Hemodynamic Parameters and Early Intimal Thickening in Branching Blood Vessels.

Intimal thickening due to atherosclerotic lesions or intimal hyperplasia in medium to large blood vessels is a major contributor to heart disease, the leading cause of death in the Western World. Balloon angioplasty with stenting, bypass surgery, and endarterectomy (with or without patch reconstruction) are some of the techniques currently applied to occluded blood vessels. On the basis of the preponderance of clinical evidence that disturbed flow patterns play a key role in the onset and progression of atherosclerosis and intimal hyperplasia, it is of interest to analyze suitable hemodynamic wall parameters that indicate susceptible sites of intimal thickening and/or favorable conditions for thrombi formation. These parameters, based on the wall shear stress, wall pressure, or particle deposition, are applied to interpret experimental/clinical observations of intimal thickening. Utilizing the parameters as "indicator" functions, internal branching blood vessel geometries are analyzed and possibly altered for different purposes: early detection of possibly highly stenosed vessel segments, prediction of future disease progression, and vessel redesign to potentially improve long-term patency rates. At the present time, the focus is on the identification of susceptible sites in branching blood vessels and their subsequent redesign, employing hemodynamic wall parameters. Specifically, the time-averaged wall shear stress (WSS), its spatial gradient (WSSG), the oscillatory shear index (OSI), and the wall shear stress angle gradient (WSSAG) are compared with experimental data for an aortoceliac junction. Then, the OSI, wall particle density (WPD), and WSSAG are segmentally averaged for different carotid artery bifurcations and compared with clinical data of intimal thickening. The third branching blood vessel under consideration is the graft-to-vein anastomosis of a vascular access graft Suggested redesigns reduce several hemodynamic parameters (i.e., the WSSG, WSSAG, and normal pressure gradient [NPG]), thereby reducing the likelihood of restenosis, especially near the critical toe region.

Particle hemodynamics analysis of Miller cuff arterial anastomosis.

OBJECTIVE: Studies of animal and human below-knee anastomoses with Miller cuffs indicate that improved graft patency results from redistribution of intimal hyperplasia away from areas critical to flow delivery, such as the arterial toe. We hypothesize that particle hemodynamic conditions are a biophysical mechanism potentially responsible for the clinically observed shift in intimal hyperplasia localization associated with better patency of the Miller configuration. METHODS: Computational fluid dynamics analysis of vortical flow patterns, wall shear stress fields, and potential for platelet interaction with the vascular surface was performed for realistic three-dimensional conventional and Miller cuff distal end-to-side anastomoses. Sites of significant platelet-wall interaction, including elevated near-wall particle concentrations and stasis, were identified with a validated near-wall residence time model, which includes shear stress-based factors for particle activation and surface reactivity. RESULTS: Particle hemodynamics largely coincide with the observed redistribution of intimal hyperplasia away from the critical arterial toe region. Detrimental changes in wall shear stress vector magnitude and direction are significantly reduced along the arterial suture line of the Miller cuff, largely as a result of increased anastomotic area available for flow redirection. However, because of strong particle-wall interaction, resulting high near-wall residence time contours indicate significant intimal hyperplasia along the graft-vein suture line and in the vicinity of the arterial heel. CONCLUSIONS: While a number of interacting mechanical, biophysical, and technical factors may be responsible for improved Miller cuff patency, our results imply that particle hemodynamics conditions engendered by Miller cuff geometry provide a mechanism that may account for redistribution of intimal hyperplasia. In particular, it appears that a focal region of significant particle-wall interaction at the arterial toe is substantially reduced with the Miller cuff configuration.

Computational analysis of effects of external carotid artery flow and occlusion on adverse carotid bifurcation hemodynamics.

OBJECTIVE: This is a computational analysis of the effects of external carotid artery (ECA) flow, waveform, and occlusion geometry on two hemodynamic wall parameters associated with intimal hyperplasia and atherosclerosis. Study design Transient three-dimensional fluid mechanics analysis was applied to a standard carotid artery bifurcation. Mean internal carotid artery (ICA) flow was maintained at 236 mL/min with a normal waveform. ECA flow was increased from zero to 151 mL/min (64% of ICA flow) with both a normal biphasic waveform and a damped waveform. Geometry of five ECA occlusions was studied: distal, proximal stump, smooth, smooth without carotid sinus, and optimal reconstruction.Primary outcome measures Two time-averaged and area-averaged hemodynamic wall parameters were computed from the velocity and wall shear stress (WSS) solutions, ie, wall shear stress angle gradient (WSSAG) and oscillatory shear index (OSI). Both local and area-averaged hemodynamic wall parameters were computed for the distal common carotid artery (CCA) and the proximal ICA. RESULTS: When ECA flow with a normal waveform is increased from zero to 151 mL/min, area-averaged WSS values increase in the CCA, from 3.0 to 4.4 dynes/cm(2) (46%), and in the ICA, from 16.5 to 17.1 dynes/cm(2) (4%); minimum local WSS values in the carotid sinus remain less than 1 dyne/cm(2); maximum local values of WSSAG and OSI are observed in the carotid sinus and increase from 3.5 to 9.1 radian/cm (160%) and 0.23 to 0.46 (100%), respectively; CCA plus ICA area-averaged WSSAG increases by 52%, and OSI increases by 144%; and damping of the ECA waveform has little effect on local or area-averaged WSSAG but reduces OSI to 68%. When the ECA is occluded, the minimum local WSS in the carotid sinus is less than 1 dyne/cm(2). However, if the carotid sinus is removed or the CCA-ICA geometry hemodynamically optimized, the minimum WSS is approximately 4 dynes/cm(2). Similarly, eliminating the carotid sinus markedly reduces local maximum WSSAG, from 3.0-3.5 radian/cm to 0.3 radian/cm, and reduces local maximum OSI from 0.22-0.49 to 0.04. Area-averaged WSSAG and OSI over the CCA and ICA are reduced by approximately 50% with elimination of the carotid sinus. CONCLUSIONS: The degree of adverse carotid bifurcation hemodynamics as measured with WSSAG and OSI is directly proportional to ECA flow. The marked difference in normal ICA and ECA flow waveforms does not contribute to adverse wall hemodynamics. Location of an ECA occlusion (distal, proximal, stump, smooth) does not affect adverse carotid hemodynamics; however, marked improvement is obtained with elimination of the carotid sinus.

Long-term geometric stability of saphenous vein patched carotid endarterectomy.

PURPOSE: This study was designed to determine whether there is a generalized trend of progressive enlargement of the common and internal carotid bulbs after carotid endarterectomy (CEA) reconstruction with saphenous vein patches. METHODS: Twenty-nine autologous greater saphenous vein-patched CEAs performed between 1983 and 1994 were examined with five to nine sequential duplex scans each that included B-mode measurements of both the common carotid bulb (CCB) and internal carotid bulb (ICB) diameters. A total of 186 scans of each of the two segments were performed from 2 to 182 months after CEA (mean, 64 months). The time from the first to the last scan ranged from 30 to 120 months (mean, 76 months). Repeated measures analysis of variance was used as a means of testing the relationship of CCB and ICB diameters with time from CEA and with time from the first scan. Simple linear regression was used as a means of analyzing the variability of individual CCB and ICB diameters and pooled normalized diameters in both time frames. RESULTS: The CCB diameters ranged from 8.4 to 18.5 mm (mean, 13.1 mm), and the ICB diameters ranged from 6.4 to 16.0 mm (mean, 11.2 mm). No significant relationship between both CCB and ICB diameters in the time from CEA or the time from the first scan (P =.643 to.913), for sex (P =.403 to.917), or for early and late post-CEA time of study onset (P =.135 to.773) was shown by means of repeated measures analysis. Low R(2) values (CCB mean, 0.17; ICB mean, 0.21) and non-significant P values for regression slope (CCB mean, 0.46; ICB mean, 0.54) were given by means of individual regression analysis. There was no correlation between individual regression coefficients and the mean diameters of the arteries. The mean change in CCB diameter was 0.023 mm/year (range, -0.37 to 0.30 mm/year), and the mean change in ICB diameter was -0.030 mm/year (range, -0.33 to 0.37 mm/year). Regression of normalized CCB and ICB diameters versus time gave R(2) values less than 0.02 and slopes not statistically significantly different from zero. The predicted 10-year average percent change in normalized diameters ranged from 0.8% to 3.3%. CONCLUSION: In a 15-year period after CEA and a 10-year sequential B-mode scan study period, there was no evidence of significant enlargement of saphenous vein-patched CEAs. This is also true for CEAs in men and women and for subsets with larger and smaller CCB and ICB diameters and early and late scan onset times. Dilatation after saphenous vein patching is most likely a rare isolated event and not the result of generalized or frequent progressive enlargement.

Balloon catheter dilatation and thrombectomy for acute aortoiliac occlusion.

A case of acute distal aortic thrombosis in an elderly high-risk patient was successfully managed with intraoperative thrombectomy and balloon catheter dilatation of the common iliac arteries. Balloon catheter dilatation may be indicated prior to bypass grafting in high-risk patients with acute aortoiliac thrombosis.