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Lack of association of restenosis following coronary angioplasty with elevated C-reactive protein levels or seropositivity to Chlamydia pneumoniae.

Seventy-five consecutive patients undergoing directional coronary atherectomy were evaluated by measuring anti-Chlamydia immunoglobulin G and anticytomegalovirus immunoglobulin G antibodies, and serum levels of C-reactive proteins (before atherectomy). The results showed that although both Chlamydia infection and elevated C-reactive protein levels are associated with coronary artery disease and coronary artery disease events, neither of these appears to play a role in the development of restenosis.

Adult↗

Features and outcome of no-reflow after percutaneous coronary intervention.

No-reflow is an uncommon complication that may occur after revascularization of patients with acute myocardial infarction, after interventions in saphenous vein bypass grafts, and after the use of some new interventional devices. However, the clinical impact of no-reflow after coronary intervention is unknown. Accordingly, this study examined the incidence, clinical presentation, angiographic characteristics, and outcome of no-reflow after percutaneous coronary intervention. No-reflow was defined as an acute reduction in antegrade flow (< or = 1, as defined by the Thrombolysis in Myocardial Infarction [TIMI] trial) not attributable to abrupt closure, high-grade stenosis, or spasm of the original target lesion. Among 10,676 coronary interventions performed between October 1988 and June 1993, no-reflow occurred in 66 patients (0.6%). These patients were compared with a subgroup of 500 consecutive patients who did not exhibit no-reflow. The incidence of no-reflow was 30 of 9,431 (0.3%) for percutaneous transluminal coronary angioplasty, 1 of 317 (0.3%) for excimer laser, 8 of 104 (7.7%) for Rotablator (Heart Technologies, Bellevue, Washington), 21 of 469 (4.5%) for extraction atherectomy, and 6 of 355 (1.7%) for directional atherectomy. Compared with those without no-reflow, patients with no-reflow experienced a 10-fold higher incidence of in-hospital death (15%) and acute myocardial infarction (31%). Correlates of in-hospital mortality included acute myocardial infarction on presentation (p = 0.006) and final flow < 3 (as defined by the TIMI trial) at completion of the procedure (p = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

Predictors of groin complications after balloon and new-device coronary intervention.

We reviewed the clinical course of 5,042 patients who underwent percutaneous transluminal coronary angioplasty (PTCA) using balloons or new devices: (stent, laser, directional and rotational atherectomy). A vascular complication was defined as the formation of a groin hematoma, bleeding, pseudoaneurysm, fistula, or the need for surgical repair. Vascular complications occurred in 309 (6.1%) patients, and 117 (2.3%) required vascular repair; among these patients, surgery was performed for correction of an an arteriovenous fistula in 12%, repair of pseudoaneurysm in 72%, repair for expanding hematoma and femoral artery lacerations in 10%, and retroperitoneal bleeding in 6%. The correlates of vascular complications were older age (66.8 vs 62.1 years; p < 0.0001), female gender (43% vs 26%; p < 0.0001), increased weight (82.1 +/- 16.46 vs 78.0 +/- 16.6 kg; p < 0.001), higher systolic blood pressure (140 +/- 25 vs 134 +/- 20 mm Hg; p < 0.001), increased heparin dose during the procedure (14,352 +/- 3,879 vs 13,599 +/- 3,508 IU; p = 0.001), administration of heparin after the procedure (232 vs 2,985 patients; p < 0.0001) and intracoronary stenting (14.9% vs 3.5%; p < 0.0001). Fifteen patients of 214 (7.0%) who underwent stent implantation had surgical repair. Vascular complications were not related to the size of the arterial sheath (8.11 +/- 0.8 vs 8.8 +/- 0.7Fr; p = 0.11) and the use of devices other than stents (laser, atherectomy) did not increase the rate of vascular complications.

Aged↗

Association between complex coronary artery stenosis and unstable angina and the extent of plaque inflammation.

PURPOSE: Patients with unstable coronary syndromes often have complex morphology of coronary stenoses at angiography. We evaluated the association between qualitative assessment of coronary stenoses and plaque inflammation determined by immunohistochemistry. METHODS: A total of 79 patients with unstable (n = 46) or stable angina (n = 33) underwent directional coronary atherectomy for culprit lesions. Qualitative analysis of coronary angiograms was performed using a modified Ambrose classification. Coronary lesions were categorized as either simple (concentric and eccentric type I, n = 29) or complex (eccentric type II and multiple irregularities, n = 50). Cryostat sections of retrieved atherosclerotic specimens were stained immunohistochemically with monoclonal antibodies, alpha-actin (smooth muscle cells), CD68 (macrophages), and CD3 (T lymphocytes). The extent of atherosclerotic inflammation within each coronary lesion was determined by the percentage of immunopositive macrophages per total tissue area (including smooth muscle cells) and the number of T lymphocytes per mm(2). RESULTS: The mean (+/- SD) percentage of macrophages in atherectomy specimens from patients with unstable angina was greater than in specimens from patients with stable angina (21% +/- 14% vs. 13% +/- 10%, P = 0.01); similar results were seen when complex coronary lesions were compared with simple lesions (23% +/- 13% vs. 9% +/- 8%, P <0.001). In multivariate linear regression models, the combination of unstable angina and lesion complexity was strongly associated with the percentage of plaque macrophages. CONCLUSION: The extent of atherosclerotic plaque inflammation is associated with angiographic grading of coronary lesion complexity and unstable angina.

Aged↗

The expression of angiotensin-I converting enzyme in human atherosclerotic plaques is not related to the deletion/insertion polymorphism but to the risk of restenosis after coronary interventions.

Plasma and tissue concentrations of the angiotensin-I converting enzyme (ACE) have been shown to be associated with the ACE insertion/deletion (I/D) polymorphism. The purpose of this study was to examine the relation of ACE levels in atherosclerotic plaques to the ACE I/D polymorphism and to restenosis after balloon angioplasty and directional atherectomy (DCA). The study included 104 patients who underwent DCA and received angiographic follow-up at 12 to 18 months. The amount of ACE protein in various morphologically defined plaque components (fibrous, atheromatous, and complicated lesions) of the atherectomy specimens was determined by qualitative and semiquantitative immunohistochemistry. ACE levels were related to the ACE genotype, to plaque morphology and to the risk of restenosis. Sequential staining revealed that pathologic ACE overexpression of the atherosclerotic lesions occurred in intimal smooth muscle cells, fibrocytes/fibroblasts and macrophage/foam cells. The ACE content of the whole plaques and of the single plaque components was not associated with the I/D polymorphism, but with restenosis after coronary interventions. In addition, ACE levels in the atherosclerotic lesions correlated with the severity of vessel wall damage. The ACE phenotype might serve as an indicator for the risk of restenosis after coronary interventions.

Angioplasty, Balloon, Coronary↗

Troponin T, creatine kinase MB mass, and creatine kinase MB isoform ratio in the detection of myocardial damage during non-surgical coronary revascularization.

The presence of myocardial injury during non-surgical coronary revascularization has been evaluated by means of highly specific and sensitive biochemical markers. Troponin T, creatine kinase-MB isoenzyme mass concentration, and creatine kinase MB2/MB1 isoform ratio have been determined in 80 patients who underwent coronary revascularization with percutaneous transluminal coronary angioplasty (PTCA). Forty-five patients underwent balloon angioplasty, 15 rotational atherectomy, 10 directional atherectomy, and 10 elective coronary stenting. Serum concentration of the evaluated markers did not increase significantly after 57 uncomplicated revascularization procedures, including 15 rotablation procedures, nor after 8 PTCAs complicated by localized coronary type B and C dissections. Significant elevation of all markers above the upper limits of the reference interval (P < 0.05) was detected after occlusion of small side branches (< 0.5 mm diameter) in 5 patients. Creatine kinase MB2/MB1 isoform ratio was the earliest marker to increase. After recanalization of occluded vessels in 8/10 patients with 6-60 days old myocardial infarction only troponin T concentrations increased from a baseline of 0.28 microgram/l to a median peak of 0.80 microgram/l. This increase was statistically not significant (P = 0.12). In conclusion, myocardial damage was not detected following uncomplicated non-surgical revascularization obtained with different techniques. Markers of myocardial injury provide high sensitivity after small side branch occlusion.

Aged↗

[Registry of activities of the Section of Hemodynamics and Interventional Cardiology in 1997].

The results of the Spanish Registry of Hemodynamic and Interventional Cardiology in 1997 are presented. The Registry collects the activity of 83 centers which constitute all the cardiac catheterization laboratories in Spain. The main activity was adult cardiac catheterization in 75 centers and exclusively pediatric cardiac catheterization in 8. A total of 72,370 diagnostic catheterization procedures, 80% coronary angiographies (57,960; 1,462 per million inhabitants), were performed which represents a 13% total increase compared to 1996. Coronary intervention increased by 23% compared to 1996, for a total number of 18,545 procedures. The ratio of coronary interventions per million inhabitants was 468. Success rates of coronary interventions (91.3%) and complications (3.7%) were similar to those registered in previous years. In the specific field of revascularization devices, there has been a dramatic increase in the use of stents. In 1997, coronary stents were employed in 11,417 cases (a 61% increase compared to 1996) which represents 61.5% of all coronary revascularizations procedures. A total of 14,170 prosthesis were implanted, 72% in a elective way, with a low rate of complications (0.95% subacute closure; 1.45% myocardial infarction and 0.75% mortality). Compared to 1996, directional coronary atherectomy (92 procedures) showed a slight decrease, whereas rotational atherectomy (554 procedures) increased by 49% with double the number of centers performing this technique. As in previous years, a slight decrease (7% compared to 1996) in adult valvuloplasties (559 vs 599) was noted. Pediatric interventional procedures decreased by 17% (465 vs 558 procedures) compared to the 1996 Registry.

Adult↗

Increased intimal apoptosis in coronary atherosclerotic vessel segments lacking compensatory enlargement.

OBJECTIVES: In a histopathologic study, we assessed the balance of cell proliferation and apoptosis by counting the number of apoptotic and proliferating cell nuclear antigen-positive cells in freshly harvested atherectomy specimens from 34 patients. BACKGROUND: Remodeling of human coronary arteries is an adaptive process that alters vascular lumen size. METHODS: Intravascular ultrasound was performed prior to atherectomy. Total vessel area (area within the external elastic lamina [EEL]), lumen area and plaque area were measured at the region of interest (ROI), and at a proximal and distal reference segment, utilizing the formula Delta(%)=100x(ROI-reference segment)/reference segment. Positive arterial remodeling (R+) resulting in luminal expansion was defined as DeltaEEL >10%. Absence of remodeling (0 < DeltaEEL <10%) and constrictive arterial remodeling (DeltaEEL <0) were considered as neutral remodeling (R0) and negative remodeling (R-), respectively. RESULTS: In R- lesions, apoptotic indices (APO) were significantly elevated (17.17 +/- 2.19%) compared with R+ lesions (4.89 +/- 1.7%; p = 0.0007). In a rabbit iliac percutaneous transluminal coronary angioplasty model intimal apoptosis was increased four weeks after balloon angioplasty injury (APO 8.8 +/- 0.03%) compared with contralateral untreated segments (APO 3.0 +/- 0.04%, n = 6). Lesions with an EEL/intimal area <3.0 showed significantly more intimal apoptosis than untreated lesions (p = 0.02). CONCLUSIONS: The data indicate that constrictive remodeling of atherosclerotic coronary lesions is associated with increased apoptosis of intimal cells. We speculate that increased apoptosis is due to extensive plaque healing after episodes of symptomatic or asymptomatic plaque rupture.

Adaptation, Physiological↗

Coronary in-stent restenosis: current status and future strategies.

In-stent restenosis (ISR) is a novel pathobiologic process, histologically distinct from restenosis after balloon angioplasty and comprised largely of neointima formation. As percutaneous coronary intervention increasingly involves the use of stents, ISR is also becoming correspondingly more frequent. In this review, we examine the available studies of the histology and pathogenesis of ISR, with particular reference to porcine and other animal models. An overview of mechanical treatments is then provided, which includes PTCA, directional coronary atherectomy and high speed rotational atherectomy. Radiation-based therapies are discussed, including a summary of current problems associated with this modality of treatment. Finally, novel strategies for the prevention of ISR are addressed, including novel developments in stents and stent coatings, conventional drugs, nucleic acid-based drugs and gene transfer. Until recently, limited pharmacologic and mechanical treatment options have been available for both treatment and prevention of ISR. However, recent advances in gene modification and gene transfer therapies and, more particularly, in local stent-based drug delivery systems make it conceivable that the incidence of ISR will now be seriously challenged.

Angioplasty, Balloon, Coronary↗

Ticlopidine and aspirin pretreatment reduces coagulation and platelet activation during coronary dilation procedures.

OBJECTIVES: It is unknown whether a therapeutic combination of aspirin (ASA) and ticlopidine might effectively decrease activation of hemostasis. BACKGROUND: Percutaneous transluminal coronary angioplasty (PTCA), rotational atherectomy and stent implantation are procedures that fracture or ablate endothelium and plaque, a situation that activates hemostasis. METHODS: In 85 patients undergoing PTCA for a 77.8 +/- 1% stenosis, we measured markers of coagulation and platelet activation (thrombin-antithrombin complexes [TAT], prothrombin fragment 1 + 2 [F1 + 2] serotonin and the presence of circulating activated platelets reacting with monoclonal antibodies against glycoproteins exposed on platelet membranes). Blood samples were drawn from a peripheral vein and from the coronary ostium before the procedures. Both immediately and 10 min after angioplasty, and 10 min afterward, samples were collected from a probing catheter (0.018 in, [0.46 cm]) positioned beyond the stenosis. All patients were being treated with antianginal drugs and ASA, 250 mg/day. Seventy of them had taken ticlopidine, 250 mg, twice daily for < or = 1 day (< or = 24 h) (n = 28) or for > or = 3 days (> or = 72 h) (n = 42). Heparin (150 U/kg) was administered before angioplasty. Thirty patients underwent PTCA; 15 of them were not treated with ticlopidine and 15 were given ticlopidine (> or = 72 h). Thirty-five patients had stent implantation, 20 rotational atherectomy. RESULTS: Before and during the procedures, there was greater thrombin generation (expressed by higher TAT and F1 + 2 plasma levels) in patients not taking ticlopidine or taking it for < or = 24 h (p < 0.05). Platelet activation and plasma serotonin levels were also significantly higher in the no ticlopidine or < or = 24-h ticlopidine groups. CONCLUSIONS: The combined use of ticlopidine, ASA and heparin effectively controls activation of coagulation in patients with stable or unstable angina undergoing coronary dilation.

Angioplasty, Balloon, Coronary↗

Six-month angiographic and clinical follow-up of patients prospectively randomized to receive either tirofiban or placebo during angioplasty in the RESTORE trial. Randomized Efficacy Study of Tirofiban for Outcomes and Restenosis.

OBJECTIVES: This study sought to investigate the effects of tirofiban versus placebo on the incidence of adverse cardiac outcomes and coronary artery restenosis at 6 months. BACKGROUND: Tirofiban is a highly selective, short-acting inhibitor of fibrinogen binding to platelet glycoprotein IIb/IIIa. In a recent clinical study, tirofiban reduced the incidence of adverse cardiovascular events at both 2 and 7 days after coronary angioplasty or directional coronary atherectomy. This reduction persisted but was no longer statistically significant at 30 days. METHODS: The Randomized Efficacy Study of Tirofiban for Outcomes and Restenosis (RESTORE) trial was a randomized, double-blind, placebo-controlled trial of tirofiban in patients undergoing balloon angioplasty or directional atherectomy within 72 h of presentation with either unstable angina pectoris or acute myocardial infarction. All patients received an initial bolus (10 microg/kg body weight over 3 min), followed by a 36-h infusion (0.15 microg/kg per min) of either tirofiban or placebo. RESULTS: At 6 months the composite end point (either death from any cause, new myocardial infarction, bypass surgery for angioplasty failure or recurrent ischemia, repeat target vessel angioplasty or stent insertion for actual or threatened abrupt closure) occurred in 1,070 placebo group patients (27.1%) and 1,071 tirofiban group patients (24.1%, p = 0.11). Analysis of 6-month coronary arteriograms by means of quantitative coronary arteriography showed no significant difference between placebo- and tirofiban-treated patients in either the incidence of a > or =50% diameter stenosis (57% vs. 51%, p = NS), a loss of > or =50% of lumen diameter gained (50% vs. 50%, p = NS) or a loss of > or =0.72 mm of lumen diameter (44% vs. 42%, p = NS). CONCLUSIONS: The 3% absolute reduction in the incidence of the composite end point at 6 months (27.1% placebo vs. 24.1% tirofiban) was similar to that previously reported at 2 days (8.7% vs. 5.4%, p < 0.005), and there does not appear to be any late effect of tirofiban on clinical end points between day 2 and 6 months. Tirofiban did not reduce the incidence of restenosis at 6 months when defined in a number of ways.

Adult↗

Mast cell infiltration in acute coronary syndromes: implications for plaque rupture.

OBJECTIVES: To define the role of mast cells in plaque destabilization. BACKGROUND: Inflammation is an essential feature of human coronary plaques. Macrophages and T lymphocytes are considered to contribute to destabilization of the plaques. The role of mast cells in this setting is less well studied. We therefore counted the mast cells in coronary atherectomy specimens from patients with chronic stable angina, unstable angina and severe unstable angina. METHODS: Patients studied had chronic stable angina (group 1, n=11), "stabilized" unstable angina (group 2; Braunwald's class I and II, n=11) and "refractory" unstable angina (group 3; Braunwald's class III, n=7). Samples of culprit lesions (n=29) were obtained by directional atherectomy, snap-frozen and analyzed immunohistochemically. The numbers of mast cells and T lymphocytes per square millimeter squared were counted and the areas containing macrophages and smooth muscle cells were measured by computed planimetry. RESULTS: We found that the numbers of mast cells and T lymphocytes increased from group 1 through groups 2 to 3. Specimens from group 3 also contained the largest numbers of tumor necrosis factor alpha (TNF-alpha)-positive mast cells and of matrix metalloproteinase (MMP)-9 (92 kD gelatinase)-positive macrophages. CONCLUSIONS: Unstable coronary syndromes are associated with increased numbers of mast cells in culprit lesions. Activated mast cells secrete neutral proteases capable of degrading the extracellular matrix and TNF-alpha, capable of stimulating macrophages to synthesize MMP-9. Our observations suggest that mast cells, in addition to macrophages, contribute to matrix degradation and, hence, to progression of coronary syndromes.

Adult↗

Histological evaluation of coronary plaque in patients with variant angina: relationship between vasospasm and neointimal hyperplasia in primary coronary lesions.

OBJECTIVES: This study was designed to determine whether coronary vasospasm in patients with variant angina pectoris (VAP) may produce focal organic lesions at the site of vasospasm that would contribute to disease progression. BACKGROUND: Recent clinical angiographic and experimental studies have demonstrated the potential role of vasospasm in the worsening of organic coronary stenosis. METHODS: We studied histologically the coronary plaques obtained at atherectomy in 202 patients with moderate to severe coronary stenosis. This population included 22 patients with VAP, 100 patients with chronic stable angina and 80 patients with restenosis following angioplasty or atherectomy. Diagnosis of VAP was based on both the clinical feature of angina at rest associated with ST elevation and a positive response to acetylcholine provocation test. RESULTS: The most common histological appearance in 92% of patients with stable angina was hypocellular fibroatheromatous plaques, whereas neointimal hyperplasia was the characteristic feature of the plaque observed in 90% of patients with restenosis. The coronary specimens at the site of spasm in 15 of the 22 patients (68%) with VAP demonstrated intimal injuries such as neointimal hyperplasia (15), thrombus formation (2), and intimal hemorrhage (3). Neointimal hyperplasia was significantly more common in the patients with VAP as compared with those with stable angina (68% vs. 8%; p < 0.0001). A rapid progression of organic stenosis within three years was angiographically found in 5 of the 22 patients with variant angina. In all five cases, neointimal hyperplasia was the main contributor to the worsening of the organic lesion at the site of spasm. These histological findings in patients with VAP extremely resembled those in restenosis. Except for vasospasm, no factors significantly predicted the presence of neointimal formations in primary coronary lesions. CONCLUSIONS: Coronary vasospasm may provoke vascular injury that leads to the formation of neointima in VAP patients similar to that seen with restenosis. Coronary spasm may thus play a key role in the rapid coronary stenosis progression in certain patients with VAP.

Adult↗

Tissue characteristics of restenosis after percutaneous transluminal coronary angioplasty in diabetic patients.

OBJECTIVES: The purposes of this study were to analyze coronary specimens from patients with diabetes mellitus (DM) and to compare them with specimens from patients without DM. BACKGROUND: Diabetes mellitus is associated with an increased incidence of restenosis after percutaneous transluminal coronary angioplasty (PTCA). Increased hypercellular smooth muscle cell proliferation with exaggerated intimal hyperplasia formation may be responsible for this predisposition. METHODS: Eighteen coronary atherectomy specimens with restenosis after PTCA from patients with DM were compared with 18 coronary atherectomy specimens with restenosis after PTCA from patients without DM. Total and segmental areas were quantified on trichrome-stained tissue of hypercellular tissue, collagen-rich sclerotic tissue, atheroma and thrombus. Demographic and angiographic data were similar in both groups. RESULTS: The percentage of total plaque area composed of hypercellular tissue was lower in restenotic specimens from patients with DM than in restenotic specimens from patients without DM (19 +/- 6% vs. 44 +/- 5%; p = 0.003). The percentage of collagen-rich sclerotic tissue area was larger in restenotic specimens from patients with DM than in restenotic specimens from patients without DM (77 +/- 9% vs. 53 +/- 4%; p = 0.004). The percentages of atheroma and thrombus were similar in both groups. CONCLUSIONS: Intimal hypercellular tissue content is reduced in restenotic tissue from patients with DM. Collagen-rich sclerotic content is increased in restenotic lesions from patients with DM. These results suggest an accelerated fibrotic rather than a proliferative response in diabetic lesions from patients with restenosis after PTCA.

Aged↗

Ultrasound-guided pseudoaneurysm compression: efficacy after coronary stenting and angioplasty.

PURPOSE: Ultrasound-guided compression of femoral pseudoaneurysms has often obviated the need for open operative repair. Increasing use of percutaneous interventional cardiac procedures has created pseudoaneurysms with a large-caliber arterial defect, often in patients who are placed immediately on anticoagulation therapy. This report describes the prospectively collected information from our vascular laboratory regarding ultrasound-guided compression of these pseudoaneurysms after cardiac procedures, both interventional and diagnostic. METHODS: Since March 1994 prospective data collection for patients who have undergone pseudoaneurysm compression in our vascular laboratory has recorded information including cardiac procedure, size of catheter or sheath, coagulation parameters, pseudoaneurysm size and location, and time to compression. Forty-one patients underwent attempted ultrasound-guided pseudoaneurysm compression after cardiac procedures: 19 after cardiac catheterization alone, seven after angioplasty, one after atherectomy, two after insertion and subsequent removal of an intraaortic balloon pump, and 12 after coronary stenting. RESULTS: Compression was successful overall in 88% of the patients (36 of 41). Successful compression of the pseudoaneurysm was seen in 95% after catheterization alone, 100% after angioplasty, 100% after atherectomy, and 100% after intraaortic balloon pumping, as compared with 67% after stenting (eight of 12 vs 28 of 29; p = 0.02). A sheath size of 9F or greater was a significant factor in predicting unsuccessful compression (three of eight vs two of 33; p = 0.04). Abnormal coagulation parameters were present in 20 of the 41 patients and was not significantly different in patients who were successfully or unsuccessfully treated (four of five vs 16 of 36; p = 0.40). CONCLUSIONS: Pseudoaneurysms after cardiac procedures and interventions can often be successfully compressed with an ultrasound-guided technique. The presence of abnormal coagulation parameters was not identified as a risk factor for compression failure and should not dissuade attempted compression. Stent placement was more likely to result in unsuccessful compression, and this appeared to be a result of the larger size of the arterial defect. Even in this setting, compression achieved obliteration of the pseudoaneurysm in more than half of the patients.

Aneurysm↗

In vivo effect of coronary laser angioplasty on atherosclerotic plaques: histopathologic analysis.

Information from histopathologic examination of coronary arterial atherosclerotic plaques treated with in vivo laser energy is sparse. Directional atherectomy provides biopsies for study of tissue changes (injury) due to coronary arterial debulking devices, including laser. Sixteen patients who presented with acute ischemic coronary syndromes underwent debulking of a total of 17 obstructive intracoronary lesions with pulsed-wave holmium:YAG laser (2.1 microm wavelength). Laser was performed with the "pulse and retreat" technique which incorporates slow catheter advancement (0.5-1 mm/s) with controlled emission of energy. Immediately postlasing, directional atherectomy was utilized to obtain irradiated plaque tissue for pathologic examination. Extent of laser-induced tissue injury to plaques was graded as 0 (no tissue damage), 1 (small foci or charring and vacuoles), 2 (large amount of charring, edge disruption and vacuoles) and 3 (extensive tissue damage). Angiographically and clinically, all 17 lesions were successfully debulked with the laser energy (mean 47+/-25 pulses), with a reduction of target lesion percent diameter stenosis from 92+/-6% to 47+/-25%. Adjunct balloon dilations further reduced the target lesions to a final of 10+/-10% stenosis. The histopathologic examination of the lased specimens demonstrated that 13 lesions (76%) had no evidence of laser-induced injury (Grade 0). Four lesions had low-level injury (Grade 1), and none had evidence of Grade 2 or 3 laser-induced trauma. Therefore, a laser debulking technique, which incorporates slow catheter advancement with controlled emission of pulses, does not cause significant injurious effects to the irradiated plaque.

Aged↗

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

AIMS: 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. METHODS: 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. RESULTS: 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). CONCLUSIONS: 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.

Angioplasty, Balloon, Coronary↗

Plaque excision for the treatment of infrainguinal arterial occlusive disease.

Lower extremity peripheral vascular disease has a broad spectrum of presentations, ranging from intermittent claudication, rest pain, to limb threatening tissue loss and gangrene. Over the last 10 to 15 years, short focal stenoses or occlusions have been treated using endovascular techniques, but conventional angioplasty and stenting is limited by high restenosis rates especially in longer lesions. Moreover, multilevel, complex disease is still generally considered best managed by surgical intervention. However, with the improvements in atherectomy technology, namely plaque excision and laser plaque ablation, the full spectrum of arterial occlusive lesions may now be addressed by percutaneous means with excellent limb salvage rates. Excisional atherectomy is currently exemplified by the SilverHawk Plaque Excision System, which is available in four sizes for the treatment of all infrainguinal vessels. As the apparatus is advanced, the rotational cutting blade excises a ribbon of plaque that is concurrently collected into a nosecone. Multiple passes are made, during which the blade is directed sequentially toward all quadrants of the vessel lumen. The stenotic lesion is grossly debulked by this technique with the proposed advantage of avoiding the arterial wall barotrauma that hampers the durability of angioplasty and stenting.

Angiography↗