Stenotic Vein Grafts Research Articles

Pericardial Hematoma Following Coronary Angiography

ntroduction: Pericardial hematoma is defined as an accumulation of blood in the pericardial space, located in close proximity to the myocardium and deep to the fibrous pericardial sac, which encloses the heart. Case Description: We present a rare case of pericardial hematoma following percutaneous coronary intervention in an individual presenting with stenotic vein graft following symptoms of a myocardial infarction. Initial computed tomography (CT) scan demonstrated hematoma in the pericardial space. This finding was managed conservatively and hematoma was deemed stable on serial CT scans. Discussion: In this urgent situation, CT imaging proves valuable due to its speed, convenience, and accuracy in visualizing the target area from different perspectives. Although patients may appear stable initially after a perforation, a pericardial hematoma can rapidly spread, leading to unstable blood flow that requires prompt intervention and long-term monitoring.

Abstract 254: The Bromo and Extraterminal Domain Protein (BET) Family Drives Endothelial-To-Mesenchymal Transition and Contributes to Vein Graft Stenosis

Background: Vein graft bypass remains the most commonly used open procedure for flow-limiting cardiovascular diseases. However, vein grafts are prone to stenosis, which ultimately leads to graft failure (4-year failure rate at ~43%). Previous studies have provided strong evidence supporting that dysfunctional endothelial cells (ECs) of the vein grafts contribute significantly to neoinitma formation (and hence stenosis) by undergoing EndoMT. Our group has recently shown that BRD4, a member of the BET epigenetic reader protein family, is up-regulated in the neointima lesion of stenotic failed vein grafts. Here we have determined whether BRD4, and possibly other BET proteins, would be involved in EndoMT in vein grafts, and ultimately vein graft stenosis/failure. Method: For in vitro experiments, we treated rat primary vascular ECs with 100ng/ml TGFβ-1 (to induce EndoMT), and/or BET inhibitors (Pan inhibitor: JQ1; Domain-selective inhibitors: Olinone and RVX208), and/or siRNAs for BRD2, 3, and 4. For in vivo experiments, we used a cuff-based technique to establish jugular vein to carotid artery interposition graft in rats, and lentiviral shRNA delivery to achieve specific knockdown of BRD4 in the graft. Results: BET pan-inhibition significantly reduced EndoMT of rat primary vascular ECs in vitro. Similar effects were observed via selective inhibition of bromodomain 2, but not bromodomain 1. Knockdown of BRD4 protein expression in vitro fully recapitulated the inhibitory effect of BET pan-inhibition on EndoMT, whereas knockdown of BRD2 and BRD3 could only lead to partial and marginal abrogation of EndoMT, respectively. In the rat vein graft model, local lentiviral delivery of BRD4 shRNA led to decrease of neointima formation. Conclusion: BET proteins, especially BRD4, play an important role in EndoMT of vascular ECs and also neointima formation in vein grafts. Blockage of BRD4 protein could potentially serve as a novel strategy to achieve prolonged patency of vein graft conduits.

Comparison of percutaneous coronary intervention in native coronary arteries vs. bypass graft in patients with prior coronary artery bypass graft surgery

Aim: Patients with coronary artery bypass grafting (CABG) represent a sizable portion of those undergoing percutaneous coronary intervention (PCI): in many instances, it is unclear whether performing PCI on the bypass graft or in the native coronary vessels can offer the best risk–benefit balance. Methods: We included patientswith prior CABGundergoingPCI at our center between July 2002 and June 2004, and we distinguished them in three groups. Those in whom PCI was performed on stenotic saphenous vein graft (SVG group), those inwhomPCIwasperformedonnativevessels despite thepresence of potentially treatable SVG disease (optional native group) and those in whom PCI had to be performed mandatorily in the native vessels because of chronic SVGocclusions or disease in nonbypassed segments (mandatory native group). The primary endpoint was long-term rate of major adverse clinical events (MACE; i.e., death, myocardial infarction or target vessel revascularization). Results: We identified 109 patients: 28 were in the SVG group, 25 were in the optional native group and 56 were in the mandatory native group. Early MACE occurred with similar frequency in the three groups (respectively, 9.1%, 0% and 5.7%; P=.35). After more than 3 years of follow-up, MACE occurred in 39.3% vs. 28% and 39.4% (P=.59), death occurred in 27.2% vs. 24.0% vs. 13.5% (P=.30) and TVR in 27.3% vs. 8.0% vs. 28.8% (P=.14). Conclusion: In selected patients, PCI of native coronary vessels despite the presence of apparently treatable SVG lesions can be envisioned.

Factors affecting symptomatic vs asymptomatic vein graft stenoses in lower extremity bypass grafts

Conclusions: Symptomatic vein graft stenosis is associated with the presence of distal vein graft lesions, alternative conduit grafts, and larger decreases in the ankle-brachial index (ABI). Graft patency after graft revision is not affected by whether the vein graft stenosis was or was not associated with symptoms. Summary: Stenosis of lower extremity vein grafts is often asymptomatic. This study was undertaken to characterize symptomatic vs asymptomatic vein grafts and to determine if the presence of symptoms influenced subsequent patency of vein grafts after revision. This was a retrospective analysis of a prospectively maintained database from a combined University and Department of Veterans Affairs Vascular Surgical Service. There were 219 lower extremity vein graft revisions performed in 161 patients between January 1995 and January 2007. Patients with vein graft stenoses were considered symptomatic if they had recurrence of the symptoms that had prompted the original placement of the vein graft. Both univariate and multivariate analysis were used to develop a model of independent predictors of symptomatic recurrence. Patency rates for symptomatic and asymptomatic stenotic vein grafts were compared after revision. There were 125 asymptomatic and 94 symptomatic vein graft lesions revised. Lesions associated with symptoms had a significantly greater drop in ABI than asymptomatic lesions (0.21 ± 0.03 vs 0.18 ± 0.02, P = .003). Vein graft stenoses that were located in the distal graft or in the outflow artery were also more likely to be associated with symptom recurrence (P = .048). By multivariate analysis, a decrease in ABI (odds ratio, 6.803; 95% confidence interval [CI], 1.418-32.258; P = .02) and use of alternative vein conduits (odds ratio. 2.633; 95% CI, 1.243-5.578; P = .01) were independent predictors of symptomatic vein graft stenosis. There were also strong trends towards symptomatic recurrence being associated with other systemic manifestations of atherosclerosis such as cerebrovascular disease or coronary artery disease (P = .06). Patients with diabetes or renal failure and current smokers were not more likely to present with recurrent symptoms. Symptomatic stenoses were more frequent in revisions performed between 1 and 2 years postoperatively (56%) than in the first year after the operation (37%, P = .003). Assisted primary patency rates of grafts revised with symptomatic vs asymptomatic stenoses were not different (82% symptomatic and 88% asymptomatic at 5 years; P = .30). Comment: The article defines, for the first time, factors associated with symptomatic vein graft stenoses. Unfortunately, although stenoses revised in alternative conduit grafts and stenoses revised >1 year after graft implantation are more frequently associated with symptoms, a significant number of patients in those groups also have asymptomatic graft stenosis of sufficient severity that the graft requires revision. At this time, a life-long policy of periodic surveillance of lower extremity vein grafts with duplex scanning still seems prudent.

Use of an aortic connector system for vein grafting

The aortic connector system was used to minimize cerebrovascular complications when performing the proximal anastomosis of vein grafts during coronary artery bypass grafting (CABG). The goal of this study was to investigate the intermediate outcomes of patients undergoing CABG with the aortic connector system. The aortic connector was used on nine patients undergoing CABG between November 2002 and July 2003. Intermediate outcomes of the patients were examined, and the results of coronary angiography, which were performed before patient discharge and at least 6 months after discharge, were evaluated. There were no operative deaths or cerebrovascular accidents. One patient died 9 months after discharge, one patient had angina, and the remaining seven patients were asymptomatic. When evaluating the results of angiography performed before patient discharge, two of the 21 distal vein graft anastomoses were occluded (patency rate, 90.5%), but there was no stenosis or occlusion at the proximal anastomoses sites that were performed using the aortic connector. When evaluating the results of the second angiography performed after patient discharge, four of the eight proximal anastomoses were patent, one was completely occluded, two had 90% stenosis and one had 75% stenosis. Further, four of the 18 distal anastomoses were occluded (patency rate, 77.8%). There was no significant difference in graft flow or device size when comparing patients with patent vein grafts and those with stenotic or occluded vein grafts. Intermediate outcomes of vein grafting using the aortic connector were suboptimal. Long-term outcome data are forthcoming.

Altered expression of vascular endothelial growth factor and its receptors in normal saphenous vein and in arterialized and stenotic vein grafts

Background Myointimal thickening is a major cause saphenous vein graft failure. The prominence of medial and adventitial microvessels in stenotic vein grafts and the known angiogenic effects of vascular endothelial growth factor (VEGF) lead us to investigate the expression of VEGF and its receptors in vein graft arterialization and stenosis. Methods Normal and arterialized vein graft segments were evaluated by reverse transcription-polymerase chain reaction (RT-PCR) for expression of VEGF-R1 (flt), VEGF-R2 (KDR), and neuropilin-1. The cells expressing VEGF, VEGF-R1, VEGF-R2, and neuropilin-1 were identified in normal, stenotic, and arterialized vein graft segments by immunohistochemistry. Results Vascular endothelial growth factor, detected in the wall in endothelial cells and adventitial microvessels in normal vein, localized to smooth muscle cells, endothelial cells and adventitial microvessels in arterialized and stenotic vein. VEGF-R1 and VEGF-R2 were expressed infrequently on endothelial cells, macrophages, and smooth muscle cells in arterialized and stenotic vein. Neuropilin-1 was detected in all specimens. RT-PCR demonstrated significantly greater expression of neuropilin-1 in normal vein compared with arterialized vein ( P <0.05). Conclusions The differential expression of VEGF and its receptors in normal, arterialized, and stenotic vein grafts suggests that alterations in VEGF/VEGF-R2/neuropilin-1 interactions may be important determinants of the adaptive response of vein grafts to arterialization.

Vein graft function improvement after percutaneous intervention: evaluation with MR flow mapping.

To provide functional reference values in single and sequential vein grafts by using magnetic resonance (MR) flow mapping and to examine the effect of percutaneous intervention (PCI) on coronary artery bypass graft function. Fast MR flow mapping at baseline and during adenosine-induced stress was performed in 39 nonstenotic single vein grafts and 20 nonstenotic sequential vein grafts, as well as in 15 stenotic vein grafts before and 7.3 weeks +/- 1.5 after successful PCI. We evaluated the following parameters (in terms of mean values +/- SDs): average peak velocity (APV) at baseline, stress APV, and velocity reserve. Parameters in nonstenotic single and sequential vein grafts were compared by means of unpaired two-tailed Student t testing. To evaluate changes in velocities before and after PCI, a paired two-tailed Student t test was used. P <.05 was considered to indicate a statistically significant difference. Reference values in single vein grafts for baseline APV, stress APV, and velocity reserve were 8.6 cm/sec +/- 3.4, 20.2 cm/sec +/- 9.5, and 2.4 +/- 0.8, respectively. In sequential vein grafts, significantly higher values for baseline APV (12.2 cm/sec +/- 5.0) and stress APV (27.2 cm/sec +/- 10.6) but a similar velocity reserve (2.3 +/- 0.7) were found. Significant improvements were observed after PCI in baseline APV (before PCI: 9.2 cm/sec +/- 6.6; after PCI: 12.9 cm/sec +/- 7.9; P =.008) and stress APV (before PCI: 12.9 cm/sec +/- 6.3; after PCI: 27.1 cm/sec +/- 13.9; P <.001). No improvement in velocity reserve was observed. Significantly higher absolute velocity and flow values were observed in sequential versus single vein grafts, underscoring the need for separate functional reference values for different graft types. Graft function showed significant improvement after PCI to the point that it was restored or nearly restored to reference values.

Proliferative activity in stenotic human aortocoronary bypass grafts

Background: Aortocoronary bypass graft disease is responsible for long-term failure of autologous vein grafts. The analyses of proliferation and cell type characterisation in human bypass grafts harvested during re-do surgery make it possible to investigate the cellular processes leading to bypass graft failure. Methods: 30 stenotic vein grafts and 25 control veins were explantated during re-do heart surgery procedures. The total area and cell count of the neointima, media and adventitia were calculated computer-assisted. Actively proliferating cells were identified using antibody to Ki-67 and positive cells were determined by double-label immunocytochemistry with SMC α-actin, CD 31 (endothelial cells), CD 68 (macrophages) and CD 45 (T-lymphocytes). Results: Active proliferation was detected in different cell types with an average proliferation index of 0.15%, 0.18% and 0.086% for neointima, media and adventitia. Only 9% of proliferating cells in the neointima were SMC (not identified cells 40%); correspondingly, 14% SMC (not identified cells 33%) were detected in the media. Endothelial cells turned out to be the predominant proliferating cell type in all sections of the vessel wall. Conclusion: Proliferation in our series of stenotic vein grafts occurred at a low level, but was significantly higher compared to native control veins. While proliferation may play an important role in early lesions, our data clearly show low proliferation activity in advanced graft lesions. The identification of proliferating macrophages and T-lymphocytes implicate an additional inflammatory component in the development of human bypass graft disease. Summary: To clarify the role of cellular proliferation in human aortocoronary bypass grafts, we characterized the cellular composition and proliferation index in 30 stenotic saphenous vein grafts in comparison to 25 native veins. Proliferation in our series of stenotic vein grafts occurred at a low level, but was significantly higher compared to native control veins.

CD40 Co-Stimulatory Molecule Expression by Dendritic Cells in Primary Atherosclerotic Lesions in Carotid Arteries and in Stenotic Saphenous Vein Coronary Artery Grafts

We have previously identified dendritic cells in the intima of human large arteries and stenotic vein coronary bypass grafts. The mechanisms by which these dendritic cells might regulate immune responses in atherosclerotic lesions and stenotic vein grafts are unknown. The aim of the present study was to investigate whether dendritic cells in carotid plaques and in stenotic aortocoronary vein grafts express an immunoregulatory molecule CD40. Segments of wall from eight carotid arteries and three stenotic aortocoronary saphenous vein grafts were obtained at operation. CD40+ cells were detected in all specimens of both occluded and stenotic grafts and carotid plaques. Although CD40+ cells of various cell types were intermingled in most areas within the plaques and stenotic grafts, there were sites where CD40+ cells were located in small groups. Consecutive sections demonstrated that a small population of CD40+ cells stained positively for S100. These CD40+/S100+ cells were clustered within the intima but were also found in the media and adventitia. This suggests that dendritic cells, which accumulate within vessels affected by atherosclerosis and graft disease, express CD40 co-stimulatory molecule. The expression of CD40 molecule on the dendritic cells may be important in regulating T cell responses within atherosclerotic plaques and stenotic vein grafts.

CD40 co-stimulatory molecule expression by dendritic cells in primary atherosclerotic lesions in carotid arteries and in stenotic saphenous vein coronary artery grafts

We have previously identified dendritic cells in the intima of human large arteries and stenotic vein coronary bypass grafts. The mechanisms by which these dendritic cells might regulate immune responses in atherosclerotic lesions and stenotic vein grafts are unknown. The aim of the present study was to investigate whether dendritic cells in carotid plaques and in stenotic aortocoronary vein grafts express an immunoregulatory molecule CD40. Segments of wall from eight carotid arteries and three stenotic aortocoronary saphenous vein grafts were obtained at operation. CD40 + cells were detected in all specimens of both occluded and stenotic grafts and carotid plaques. Although CD40 + cells of various cell types were intermingled in most areas within the plaques and stenotic grafts, there were sites where CD40 + cells were located in small groups. Consecutive sections demonstrated that a small population of CD40 + cells stained positively for S100. These CD40 +/S100 + cells were clustered within the intima but were also found in the media and adventitia. This suggests that dendritic cells, which accumulate within vessels affected by atherosclerosis and graft disease, express CD40 co-stimulatory molecule. The expression of CD40 molecule on the dendritic cells may be important in regulating T cell responses within atherosclerotic plaques and stenotic vein grafts.

Intimal growth and neovascularization in human stenotic vein grafts

Background: Myointimal thickening and microvessel ingrowth are commonly observed in vein graft stenosis, which complicates a third of infrainguinal bypass procedures. But a direct correlation between these two features has not been established. Our purpose was to analyze the relationship between neovascularity and intimal thickness in human vein grafts. Study Design: Twenty-two explant stenotic vein grafts (STVG), 8 nonstenotic arterialized vein grafts (AVG), and 20 age-matched control greater saphenous veins (CGSV) were analyzed histologically and compared morphologically by light microscopy. Digitized computer image analysis was used to measure intimal thickness and quantitate microvessel ingrowth. Immunolocalization of endothelial cells around the lumen and in microvessels was determined using antibodies to factor VIII and to endothelial nitric oxide synthase (eNOS), respectively. Results: Focal areas of endothelial disruption and thrombus deposition were present in 23% (5 of 22) of stenotic vein grafts. The neointima of STVG grafts was two- and fourfold thicker than that of AVG and CGSV, respectively (p < 0.0001). Microvessels were most frequently observed in the adventitia and media of STVG and increased in number with increasing intimal thickness (p < 0.001 by ANOVA). Conclusions: A fourfold increased neointimal thickness in critically stenotic vein grafts is associated with increased medial and adventitial neovascularization. Remodeling alone with doubling of the intimal thickness in nonstenotic arterialized vein grafts does not appear to be associated with enhancement of the graft microvasculature. More specific observations using an experimental model may allow us to further define the role of angiogenesis in vein graft stenosis and to determine the therapeutic implications of such observations.

Characterization of cellular density and determination of neointimal extracellular matrix constituents in human lower extremity vein graft stenoses

Arterial restenosis has been attributed to a hyperproliferative smooth muscle cell response. Paradoxically, studies of human coronary atherectomy and vein graft stenotic lesions have demonstrated a relatively low nuclear proliferative rate with the majority of the neointimal mass consisting of extracellular matrix. The purpose of the present study was to characterize the cellular density and determine the relative composition of the extracellular matrix protein constituents in stenotic, human lower extremity vein-bypass graft lesions. Methods: Duplex surveillance of 148 consecutive infrainguinal bypass grafts identified 17 patients with 22 pre-occlusive autogenous vein graft stenoses (mean graft age 7 months). Morphological analyses of these stenotic lesions were compared with excised samples of 20 greater saphenous vein segments taken at the time of graft implantation from matched control patients. Intimal and medial areas were compared and cell density was determined with fluorescent nuclear (Bisbenzimide) staining. Differential light microscopy with pentachrome staining was performed to determine the relative percent composition of intimal matrix constituents by stereological morphometric (point-count) techniques. Results: The intimal areas for control and stenotic vein segments were 1.64×10 6 μm 2 and 3.85×10 6 μm 2, P<0.0001, whereas the intimal nuclear densities (cells/unit volume) were 1.42×10 3 and 1.70×10 3 cells/ μm 2, P=0.03, respectively. The corresponding medial area and medial nuclear densities were 5.01×10 6 μm 2, 3.31×10 6 μm 2; P=0.08, and 2.27×10 3, 3.29×10 3; P=0.001, for control and stenotic specimens, respectively. The intima:media area ratios were much greater, whereas the intimal and medial cell densities were only slightly greater in the stenotic compared with control veins. The relative composition of intimal extracellular matrix proteins of stenotic vein graft segments consisted of 21% cellular (fibrous) material, 33% collagen, and 46% glycosaminoglycan ground substance. Conclusion: The intimal lesions responsible for lower extremity vein graft stenosis are more hypertrophic than hyperplastic. Therapies aimed at preventing arterial and vein graft restenosis may thus need to inhibit matrix biosynthetic processes in addition to cellular proliferation.

Characterization of Cellular Density and Determination of Neointimal Extracellular Matrix Constituents in Human Lower Extremity Vein Graft Stenoses

Arterial restenosis has been attributed to a hyperproliferative smooth muscle cell response. Paradoxically, studies of human coronary atherectomy and vein graft stenotic lesions have demonstrated a relatively low nuclear proliferative rate with the majority of the neointimal mass consisting of extracellular matrix. The purpose of the present study was to characterize the cellular density and determine the relative composition of the extracellular matrix protein constituents in stenotic, human lower extremity vein-bypass graft lesions. Methods: Duplex surveillance of 148 consecutive infrainguinal bypass grafts identified 17 patients with 22 preocclusive autogenous vein graft stenoses (mean graft age 7 months). Morphological analyses of these stenotic lesions were compared with excised samples of 20 greater saphenous vein segments taken at the time of graft implantation from matched control patients. Intimal and medial areas were compared and cell density was determined with fluorescent nuclear (Bisbenzimide) staining. Differential light microscopy with pentachrome staining was performed to determine the relative percent composition of intimal matrix constituents by stereological morphometric (point-count) techniques. Results: The intimal areas for control and stenotic vein segments were 1.64 × 106 μm2 and 3.85 × 106 μm2, P &lt; 0.0001, whereas the intimal nuclear densities (cells/unit volume) were 1.42 × 103 and 1.70 × 103 cells/μm2, P = 0.03. respectively. The corresponding medial area and medial nuclear densities were 5.01 × 106 μm2, 3.31 × 106 μm2; P = 0.08. and 2.27 × 103, 3.29 × 103; P = 0.001, for control and stenotic specimens, respectively. The intima: Media area ratios were much greater, whereas the intimal and medial cell densities were only slightly greater in the stenotic compared with control veins. The relative composition of intimal extracellular matrix proteins of stenotic vein graft segments consisted of 21% cellular (fibrous) material, 33% collagen, and 46% glycosaminoglycan ground substance. Conclusion: The intimal lesions responsible for lower extremity vein graft stenosis are more hypertrophic than hyperplastic. Therapies aimed at preventing arterial and vein graft restenosis may thus need to inhibit matrix biosynthetic processes in addition to cellular proliferation.

At what peak velocity ratio value should duplex-detected infrainguinal vein graft stenoses be revised?

To determine the peak velocity ratio (PVR) threshold at which to intervene and correct duplex detected vein graft stenoses. Prospective study. Infrainguinal vein grafts in patients attending the vascular studies for routine postoperative surveillance. Colour duplex detected stenotic vein graft lesions with a peak velocity ratio (PVR) between 2.0 and 2.9 were identified and monitored by serial duplex scans performed monthly for 3 months and then at 3-monthly intervals thereafter. At the end of the study period, the outcome of these lesions were analysed. Thirty-eight lesions were identified from 32 grafts. Of these lesions, sixteen (42%) resolved, 11 (29%) remained stable and 11 (29%) progressed to a PVR of > or = 3.0 and underwent angioplasty. There were no occlusions in any of the grafts during the period of study. Colour duplex detected vein graft stenoses with a PVR of less than 3.0 can be treated expectantly if grafts with stenoses with a PVR 2.0-2.9 are scanned every month for at least 3 months after detection.

Hemodynamic impact of vein graft stenoses and their prediction in the vascular laboratory.

We undertook this prospective evaluation to define the direct hemodynamic impact of vein graft stenoses and to correlate intraoperative hemodynamic findings with the preoperative duplex scan. Twelve consecutive isolated vein graft stenoses were identified in the vascular laboratory during our routine duplex scanning surveillance protocol over 10 months. Peak systolic flow velocity ratios (PSFVRs; velocity within stenosis/velocity proximal to the stenosis) at the stenoses ranged from 2.7 to 10 (mean, 5.5), and ankle-brachial indexes ranged from 0.47 to 0.94 (mean, 0.68) Preoperative arteriograms were obtained and confirmed the isolated stenoses, which radiographically ranged from 20% to 83% diameter reduction (mean, 64%). At the time of surgery the stenotic graft segment was isolated, and simultaneous pressure measurements proximal and distal to the graft stenosis were measured, along with ultrasound transit-time blood flow measurements. Pressure and flow wave forms were recorded for 10 seconds at 200 Hz and were stored on a personal computer-based digital acquisition system. The graft stenoses were then repaired with either a vein patch or short interposition graft, and the hemodynamic measurements were repeated. Fourier transformation of the pressure and flow curves was performed, and the resistance and longitudinal impedance were calculated for each graft segment. Before repair, mean pressure gradients across the stenotic graft segments (delta P) ranged from 1.0 to 74.6 mm Hg (mean, 20.4 mm Hg), and vein graft flow ranged from 4.9 to 140 ml/min (mean, 45.2 ml/min). After repair of the stenotic segments, the mean pressure gradient was decreased to a mean of 1.3 mm Hg, and vein graft flow increased to a mean of 104.8 ml/min. The PSFVR recorded in the vascular laboratory correlated significantly with delta P (r = 0.71; p = 0.01) and allowed prediction of delta P as: delta P = 7.4 (PSFVR) - 19.8. PSFVR also correlated with measured resistance across the stenosis (r = 0.79; p = 0.004). Conversely, the angiographic measurement of stenosis did not correlate significantly with these parameters. The angiographic measurement of stenosis showed a moderate correlation with the PSFVR (r = 0.58; p = 0.046). The PSFVR, as measured in the laboratory, is an accurate and useful indicator of the hemodynamic impact of vein graft stenosis. Revision of stenotic vein graft segments resulted in a significant improvement in graft hemodynamics.

Systolic flow limitation in stenotic lower-extremity vein grafts

Our purpose was to investigate the hemodynamic theory that the blood flow rate through a stenotic arterial graft is limited by the onset of turbulence, which acts as a barrier at peak systole against further increases in systolic flow. We used duplex ultrasonography to examine 25 stenotic infrainguinal vein grafts. Theory predicts that the flow limitation occurs at peak systole at a stenotic velocity greater than 250 cm/sec, which corresponds to a residual stenotic lumenal diameter of 0.36 cm (Reynolds No. 2000). These numbers are based on the assumption that the 68 ml/min blood flow is supplied by the femoropopliteal graft to the resting lower leg only during systole. When the lumen is smaller than 0.36, peak systolic velocity (PSV) must exceed 250 cm/sec. The increased velocity results in poststenotic turbulence. This turbulent condition restricts the average graft systolic flow to less than the 68 ml/min required by the lower leg, so diastolic flow is needed to make up the deficit. Twenty vein grafts with PSVs of 250 cm/sec or greater had end-diastolic velocities of 50 cm/sec or greater as predicted; three grafts with PSVs of 256 to 300 cm/sec and two grafts with PSVs of less than 250 cm/sec had no forward diastolic flow. The onset of turbulence in a stenotic vein graft supplying the lower leg occurs at a PSV of 250 cm/sec or greater. The appearance of diastolic flow maintains the average graft volume flow.

Hemodynamics of Stenotic Infrainguinal Vein Grafts: Theoretic Considerations

We developed a theoretic model of arterial stenosis to study the relationship between perfusion pressure and regional hemodynamics in stenotic infrainguinal vein grafts in an attempt to identify grafts at high risk for failure. Our model was based on the concept of energy and mass conservation of the flowing blood. We used the modified Bernoulli equation (delta P = 4 delta V2) to calculate the maximum possible intrastenotic peak systolic velocity (PSV) from the systolic blood pressure. PSV was measured by means of duplex ultrasonography in infrainguinal bypasses up to the time of revision (nine grafts) or spontaneous thrombosis (two grafts). We related arm systolic blood pressure, intrastenotic PSV, and prestenotic PSV obtained from duplex examinations conducted prior to graft thrombosis or revision and applied our model to these stenotic vein grafts. Intrastenotic PSV was consistently lower than maximum PSV predicted from the Bernoulli equation. The highest measured intrastenotic PSV of 600 cm/sec would require a minimum perfusion pressure of 144 mm Hg. The lowest measured PSV (20 cm/sec) was considered the minimum "thrombotic threshold velocity." This model predicts that for parabolic profile flow in an 80% diameter-reducing axisymmetric stenosis (96% cross-sectional area reduction), a prestenotic PSV of 20 cm/sec would produce an intrastenotic PSV of 500 cm/sec requiring the equivalent potential energy of 100 mm Hg systolic blood pressure. Our theory implies that in patients with nocturnal hypotension thrombosis of stenotic vein grafts may occur.

Hemodynamic parameters of failing infrainguinal bypass grafts

To assess the relationship of duplex ultrasound hemodynamic parameters in stenotic vein grafts with events such as graft thrombosis or surgical revisions. We studied 35 patent infrainguinal bypass grafts that were observed by means of color duplex graft mapping using a surveillance protocol. During the 11.2 month mean follow-up interval, 10 grafts developed complications. Two stenotic grafts (1 already revised) thrombosed spontaneously, and arteriography was obtained on the basis of either clinical indications or a decreased ankle/brachial index of greater than 0.15 on 9 bypasses, leading to 12 procedures (multiple procedures on 2 grafts). The 14 duplex examinations preceding an event showed these bypasses had increased focal peak systolic velocities that ranged from 250 to 600 cm/s and velocity ratios that ranged from 3.4 to 25.0 at the stenotic segment of the graft, anastomosis, or outflow artery. None of the grafts with a stenotic peak systolic velocity less than 250 cm/s or a velocity ratio less than 3.4 thrombosed spontaneously or required revision. We conclude that stenotic vein grafts with a focal peak systolic velocity of at least 250 cm/s or a velocity ratio of at least 3.4 are at increased risk for thrombosis or need for revision. Asymptomatic stenotic vein grafts with focal peak systolic velocities and ratios less than the above values may be safely observed without immediate risk for thrombosis.

Coronary reoperation: Results of adding an internal mammary artery graft to a stenotic vein graft

Although it is desirable at coronary reoperation to replace a stenotic vein graft to the left anterior descending coronary artery (LAD) with an internal mammary artery (IMA) graft, previous reports have shown that if the stenotic vein graft is removed, that strategy can be complicated by severe hemodynamic deterioration and increased perioperative mortality. We report the results for 90 patients in whom an IMA was used to graft a completely obstructed LAD with the stenotic vein graft left intact. For 10 patients, reoperation involved only an IMA-LAD graft, and in 80 patients, a second IMA, veins, or both were used to graft other vessels. There were no hospital deaths. One patient had a perioperative myocardial infarction. Follow-up at a mean postoperative interval of 58 months documented 11 late deaths (eight cardiac related) and actuarial 5-year survival of 88%. Twenty-two patients underwent coronary angiography at a mean postoperative interval of 48 months. The IMA-LAD graft was found to be perfectly patent in 20 and obstructed in 2. The strategy of adding an IMA graft to the LAD and leaving a stenotic vein graft intact has been associated with a low risk of perioperative myocardial infarction, the late clinical results are favorable, and repeat angiography indicates that serious competitive flow from the stenotic vein graft is uncommon.

Placement of "biliary" stents in saphenous vein coronary bypass grafts.

Angioplasty of coronary saphenous vein grafts has been associated with less favorable results than in native coronary arteries owing to a higher acute complication rate and an increased incidence of restenosis. We placed 16 nonarticulated balloon expandable stainless steel "biliary" stents at the sites of 13 stenotic or occluded aortocoronary saphenous vein graft lesions in 11 patients. All of the lesions were stented successfully. There were no instances of stent thrombosis or stent embolism. The percent diameter stenosis was reduced from 85.5 +/- 14.1% to 3.5 +/- 4.4% (p < .001), and the minimal lumen diameter of the lesion increased from 0.7 +/- 0.7 mm at baseline to 3.7 +/- 0.2 mm (p < .001) after stent placement. We conclude that this noncoronary stent appears to be safe and effective for treating saphenous vein coronary bypass grafts. The high procedural success rate and excellent angiographic results are very encouraging, while the restenosis rates remain to be determined.