Jennifer Griffin

Patterns and Mechanisms of In-Stent Restenosis A Serial Intravascular Ultrasound Study

BACKGROUND Studies have suggested that restenosis within Palmaz-Schatz stents results from neointimal hyperplasia or chronic stent recoil and occurs more frequently at the articulation. METHODS AND RESULTS Serial intravascular ultrasound (IVUS) was performed after intervention and at follow-up in 142 stents in 115 lesions. IVUS measurements (external elastic membrane [EEM], stent, and lumen cross-sectional areas [CSAs] and diameters) were performed, and plaque CSA (EEM lumen in reference segments and stent lumen in stented segments), late lumen loss (delta lumen), remodeling (delta EEM in reference segments and delta stent in stented segments), and tissue growth (delta plaque) were calculated. After intervention, the lumen tended to be smallest at the articulation because of tissue prolapse. At follow-up, tissue growth was uniformly distributed throughout the stent; the tendency for greater neointimal tissue accumulation at the central articulation reached statistical significance only when normalized for the smaller postintervention lumen CSA. In stented segments, late lumen area loss correlated strongly with tissue growth but only weakly with remodeling. Stents affected adjacent vessel segments; remodeling progressively increased and tissue growth progressively decreased at distances from the edge of the stent. These findings were similar in native arteries and saphenous vein grafts and in lesions treated with one or two stents. There was no difference in the postintervention or follow-up lumen (at the junction of the two stents) when overlapped were compared with nonoverlapped stents. CONCLUSIONS Late lumen loss and in-stent restenosis were the result of neointimal tissue proliferation, which tended to be uniformly distributed over the length of the stent.

Intravascular ultrasound predictors of restenosis after percutaneous transcatheter coronary revascularization

OBJECTIVES This study sought to evaluate preintervention and postintervention intravascular ultrasound studies for potential predictors of angiographic restenosis and to use ultrasound predictors of restenosis to enhance our understanding of the pathophysiology of the restenosis disease process. BACKGROUND Restenosis remains the major limitation of percutaneous transcatheter coronary revascularization. Although its mechanisms remain incompletely understood, numerous studies have identified some of the clinical, anatomic and procedural risk factors for restenosis. Intravascular ultrasound imaging of target lesions before and after catheter-based treatment consistently demonstrates more target lesion calcium, more extensive reference segment atherosclerosis, smaller final lumen dimensions, significant residual plaque burden and a greater degree of tissue trauma than is evident by angiography. METHODS Intravascular ultrasound studies were performed in 360 nonstented native coronary artery lesions (final diameter stenosis 18 +/- 11%) in 351 patients for whom follow-up angiographic data were available 6.4 +/- 3.6 months later. Hospital charts were reviewed, and qualitative and quantitative coronary angiographic and intravascular ultrasound analyses were performed by independent core laboratories. Four dependent angiographic end points were tested: restenosis as a binary definition (> or = 50% diameter stenosis at follow-up) was the primary end point; follow-up diameter stenosis, late lumen loss and follow-up minimal lumen diameter were the secondary end points. RESULTS Reference vessel size, the preintervention quantitative coronary angiographic assessment of lesion severity and the postintervention intravascular ultrasound cross-sectional measurements predicted the late angiographic results. In particular, the intravascular ultrasound postintervention cross-sectional narrowing (plaque plus media cross-sectional area divided by external elastic membrane cross-sectional area) predicted the primary end point (restenosis) and two of the three secondary end points (follow-up diameter stenosis and late lumen loss) and was therefore the most consistent predictor of restenosis. CONCLUSIONS Intravascular ultrasound variables are more powerful and consistent predictors of angiographic restenosis than currently accepted clinical or angiographic risk factors.

Mechanisms and results of balloon angioplasty for the treatment of in-stent restenosis.

Restenosis within tubular slotted stents is secondary to intimal hyperplasia and is usually treated with percutaneous transluminal coronary angioplasty (PTCA). Sequential intravascular ultrasound (IVUS) was used to assess the mechanisms and results of PTCA for in-stent restenosis. Sixty-four restenotic Palmaz-Schatz stents were studied by IVUS imaging before and after PTCA. IVUS measurements of stent and lumen cross-sectional areas (CSAs) at 5 segments (proximal and distal stent edges, proximal and distal stent bodies, and the central articulation) were used to calculate intimal hyperplasia CSA (stent-lumen CSA). The results of the 5 segments were then averaged. Mean and minimum CSAs were compared before and after PTCA. Quantitative angiographic measurements showed a minimal lumen diameter increase from 1.05 +/- 0.63 mm (mean +/- 1 SD) before intervention to 2.77 +/- 0.51 mm after PTCA (p < 0.0001). Conversely, the diameter stenosis decreased from 63 +/- 19% to 18 +/- 12% (p < 0.0001). IVUS measurements showed a minimum lumen CSA increase from 2.3 +/- 1.3 mm2 to 6.1 +/- 2.2 mm2 (p < 0.0001) as a result of an increased minimum stent CSA (7.2 +/- 2.4 mm2 to 8.7 +/- 2.6 mm2, p < 0.0001) and a decreased intimal hyperplasia CSA within the stent (4.9 +/- 2.2 mm2 to 2.7 +/- 2.0 mm2, p < 0.0001). Of the total mean lumen enlargement, 56 +/- 28% was the result of additional stent expansion and 44 +/- 28% was the result of a decrease in neointimal tissue. The minimum lumen CSA after PTCA was significantly smaller than the minimum stent CSA before PTCA (presumably an accurate reflection of lumen dimensions immediately after stent implantation; p = 0.0002). The mechanism of PTCA for restenosis is a combination of additional stent expansion and tissue extrusion out of the stent; there is a relatively high residual stenosis (angiographic diameter stenosis of 18 +/- 12%).

Reproducibility of the intravascular ultrasound assessment of stent implantation in saphenous vein grafts

IVUS measurements of stent and reference lumen dimensions and cross-sectional areas are highly reproducible. Furthermore, paramedical personnel can be trained to perform these measurements accurately. Thus, IVUS measurements may become the gold standard for the acute, chronic, and serial assessment of stent implantation procedures.

Intravascular ultrasound identification of calcified intraluminal lesions misdiagnosed as thrombi by coronary angiography

Accurate identification of coronary atherosclerotic plaque composition is important for optimum patient management and transcatheter therapy. In particular, the presence ofthrombus typically leads to protracted hospitalization, intravenous or intracoronary thrombolysis, prolonged systemic anticoagulation, and the use oftranscatheter devices designed to remove thrombi. Furthermore, thrombi may be implicated in poor outcome after transcatheter therapy. Intraluminal filling defects are believed to be the most specific angiographic markers of thrombus. We report three patients with intracoronary filling defects initially diagnosed as thrombus; however, intravascular ultrasound (IVUS) imaging showed that these filling defects represented calcified nodules. IVUS studies were performed with one of two commercially available systems. The first (Cardiovascular Imaging Systems Inc./InterTherapy Inc., Sunnyvale, Calif.) incorporated a single element 25-MHz transducer and an angled mirror mounted on the tip of a flexible shaft that was rotated at 1800 rpm within a 3.9F short monorail polyethylene imaging sheath to form planar cross-sectional images in real time. The second (Cardiovascular Imaging Systems) incorporated a single element 30-MHz beveled transducer within either a 2.9F long monorail imaging catheter having a common distal lumen design (the distal lumen alternatively accommodates the imaging core or the guide wire, but not both) or within a 3.2F short monorail imaging catheter. With both systems the imaging catheter was advanced 5 to 10 mm beyond the target lesion and the transducer was withdrawn automatically at 0.5 mm/sec within the imaging sheath to perform the imaging sequence. IVUS studies were recorded on ~-inch high resolution s-VHS tape for offiine analysis. Patient 1. A 78-year-old white man with a history of pneumoconiosis, gastrectomy for stomach cancer, congestive heart failure from dilated cardiomyopathy, and coronary artery disease was seen for progressive angina. A

Mechanisms and immediate and long-term results of adjunct directional coronary atherectomy after rotational atherectomy

OBJECTIVES The purpose of this study was to confirm the mechanisms and the immediate and long-term results of rotational atherectomy and adjunct directional coronary atherectomy. BACKGROUND Rotational atherectomy is best suited for treating calcific stenoses, but the ability of rotational atherectomy alone to optimize lumen dimensions in large vessels is limited; this is only partly improved by adjunct balloon angioplasty. METHODS We treated 165 lesions in 163 patients by use of rotational atherectomy and adjunct directional coronary atherectomy. Quantitative angiography and intravascular ultrasound were used for lesion analysis. A matched comparison with 208 lesions treated with rotational atherectomy and adjunct coronary angioplasty was performed. Patients were then followed up for at least 9 months, and target-lesion revascularization was assessed. RESULTS In the 61 lesions imaged sequentially, lumen area increased from 1.7 +/- 0.8 (mean +/- 1 SD) to 3.9 +/- 1.1 mm(2) after rotational atherectomy, owing to a decrease in plaque plus media area from 16.8 +/- 5.0 to 15.2 +/- 5.2 mm(2) (both p < 0.0001). After adjunct directional coronary atherectomy, lumen area increased even more to 6.7 +/- 2.0 mm(2) (vs. 5.1 +/- 1.4 mm(2) after adjunct coronary angioplasty, p < 0.0001) as a result of both vessel expansion (18.8 +/ 5.3 to 20.8 +/- 5.7 mm(2)) and additional plaque removal (to 14.1 +/- 5.0 mm(2), all p < 0.0001). The total arcs of calcium decreased from 207 +/- 107 degrees to 166 +/- 93 degrees after rotational atherectomy and to 145 +/- 87 degrees after directional coronary atherectomy. Overall, procedural success was 96%, and final diameter stenosis was 15 +/- 17%. Target-lesion revascularization was 23%. The only independent predictor of target-lesion revascularization was a larger overall atherectomy index (84% vs. 59%, p = 0.048). CONCLUSIONS There is a synergistic relationship between rotational atherectomy and directional coronary atherectomy in the treatment of calcific lesions. The immediate results show a high procedural success--lumen dimensions were larger and late target-lesion revascularization was lower in lesions treated with rotational atherectomy and directional coronary atherectomy than in those treated with rotational atherectomy and adjunct balloon angioplasty.