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At least 19 recordsLinked to original sources
PubMed1990

Predicting late restenosis after coronary angioplasty by very early (12 to 24 h) thallium-201 scintigraphy: implications with regard to mechanisms of late coronary restenosis.

To examine whether late coronary restenosis may be predicted by abnormalities of myocardial perfusion in the early hours after successful percutaneous transluminal coronary angioplasty and to study in greater detail the mechanisms involved in the development of late coronary restenosis after angioplasty, a prospective study was undertaken in 90 consecutive patients. Thallium-201 scintigrams were recorded at rest and during the stress of atrial pacing, 12 to 24 h after angioplasty, and the results were related to the findings at angiography in 70 patients undergoing late cardiac catheterization. A reversible thallium-201 perfusion defect was found in 39 (38%) of 104 myocardial regions supplied by the dilated coronary vessel and identified a subset of patients at high risk of late (6 to 12 months) angiographic restenosis (sensitivity 77%, specificity 67%). In contrast, late coronary restenosis developed in only 7 (11%) of 65 vessels and in 5 (14%) of 37 patients with a nonischemic thallium-201 scintigram on day 1 (p less than 0.005). Multivariate logistic regression analysis of 14 possible preangioplasty and periangioplasty clinical and angiographic variables selected reversible perfusion defect on the thallium-201 scintigram on day 1 (p = 0.016) and immediate postangioplasty residual coronary narrowing (p = 0.004) as significant independent predictors of late restenosis, with younger patient age as an additional less powerful predictor (p less than 0.05). The findings have important implications regarding the pathogenesis of late coronary restenosis in patients undergoing successful angioplasty and they imply that in the majority of these patients pathophysiologic events in the early minutes and hours after angioplasty may determine the development of late restenosis.

Adult↗
PubMed2005

Nocturnal oxygen desaturation as a predictive risk factor for coronary restenosis after coronary intervention.

BACKGROUND: Sleep-disordered breathing may affect coronary artery disease, so patients treated by percutaneous transluminal coronary angioplasty were studied to investigate the relationship between nocturnal oxygen desaturation (NOD) and the loss index. METHODS AND RESULTS: The nocturnal oxygen desaturation index (ODI) was determined by means of a pulse oximeter in 35 patients with coronary artery disease treated by stent placement. The patients were divided into 3 groups according to ODI: <5 events/h (group N, n=6), between 5 and 14 events/h (group A, n=19), and >or=15 events/h (group B, n=10). The relationship between the ODI and loss index was examined in each group. The loss index, 0.27+/-0.23 in group N, 0.30+/-0.27 in group A, and 0.70+/-0.32 in group B, differed significantly between groups N and B (p=0.007). In all patients, the loss index showed a significant positive correlation with the ODI (R=0.585, p=0.002). CONCLUSIONS: These findings suggest that NOD may be an important contributor to coronary restenosis in patients treated with stent placement.

Aged↗
PubMed2002

Detection of coronary restenosis after coronary angioplasty by contrast-enhanced transthoracic echocardiographic Doppler assessment of coronary flow velocity reserve.

OBJECTIVES: This study sought to evaluate the diagnostic potential of contrast-enhanced transthoracic echocardiography (CE-TTE) during adenosine infusion, a noninvasive method for evaluating coronary flow reserve (CFR), in detecting restenosis after successful percutaneous transluminal coronary angioplasty (PTCA). BACKGROUND: Restenosis is the most important limitation of PTCA, and CFR can be impaired in patients with angiographically documented significant coronary stenosis. METHODS: We performed 6 +/- 2 months of follow-up of 53 patients after successful elective PTCA in the left anterior descending coronary artery (LAD). Coronary angiography was performed at the end of the planned follow-up period or even before, if clinically indicated. Thus, of the 53 patients, a total of 63 angiographic studies were performed; CE-TTE assessment of CFR was achieved before each of the 63 angiographic studies. RESULTS: Coronary angiography revealed the presence of restenosis (defined as >50% stenosis at a previous PTCA site) in 32 angiographic examinations (group A) and no coronary restenosis in the remaining 31 examinations (group B). Coronary flow reserve was significantly reduced in group A compared with group B (1.65 +/- 0.5 vs. 3.17 +/- 0.8, p < or = 0.001). A noninvasive CFR value < or = 2 was 93% specific and 78% sensitive for detecting significant restenosis, with positive and negative diagnostic accuracies of 92% and 80%, respectively. CONCLUSIONS: Noninvasive CFR assessment by CE-TTE is an accurate method of monitoring significant restenosis in the LAD when following up patients submitted to elective PTCA.

Adult↗
PubMed2005

Clinical and economic effects of coronary restenosis after percutaneous coronary intervention in a managed care population.

PURPOSE: The epidemiology of coronary restenosis after percutaneous coronary intervention (PCI) has been documented extensively in clinical trials, but no data exist on the clinical and economic burden of restenosis in a managed care population. DESIGN: Retrospective cohort with a nationally representative managed care claims database (IHCIS, Waltham, Mass.) representing 2.8 million members. METHODOLOGY: Patients undergoing initial PCI between 1/1/00 and 12/31/00 (N=3,258) were identified and followed to 1 year. Clinical events, resource use, and costs between 1 month and 1 year after the initial PCI were identified. The clinical restenosis rate was estimated by multiplying the observed repeat revascularization rate by 0.85, based on previously published studies. All costs are reported from a managed care perspective in Year 2000 dollars. PRINCIPAL FINDINGS: Overall, 14.7 percent of patients required 1 or more repeat revascularization procedures between 1 month and 1 year after initial PCI, which implies an estimated clinical restenosis rate of 12.5 percent. Mean 1-year costs were nearly 6-fold higher among patients with and without repeat revascularization (dollars 31,954 +/- dollars 31,857 vs. dollars 5,474 +/- dollars 12,006, P<.001). After adjusting for baseline imbalances, the independent incremental cost for each patient with repeat revascularization was dollars 24,955 (95 percent confidence interval, dollars 23,401-dollars 26,510). Annual follow-up costs attributable to restenosis were dollars 3,118 per initial PCI recipient (i.e., dollars 24,955 x 12.5 percent). CONCLUSION: Clinical restenosis occurred in approximately 12.5 percent of real-world managed care PCI patients and increased health care costs by an average of dollars 3,118 per patient. These findings have important implications for the cost-effectiveness of new treatments that substantially reduce restenosis.

Aged↗
PubMed2001

The effect of magnetic stent on coronary restenosis after percutaneous transluminal coronary angioplasty in dogs.

OBJECTIVE: To investigate the effects of magnetic stents on coronary restenosis after percutaneous transluminal coronary angioplasty (PTCA). METHODS: Twenty dogs were randomly divided into the control and experimental groups, each with 10 dogs. The control group was given common Palmaz-stents in the 6-8 segment of left anterior descending coronary artery or in the 11-14 segment of the left circumflexus. The experimental group was given magnetic stents in the same parts of the coronary arteries. The dogs were not given antiplatelet or anticoagulant drugs before or after the operation. Six months later, the 20 dogs were subjected to coronary angiographies, and then were sacrificed. Three centimeter long segments of the target vessels were cut for pathological examination. RESULTS: The degree of restenosis in 3 dogs of the control group was more than 50%, but none in the experimental group experienced restenosis. The average thickness of the tunica intima of the target artery was 2.98 +/- 0.56 mm in the control and 1.13 +/- 0.41 mm in the experimental group (P < 0.05). CONCLUSION: Magnetic stents could have a significant preventive effect on coronary restenosis.

Angioplasty, Balloon, Coronary↗
PubMed1989

[Effects and chronology of coronary restenosis after percutaneous transluminal coronary angioplasty. Quantitative angiographic analysis at 1, 2, 3, 4 and 5 months].

Coronary restenosis occurs fairly early after transluminal coronary angioplasty, as suggested by anatomico-clinical, isotopic and angiographic studies. Its incidence, as reported in the literature, varies according to the clinical selection of patients, to the number of patients with follow-up angiography and the timing of this procedure, and to the criteria used to define restenosis. In this prospective study we endeavoured to determine the exact date at which restenosis takes place, as well as its true incidence, by means of 6 different angiographic criteria. The population studied was divided into five groups and each group underwent coronary arteriography at a different date: during the 1st, 2nd, 3rd, 4th and 5th post-angioplasty months respectively. In 424 of the 500 patients thus examined (84.8 p. 100), coronary angiography involved automatic detection of contours and made quantitative analysis possible. Coronary restenosis was found to occur early, with a peak of incidence in the 3rd month. Its incidence varied considerably depending on the criterion used. A critical analysis of the data has prompted us to use a criterion based on absolute values determined by quantitative angiographic analysis.

Adolescent↗
PubMed1999

Detection of angiographic coronary restenosis after percutaneous transluminal coronary angioplasty (PTCA): usefulness of angina combined with rest electrocardiogram.

PURPOSE: To evaluate the value of recurrent anginal symptoms combined with seriation of conventional EKG in detecting coronary restenosis (renarrowing > or = 50% at the site dilated) after PTCA. Two hundred and seventy patients (204 men, mean age 53.1 +/- 9.4 years) with angina who submitted to successful PTCA of single-vessel coronary disease were followed and restudied angiographically 5.2 +/- 1.6 months after the procedure. At any moment from PTCA to follow-up: 1) typical angina pectoris was classified as either absent or present; 2) a 12-lead EKG was classified as improved, unchanged or worsened in comparison with the EKG either before or early after PTCA on the basis of ST-T alterations; 3) all patients underwent coronariography and were then classified as either having or lacking restenosis. The sensitivity and predictive positive value of recurrent angina, worsened EKG, or both, in detecting restenosis were respectively: 74.6% and 68.6%, 44.3% and 85.3%, and 55.9 and 91.7%. The specificity and predictive negative value of no recurrence of angina, improved EKG, or both, in detecting the absence of restenosis were respectively: 85.8% and 89.1%; 69.6% and 91.0%; and 75.6% and 93.9%. CONCLUSION: In single-vessel coronary disease, the detection of coronary restenosis after PTCA based on behavior of the symptoms plus rest EKG seriation shows acceptable degrees of sensitivity, specificity and mainly of predictive values when comparison with respective historical values of the ergometric test is considered.

Adult↗
PubMed1989

[Treatment of coronary restenosis by repeated coronary transluminal angioplasty. Immediate and medium-term results].

To assess the immediate and medium term efficacy of percutaneous transluminal coronary angioplasty (PTCA) for restenosis, we retrospectively studied 102 patients undergoing a second PTCA between August 1983 and October 1987. The patients were 89 males and 13 females, mean age 61 +/- 7 years. Before the second PTCA, 13 patients were asymptomatic, 31 had effort angina and 58 resting angina. Exercise stress test performed in 50 patients was positive in 40 cases, negative in 9 and uninterpretable in 1. The coronary lesions were: 59 one vessel disease (58 p. 100) and 43 multivessel disease in which PTCA was performed on 1 lesion in 40 and on 2 lesions in 3. Primary success of PTCA was obtained in 100 patients (98 p. 100); 2 patients underwent coronary artery bypass graft (CABG), 1 as an emergency. At 6 months 45 patients had recurrent chest pain (46 p. 100) and 52 were asymptomatic. Control coronary angiogram performed in 70 patients (72 p. 100) after a mean delay of 7.4 +/- 6 months showed a second restenosis in 34, symptomatic in 31. Medium term follow-up was obtained for 96 patients (96 p. 100) with a mean follow-up period of 22.3 +/- 13.2 months. There were 5 cardiac deaths (5.2 p. 100) and 4 non fatal myocardial infarctions (4.2 p. 100). A new revascularization procedure after the second PTCA was performed in 33 patients (34.4 p. 100). Twenty-five patients underwent a third PTCA (26 p. 100), 5 patients a fourth PTCA (5.2 p. 100) and 11 patients underwent a CABG (11.4 p. 100).(ABSTRACT TRUNCATED AT 250 WORDS)

Angioplasty, Balloon, Coronary↗
PubMed1996

Deposition of PG-M/versican is a major cause of human coronary restenosis after percutaneous transluminal coronary angioplasty.

To clarify the mechanisms of restenosis, restenotic human tissue specimens obtained by directional coronary atherectomy (DCA) in 43 patients were immunohistochemically analysed for cell proliferation and deposition of PG-M/versican, an important extracellular matrix proteoglycan of the vessel wall. The patients were classified into five groups according to the period after percutaneous transluminal coronary angioplasty (PTCA): 0-1 month (N = 6), 1-3 months (N = 12), 3-6 months (N = 11), more than 6 months (N = 6) and de novo lesions (N = 8). The tissue specimens were of 35 restenotic lesions following PTCA and eight primary stenotic lesions with no prior PTCA. Total cell numbers in the atherectomy specimens increased significantly up to 3 months after PTCA. Most cells were alpha-smooth muscle actin (alpha-SMA)-positive. To evaluate cell proliferation, the specimens were immunostained for Ki-67 antigen (clone MIB-1). A significant increase in the positive ratio was observed up to 1 month after PTCA, although the labelling index was less than 1 per cent at every stage. The deposition of PG-M/versican, as analysed by immunohistochemistry, was greatest during the period 1-3 months after primary angioplasty, when restenosis detected by angiography progresses most actively. These results suggest that the peak of cell proliferation in the neointima occurs earlier than angiographic restenosis and that the deposition of PG-M/versican may be a major factor in restenosis following angioplasty.

Aged↗
PubMedDate not supplied

Initial studies with gamma radiotherpay to inhibit coronary restenosis.

BACKGROUND: Early studies indicate brachytherapy is a potential clinical treamtent for restenosis after coronary angioplasty procedures. The objective of this study was to evaluate the safety and efficacy of gamma radiation plus stenting in patients' previous restenosis. METHODS: In patients with previous coronary restenosis, balloon dilatation and/or coronary stenting was undertaken and then patients were randomly assigned to receive either Iridium-192 or placebo. Quantitative coronary angiographic, intravascular ultrasonographic, and clinical follow-up was obtained. RESULTS: Of the 55 patients enrolled, 26 were treated with Iridium-192 and 29 were in the placebo group. Late luminal loss was significantly lower in the treated group compared to the placebo group (0.38 +/- 1.06 mm vs. 1.03 +/- 0.97 mm, p = 0.03). Restenosis (stenosis of > or = 50% at follow-up) was found in 17% of treated patients compared to 54% of placebo patients (p = 0.01). The need for target lesion revascularization was observed in 12% of patients in the treated group compared to 45% in the placebo group (p = 0.01). CONCLUSIONS: In this initial trial, at 12 months follow-up, patients with previous restenosis were benefited by catheter-based gamma radiation therapy.

Angioplasty, Balloon, Coronary↗
PubMed2005

Insulin resistance, hyperleptinemia and endothelial dysfunction in coronary restenosis.

Impaired insulin sensitivity and endothelial dysfunction are important markers in the development of restenosis after coronary stenting. In addition, new markers of inflammation and endothelium activation, such as increased leptin levels, also have to considered. Many studies have shown that hyperinsulinemia and insulin resistance increase neointimal index measured six months after coronary stenting, and that insulin-sensitizers have beneficial effects by decreasing the rate of restenosis. The role of endothelial dysfunction in the process of restenosis is a fascinating problem. The pathobiology of restenosis in stented arteries is largely related to neointimal hyperplasia, which is dependent upon several factors, such as a reduction in nitric oxide activity that determines endothelial dysfunction and oxidative stress. Abnormal endothelium-dependent vasodilation (related to decreased nitric oxide production in the insulin-resistant state) might be explained by alterations in intracellular signaling and increased endothelin-1 production. Leptin is a hormone related to both fat metabolism and insulin resistance that has been recognized as an independent predictor of coronary restenosis. Chronic hyperleptinemia can reduce the synthesis of nitric oxide owing to the increased oxidative stress in endothelial cells. As a result, the goal in prevention of in-stent restenosis is to develop drugs that are able to act both as insulin- and endothelium-sensitizers.

Animals↗
PubMed1993

Coronary restenosis: prospects for solution and new perspectives from a porcine model.

Coronary restenosis, a major unresolved problem for percutaneous coronary revascularization procedures, has thus far been resistant to all therapeutic strategies. In part, ineffective treatment or prevention of coronary restenosis may be due to reliance on a conceptualization of the restenosis process that incompletely reflects the pathophysiologic factors associated with neointimal formation after arterial injury. In a porcine coronary restenosis model, three stages of neointimal growth after arterial injury have been identified: an early thrombotic stage, with platelets, fibrin, and erythrocytes; a cellular recruitment stage, with endothelialization and an infiltration by lymphocytes and monocytes; and a proliferative stage, in which smooth muscle cells migrate into and proliferate within the fibrin-rich degenerating thrombus. Evaluation of basic mechanisms responsible for neointimal formation has been possible with this model. In particular, a direct relationship exists between the depth of arterial injury and subsequent neointimal thickness. This relationship can be used for investigating the efficacy of new therapies. Treatment strategies for restenosis should be directed toward interference with the cellular or humoral events that lead to neointimal formation, with the specific goal of decreasing the neointimal volume. These strategies may include delivery of drugs to the site of arterial injury to limit the amount of early mural thrombus or decreasing subsequent cellular recruitment and proliferation as well as synthesis of extracellular matrix.

Animals↗
PubMed1994

Percutaneous transluminal in vivo gene transfer by recombinant adenovirus in normal porcine coronary arteries, atherosclerotic arteries, and two models of coronary restenosis.

BACKGROUND: Gene therapy has been proposed as a possible solution to the problem of restenosis after coronary angioplasty. The current study was undertaken to assess conventional methods of gene transfer and to develop percutaneous techniques for introducing genes directly into the coronary arteries of large mammals. Since the anticipated targets of gene therapy against restenosis include atherosclerotic and previously instrumented arteries, we also evaluated gene transfer in atherosclerotic coronary arteries and in two porcine models of restenosis: one using intracoronary stents and a second using balloon overstretch angioplasty. METHODS AND RESULTS: The conventional method of using perforated balloon catheters to deliver Lipofectin-DNA complexes directly into the coronary arteries of intact animals was applied to 18 porcine coronary arteries including normal arteries, hypercholesterolemic arteries, and those simulating restenosis. The results of this study were consistent with previously published results indicating that only low levels of luciferase gene expression could be obtained by Lipofectin-mediated gene transfer. We therefore undertook a second, parallel study to evaluate percutaneous transluminal in vivo gene transfer using a replication-deficient adenoviral vector. A comparison of the two studies revealed that the mean level of reporter gene expression in the cohort undergoing adenoviral infection was 100-fold higher than in the cohort undergoing Lipofection. Analysis of luciferase activity over time in normal arteries revealed that recombinant gene expression was half-maximal after 1 day, peaked within 1 week, was still half-maximal at 2 weeks, and declined to low levels by 4 weeks. Histochemical analysis of coronary arteries treated with a second adenovirus expressing a nuclear-localized beta-galactosidase gene demonstrated gene transfer to a limited number of cells in the media and adventitia. Immunohistochemical analysis of Ad5-infused arteries using a monoclonal antibody directed against CD44 identified a periadventitial infiltrate composed of leukocytes. CONCLUSIONS: The recombinant adenoviral vectors proved to be far more effective than Lipofectin at delivering foreign genes directly into the coronary arteries of living mammals. Furthermore, the influences of hypercholesterolemia and arterial injury appeared to have little effect on the levels of gene expression obtained using either method. The results demonstrate that low-level recombinant gene expression, the major obstacle impeding gene therapy for the prevention of restenosis, can potentially be overcome by using adenoviral vectors to mediate coronary gene transfer in vivo. The duration of gene expression provided by these vectors and their effective deployment in atherosclerotic, balloon-overstretched, and stented coronary arteries suggest that recombinant adenovirus may have potential for evaluating gene therapy in the clinically informative porcine models of coronary restenosis.

Adenoviridae↗
PubMed2005

Novel site-specific systemic delivery of Rapamycin with perfluorobutane gas microbubble carrier reduced neointimal formation in a porcine coronary restenosis model.

Earlier studies demonstrated that perfluorobutane gas microbubble carrier (PGMC) adheres to injured arteries and enhances the drug uptake specifically into the cells of the denuded vessel segment. The purpose of this study was to investigate the effect of PGMC-based systemic delivery of Rapamycin on expression of p27 in vascular tissue and restenosis in porcine coronary arteries after stent implantation. Eight pigs underwent coronary stent implantation (three stents per animal). Five pigs were treated with i.v. injection of PGMC with 2 mg of Rapamycin and three animals served as control. Four hours postprocedure, three pigs were sacrificed and stented segments were analyzed by high-performance liquid chromatography (HPLC) and Western blot. In chronic experiments, five pigs (15 stent sites) were sacrificed at 28 days following intervention and vessels were perfusion-fixed. HPLC of the treated arteries demonstrated high drug concentration in the vessel tissue, and Western blot analysis showed elevated expression of p27 at 4 hr postprocedure. Histomorphometry revealed significantly reduced (by 40%) neointimal formation in the PGMC/Rapamycin group compared with controls (1.84 +/- 0.84 vs. 4.77 +/- 1.71 mm2, respectively; P < 0.001). In the porcine coronary model, site-specific systemic delivery of Rapamycin utilizing PGMC resulted in overexpression of p27 and a significant reduction of neointimal formation within the stented segments.

Animals↗
PubMed1997

Management of Coronary Restenosis via the Radial Artery: An Elegant Approach to the AchillesÕ Heel of PTCA.

In spite of many efforts, the most effective treatment for restenosis after coronary angioplasty remains repeat angioplasty. Although the second procedure is known to be at lower risk, it is usually performed by the same technique, thus requiring hospitalization. In such a group of patients, the feasibility of using the radial route for repeat coronary angiography and angioplasty when needed and the safety of early discharge were evaluated prospectively. Coronary angiography via the radial artery was attempted in 51 patients referred within 6 months of initial coronary angioplasty with the clinical suspicion of restenosis. Successful cannulation of the radial artery was possible in 48 (94%). Following placement of a 4 Fr arterial sheath, coronary angiography was completed successfully in all but one patient. Restenosis was confirmed angiographically in 25 patients (one via the femoral route) and a new lesion was observed in 3. Repeat angioplasty was attempted via the radial route (25 patients) or via the femoral route (one patient) using a fixed-wire balloon catheter through the 4 Fr diagnostic catheter (n=22). Angioplasty via the radial route including elective stent implantation (5 patients) was a technical success in 92% of the patients. Immediate arterial sheath withdrawal and mechanical compression of the radial artery provided satisfactory hemostasis after 186 +/- 126 minutes. The radial pulse was absent post-procedure without clinical consequence in 3 patients (6%). Of the 46 patients without a femoral artery puncture, 39 (85%) were discharged the same day without any cardiac or local complications. Thus, early discharge after repeat coronary angiography and angioplasty for restenosis is feasible and safe using the transradial route in the majority of patients.

Journal Article↗
PubMed2001

Monocyte integrin expression and monocyte-platelet complex formation in humans with coronary restenosis.

1. In the present study, we sought to determine whether patients with restenosis after coronary stenting possess increased monocyte reactivity, as manifested by a higher level of adhesion molecule expression and an enhanced propensity to form monocyte-platelet aggregates after activation in vitro. 2. Anti-coagulated peripheral venous blood from 24 patients, 10 with and 14 without angiographically verified restenosis, was obtained. Leucocyte antigen expression and the number of leucocyte-platelet complexes were measured by flow cytometry after activation in whole blood. 3. Surface integrin Mac-1 (CD11b/CD18) and VLA-4 (CD49d/ CD29) expression on monocytes and the relative number of monocyte-platelet complexes after in vitro activation were significantly elevated in patients with restenosis compared with patients without restenosis (fluorescence intensities of 1425 +/- 76 vs 1195 +/- 71, 87 +/- 7 vs 65 +/- 6 and 47 +/- 4 vs 29 +/- 3% for for Mac-1, VLA-4 and monocyte-platelet complexes, respectively; P < 0.05 for each parameter). 4. The results suggest that restenosis is associated with increased monocyte VLA-4 and Mac-1 integrin expression and monocyte-platelet complex formation, which can be revealed after activation in vitro.

Blood Platelets↗
PubMed1992

A decrease in plasminogen activator inhibitor-1 activity after successful percutaneous transluminal coronary angioplasty is associated with a significantly reduced risk for coronary restenosis.

To determine a possible relation of changes in plasma levels of plasminogen activator inhibitor 1 (PAI-1) and tissue plasminogen activator (t-PA) to the development of coronary restenosis after successful coronary angioplasty (PTCA), we followed 104 patients with a low grade residual stenosis after PTCA (less than 30%) for a period of 12 months. PAI-1 plasma levels (functional activity) and t-PA antigen were determined 1 day before PTCA and 3 days, 3 months and 6 months thereafter. Thirty-four patients (32.69%) developed angiographically proven coronary restenosis (group A) within a time range of 4-48 weeks (median 12.5 weeks) after PTCA while the remaining patients (group B) had neither clinical signs nor angiographic evidence of restenosis after 6 months. No significant differences could be demonstrated in t-PA antigen or PAI-1 activity (plasma levels between the two groups of patients the day before PTCA). During the whole observation period t-PA plasma levels were not significantly different between the two groups; however, PAI-1 plasma levels were significantly higher at 3 months and 6 months after PTCA in patients of group A (p less than 0.005). When the pattern of PAI-1 plasma levels over time (increase or decrease between two consecutive time points of blood collection) was used to discriminate between the two study groups only 3.5-18% of patients with a decrease in PAI-1 developed coronary restenosis within the following observation period in contrast to 25-58% of patients with an increase in PAI-1 plasma levels (p less than 0.05 to p less than 0.0005).

Aged↗
PubMedDate not supplied

Prevention of coronary restenosis.

Percutaneous transluminal coronary angioplasty (PTCA) was introduced 22 years ago as a nonsurgical catheter-based treatment for obstructive coronary artery disease. Over the following 2 decades, major advances in equipment and techniques led to tremendous growth in the use of PTCA to treat coronary artery disease and angina. Restenosis persists as the limiting factor in the maintenance of vessel patency after PTCA, occurring in 30% to 50% of patients and accounting for significant morbidity and health care expenditures. Plaque persistence and vessel recoil, thrombus formation, constrictive remodeling, and neointimal proliferation are the primary contributors to the development of restenosis after PTCA. Early clinical trials in restenosis prevention using various revascularization devices, antiplatelet drugs, antithrombotic drugs, and antiinflammatory drugs were uniformly negative. Coronary stents are the only devices that have shown a reduction in the incidence of restenosis. Recently, novel therapies, such as intracoronary radiation, antioxidant drugs, and platelet-derived growth factor antagonists, have shown reductions in the incidence of restenosis in small randomized trials. This review focuses on the etiology and pathophysiology of restenosis and discusses current and future therapies that may reduce the incidence of restenosis.

Angioplasty, Balloon, Coronary↗