Role of intravascular ultrasound and Doppler flow studies in coronary interventions.
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Blood Flow Velocity↗
Biomedical subjects
A D Pichard
Publications and source records attributed to A D Pichard.
Insights into the mechanism of restenosis after PTCA and stenting.
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Angioplasty, Balloon, Coronary↗
Predictors of acute and long-term outcome with transluminal extraction atherectomy: the New Approaches to Coronary Intervention (NACI) registry.
The New Approaches to Coronary Intervention (NACI) registry was established to define the role of new coronary devices in overcoming the limitations of balloon angioplasty. The purpose of the present study was to evaluate the acute and long-term efficacy of the transluminal extraction catheter (TEC) device utilizing data from the NACI registry and identify clinical and anatomic patient subsets who may benefit from this device. From 1990-1994, >4,300 patients from 39 clinical sites enrolled consecutive patients treated with one of the 7 new devices to the NACI registry. The study population consists of 331 patients (385 lesions) treated with planned TEC as the sole new device. Of these patients, 243 (292 lesions) were treated for saphenous vein graft (SVG) disease and 88 (93 lesions) for native disease. Patients undergoing SVG treatment were older and more likely to be male. They had lower ventricular function, more unstable angina, and a higher incidence of congestive heart failure. Multivessel disease was more prevalent in the SVG cohort, as was evidence of thrombus before treatment. Although device success was achieved in 50% of SVG lesions and 41% of native lesions, lesion success was achieved in 90% and 78%, respectively, after adjunctive balloon angioplasty, and procedure success rates were 86% and 79%, respectively. The in-hospital major complication (death/Q-wave myocardial infarction/emergency coronary artery bypass graft [CABG] surgery) rate was higher in the SVG cohort (6.2% vs 2.3%), mainly due to higher mortality rate (5.3% vs 1.1%). Multivariate analysis showed that SVG was not an independent predictor for either an in-hospital major complication or clinical failure. The risk factors for major in-hospital complications were history of congestive heart failure (odds ratio = 3.17) and thrombus (odds ratio = 3.36). For clinical failure the risk factors were diabetes (odds ratio = 1.88), thrombus (odds ratio = 2.08), and calcium (odds ratio = 3.09). One-year rates of death, Q-wave myocardial infarction, or any repeat revascularization were 51% in the SVG cohort and 41% in the native cohort. Following adjustment, patients treated for SVG disease did not have a higher risk when compared with those treated for native disease. The factors significantly associated with this composite event at 1 year are male (relative risk = 1.41), patients with history of congestive heart failure (relative risk = 1.56), and total occlusions (relative risk = 1.52). This study shows that for both SVG and native cohorts, device success rates were low with TEC alone, but acceptable lesion success rates were achieved when adjunctive PTCA was used. In-hospital as well as 1-year major complications were higher in the SVG cohort. However, after adjusting for other risk factors, SVG attempt was not significantly associated with either in-hospital or 1-year events.
Aged↗
Overestimation of acute lumen gain and late lumen loss by quantitative coronary angiography (compared with intravascular ultrasound) in stented lesions.
The accurate measurement of lumen dimensions is essential for guidance of interventional procedures and the assessment of acute and late results. This study compared intravascular ultrasound (IVUS) with quantitative coronary angiography (QCA) in the assessment of lumen dimensions before and after intervention, and at follow-up. Two hundred thirty-one consecutive patients treated with Palmaz-Schatz stents and evaluated using serial (before and after intervention, and follow-up) IVUS and QCA were screened. Because IVUS cannot measure dimensions smaller than the imaging catheter, patients having an angiographic minimal lumen diameter (MLD) less than the IVUS catheter (1.0 mm) during any study were excluded, leaving 71 patients in the final study group. IVUS and QCA measurements (reference dimensions and MLD) and calculations (percent diameter stenosis, acute lumen gain, late lumen loss, loss index, and restenosis rates) were compared. Correlation coefficients ranged from 0.641 to 0.816 for measured variables and from 0.280 to 0.680 for calculated variables. Reference lumen dimensions were consistently larger by IVUS than by QCA: 0.50 +/- 0.52 mm before intervention (p <0.0001), 0.46 +/- 0.45 mm after intervention (p <0.0001), and 0.38 +/- 0.53 mm at follow-up (p <0.0001). MLDs measured by IVUS were larger before intervention (0.17 +/- 0.28 mm, p <0.0001), smaller after intervention (0.17 +/- 0.34 mm, p <0.0001), and larger at follow-up (0.14 +/- 0.41 mm, p <0.0001). This resulted in a smaller acute gain and late loss measured by IVUS (0.33 +/- 0.39 and 0.30 +/- 0.47 mm, respectively, both p <0.0001). Although measures of restenosis (i.e., loss index and restenosis rates) were similar, the classification of lesions in individual patients (as restenotic vs nonrestenotic) was significantly different (p = 0.002, concordance rate = 73%). There are systematic differences between IVUS and QCA in the measurement of reference and lesion lumen dimensions. Although indexes of restenosis were similar, classification of lesions in individual patients was different.
Aged↗
Treatment of in-stent restenosis with excimer laser coronary angioplasty: mechanisms and results compared with PTCA alone.
BACKGROUND: This study determined the clinical safety, mechanisms, and 6-month results of excimer laser angioplasty (ELCA)+adjunct PTCA for the treatment of in-stent restenosis and (via lesion matching) compared the results of ELCA+PTCA to PTCA alone. METHODS AND RESULTS: Using quantitative angiography (QCA) and intravascular ultrasound (IVUS), we studied 107 restenotic previously stented lesions in 98 patients before and after intervention. QCA measurements included minimum lumen diameter (MLD) and diameter stenosis (DS). IVUS measurements included stent, lumen, and intimal hyperplasia (IH=stent-lumen) cross-sectional areas (CSA) and volumes. In the 54 lesions treated with ELCA+PTCA, the MLD increased from 0.73+/-0.38 mm before ELCA to 2.10+/-0.47 mm after ELCA+PTCA (P<.0001); the DS decreased from 70+/-14% to 25+/-12% (P<.0001). By IVUS, the minimum lumen CSA increased from 1.58+/-0.78 mm2 before ELCA to 6.34+/-1.75 mm2 after ELCA+PTCA (P<.0001) as a result of an increase in minimum stent CSA from 7.70+/-2.41 to 9.10+/-2.60 mm2 (P<.0001) and a decrease in IH CSA from 5.25+/-2.84 to 2.63+/-1.41 mm2 (P<.0001). Volumetric analysis showed that tissue ablation (during ELCA) contributed 29+/-15%, tissue extrusion (during adjunct PTCA) contributed 31+/-14%, and additional stent expansion (during adjunct PTCA) contributed 40+/-16% to the overall lumen gain. There were no ELCA-related complications. Matched to lesions treated with PTCA alone, ELCA+PTCA resulted in greater lumen gain, more IH ablation/extrusion, larger final lumen CSA (IVUS), and a tendency for less frequent need for subsequent target vessel revascularization (TVR, 21% versus 38%, P=.0823). CONCLUSIONS: ELCA safely and effectively ablates in-stent neointimal tissue. Adjunct PTCA extrudes neointimal tissue out of the stent and also further expands the stent. Compared with PTCA alone, ELCA+PTCA achieves better short-term and, potentially, better long-term results.
Angioplasty, Balloon, Coronary↗
Comparison of men versus women in cross-sectional area luminal narrowing, quantity of plaque, presence of calcium in plaque, and lumen location in coronary arteries by intravascular ultrasound in patients with stable angina pectoris.
Women have an increased mortality after coronary interventions compared with men, which may be partly explained by differences in comorbid clinical conditions. However, whether women also have quantitative differences in coronary atherosclerosis is not known. Preinterventional intravascular ultrasound (IVUS) was used to study de novo, nonostial native coronary lesions in 169 women and 549 men with chronic angina. The external elastic membrane (EEM), lumen, and plaque + media (P + M) areas, plaque burden, plaque eccentricity, and calcium were measured at the target lesion and at a proximal reference site. All cross-sectional IVUS measures were also corrected for body surface area. Results are reported as mean +/- 1 SD. Women had significantly smaller reference site EEM (16.5 +/- 5.3 vs 19.4 +/- 6.3 mm2, p <0.0001), lumen (8.7 +/- 3.0 vs 9.9 +/- 4.0 mm2, p = 0.0020), and P + M areas (7.8 +/- 3.7 vs 9.5 +/- 4.2 mm2, p = 0.0001). Women also had significantly smaller lesion site EEM (16.2 +/- 5.9 vs 18.3 +/- 6.7 mm2, p = 0.0028), lumen (2.4 +/- 1.7 vs 2.9 +/- 2.6 mm2, p = 0.0273), and P + M areas (13.6 +/- 5.7 vs 15.3 +/- 6.4 mm2, p = 0.0112). However, when corrected for BSA, these differences were no longer significant. Women and men also had similar reference and lesion plaque burden, eccentricity, and calcium. Preinterventional IVUS analysis failed to detect any quantitative or qualitative differences in coronary atherosclerosis in men compared with women.
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Serial intravascular ultrasound predictors of restenosis at the margins of Palmaz-Schatz stents.
To evaluate predictors of restenosis at margins of Palmaz-Schatz stents, intravascular ultrasound studies were performed after intervention and at follow-up (5.4 months) in 161 stented lesions. Of 301 stent margins, 77 (26%) were restenotic at follow-up (>50% late lumen loss). Intimal hyperplasia was greater for restenotic than for nonrestenotic stents margins. The dominant periprocedural predictor of stent margin restenosis was the plaque burden of the continuous reference segment.
Coronary Disease↗
Contribution of inadequate arterial remodeling to the development of focal coronary artery stenoses. An intravascular ultrasound study.
BACKGROUND: Adaptive remodeling occurs to compensate for the accumulation of atherosclerotic plaque. Lumen reduction depends on the relative rates of plaque deposition and adaptive remodeling responses. Intravascular ultrasound permits detailed, high-quality, cross-sectional imaging of the coronary arteries in vivo. METHODS AND RESULTS: Preintervention intravascular ultrasound was used to study 603 focal, new, nonostial significant coronary artery stenoses in patients with chronic stable angina. Measurements of the target lesion of the external elastic membrane (EEM), lumen, and plaque plus media (P&M; P&M = EEM - Lumen) cross-sectional areas (CSAs) were compared with a proximal reference segment (most normal-looking cross section within 10 mm proximal to the lesion but distal to any side branch). Inadequate remodeling was defined as lesion/ reference EEM CSA that exceeded the upper limits of normal arterial tapering (lesion/reference EEM CSA ratio < or = 0.78 or a 21% reduction in EEM CSA per 10-mm length). Overall, the lesion/reference EEM CSA ratio was 1.00 +/- 0.22; 15% of lesions had inadequate remodeling, and 37% of the 603 lesions had less plaque than expected. This represented a lesion-specific response. The only predictor of inadequate remodeling was the arc of superficial lesion calcium. CONCLUSIONS: Inadequate remodeling is present in at least 15% of chronic, focal, new coronary arterial stenoses in patients with stable angina. The magnitude of arterial remodeling appears to be a lesion-specific response.
Adaptation, Physiological↗
Increased restenosis in diabetes mellitus after coronary interventions is due to exaggerated intimal hyperplasia. A serial intravascular ultrasound study.
BACKGROUND: The increased risk of restenosis after catheter-based coronary interventions in diabetic patients has not been determined. Intravascular ultrasound (IVUS) has shown that the decrease in arterial area is responsible for most of the late lumen loss in nonstented lesions and that intimal hyperplasia is responsible for all of the late lumen loss in stented lesions. METHODS AND RESULTS: Serial (postintervention and follow-up at 5.6 +/- 3.3 months) IVUS was used to study 251 native coronary lesions in 241 patients; 63 patients had treated diabetes mellitus (oral hypoglycemic drugs or insulin). Interventional procedures included percutaneous transluminal coronary angioplasty, directional or rotational atherectomy, excimer laser angioplasty, or Palmaz-Schatz stents. The external elastic membrane (EEM), stent, and lumen areas were measured. The plaque+media (P+M) area in nonstented lesions was calculated as EEM minus lumen area, and the intimal hyperplasia (IH) area in stented lesions was calculated as stent minus lumen area. The anatomic slice selected for serial analysis had an axial location within the target lesion at the smallest follow-up lumen area. Nonstented lesions in diabetics and nondiabetics had a similar decrease in EEM cross-sectional area (CSA; 1.9 +/- 2.8 versus 1.8 +/- 4.2 mm2; P = .6350). However, nonstented lesions in diabetics had a greater increase in P+M CSA (1.3 +/- 2.8 versus 0.6 +/- 2.5 mm2, P = .0720), and the increase in P+M CSA contributed a greater percentage to the decrease in lumen CSA. In stented lesions, the decrease in lumen CSA (5.2 +/- 2.5 versus 2.0 +/- 2.3 mm2) and the increase in IH CSA (5.0 +/- 2.8 versus 1.8 +/- 2.0 mm2) were greater in diabetics than nondiabetics (P = .0009 and P = .0007, respectively). These findings were even more striking in (nonstented and stented) restenotic lesions. CONCLUSIONS: Serial IVUS analysis showed that the main reason for increased restenosis in diabetes mellitus was exaggerated intimal hyperplasia in both stented and nonstented lesions.
Aged↗
Intravascular ultrasound insights into mechanisms of stenosis formation and restenosis.
Using intravascular ultrasound (IVUS), stenosis formation and restenosis (or late lumen loss following coronary angioplasty procedures) can be subdivided into two distinct underlying components: tissue accumulation and arterial remodeling. Arterial remodeling is defined as a change in total arterial cross-sectional area over time; it can be adaptive (an increase in arterial cross-sectional area as a compensatory response to plaque accumulation) or pathologic (a decrease in arterial cross-sectional area or chronic arterial shrinkage). Adaptive arterial remodeling can delay the development of coronary artery stenoses and prevent restenosis; pathologic remodeling can contribute to de novo lesion formation and has been shown to be the dominant mechanism of restenosis following coronary intervention. Serial IVUS studies have also been used to study the natural history of the restenosis process; adaptive remodeling occurs early (within 1 month) and pathologic remodeling occurs late (between 1 and 6 months) after intervention. The residual plaque burden postintervention acts as an amplifier in this process.
Animals↗
Determinants and correlates of target lesion calcium in coronary artery disease: a clinical, angiographic and intravascular ultrasound study.
OBJECTIVES: This report used intravascular ultrasound and quantitative coronary angiography to explore the relation between lesion-associated calcium and risk factors, clinical presentation and angiographic severity of coronary artery stenoses. BACKGROUND: Coronary artery calcium is a marker for significant coronary atherosclerosis. Noninvasive procedures are being proposed as screening tests for coronary artery disease. Intravascular ultrasound identification of tissue calcium has been validated in vitro. METHODS: Independent chart review, preintervention intravascular ultrasound imaging and coronary angiography were used to study primary native vessel lesions in 1,442 patients. Target lesions and reference segments were evaluated according to previously published quantitative and qualitative methods. Results are presented as mean value +/- SD. RESULTS: Overall, 1,043 lesions contained target lesion calcium (72%); the arc of target lesion calcium was 110 +/- 109 degrees. Lesions with an ultrasound plaque burden > 0.75 or an angiographic diameter stenosis > 0.25 had a prevalence of calcium of at least 65%, with a mean arc > 100 degrees. Intermediate lesions had as much target lesion calcium as did angiographically severe lesions. Using multivariate linear regression analysis, patient age, stable (vs. unstable) angina and the intravascular ultrasound lesion site and reference segment plaque burden (but not the angiographic diameter stenosis) were the independent predictors of the arc of target lesion calcium (all p < 0.0001). CONCLUSIONS: Intravascular ultrasound analysis shows that coronary calcification correlates with plaque burden but not with degree of lumen compromise. Thus, the noninvasive detection of coronary calcium is predictive of future cardiac events, presumably because coronary calcification is a marker for overall atherosclerotic plaque burden. Coronary calcium increases with increasing patient age and is less common in unstable lesion subsets.
Adult↗
Is intravascular ultrasound clinically useful or is it just a research tool?
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Coronary Angiography↗
[Clinical application of intracoronary ultrasound].
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Coronary Disease↗
Chronic arterial responses to stent implantation: a serial intravascular ultrasound analysis of Palmaz-Schatz stents in native coronary arteries.
OBJECTIVES: We used intravascular ultrasound (IVUS) imaging to evaluate the chronic vessel responses to Palmaz-Schatz stents. BACKGROUND: Palmaz-Schatz stents have been shown to inhibit early elastic recoil and late arterial remodeling while triggering neointimal hyperplasia. However, changes occurring in native vessels surrounding stent struts have not been well studied. METHODS: Postintervention and follow-up (mean [+/-SD] 5.4 +/- 3.8 months) serial IVUS imaging was performed in 25 stents without restenosis and 24 with in-stent restenosis. Intravascular ultrasound imaging using automatic transducer pullback at 0.5 mm/s allowed measurement at 1-mm axial increments of external elastic membrane (EEM), stent and lumen cross-sectional areas (CSAs) and calculation of peristent plaque plus media (P + M = EEM - stent) CSA, intrastent plaque (stent-lumen) CSA, arterial remodeling (delta EEM CSA), tissue growth outside the stent (delta P + M CSA) and tissue growth within the stent (delta stent-lumen CSA). Volumes were calculated using the Simpson rule. RESULTS: Mean EEM CSA increased significantly from 16.9 +/- 5.0 mm2 after intervention to 18.4 +/- 4.9 mm2 at follow-up (p < 0.0001), reflecting an increase in P + M CSA surrounding the stent (1.6 +/- 1.3 mm2). Greater tissue growth within the stent (2.4 +/- 2.2 mm2) correlated weakly, but directly with tissue growth surrounding the stent (r = 0.356, p = 0.0121). The ratio of peristent/intrastent tissue growth correlated weakly with arterial remodeling (r = 0.282, p = 0.0525). Restenotic stents had more tissue growth both within and surrounding the stent than did nonrestenotic stents. Volumetric measurements, which could be obtained in 15 lesions, showed similar results. CONCLUSIONS: After implantation there is a chronic increase in plaque mass both within and surrounding the stents. The increase in peristent plaque mass is associated with adaptive remodeling.
Aged↗
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%).
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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.
Aged↗
Intravascular ultrasound to discern device-specific effects and mechanisms of restenosis.
Restenosis continues to be the "Achilles heel" of transcatheter interventions. While attempts to reduce restenosis by inhibiting cellular proliferation through pharmacologic or mechanical means have been unsuccessful, stents, which inhibit acute recoil and chronic remodeling, have been shown convincingly to reduce restenosis in 2 randomized clinical trials. Intravascular ultrasound (IVUS) allows transmural, tomographic imaging of coronary arteries in humans in vivo to subdivide restenosis into the two basic underlying components: tissue proliferation and arterial remodeling. In studies performed at the Washington Hospital Center, in nonstented lesions 73% of late lumen loss was due to arterial remodeling (a decrease in arterial, or external elastic membrane cross-sectional area) and 27% was due to tissue growth (an increase in plaque plus media cross-sectional area). These findings were confirmed by 2 other studies: the Optimal Atherectomy Restenosis Study (OARS) and the Serial Ultrasound analysis of REstenosis (SURE) Trial. IVUS was also used to study the mechanisms by which stents reduce restenosis. Stents created a larger final lumen cross-sectional area and, for all practical purposes, abolished arterial remodeling to offset a stent-related increase in neointimal tissue accumulation. Neointimal hyperplasia is solely responsible for in-stent restenosis and therefore appears to be a pure model for studying strategies to limit tissue proliferation.
Angioplasty, Balloon, Coronary↗
Arterial remodeling after coronary angioplasty: a serial intravascular ultrasound study.
BACKGROUND: Restenosis occurs after 30% to 50% of transcatheter coronary procedures; however, the natural history and pathophysiology of restenosis are still incompletely understood. METHODS AND RESULTS: Serial (postintervention and follow-up) intravascular ultrasound imaging was used to study 212 native coronary lesions in 209 patients after percutaneous transluminal coronary angioplasty, directional coronary atherectomy, rotational atherectomy, or excimer laser angioplasty. The external elastic membrane (EEM) and lumen cross-sectional areas (CSA) were measured; plaque plus media (P+M) CSA was calculated as EEM minus lumen CSA. The anatomic slice selected for serial analysis had an axial location within the target lesion at the smallest follow-up lumen CSA. At follow-up, 73% of the decrease in lumen (from 6.6+/-2.5 to 4.0+/-3.7 mm2, P<.0001) was due to a decrease in EEM (from 20.1+/-6.4 to 18.2+/-6.4 mm2, P<.0001); 27% was due to an increase in P+M (from 13.5+/-5.5 to 14.2+/-5.4 mm2, P<.0001). Delta Lumen CSA correlated more strongly with delta EEM CSA (r=.751, P<.0001) than with delta P+M CSA (r=.284, P<.0001). Delta EEM was bidirectional; 47 lesions (22%) showed an increase in EEM. Despite a greater increase in P+M (1.5+/-2.5 versus 0.5+/-2.0 mm2, P=.0009), lesions exhibiting an increase in EEM had (1) no change in lumen (-0.1+/-3.3 versus 3.6+/-2.3 mm2, P<.0001), (2) a reduced restenosis rate (26% versus 62%, P<.0001), and (3) a 49% frequency of late lumen gain (versus 1%, P<.0001) compared with lesions with no increase in EEM. CONCLUSIONS: Restenosis appears to be determined primarily by the direction and magnitude of vessel wall remodeling (delta EEM). An increase in EEM is adaptive, whereas a decrease in EEM contributes to restenosis.
Aged↗