Stent Volume Research Articles

Extent and distribution of in-stent intimal hyperplasia and edge effect in a non-radiation stent population

Intimal hyperplasia within the body of the stent is the primary mechanism for in-stent restenosis; however, stent edge restenosis has been described after brachytherapy. Our current understanding about the magnitude of in vivo intimal hyperplasia and edge restenosis is limited to data obtained primarily from select, symptomatic patients requiring repeat angiography. The purpose of this study was to determine the extent and distribution of intimal hyperplasia both within the stent and along the stent edge in relatively nonselect, asymptomatic patients scheduled for 6-month intravascular ultrasound (IVUS) as part of a multicenter trial: Heparin Infusion Prior to Stenting. Planar IVUS measurements 1 mm apart were obtained throughout the stent and over a length of 10 mm proximal and distal to the stent at index and follow-up. Of the 179 patients enrolled, 140 returned for repeat angiography and IVUS at 6.4 ± 1.9 months and had IVUS images adequate for analysis. Patients had 1.2 ± 0.6 Palmaz-Schatz stents per vessel. There was a wide individual variation of intimal hyperplasia distribution within the stent and no mean predilection for any location. At 6 months, intimal hyperplasia occupied 29.3 ± 16.2% of the stent volume on average. Lumen loss within 2 mm of the stent edge was due primarily to intimal proliferation. Beyond 2 mm, negative remodeling contributed more to lumen loss. Gender, age, vessel location, index plaque burden, hypercholesterolemia, diabetes, and tobacco did not predict luminal narrowing at the stent edges, but diabetes, unstable angina at presentation, and lesion length were predictive of in-stent intimal hyperplasia. In a non-radiation stent population, 29% of the stent volume is filled with intimal hyperplasia at 6 months. Lumen loss at the stent edge is due primarily to intimal proliferation.

Three-dimensional intravascular ultrasonic volumetric quantification of stent recoil and neointimal formation of two new generation tubular stents

Currently, several different designs of coronary stents are available. However, only a few of the new generation stents have been investigated in large randomized trials. Mechanical behavior of first-generation stents (Palmaz-Schatz, Gianturco-Roubin) may not be applied to the new designs. We investigated the chronic mechanical behavior (recoil) of 2 stents recently approved by the Food and Drug Administration (MULTILINK and NIR). Forty-eight patients with single-stent implantation (23 MULTILINK and 25 NIR) were assessed by means of volumetric 3-dimensional intravascular ultrasound analysis after the procedure and at 6-month follow-up. In addition, volumetric assessment of neointimal formation was performed. No significant chronic stent recoil was detected in both groups (Δ MULTILINK stent volume: +5.6 ± 41 mm 3 [p = NS] and Δ NIR stent volume + 2.1 ± 26 mm 3 [p = NS]). A similar degree of neointimal formation at 6 months was observed between the 2 stents (MULTILINK 46 ± 31.9 mm 3 vs NIR 39.9 ± 27.6 mm 3, p = NS). In conclusion, these 2 second-generation tubular stents did not show chronic recoil and appeared to promote similar proliferative response after implantation in human coronary arteries.

Early lumen loss after treatment of in-stent restenosis: an intravascular ultrasound study.

Mechanisms of recurrence after treatment of in-stent restenosis are unknown. We prospectively performed quantitative coronary angiography (QCA) and intravascular ultrasound (IVUS) in 37 lesions with Palmaz-Schatz stents enrolled in a study of intracoronary radiation for in-stent restenosis. Primary treatment was at the discretion of the operator: PTCA (n=8) or ablation+adjunct PTCA (n=29). Lesions were studied before intervention, immediately after primary intervention, and 42+/-8 minutes later. QCA measurements included minimal luminal diameter and diameter stenosis. Planar IVUS measurements included arterial, stent, lumen, and in-stent tissue areas. Stent, lumen, and in-stent tissue volumes were calculated by use of Simpson's rule. Compared with immediately after intervention, the delayed (42+/-8 minutes) minimal lumen area decreased by 20% (5.8+/-1.9 to 4.5+/-1.3 mm2, P<0.0001) and the lumen volume by 12% (58+/-41 to 52+/-37 mm3, P=0.0001). Ten lesions (27%) had a > or = 2.0-mm2 decrease in minimum lumen area. Lumen loss (1) resulted from increased tissue with the stent, (2) correlated with lesion length and preintervention in-stent tissue, and (3) was not seen angiographically. There is significant tissue reintrusion shortly after catheter-based treatment of in-stent restenosis. This was greater in longer lesions and those with a larger in-stent tissue burden, was not reflected in the QCA measurements, and may contribute to recurrence.

THE USE OF BLADDER FOR TOTAL TRANSPLANT URETERAL RECONSTRUCTION

Purpose Although complete necrosis of a transplanted renal allograft ureter is uncommon, it is a difficult complication to manage. Long or multisegment ureteral strictures, most commonly ischemic in nature, are formidable problems for the reconstructive surgeon. We reviewed 655 consecutive renal allografts to determine the incidence of these complex ureteral complications, and the effectiveness and morbidity of complete ureteral reconstruction using bladder alone. Materials and Methods Of 20 patients (3.0%) who required ureteral reconstruction 9 had complete ureteral necrosis and 11 had long (4) or multisegment (7) ureteral strictures. Total ureteral reconstruction was performed using a modified Boari flap in 15 patients and direct pyelovesicostomy in 5. All patients were followed postoperatively with renal ultrasound as well as 99mtechnetium mercaptoacetyltriglycine-3 diuretic renal scans. Mean followup was 28 months. Results All 20 patients had successful reconstruction of the transplant ureter using bladder for substitution. Four patients had persistent dilatation of the renal collecting system without evidence of obstruction as measured by diuretic renal scan (half-time less than 20 minutes). Reflux into the transplant renal pelvis occurred in 6 patients. Two patients had reversible deterioration in renal function secondary to rejection episodes. Of the group reconstructed via Boari bladder flap prolonged stenting (mean 27 days) and prolonged high volume drain output (mean 22 days) were not uncommon. Conclusions Complete ureteral reconstruction is a complex problem in the renal allograft recipient. Using the bladder for reconstruction via Boari flap or direct pyelovesicostomy is an effective technique with minimal morbidity.

Serial follow-up after optimized ultrasound-guided deployment of Palmaz-Schatz stents. In-stent neointimal proliferation without significant reference segment response.

The effects of ultrasound-guided high-pressure stenting on late stent and reference segment dimensions are unknown. In this study, we report about angiographic and ultrasound measurements to assess the amount and distribution of neointimal ingrowth within the stent and the changes of plaque burden and dimensions within the reference segments. Sixty-eight consecutive patients with 72 lesions received single or multiple Palmaz-Schatz coronary stents with a standardized protocol for stent optimization under ultrasound guidance. The residual angiographic diameter stenosis was 3 +/- 12% (reference diameter, 3.16 +/- 0.61 mm). At follow-up 4.8 +/- 2.5 months later, angiography revealed a diameter stenosis of 27 +/- 21% with a restenosis rate of 15.3% (confidence interval: 7.8% to 25.6%). Lumen renarrowing within the stent was exclusively due to neointimal ingrowth; no stent compression was observed. The neointima covered 20 +/- 20% of the stent area and was more pronounced in the midportion of the stent. Volumetric assessment performed in 26 patients resulted in 13 +/- 14% or 65 +/- 28% of the stent volume occupied by neointimal ingrowth in patients without or with restenosis, respectively. Vessel remodeling had an impact on lumen dimensions only at reference sites but not within the stent. Plaque burden of 46 +/- 11% and 48 +/- 11% at the proximal and distal reference sites, respectively, did not show a relevant progression during the follow-up. Serial ultrasound analyses did not show any evidence of stent compression or relevant vessel remodeling. Restenosis was solely due to neointimal ingrowth. Despite a considerable plaque burden within the reference segments, there was no relevant progression of the disease adjacent to the stent.

Small stent size and intimal hyperplasia contribute to restenosis: A volumetric intravascular ultrasound analysis

The purpose of this study was to use volumetric intravascular ultrasound analysis of Palmaz-Schatz stents to assess the in-stent restenotic process. By reducing lesion elastic recoil and chronic arterial remodeling, stents improve the long-term results of coronary angioplasty. However, stents are prone to the development of neointimal hyperplasia. Angiographic studies of stent restenosis have suggested that these hyperplastic responses are the cause of in-stent restenosis; however, it is difficult to visualize the radiolucent Palmaz-Schatz stent by angiography. Intravascular ultrasound provides detailed cross-sectional imaging of the coronary arteries, especially the intense metallic reflection of endovascular stents. Forty-four patients with 60 Palmaz-Schatz stents underwent intravascular ultrasound imaging at follow-up ([mean +/- SD] 8.8 +/- 7.2 months after implantation). Thirty-four stents were placed in saphenous vein grafts and 26 in native coronary arteries; 30 were placed in restenotic lesions. Intravascular ultrasound with automatic transducer pullback at 0.5 mm/s allowed measurement of stent, lumen and intimal hyperplasia cross-sectional areas at 1-mm axial increments within the stents. Using Simpson's rule, stent, lumen and intimal hyperplasia volumes were calculated. Patterns of in-stent restenosis were then identified. Restenotic stents had smaller stent volumes (120 +/- 41 vs. 147 +/- 43 mm3, p = 0.016) and lumen volumes (62 +/- 28 vs. 118 +/- 42 mm3, p < 0.0001) but larger intimal hyperplasia volumes (58 +/- 36 vs. 29 +/- 18 mm3, p < 0.001) than nonrestenotic stents. A focal restenosis pattern was more common (20 [77%] of 26) than a diffuse restenosis pattern (6 [23%] of 26). Stents with focal restenosis and stents with diffuse restenosis had equally small stent volumes (120 +/- 44 vs. 120 +/- 31 mm3, respectively, p = NS); however, stents with diffuse restenosis had larger intimal hyperplasia volumes (84 +/- 30 vs. 50 +/- 34 mm3, p < 0.05). Focal restenosis was most commonly located at the central articulation (45%); the location of focal restenosis was related to the focal accumulation of neointimal tissue. Stent volume and magnitude and distribution of intimal hyperplasia are important in the development of in-stent restenosis. Stent volume was smaller and intimal hyperplasia volume greater in restenotic stents. Stent restenosis is more commonly focal in nature and located at the central articulation.

Short- and long-term hemodynamic effects of transjugular intrahepatic portosystemic shunts: a Doppler/manometric correlative study.

The purposes of this study were to evaluate the effect of a well-functioning transjugular intrahepatic portosystemic shunt (TIPS) on the splanchnic and intrahepatic circulation, to determine if sonographic measurements can predict shunt dysfunction before clinical manifestations of portal hypertension occur, and to compare Doppler sonographic findings with portocaval gradient measurements before and after shunt revision. Forty-four patients with cirrhosis (n = 43) and myelofibrosis (n = 1) who underwent successful TIPS insertion were included in this prospective study. Indications for TIPS placement were: refractory ascites (24 patients), bleeding esophageal varices (17 patients), portal hypertensive gastropathy (two patients), and bleeding colonic varices (one patient). The portal vein and the inferior vena cava were catheterized; and the portocaval gradient was recorded before TIPS placement, at 2 and 12 months after TIPS placement, and when clinical or Doppler findings suggested shunt dysfunction. Doppler studies were done within 1 week before TIPS placement, within 2 days after TIPS placement, every 2-3 months thereafter, and before and after a TIPS revision. The Doppler studies included flow volume measurements in the portal vein and in the stent, as well as determination of the direction of flow in the segmental branches of the portal vein, in the splanchnic veins, and in portosystemic collaterals. Changes in Doppler findings and in catheter pressure measurements were compared using Spearman's rank correlation test. Significance was set at the .05 level. A marked decrease (-51%) in portocaval gradient was observed after TIPS placement. At Doppler sonography, portal vein velocity and diameter were both higher after TIPS placement, resulting in a marked increase in portal venous flow (170%). Mean flow velocity in the shunt was 55.8 +/- 3.6 cm/sec, and flow volumes in the shunt and in the main portal vein were 1596 ml/min and 1731 ml/min, respectively (p = nonsignificant). Dysfunction of the stent occurred in 27% of the patients. Changes in stent blood flow volume were closely related to changes in the portocaval gradient (r = -0.67, p < .001). Reduction of blood flow volume in the stent or change of direction of flow in intrahepatic portal veins or in collateral veins signaled shunt dysfunction (84% sensitivity, 89% specificity). Marked hemodynamic changes in the portal venous system occur soon after a TIPS procedure. Monitoring of shunt function with periodic Doppler sonography, including calculation of shunt blood flow, is useful in detecting shunt dysfunction before clinical signs occur.

1018-52 Volumetric Intravascular Ultrasound Volumetric Analysis Shows that Small Stent Size and Intimal Hyperplasia Contribute to Restenosis

To explore the mechanisms and patterns of stent restenosis, we performed volumetric intravascular ultrasound analysis (IVUS) in 60 tubular-slotted stents a mean of 8 months after implantation. Motorized transducer pullback (@ 0.5 mmls within a stationary imaging sheath) permitted measurement of stent and lumen cross-sectional areas in 1 mm axial increments and calculation of stent, lumen, and neointimal hyperplasia (IH = stent–lumen) volumes using Simpson's Rule. Lumen areas were normalized for a reference lumen cross-sectional area to calculate a % area stenosis (AS) for each cross-section. Restenosis was defined as a quantitative angiographic % diameter stenosis ≥50 or an IVUS %AS ≥75.s Restenosis (N = 6) No Restenosis (N = 20) P Stent volume (mm 3 ) 120 ± 41 147 ± 43 0.016 Lumen volume (mm 3 ) 62 ± 28 118 ± 42 &lt;0.001 IH volume (mm 3 ) 58 ± 36 29 ± 18 &lt;0.001 We then defined diffuse and focal patterns of restenosis: (1) diffuse = more than 50% of the stent length having a %AS ≥ 75 and (2) focal = less than 50% of the stent length having a %AS ≥75. Diffuse (N = 6) Focal (N = 20) P Stent volume (mm 3 ) 120 ± 31 120 ± 44 NS Lumen volume (mm 3 ) 36 ± 15 70 ± 26 &lt;0.005 IH volume (mm 3 ) 84 ± 30 50 ± 34 &lt;0.05 In pts with focal in-stent restenosis, the region of greatest %AS was at the central articulation in 9 (45%), at the stent margins in 6 (30%), and within a stent segment in 5 (25%). (1) IVUS imaging with automated transducer pullback allows detailed volumetric analysis of in-stent restenosis. (2) In-stent restenosis is due to a combination of reduced stent volume and greater IH. (3) Diffuse in-stent restenosis is seen in less than 1/3 of restenotic stents and is associated with more aggressive neointimal growth than the more common pattern of focal restenosis. Further studies are required to determine if differing patterns of in-stent restenosis are associated with subsequent clinical outcomes.

Enteral pancreatic enzyme feedback inhibition of the exocrine secretion of the human transplanted pancreas.

The mechanism of regulation of negative feedback inhibition of the exocrine pancreas and its possible role in decreasing the exocrine secretion of the grafted human pancreas is unknown. To evaluate this we studied the effect of oral pancreatic enzymes on the stimulated transplanted pancreatic exocrine secretion in eight patients with allograft pancreaticocystostomies. After an 8-hr fast, all graft exocrine secretions via graft stent, fistula, and urinary anastomosis were collected for a 1-hr basal period. A standard 300-ml Lundh test meal was then ingested, and all exocrine secretions were collected in 30-min intervals for 3 hr. This test was repeated with 6 capsules of pancrelipase (24,000 units of lipase, 120,000 units of amylase, and 150,000 units of protease) given with the Lundh test meal. Stent, urine and fistula volume, amylase, and pH were measured for each collection period. The total 3-hr amylase secreted after the test meal and the test meal plus pancrelipase were compared. The period of peak amylase secretion after the test meal alone was compared with the same period after the test meal plus pancrelipase and the premeal basal period. The total amylase decreased 34% from 5550 +/- 1000 to 3680 +/- 740 IU/3 hr (P < .03) with pancrelipase. The peak amylase secretion decreased 63% from 1520 +/- 271 to 567 +/- 185 IU/30 min (P < .02) with the addition of pancrelipase to the test meal. Pancrelipase eliminated all meal-stimulated amylase secretion with the mean secretion 16% below the basal secretion of 674 +/- 117 IU/30 min. We conclude that pancreatic negative feedback inhibition significantly decreases meal-stimulated and basal exocrine secretion in the transplanted human pancreas.