotic arterial tissue during in vitro balloon angioplasty to characterize type and severity of induced trauma. METHODS AND RESULTS: Thirty-two postmortem human peripheral arterial specimens 1.0 cm long were subjected to in vitro balloon angioplasty with simultaneous acoustic emission monitoring. Specimens were examined before and after angioplasty to ascertain the extent of angioplasty-induced injury. Gross observation was used to identify dissection. A three-dimensional intravascular ultrasound reconstruction technique was used to estimate the luminal surface area of the specimen. Change in luminal surface area (postangioplasty minus preangioplasty) was used to quantify induced injury. The energy content and spectral distribution of the digitally acquired vascular acoustic emission (VAE) signals were computed. Comparisons of angioplasty-induced trauma with VAE signal characteristics were made. Dissection (mural laceration of variable depth) was observed in 15 of 32 specimens. Eleven showed no evidence of induced dissection, and 6 had preexisting intimal disruptions. The energy content of the VAE signals collected from specimens with dissection was greater than that obtained from those in which dissection was absent: 845 +/- 89.4 mJ (mean +/- SEM; n = 15) versus 128 +/- 40.8 mJ (n = 1 l; P < .001). Comparison of induced trauma and VAE signal energy demonstrated a proportional relationship (r = .87, P < .001, n = 32). CONCLUSIONS: VAE signals contain information characterizing type and severity of angioplasty-induced arterial injury. Because vascular injury is related to adverse procedural outcome, development of VAE technology as an adjunct to conventional diagnostic modalities may facilitate optimal balloon angioplasty delivery and postprocedural care.