Angiographic Follow-up after Placement of a Self-Expanding Coronary-Artery Stent

Serruys, Patrick W.; Strauss, Bradley H.; Beatt, Kevin J.; Bertrand, Michel E.; Puel, Jacques; Rickards, Anthony F.; Meier, Bernhard; Goy, Jean‐Jácques; Vogt, Pierre; Kappenberger, Lukas; Sigwart, Ulrich

doi:10.1056/nejm199101033240103

Cited by 683 publications

(219 citation statements)

References 14 publications

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“…For clinically defined stent thrombosis events, the associated 6-month mortality was 20.8%. These findings are consistent with the disastrous consequences of stent thrombosis reported in early studies 1,6,19,21,23,24 and are somewhat surprising because stent thrombosis events in our study patients were much more likely to occur while patients were still hospitalized. This is consistent, however, with a report by Hasdai et al 25 that showed poor clinical outcomes despite prompt restoration of blood flow after stent thrombosis.…”

Section: Cutlip Et Al Stent Thrombosissupporting

confidence: 82%

“…[1][2][3][4] These studies also showed a reduction in the previously alarmingly high rates of stent thrombosis from 20% [5][6][7] to Ϸ3.5%, although this was achieved at the cost of aggressive anticoagulation with an associated high rate of bleeding complications. 1,2 More recently, studies using either routine high-pressure postdilation stenting or intravascular ultrasound guidance and antiplatelet therapy with aspirin and ticlopidine have reported reduced rates of stent thrombosis of 0.5% to 1.9% without an associated increased bleeding risk.…”

mentioning

confidence: 90%

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Stent Thrombosis in the Modern Era

Cutlip

Baim²,

Ho³

et al. 2001

Circulation

761

203

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Background-There are limited studies of stent thrombosis in the modern era of second-generation stents, high-pressure deployment, and current antithrombotic regimens. Methods and Results-Six recently completed coronary stent trials and associated nonrandomized registries that enrolled 6186 patients (6219 treated vessels) treated with Ն1 coronary stent followed by antiplatelet therapy with aspirin and ticlopidine were pooled for this analysis. Within 30 days, clinical stent thrombosis developed in 53 patients (0.9%). The variables most significantly associated with the probability of stent thrombosis were persistent dissection NHLBI grade B or higher after stenting (OR, 3.7; 95% CI, 1.9 to 7.7), total stent length (OR, 1.3; 95% CI, 1.2 to 1.5 per 10 mm), and final minimal lumen diameter within the stent (OR, 0.4; 95% CI, 0.2 to 0.7 per 1 mm). Stent thrombosis was documented by angiography in 45 patients (0.7%). Clinical consequences of angiographic stent thrombosis included 64.4% incidence of death or myocardial infarction at the time of stent thrombosis and 8.9% 6-month mortality. Conclusions-Stent thrombosis occurred in Ͻ1.0% of patients undergoing stenting of native coronary artery lesions and receiving routine antiplatelet therapy with aspirin plus ticlopidine. Procedure-related variables of persistent dissection, total stent length, and final lumen diameter were significantly associated with the probability of stent thrombosis. Continued efforts to eliminate this complication are warranted given the serious clinical consequences. (Circulation.

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Section: Cutlip Et Al Stent Thrombosissupporting

confidence: 82%

mentioning

confidence: 90%

Stent Thrombosis in the Modern Era

Cutlip

Baim²,

Ho³

et al. 2001

Circulation

761

203

View full text Add to dashboard Cite

show abstract

“…ST occurred in up to 25% of the cases within the first 14 days in early experience. 3 ST is a very serious clinical event typically resulting in ST-elevation myocardial infarction (MI) in 70-80% of cases 4 with mortality rates that may be as high as 20-40%. 5 Aggressive initial attempts to tackle ST with high dose heparin, dextran and urokinase infusions lead to considerable morbidity and mortality with major bleeding occurring in up to 9% of the cases.…”

Section: Bare Metal Stents (Bms) -The Rise and Fallmentioning

confidence: 99%

Drug eluting stents: To evolve or dissolve?

Bharadwaj¹,

Chadha²

2016

Medical Journal Armed Forces India

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“…The inability of the smooth muscle cells to regulate their own growth effectively results in neointimal hyperplasia, and vascular remodeling that may eventually hinder adequate blood flow due to luminal size reduction ultimately inducing major cardiac events (MACE) i.e. myocardial ischemia, infarction, thrombosis, or death (Serruys et al 1991;Serruys et al 1994;Sigwart et al 1987). The two major categories of restenosis for balloon angioplasty are angiographic restenosis, which is defined as a 50% reduction of luminal diameter at follow-up angiography, which is 25 to 50% of all cases, and clinical restenosis, which is defined as recurrent angina (chest discomfort), which occurs in 20 to 30% of patients (Hansrani, 2002).…”

Section: Pci and Coronary Restenosismentioning

confidence: 99%

“…Intracoronary stent implantation along with balloon angioplasty is highly effective in the treatment of acute vessel closure (Sigwart et al 1987;Roubin et al 1992;de Jaegere et al 1993a;Fischman et al 1994). However, bare metal stents are thrombogenic, and the benefit achieved at the expense of high-risk vascular complications (Schatz et al 1991;Serruys et al 1994;de Jaegere et al 1993b;Serruys et al 1991) must be considered. The use of stents has significantly improved the outcome of PCI.…”

Section: Hypothesismentioning

confidence: 99%

Homocysteine and Malondialdehyde as Predictors of Restenosis Following Percutaneous Coronary Intervention

et al. 2006

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Restenosis is one of the major adverse outcomes of Percutaneous CoronaryIntervention (PCI). Previous studies have shown conflicting reports for homocysteine as a predictor of restenosis following PCI. The conflicting reports may be due to oxidative factors (stimulation of polymorphonuclear leukocyte [PMNL]-induced reactive oxygen species generation, xanthine-xanthine oxidase, and arachidonic acid metabolism) other than homocysteine which could cause endothelial cell dysfunction leading to restenosis.Malondialdehyde (MDA), a lipid peroxidation product, is a marker for oxidative stress and is related to all oxidative factors. Therefore, it is possible that serum MDA may be a better predictor of restenosis than plasma homocysteine. The purpose of this study is to determine whether or not the pre-procedural serum MDA and plasma homocysteine levels are elevated in patients who develop restenosis post PCI.The study included fifty-one patients undergoing elective PCI who consented to participate in a protocol that was approved by the Ethics Committee of the University of Saskatchewan. Homocysteine and malondialdehyde were measured in the plasma and serum respectively. Blood samples were collected pre-procedural, 0 time, 8 hours, 24 hours, and 6 months post-procedure. Exercise tolerance tests were performed at two weeks, and six months post-procedure to determine if there was any evidence of restenosis.The results of the study showed that pre-procedural values of plasma homocysteine in the restenosis and non-restenosis groups were 10.37 ± 0.46 and 10.73 ± 0.49 respectively. These values were not significantly different (p=0.60) between the groups. The pre-procedural levels of plasma homocysteine were not significantly ii different (p=0.08) from the post-PCI values of those patients who did not develop restenosis at the 6-month time interval. However, the pre-procedural levels of plasma homocysteine were significantly different from the post-PCI values of those patients in the restenosis group at the 24hr (p=0.04) and 6-month (p=0.002) time intervals. In the restenosis group there was a significant increase (24%) after six months in the values of homocysteine from the pre-procedural levels. Thus, this indicates that restenosis is associated with higher post-PCI levels of homocysteine.The pre-procedural levels of serum MDA in the restenosis and non-restenosis groups were 0.124± 0.16 and 0.147± 0.02 respectively. There was no significant difference (p=0.60) between the two groups. There was also no significant difference The results suggest that pre-procedural levels of plasma homocysteine and serum MDA were not predictors of restenosis following PCI. However, the post-PCI sixmonth levels of both homocysteine and MDA are predictors of restenosis. Moreover, the post-PCI levels of MDA were better predictors of restenosis than the post-PCI levels of homocysteine because the increase in MDA levels were greater at six months than the rise in homocysteine levels at the same time interval.iii ACKNOWLEDGEMENTS

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Angiographic Follow-up after Placement of a Self-Expanding Coronary-Artery Stent

Abstract: Early occlusion remains an important limitation of this coronary-artery stent. Even when the early effects are beneficial, there are frequently late occlusions or restenosis. The place of this form of treatment for coronary artery disease remains to be determined.

Cited by 683 publications

References 14 publications

Stent Thrombosis in the Modern Era

Stent Thrombosis in the Modern Era

Drug eluting stents: To evolve or dissolve?

Homocysteine and Malondialdehyde as Predictors of Restenosis Following Percutaneous Coronary Intervention

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