Loss In Lumen Diameter Research Articles

Predictors of In-Stent Stenosis Following the Implantation of Pipeline Embolization Devices for the Treatment of Aneurysms Located at or beyond the Circle of Willis in the Anterior Circulation.

In-stent stenosis is commonly observed after stent implantation. There is no consensus on the contributing factors for in-stent stenosis, especially for aneurysms located at or beyond the circle of Willis in the anterior circulation. This study aimed to investigate the morbidity and determinants of in-stent stenosis in distal anterior circulation aneurysms following the implantation of Pipeline Embolization Devices. Patients who underwent Pipeline Embolization Device treatment at our center between January 1, 2018, and June 15, 2023, were enrolled. Distal anterior circulation aneurysms were defined as those occurring at or beyond the circle of Willis, including anterior communicating artery aneurysms, anterior cerebral artery aneurysms, and MCA aneurysms. Baseline information, aneurysm characteristics, and follow-up data of patients were analyzed. Patients were divided into 2 groups: the in-stent stenosis group (patients with a loss of >25% of the lumen diameter of the parent artery) and the non-in-stent stenosis group. Binary logistic regression and restricted cubic spline curves were used to explore risk factors. We included 85 cases of 1213 patients treated with flow-diverter devices at our hospital. During an average follow-up period of 9.07 months, the complete occlusion rate was 77.64%. The overall incidence of in-stent stenosis was 36.47% (31/85), of which moderate stenosis accounted for 9.41% (8/85), and severe stenosis, 5.88% (5/85) (triglyceride-glucose index ≥ 8.95; OR = 6.883, P = .006). The difference in diameters between the stent and parent artery of ≥0.09 mm (OR = 6.534, P = .015) and 55 years of age or older (OR = 3.507, P = .036) were risk factors for in-stent stenosis. The restricted cubic spline curves indicated that the risk of in-stent stenosis increased as the difference in diameter between stent and parent artery and the triglyceride-glucose index increased. Compared with the on-label use of Pipeline Embolization Devices, the rate of in-stent stenosis did not obviously increase when treating distal anterior circulation aneurysms with these devices. The incidence of in-stent stenosis was 36.47% when defined as a lumen diameter loss of >25%, and 15.2% when defined as a lumen diameter loss of >50%. Stent-size selection and biochemical indicators can potentially impact the incidence of in-stent stenosis.

Biodegradable Magnesium Alloy Stents as a Treatment for Vein Graft Restenosis.

PurposeTo explore the effects of biodegradable magnesium alloy stents (BMAS) on remodeling of vein graft (VG) anastomotic restenosis.Materials and MethodsTo establish a VG restenosis model, seventy two New Zealand rabbits were randomly divided into three groups according to whether a stent was implanted in the graft vein or not. BMASs and 316L stainless steel stents were implanted in BMAS and 316L groups, respectively, while no stent was implanted in the no-treatment control group (NC group). Loss of lumen diameter in the graft vein was measured in all three groups. Upon harvesting VG segments to evaluate intimal proliferation and re-endothelization, the degradation and biological safety of the stents were observed to explore the effects of BMAS on VG remodeling.ResultsModel establishment and stent implantation were successful. The BMAS reduced lumen loss, compared with the control group (0.05±0.34 mm vs. 0.90±0.39 mm, p=0.001), in the early stage. The neointimal area was smaller in the BMAS group than the 316L group after 4 months (4.96±0.66 mm2 vs. 6.80±0.69 mm2, p=0.017). Re-endothelialization in the BMAS group was better than that in the 316L group (p=0.001). Within 4 months, the BMAS had degraded, and the magnesium was converted to phosphorus and calcium. The support force of the BMAS began to reduce at 2–3 months after implantation, without significant toxic effects.ConclusionBMAS promotes positive remodeling of VG anastomosis and has advantages over the conventional 316L stents in the treatment of venous diseases.

Increasing our IQ of vascular smooth muscle cell migration with IQGAP1. Focus on “IQGAP1 links PDGF receptor-β signal to focal adhesions involved in vascular smooth muscle cell migration: role in neointimal formation after vascular injury”

<i>Increasing our IQ of vascular smooth muscle cell migration with IQGAP1</i>. Focus on “IQGAP1 links PDGF receptor-β signal to focal adhesions involved in vascular smooth muscle cell migration: role in neointimal formation after vascular injury”

Acute myocardial infarction as presentation of an infiltrative lung neoplasia

We report the case of a 51-year-old woman who presented with acute myocardial infarction as initial symptom of an infiltrative lung neoplasia. The patient was admitted to our center following an out-of-hospital cardiac arrest due to ventricular fibrillation which was cardioverted. On electrocardiography an anterior wall ST-elevation was found and urgent coronary angiography was performed. Left anterior descending coronary artery was occluded and after thrombus aspiration, an image of diffuse loss of lumen diameter and absence of coronary branches was compatible with an extrinsic compression. Such findings along with a lingula consolidation on chest X-ray examination suggested a thoracic neoplasia. Enhanced-chest computed tomography showed a mass located in the lingula with extensive mediastinal infiltration involving pericardium and myocardium. Anatomopathologic examination confirmed the presence of lung adenocarcinoma.<Learning objective: In patients with neoplasms should be suspected cardiac tumor infiltration in those with acute myocardial infarction. Since differential diagnosis between true AMI electrocardiographic (ECG) changes and pseudo-AMI ECG changes in patients with secondary cardiac tumors assumed to be difficult, such TTE or IVUS findings of extra-cardiac tumor could help physicians to make an accurate diagnosis.>

Reduction of Late In-Stent Stenosis in a Porcine Coronary Artery Model by Cobalt Chromium Stents with a Nanocoat of Polyphosphazene (Polyzene-F)

The purpose of this study was to investigate the potential of nanoscale coating with the highly biocompatible polymer Polyzene-F (PZF), in combination with cobalt chromium and stainless steel stents, to reduce in-stent stenosis, thrombogenicity, and vessel wall injury and inflammation. One bare cobalt chromium, PZF-nanocoated stainless steel or PZF-nanocoated cobalt chromium stent was implanted in right coronary artery of 30 mini-pigs (4- or 12-week follow-up). Primary study end points were in-stent stenosis and thrombogenicity. Secondary study end points were vessel wall injury and inflammation as evaluated by microscopy and a new immunoreactivity score applying C-reactive protein (CRP), tumor-necrosis factor alpha (TNFalpha), and TGFbeta. At 12 weeks, angiography showed a significantly lower average loss in lumen diameter (2.1% +/- 3.05%) in PZF-nanocoated cobalt chromium stents compared with stents in the other groups (9.73% +/- 4.93% for bare cobalt chromium stents and 9.71% +/- 7% for PZF-nanocoated stainless steel stents; p = 0.04), which was confirmed at microscopy (neointima 40.7 +/- 16 lm in PZF-nanocoated cobalt chromium stents, 74.7 +/- 57.6 lm in bare cobalt chromium stents, and 141.5 +/- 109 lm in PZF-nanocoated stainless steel stents; p = 0.04). Injury and inflammation scores were low in all stents and were without significant differences. PZF-nanocoated cobalt chromium stents provided the highest efficacy in reducing in-stent stenosis at long-term follow-up. The PZF nanocoat proved to be biocompatible with respect to thromboresistance and inflammation. Our data suggest that its combination with cobalt chromium stents might provide an interesting passive stent platform.

Sirolimus-Eluting Stent Versus Paclitaxel-Eluting Stent for Patients With Long Coronary Artery Disease

Outcomes remain relatively unfavorable for stent-based coronary intervention of lesions with long diseased segments. This study compared sirolimus-eluting stents (SES) and paclitaxel-eluting stents (PES) for long coronary lesions. The present randomized, multicenter, prospective study compared the use of long (> or =32 mm) SES with PES in 500 patients with long (> or =25 mm) native coronary lesions. The primary end point of the trial was the rate of binary in-segment restenosis according to follow-up angiography at 6 months. The SES and PES groups had similar baseline characteristics. Lesion length was 33.9+/-11.6 mm in the SES group and 34.5+/-12.6 mm in the PES group (P=0.527). The in-segment binary restenosis rate was significantly lower in the SES group than in the PES group (3.3% versus 14.6%; relative risk 0.23; P<0.001). In-stent late loss of lumen diameter was 0.09+/-0.37 mm in the SES group and 0.45+/-0.55 mm in the PES group (P<0.001). In patients with restenoses, a pattern of focal restenosis was more common in the SES group than in the PES group (100% versus 53.3%, P=0.031). Consequently, SES patients had a lower rate of target-lesion revascularization at 9 months (2.4% versus 7.2%, P=0.012). The incidence of death (0.8% in SES versus 0% in PES, P=0.499) or myocardial infarction (8.8% in SES versus 10.8% in PES, P=0.452) at 9 months of follow-up was not statistically different between the 2 groups. For patients with long native coronary artery disease, SES implantation was associated with a reduced incidence of angiographic restenosis and a reduced need for target-lesion revascularization compared with PES implantation.

Neointima Inhibition: Comparison of Effectiveness of Non–Stent-based Local Drug Delivery and a Drug-eluting Stent in Porcine Coronary Arteries

To compare the inhibition of neointimal proliferation by using non-stent-based local drug delivery and a drug-eluting stent in porcine coronary arteries. Experiments were conducted with permission of the animal protection committee of the local government. Paclitaxel was either dissolved in a nonionic contrast medium or coated on balloons. Stents were crimped on the coated balloons. Effectiveness was tested in 22 pigs. Two coronary stents were placed in each pig, and slight overstretch was applied. The animals were treated as follows: group A (control group), uncoated balloons, bare stents, and "plain" contrast medium; group B, same treatment as group A, but with paclitaxel in the contrast medium; group C, paclitaxel-coated balloons, with premounted bare stents and plain contrast medium; and group D, sirolimus-eluting stents, noncoated balloons, and plain contrast medium. Stenosis was assessed 4 weeks later at angiography and histomorphometry. For exploratory purposes, continuous variables of quantitative coronary angiography and histomorphometry were compared by using analysis of variance. Results at follow-up angiography indicated a mean of 1.00 mm +/- 0.18 (standard deviation) lumen diameter loss in the control group and 0.14 mm +/- 0.18 loss in the group treated with the paclitaxel-coated balloon (group C; P < .001). Findings at histomorphometry confirmed the effectiveness of drug delivery, with the most impressive inhibition of neointimal proliferation from coated balloons-the neointimal area was 2.4 mm2 +/- 0.3 (P < .01 vs all other groups), compared with 5.2 mm2 +/- 0.3 in group A (control group), 4.3 mm2 +/- 0.3 in group B, and 3.8 mm2 +/- 0.3 in group D. In spite of the short intima contact time, paclitaxel coated on the balloon inhibits neointimal formation in the porcine model of coronary stent placement.

Impaired Left Ventricular Systolic Function Early After Heart Transplantation is Associated with Cardiac Allograft Vasculopathy

Cardiac allograft vasculopathy (CAV) is a major cause of death more than 1 year after heart transplantation. We evaluated the role and possible predictive value of different etiological factors on development of CAV as diagnosed by quantitative coronary angiography (QCA). A total of 121 patients were studied with baseline QCA and 117 had a follow-up study at 1 year to assess the relationship of mean lumen diameter loss (MLDL) in main coronary arteries to immunological and non-immunological factors potentially affecting long-term survival. Out of them, 103 patients were males (85%), 114 (94%) patients were Caucasians and mean age was 48.5 +/- 10 years. Univariate analysis showed that MLDL at 1 year was inversely related to echocardiographic fractional shortening (FS) measured within the first week after transplantation (p = 0.0098) and to intracranial hemorrhage as cause of donor death (p = 0.04) and was directly related to male donors (p = 0.0008), domino transplants (p = 0.037) and donor negative cytomegalovirus (CMV) status (p = 0.022). Multivariate analysis showed that initial FS (p = 0.006) and donor intracranial hemorrhage as a cause of death (p = 0.042) were inversely related to MLDL whereas donor male sex (p = 0.003) and prednisolone treatment throughout the first year (p = 0.012) were directly related. Thus, left ventricular systolic dysfunction early after heart transplantation was associated with subsequent development of CAV.

Letter Regarding Article by Mauri et al, “Late Loss in Lumen Diameter and Binary Restenosis for Drug-Eluting Stent Comparison”

Letter Regarding Article by Mauri et al, “Late Loss in Lumen Diameter and Binary Restenosis for Drug-Eluting Stent Comparison”

Late Loss in Lumen Diameter and Binary Restenosis for Drug-Eluting Stent Comparison

Late Loss in Lumen Diameter and Binary Restenosis for Drug-Eluting Stent Comparison

Late Loss in Lumen Diameter and Binary Restenosis for Drug-Eluting Stent Comparison

Published rates of coronary restenosis have fallen below 10% in drug-eluting stent trials. Early evaluations of new stents have used continuous end points that are presumed surrogates for restenosis, but the generalizability and power of such end points have not been examined systematically. We examined the relationship between incremental changes in observed late loss in lumen diameter and the probability of restenosis using reported late loss from 22 published trials of various types of stents (bare-metal, drug-eluting, and small-vessel stents). Next, the power of late loss differences was compared with that of corresponding binary restenosis rates. The relationship between mean late loss and its SD was linear and did not vary with stent type (drug-eluting or bare-metal) or vessel diameter. At all levels of late loss examined (0 to 1 mm), incremental changes were associated with increasing restenosis risk (with an increasing magnitude of effect at higher levels of late loss). The power to detect a treatment effect was greater for late loss than for binary angiographic restenosis (> or =32% relative increase in power, > or =24% absolute increase for late loss between 0.2 and 0.6 mm). Late loss is monotonically related to restenosis risk in published stent trials. It is a generalizable and powerful angiographic end point in early or small trials of new drug-eluting stents.

Relationship of Late Loss in Lumen Diameter to Coronary Restenosis in Sirolimus-Eluting Stents

Relationship of Late Loss in Lumen Diameter to Coronary Restenosis in Sirolimus-Eluting Stents

Relationship of Late Loss in Lumen Diameter to Coronary Restenosis in Sirolimus-Eluting Stents

Observed rates of restenosis after drug-eluting stenting are low (<10%). Identification of a reliable and powerful angiographic end point will be useful in future trials. Late loss (postprocedural minimum lumen diameter minus 8-month minimum lumen diameter) was measured in the angiographic cohorts of the SIRIUS (n=703) and E-SIRIUS (n=308) trials. Two techniques, the standard normal approximation and an optimized power transformation, were used to predict binary angiographic restenosis rates and compare them with observed restenosis rates. The mean in-stent late loss observed in the SIRIUS trial was 0.17+/-0.45 mm (sirolimus) versus 1.00+/-0.70 mm (control). If a normal distribution was assumed, late loss accurately estimated in-stent binary angiographic restenosis for the control arm (predicted 35.4% versus observed 35.4%) but underestimated it in the sirolimus arm (predicted 0.6% versus observed 3.2%). Power transformation improved the reliability of the estimate in the sirolimus arm (predicted 3.2% [CI 1.0% to 6.7%]) with similar improvements in the E-SIRIUS trial (predicted 4.0% [CI 1.2% to 7.0%] versus observed 3.9%). In the sirolimus-eluting stent arm, in-stent late loss correlated better with target-lesion revascularization than in-segment late loss (c-statistic=0.915 versus 0.665). Because distributions of late loss with a low mean are right-skewed, the use of a transformation improves the accuracy of predicting low binary restenosis rates. Late loss is monotonically correlated with the probability of restenosis and yields a more efficient estimate of the restenosis process in the era of lower binary restenosis rates.

AIF-1 is an actin-polymerizing and Rac1-activating protein that promotes vascular smooth muscle cell migration.

Development of vascular restenosis is a multifaceted process characterized by migration and proliferation of vascular smooth muscle cells (VSMCs), resulting in loss of lumen diameter. Characterization of proteins that mediate this process is essential in our understanding of the pathogenesis of arterial injury. Allograft inflammatory factor-1 (AIF-1) is a cytoplasmic, calcium-binding protein that is expressed in VSMCs by allograft and balloon angioplasty injury. AIF-1 is not present in cultured human VSMCs but is induced by cytokines, and overexpression of AIF-1 results in increased VSMC growth and cell-cycle gene expression. To characterize AIF-1 modulatory effects in primary human VSMCs, AIF-1-interacting proteins were identified by an AIF-1/glutathione S transferase fusion protein affinity assay. MALDI-TOF mass spectrophotometric amino analysis identified actin as an AIF-1 interacting protein. This interaction was verified by coimmunoprecipitation. This is a functional interaction, because AIF-1 binds to and polymerizes F-actin in vitro. In unstimulated VSMCs, AIF-1 colocalizes with F-actin but translocates to lamellipodia on stimulation with platelet-derived growth factor. VSMCs stably transduced with AIF-1 retrovirus migrate 2.6-fold more rapidly (85.1+/-2.9 versus 225.5+/-16.6; P<0.001) in response to platelet-derived growth factor versus control cells. AIF-1 colocalizes with Rac1, and AIF-1-transduced VSMCs show a constitutive and enhanced activation of Rac1, providing a mechanism for the increased migration. These data indicate that AIF-1 binds and polymerizes F actin and also regulates Rac1 activity and VSMC migration. Considering the AIF-1 expression pattern in injured arteries, this suggests that AIF-1 may be involved in the cytoskeletal signaling network leading to vascular remodeling.

Allograft-induced proliferation of vascular smooth muscle cells: potential targets for treating transplant vasculopathy.

Despite advances in immunosuppressive drugs, coronary artery transplant vasculopathy (CATV) is the major cause of graft failure that limits long-term survival of cardiac transplantation. The pathogenesis of CATV involves a chronic immune response of the recipient to the donor vasculature in which activated recipient immune cells damage the endothelium and produce cytokines, resulting in vascular smooth muscle cell (VSMC) activation. Activated VSMC migrate from the media into the lumen, proliferate, and elaborate cytokines and matrix proteins, resulting in loss of lumen diameter and vascular contractility. Because of its extensive nature, interventions which are successful in patients with conventional coronary artery disease are often not applicable to the majority of patients with CATV. Although intended for immune suppression, many immunosuppressive agents owe at least part of their efficacy to their anti proliferative effects on VSMC, including rapamycin, mycophenolic acid, cyclosporin, calcium channel blockers, and HMG CoA reductase inhibitors. Because activation of VSMC is responsible for most of the obliterative arterial intimal thickening present in solid organ allografts, the induction of expression of a selected set of genes may reflect the status of acceptance of the vasculature by the recipient, and the activation, migration, and proliferation of VSMC represent potential points for therapeutic intervention. The risk of infection and malignancy associated with immunosuppressive therapy further promote the need to identify a molecular target which directly modulates the VSMC response to injury. This review will summarize the anti proliferative effects that immunosuppressive drugs have on VSMC proliferation. We will also describe efforts to define the genes which regulate the vascular response to allograft injury, and describe how some of these proteins may represent targets to reduce VSMC proliferation and attenuate CATV.

Early lumen diameter loss after percutaneous transluminal coronary angioplasty is related to coronary plaque burden: a role for viscous plaque properties in early lumen diameter loss.

We tested the hypothesis that lumen diameter loss within 1 h after percutaneous transluminal coronary angioplasty is related to plaque volume parameters. Early lumen diameter loss after coronary balloon angioplasty may predict restenosis and may paradoxically decrease late lumen diameter loss. Viscous properties of the vessel wall, as would be determined by tissue volume and composition, may be involved in early lumen diameter loss. Early lumen diameter loss was measured with quantitative coronary angiography as the loss in lesion lumen diameter (significant loss 0.4 mm) occurring between 5 min and a median of 40 min after successful coronary balloon angioplasty in 68 patients. Thirty-nine patients were evaluated with intravascular ultrasound at the narrowest lumen cross-section of the dilated lesion, 29 patients formed a control group without intravascular ultrasound imaging. We tested the relation between intravascular ultrasound parameters and early lumen diameter loss. Early lumen diameter loss of > or = 0.4 mm was present in eight patients (12%), decreasing lumen diameter from 2.26 +/- 0.36 mm to 1.73 +/- 0.43 mm. There was no difference in the frequency of early lumen diameter loss between the groups with or without intravascular ultrasound imaging. Univariate intravascular ultrasound determinants of early lumen diameter loss were media bounded area (p = 0.01), maximal plaque thickness (p = 0.02), eccentricity index (p = 0.03) and the presence of hard lesions (p = 0.02). Early lumen diameter loss in the first hour after successful coronary balloon angioplasty occurs in a small proportion of patients. It is related to hard lesion type, maximal plaque thickness and eccentricity index, favoring a role for viscous plaque properties in early lumen diameter loss.

Effect of direct thrombin inhibition with Bivalirudin (Hirulog) on restenosis after coronary angioplasty

The direct antithrombin, bivalirudin, did not reduce angiographic restenosis measured either as the dichotomous restenosis rate of 62% for bivalirudin and 58% for heparin (p = 0.70), or as the late loss in lumen diameter of 0.44 +/- 0.47 mm for bivalirudin and 0.39 +/- 0.53 mm for heparin (p = 0.62). Direct thrombin inhibition with bivalirudin neither reduces angiographic restenosis nor alters the impact of several established risk factors for restenosis.

In Vivo experiments with mesothelial cell seeded ePTFE vascular grafts

To investigate the influence of mesothelial cell (MC) seeding on patency and neointimal formation of small diameter ePTFE grafts in a canine model. MC were isolated from the omentum, cultured, seeded on fibronectin-coated ePTFE grafts (4 cm, 4 mm ID), and implanted in the carotid artery of five Beagle dogs. Each dog also received a non-seeded control graft. Patency was assessed by palpation immediately after implantation, and non-invasively by magnetic resonance angiography (MRA) after 1 week and just prior to sacrifice (4 weeks). Intimal thickness was quantified on histological sections by use of computer-aided morphometry. All grafts were patent after implantation. After 1 week, MRA showed the loss of lumen diameter in two seeded grafts. After 4 weeks, two seeded grafts were occluded, one seeded graft was severely stenosed, and all others were without angiographic lumen reduction. Histology and morphometry confirmed that two seeded grafts were occluded, and demonstrated that the other three seeded grafts showed significantly more intima formation (0.22-1.34 mm) than the control grafts (< 0.08 mm; p < 0.01). The MC seeding process decreases patency and increases neointimal formation of small diameter ePTFE grafts in dogs and does not seem to be useful for reduction of graft thrombogenicity.

Angioscopy variables predictive of early angiographic outcome after excimer laser-assisted coronary angioplasty

This study attempted to determine whether anatomic findings at angioscopy were associated with adverse early angiographic outcomes following excimer laser-assisted coronary angioplasty. Predictive factors of either coronary abrupt vessel closure or early (≤24 hours) restenosis after percutaneous coronary angioplasty, including clinical and angiographic variables, have been widely evaluated. The role of angioscopic findings may contribute to identification of patients at risk for early poor outcome. Thirty-seven patients with severe lesions, including 23 total occlusions which underwent successful percutaneous transluminal coronary angioplasty (PTCA) with laser irradiation and adjunctive balloon dilatation (n = 35), or stand alone laser (n = 2), had concomitant angioscopic imaging of the target vessel. All patients had a 24-hour angiographic follow up. Early unfavorable outcome (n = 15) was defined as abrupt vessel closure or restenosis (≥50% stenosis) at 24 hours. By multivariate logistic regression analysis, immediate post-PTCA residual percent stenosis was associated with a poor outcome (restenosis: 33 ± 22% vs no restenosis: 21 ± 14%, p = 0.05). Angioscopic red thrombus aspect was the most significant correlate for early closure or restenosis (7 of 15 patients with unfavorable outcome vs 2 of 22 patients with favorable outcome, odds ratio, 22.9; p < 0.01) and was associated with a significantly higher early minimal lumen diameter loss (1 ± 0.8 mm in the presence of a red thrombus vs 0.3 ± 0.5 mm without thrombus, p < 0.005). Red thrombus appearance is associated with an unfavorable early angiographic outcome in patients who undergo laser-assisted coronary angioplasty.

Remodeling rather than neointimal formation explains luminal narrowing after deep vessel wall injury: insights from a porcine coronary (re)stenosis model.

Oversized balloon dilatation of normal porcine coronary arteries usually heals without stenosis formation. With the purpose of developing a stenotic model and examining the mechanisms of luminal narrowing after angioplasty, we produced a circumferential deep vessel wall injury by inflating and withdrawing an oversized chain-encircled angioplasty balloon in the left anterior descending coronary artery (LAD) of 20 pigs. Three pigs died and did not complete the study. In 8 pigs (group 1), serial coronary arteriography was performed. The lumen diameter (mean+/-SD) before dilation was 3.4 +/- .4 mm; after dilation, 4.2 +/- 0.6 mm; and at follow-ups 2 and 4 weeks later, 1.6 +/- 0.4 mm (P<.0001). In 9 pigs (group 2) examined postmortem 3 weeks after dilatation, histology revealed that the injury was deep (out to adventitia) in all arteries and completely circumferential (360 degrees) in all but two arteries. Adventitia was markedly thickened as a result of neoadventitial formation. Injury correlated strongly with neointimal formation (middle LAD, r=.71, P=.00001, but neither injury nor neointima correlated with lumen size (r=.14, P=.46 and r=.34, P=.07, respectively); ie, neointimal formation did not explain late luminal narrowing. Lumen size, however, did correlate strongly with vessel size (r=.74, P=000005). The late loss in lumen diameter observed angiographically in group 1 substantially exceeded that caused by neointimal formation seen by histology in group 2. The chain-encircled angioplasty balloon produced a circumferential deep vessel wall injury that healed by luminal narrowing. In this porcine model, arterial remodeling was more important than neointimal formation in late luminal narrowing.