Mechanisms Of Lumen Enlargement Research Articles

Residual coronary dissections after drug-eluting stenting: the good, the bad, and the uglyThe opinions expressed in this article are not necessarily those of the Editors of the European Heart Journal or of the European Society of Cardiology.

This editorial refers to ‘Incidence, predictors, and outcomes of coronary dissections left untreated after drug-eluting stent implantation’† by G.G.L. Biondi-Zoccai et al ., on page 540 The article of Biondi-Zoccai et al. 1 provides a unique opportunity to review the management of coronary dissections induced during percutaneous coronary interventions. For more than 25 years, interventional cardiologists have been facing this challenging situation using different approaches.2–5 Initially, prolonged balloon inflation was the only available therapy. If unsuccessful, patients with acute or threatened vessel closure had only urgent coronary artery bypass surgery as a therapeutic alternative to prevent or limit myocardial damage. The introduction of coronary stents, with their inherent scaffolding properties, dramatically changed this scenario and allowed the dissection flap to be readily tackled. However, whether or not routine stenting is systematically required to seal even minor residual coronary dissections has been a matter of continuous debate for the last decade.2–5 Currently, the soliloquy ‘ To stent or not to stent : that is the question ’4 is being revisited in the new era of drug-eluting stents. Only inquiring into the facts (the good, the bad, and the ugly) may guide us in solving this dilemma. However, what do we know about the pathophysiology, predisposing factors, prognostic implications, and management of residual coronary dissections? Coronary dissections represent the ‘natural’ response of the coronary wall to the mechanical injury of vessel stretching caused by high-pressure balloon inflation. In fact, the mechanism of lumen enlargement after balloon angioplasty relies upon the occurrence of a ‘controlled’ coronary dissection. If this ‘therapeutic’ dissection is relatively confined, both in depth and in length, the lumen gain obtained guarantees a high coronary flow that largely offsets the associated drawbacks of high/low shear stress zones caused by winding dissection planes and the … *Corresponding author. Tel: +34 91 3303289; fax: +34 91 3303289. E-mail address : falf{at}hotmail.com

Preintervention arterial remodeling affects vessel stretch and plaque extrusion during coronary stent deployment as demonstrated by three-dimensional intravascular ultrasound

The mechanisms of lumen enlargement during stent implantation may be significantly affected by arterial remodeling. To assess effects of lesion remodeling, we performed 3-dimensional intravascular ultrasound (IVUS) analyses in 55 coronary lesions before and after deployment of balloon-expandable stents. Standard quantitative analysis was performed, and arterial remodeling was assessed by the remodeling index (target site divided by mean of proximal and distal reference segment vessel areas), which classified lesions into group A (remodeling index ≤1, negative or intermediate remodeling, n = 40) or group B (remodeling index >1, positive remodeling, n = 15) lesions. Characteristics of the 55 patients and the interventional procedures were similar in the 2 groups. IVUS demonstrated that stenting resulted in increased lumen and vessel dimensions and in a reduced plaque size (p ≤0.001 each) in both group A and group B lesions. The extent of lumen increase inside the stents was almost identical, but resulted from different mechanisms: (1) vessel stretch was greater in group A (p <0.002 at minimum lumen site); (2) plaque compression (or embolization) tended to be greater in group B (p = 0.05, along entire stented segment); (3) plaque redistribution within the stent was observed in both groups (p <0.005 both); and (4) significant (p <0.01) plaque extrusion into the distal reference segment was found in group B only. Thus, the remodeling pattern of coronary lesions has a significant impact on the mechanisms of lumen enlargement during stent deployment. Lesions with positive remodeling show more plaque extrusion into the distal reference and less stent-induced vessel stretch than those with negative remodeling.

Mechanisms of lumen enlargement during stenting of acute myocardial infarction lesions: A volumetric intravascular ultrasound study

Mechanisms of lumen enlargement during stenting of acute myocardial infarction lesions: A volumetric intravascular ultrasound study

Does directional atherectomy before stenting reduce wall stretch? A serial intravascular ultrasound evaluation of the mechanisms of lumen enlargement

Does directional atherectomy before stenting reduce wall stretch? A serial intravascular ultrasound evaluation of the mechanisms of lumen enlargement

Intravascular ultrasonic evaluation of the magnitude of stent expansion and the mechanisms of lumen enlargement after direct stenting and after conventional stenting with balloon predilatation

Intravascular ultrasonic evaluation of the magnitude of stent expansion and the mechanisms of lumen enlargement after direct stenting and after conventional stenting with balloon predilatation

Different mechanism of lumen enlargement during balloon angioplasty between focal and diffuse in-stent restenosis

Different mechanism of lumen enlargement during balloon angioplasty between focal and diffuse in-stent restenosis

Different mechanism of lumen enlargement in lesions with stent underexpansion after balloon angioplasty for in-stent restenosis compared to those with optimal stent expansion: an intravascular ultrasound study

Different mechanism of lumen enlargement in lesions with stent underexpansion after balloon angioplasty for in-stent restenosis compared to those with optimal stent expansion: an intravascular ultrasound study

Comparison of luminal enlargement by direct coronary stenting versus predilation coronary stenting by three-dimensional volumetric intravascular ultrasound analysis

S tudies using planar intravascular ultrasound (IVUS) have shown that during intracoronary stent implantation, the mechanisms of lumen enlargement are similar to those of balloon angioplasty, with significant plaque redistribution and extrusion, vessel expansion, and plaque reduction. However, these assessments were performed with stents implanted after predilation by balloon. New stents, crimped onto their low-profile flexible delivery systems, with more rapid tapering of the balloon outside of the conical markers, are suitable for direct stenting (DS). DS has become routine in some laboratories. This new therapeutic approach of DS without predilation provides a way to rationalize stent implantation with the potential of less ischemic complications, less use of balloons, and less x-ray exposure. Although DS has become widespread, the mechanism by which it causes lumen enlargement is still unknown. Furthermore, there remains concern about the risk of microplaque embolization with DS. The present 3-dimensional volumetric IVUS study compares the mechanisms of lumen enlargement with DS versus predilation stenting (PDS) using the same contemporary stent design and the same stent length. • • • We retrospectively studied 30 patients with DS and 30 patients with PDS of nonostial, noncalcified, native coronary lesions treated with the same stent design and dimensions (ACS Multilink DUET or TRISTAR stent, Guidant Corporation, Santa Clara, California) and the same stent length (13 mm). The decision to predilate or not to predilate was partly based on general operator attitude. All lesions in both groups had met the inclusion criterion of the physical feasability of preintervention IVUS examination. Consequently, the DS success rate was 100%. For each procedure, the number of inflations, the maximum balloon inflation pressure, and the diameter of the stent used were recorded. Stent-to-artery ratio was defined as the diameter of the stent (according to the linear compliance curve of the balloon and the maximum balloon inflation pressure) divided by the reference luminal diam-

Impact of coronary plaque morphology as assessed by IVUS computer‐aided analysis on mechanisms of balloon angioplasty and stenting

This study was performed in order to quantitate structural coronary plaque modifications after balloon angioplasty and stenting and to evaluate the impact of plaque morphology on the mechanisms of lumen enlargement during angioplasty. Plaque morphology was studied by computer-aided analysis of 60 cross-sectional intravascular ultrasound (IVUS) images of the target lesion in 20 patients undergoing percutaneous coronary angioplasty. Based on a computer-aided video densitometry classification of plaque morphology, three groups of plaques were defined based on the slope value of a fifth polynomial regression of the plaque gray-level distribution. In groups A and B, balloon angioplasty provided significant increases in lumen area (P < 0.0001) and vessel area (P < 0.05) without a reduction in plaque area; neither parameter increased in group C. In group A, stenting was associated with an additional lumen enlargement (P < 0.0001) due to plaque reduction (P < 0.05). In groups B and C, stenting further increased lumen area (P < 0.0001) by improving vessel area (P < 0.001) but without plaque reduction. Balloon angioplasty and stenting provided a significant decrease in plaque area in group A as compared to groups B (P < 0.05) and C (P < 0.01). Finally, vessel area improvement was greater in group B than in groups A (P < 0.01) and C (P < 0.05). The mechanisms underlying lumen enlargement after coronary angioplasty are highly dependent on plaque morphology as defined by an IVUS computer-aided analysis and may differ between balloon angioplasty and stenting.

Influence of coronary atherosclerotic remodeling and plaque characteristics on mechanisms of lumen enlargement during stent implantation Gerard Finet, Neil J. Weissman, Marco T. Castagna, Kenneth M. Kent, Lowell F. Satler, John R. Laird, Augusto D. Pichard. Washington Hospital Center, Washington, DC

Influence of coronary atherosclerotic remodeling and plaque characteristics on mechanisms of lumen enlargement during stent implantation Gerard Finet, Neil J. Weissman, Marco T. Castagna, Kenneth M. Kent, Lowell F. Satler, John R. Laird, Augusto D. Pichard. Washington Hospital Center, Washington, DC

Mechanism of lumen enlargement during cutting balloon angioplasty for in-stent restenosis: An intravascular ultrasound study Javed M. Ahmed, Gary S. Mintz, Marco Castagna, Neil J. Weissman, Lowell F. Satler, Kenneth M. Kent, Augusto D. Pichard. Washington Hospital Center, Washington, DC

Mechanism of lumen enlargement during cutting balloon angioplasty for in-stent restenosis: An intravascular ultrasound study Javed M. Ahmed, Gary S. Mintz, Marco Castagna, Neil J. Weissman, Lowell F. Satler, Kenneth M. Kent, Augusto D. Pichard. Washington Hospital Center, Washington, DC

Is there a difference in the mechanisms of lumen enlargement with direct stenting as compared to stenting with predilatation? A three-dimensional intravascular ultrasound analysis Gerard Finet, Neil J. Weissman, Lowell F. Satler, Kenneth M. Kent, Marco T. Castagna, Augusto D. Pichard. Washington Hospital Center, Washington, DC

Is there a difference in the mechanisms of lumen enlargement with direct stenting as compared to stenting with predilatation? A three-dimensional intravascular ultrasound analysis Gerard Finet, Neil J. Weissman, Lowell F. Satler, Kenneth M. Kent, Marco T. Castagna, Augusto D. Pichard. Washington Hospital Center, Washington, DC

Predictors of event-free survival after repeat intracoronary procedure for in-stent restenosis; study with angiographic and intravascular ultrasound imaging.

Lumen enlargement during repeat percutaneous coronary intervention for in-stent restenosis has been shown to be the result of both stent over-expansion and decrease in neointimal tissue. How these two different mechanisms of action may influence outcome and target lesion revascularization after repeat intervention for in-stent restenosis is unclear. Intravascular ultrasound guided repeat intervention for in-stent restenosis was carried out either with balloon angioplasty, or with a combination of rotational atherectomy plus balloon angioplasty. Clinical follow-up at 1 year, including death, myocardial infarction, or need for revascularization, was obtained. Seventy patients were included in this study; 40 were treated by balloon alone, and 30 by combination of rotational atherectomy plus balloon. Event-free survival probability was 76+/-5%. The mechanism of lumen enlargement, be it stent over-expansion or tissue removal, had no influence on long-term clinical evolution. The only independent predictor was the minimal lumen cross-sectional area at the end of the procedure, the larger the lumen cross-sectional area, the higher the event-free probability. The cut-off point of the lumen cross-sectional area was set at 4.7 mm(2)by discriminant analysis. Event-free survival was 69+/-15% in patients with <4.7 mm(2)lumen cross-sectional area and 91+/-8% in patients with >4.7 mm(2)lumen cross-sectional area (P=0. 008). This study showed that the only independent predictor of late clinical outcome after percutaneous re-intervention for in-stent restenosis was final lumen size, no matter which means were used to achieve it.

Effect of balloon material and inflation strategy on arterial trauma and mechanisms of percutaneous transluminal coronary angioplasty as determined by intracoronary ultrasound

Twenty-three patients were randomized to a minimally invasive strategy or to standard percutaneous transluminal coronary angioplasty followed by intracoronary ultrasound. There was no difference in intracoronary ultrasound-determined dissection after the procedure in the 2 groups, and the mechanism of lumen enlargement by percutaneous transluminal coronary angioplasty in both groups predominantly was due to vessel stretch.

Effect of Rotational Atherectomy in Noncalcified Atherosclerotic Plaque: A Volumetric Intravascular Ultrasound Study

Objectives. This study used pre-rotational and post-rotational atherectomy volumetric intravascular ultrasound analysis to determine whether rotational atherectomy causes ablation of noncalcified atherosclerotic plaque.Background. Rotational atherectomy is currently the preferred treatment for heavily calcified coronary lesions. However, the mechanism of lumen enlargement in noncalcified lesions has not been studied in detail. Intravascular ultrasound allows detailed, cross-sectional imaging of the coronary arteries in vivo. The normal coronary artery wall, the major components of the atherosclerotic plaque and the quantitative changes in vessel, lumen and plaque cross-sectional areas and volumes that occur as a result of the atherosclerotic disease process and during transcatheter therapy can be studied in a manner otherwise not possible.Methods. Eighteen noncalcified native vessel lesions in 18 patients were imaged before and after rotational atherectomy using intravascular ultrasound systems incorporating motorized transducer pullback through a stationary imaging sheath. External elastic membrane, lumen and plaque plus media cross-sectional areas were measured every 1 mm of lesion length (for a total of 10 image slices), and external elastic membrane, lumen and plaque plus media volumes were calculated using Simpson's rule.Results. After rotational atherectomy, the minimal lumen cross-sectional area increased from 1.37 ± 0.50 to 2.99 ± 0.60 mm2 (mean value ± 1 SD, p < 0.0001). Lumen volume increased from 23.2 ± 9.0 to 38.0 ± 8.0 mm3 (p < 0.0001) as a result of a decrease in plaque plus media volume (from 102.2 ± 50.9 to 85.8 ± 47.7 mm3, p < 0.0001), with no change in total vessel (external elastic membrane) volume (125.3 ± 54.2 to 123.8 ± 52.9 mm3, p = 0.119).Conclusions. Rotational atherectomy effectively ablates noncalcified plaque in non-calcium-containing lesions.

Coronary artery morphologic features after coronary rotational atherectomy: Insights into mechanisms of lumen enlargement and embolization: A. Fart, D.K. Roberts, A.D. Pichard, K.M. Kent, R. Virmani. Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, DC. Am Heart J 1995;129:1058–67

Coronary artery morphologic features after coronary rotational atherectomy: Insights into mechanisms of lumen enlargement and embolization: A. Fart, D.K. Roberts, A.D. Pichard, K.M. Kent, R. Virmani. Department of Cardiovascular Pathology, Armed Forces Institute of Pathology, Washington, DC. Am Heart J 1995;129:1058–67

Mechanisms of lumen enlargement after excimer laser coronary angioplasty. An intravascular ultrasound study.

The mechanisms of excimer laser coronary angioplasty (ELCA) have never been studied in human coronary arteries in vivo. ELCA was used to treat 202 lesions in 190 patients. Forty-nine lesions in 48 patients were studied by use of sequential (before and after ELCA and after adjunctive device therapy) intravascular ultrasound (IVUS). External elastic membrane (EEM), lumen, and plaque+media (P+M = EEM-lumen) cross-sectional areas (CSAs) and lesion arcs of calcium were measured before and after ELCA and after adjunct device use. Lumen improvement after ELCA (1.4 +/- 0.5 to 2.7 +/- 0.8 mm2) was the result of both tissue ablation (decrease in P+M CSA from 16.8 +/- 7.1 to 15.9 +/- 6.7 mm2, P < .0001) and vessel expansion (increase in EEM CSA from 18.2 +/- 7.1 to 18.6 +/- 6.8 mm2, P = .0245), with no change in calcium. The decrease in P+M CSA was 39% of the CSA of the laser catheter used. Dissections were present in 39% of lesions, 84% within superficial calcium; fibrocalcific deposits developed a "fragmented" appearance. ELCA increased lumen CSA by both atheroablation and vessel expansion without calcium ablation. Superficial fibrocalcific deposits developed a characteristic fragmented appearance. These findings support both photoablation and forced vessel expansion as mechanisms of lumen enlargement and plaque dissection after ELCA.

Angiographic, ultrasonic, and angioscopic assessment of the coronary artery wall and lumen area configuration after directional atherectomy: The mechanism revisited

The purpose of the present study was to use the complementary information of angiography, intravascular ultrasound, and intracoronary angioscopy before and after directional atherectomy to characterize the postatherectomy appearance of vessel wall contours and the mechanism of lumen enlargement. Directional coronary atherectomy aims at debulking rather than dilating a coronary artery lesion. The selective removal of the plaque may potentially minimize the vessel wall damage and lead to subsequent better late outcome. Whether plaque removal is the main mechanism of action has only to be assessed indirectly by angiography and warrants further investigation with detailed analysis of luminal changes and vessel wall damage by ultrasound and direct visualization with angioscopy. Twenty-six patients have been investigated by quantitative angiography, intravascular ultrasound, and intracoronary angioscopy ( n = 19) before and after atherectomy. In addition, all retrieved specimens were microscopically examined. Ultrasound imaging showed an increase in lumen area from 1.95 ± 0.70 mm 2 to 7.86 ± 2.16 mm 2 at atherectomy. The achieved gain mainly resulted from plaque removal because plaque plus media area decreased from 18.16 ± 4.47 mm 2 to 13.13 ± 3.10 mm 2. Vessel wall stretching (i.e., change in external elastic lamina area) accounted for only 15% of lumen area gain. Luminal gain was higher in noncalcified (6.52 ± 2.12 mm 2) lesions than in lesions containing deeply located calcium (5.19 ± 0.99 mm 2) and lowest in superficially calcified lesions (5.41 ± 2.41 mm 2). Ultrasound imaging identified an atherectomy byte in 85% of the cases, whereas angioscopy revealed such a crevice in 74%. The complementary use of the three techniques revealed an underestimation of the presence of dissection/tear and new thrombus by angiography (10% and 4%) and ultrasound imaging (12% and 0%) compared with angioscopy (26% and 21%). The combined use of angiography, ultrasound, and angioscopy reveals that the postatherectomy luminal lining is not as regular and smooth as that seen by angiography. Luminal enlargement with atherectomy is achieved by plaque excision rather than arterial expansion.

Atherectomy (directional, rotational, extractional) and its role in percutaneous revascularization

After an initial wave of enthusiasm, atherectomy devices face a number of difficult issues today. The first two randomized studies comparing balloon angioplasty with directional atherectomy, the Coronary Angioplasty Versus Excisional Atherectomy Trial (CAVEAT) and the Canadian Coronary Atherectomy Trial (CCAT), showed no clinical benefit for atherectomy. Data from these trials, as well as other studies, suggest that the mechanism of lumen enlargement with atherectomy may be less beneficial than expected. A number of investigations are currently evaluating the benefit of even more aggressive debulking with directional coronary atherectomy, but in view of the increased incidence of acute complications, it is unlikely that this technique will increase its share in routine coronary angioplasty in the near future. Clinical evaluation of rotational and extractional atherectomy has not reached a conclusive phase yet, but results from registries and single-center observations show that these devices require adjunctive balloon angioplasty in a large proportion of cases, on the one hand, and that they do not solve the issue of restenosis, on the other. The difficulty in delineating the rationale for use of these devices highlights the urgent need for controlled and carefully designed device trials.

Coronary artery morphologic features after coronary rotational atherectomy: Insights into mechanisms of lumen enlargement and embolization

The coronary arteries and myocardium from two patients who died after coronary rotational atherectomy were analyzed to gain insights into the mechanisms of lumen enlargement and to document embolization of calcified plaque. Rotational atherectomy resulted in sharp cuts in plaque, producing a relatively smooth luminal surface. When extensive nodular calcific atherosclerosis was present, the luminal surface was focally uneven with exposure of jagged calcified plaque to blood flow. Deep plaque fissures and medial dissections were also seen. These fissures may have been created by the rotoblator or by adjunctive balloon angioplasty. Multiple calcific atheroemboli were present after rotoblator use in plaques containing extensive nodular calcification; in moderately calcified plaque only one small atheroembolus was found. Thus embolization of calcified plaque can occur after rotational atherectomy and may correlate with the severity of plaque calcification. Rotational atherectomy produces a focally smooth, sharp-edged, luminal surface, a lumen enlargement mechanism different from balloon angioplasty.