Angioplasty Strategies in ST-Segment–Elevation Myocardial Infarction
2008; Lippincott Williams & Wilkins; Volume: 118; Issue: 5 Linguagem: Inglês
10.1161/circulationaha.107.756494
ISSN1524-4539
Autores Tópico(s)Cardiac Imaging and Diagnostics
ResumoHomeCirculationVol. 118, No. 5Angioplasty Strategies in ST-Segment–Elevation Myocardial Infarction Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBAngioplasty Strategies in ST-Segment–Elevation Myocardial InfarctionPart I: Primary Percutaneous Coronary Intervention Gregg W. Stone, MD Gregg W. StoneGregg W. Stone From Columbia University Medical Center and the Cardiovascular Research Foundation, New York, NY. Originally published29 Jul 2008https://doi.org/10.1161/CIRCULATIONAHA.107.756494Circulation. 2008;118:538–551is corrected byCorrectionCardiovascular disease is the most common cause of mortality in most developed nations; ≈838 000 in-hospital discharges in the United States in 2005 were for acute myocardial infarction, 29% to 47% of which were acute ST-segment-elevation myocardial infarction (STEMI).1 The case fatality rate of STEMI has fallen dramatically in the last 3 decades, in part because of the widespread use of reperfusion therapy.1–4 STEMI is in most cases due to rupture of an inflamed thin-capped fibroatheroma containing a lipid-rich necrotic core with superimposed secondary thrombosis resulting in coronary artery occlusion.5,6 From the seminal demonstration by Reimer et al7 that canine coronary occlusion results in a several-hour wave front of necrosis spreading from the subendocardial to the subepicardial myocardium arose the hypothesis that timely restoration of flow in the occluded coronary artery would salvage jeopardized myocardium and enhance survival. Effective reperfusion in STEMI can be achieved by either fibrinolytic therapy or primary percutaneous coronary intervention (PCI) without antecedent fibrinolysis (also generally known as primary angioplasty). Fibrinolysis and PCI also may be combined in a variety of ways, depending on the timing of PCI after fibrinolytic administration, the clinical condition of the patient, and whether PCI is applied routinely or selectively after lytic therapy. Randomized trials have collectively demonstrated enhanced survival and freedom from major adverse cardiovascular events with primary PCI compared with fibrinolysis, and as a result, the expeditious performance of primary PCI has become the preferred reperfusion modality for patients with STEMI presenting at appropriately equipped centers.The introduction of new devices such as bare metal stents (BMS) and drug-eluting stents (DES) and novel potent antiplatelet and antithrombotic agents have transformed the interventional approach to the patient with STEMI. Important studies have been completed that have addressed previously unsettled issues such as the importance of time to intervention and the utility of late reperfusion. It is thus appropriate and timely to review the data underlying the contemporary interventional approach to STEMI. The first part of this 2-part series will review the essentials of primary PCI in STEMI, including comparison with fibrinolytic therapy, the impact of PCI-related delays, the evidence for and against delayed infarct artery intervention, the role of BMS and DES, appropriate use of adjunctive antiplatelet and antithrombotic agents, and strategies to expand access to primary PCI, including angioplasty without surgical backup and interhospital transfer. Part 2 reviews interventional strategies after fibrinolytic therapy, discusses volume-quality relationships for PCI outcomes, offers summary recommendations for the patient presenting with STEMI at hospitals with and without interventional facilities, and reviews recent and ongoing investigations to further improve outcomes after catheter-based reperfusion therapy. The conclusions reached rely heavily on the results from randomized controlled trials, with the greatest weight placed on the largest and most contemporary studies. A distinction is drawn in which the evidence-based recommendations in this article differ substantially from the 2004 task force guidelines of the American College of Cardiology (ACC) and American Heart Association,8 which recently received a focused update in 2007.9 It should be noted, however, that surprisingly few definitive (adequately powered) randomized trials with meaningful (noncomposite) clinical end points such as mortality have been performed to address many of these critical issues, often leading to reliance on meta-analysis to guide treatment recommendations. Given the well-known methodological limitations of meta-analysis10,11 and recognition that the results of meta-analysis often conflict with more definitive conclusions reached from subsequently performed, appropriately sized randomized trials,12 caution should be applied in their interpretation, especially when heterogeneity is present or if the results are of borderline significance.Primary PCI in STEMIComparison With Fibrinolytic TherapyDetailed data are available from 23 prospective controlled trials in which 7739 patients presenting with acute MI (AMI) within 12 hours of symptom onset were randomized to primary PCI or fibrinolytic therapy, including 8 trials of primary PCI versus streptokinase (n=1837) and 15 trials of primary PCI versus fibrin-specific agents (n=5902). Primary PCI compared with fibrinolysis resulted in a 25% reduction in death, a 64% reduction in reinfarction, a 95% reduction in intracranial hemorrhage, and a 53% reduction in stroke (Figure 1).13 The odds ratios (ORs) for mortality with primary PCI compared with streptokinase and fibrin-specific agents were 0.53 (95% CI, 0.37 to 0.75; P=0.0005) and 0.80 (95% CI, 0.66 to 0.96; P=0.02). Overall, treatment with primary PCI rather than fibrinolysis saved ≈2 lives per 100 patients so treated (even when patients in shock were excluded), similar to the ≈2 lives saved per 100 patients treated with fibrinolytic therapy rather than placebo, although major bleeding was increased (7% versus 5%; P=0.032).14 The absolute mortality advantage of primary PCI is greatest in high-risk patients such as those with cardiogenic shock in whom emergency revascularization may save as many as 13 lives per 100 patients treated at 6 months compared with more conservative management.15 The relative survival benefit of primary PCI may extend to low-risk patients as well, although the absolute reduction in mortality would be proportionately less.16 Primary PCI also has been shown to salvage more myocardium at risk than fibrin-specific fibrinolytic agents, thus resulting in smaller infarcts.17,18 Primary PCI compared with fibrinolysis also reduces recurrent ischemia, resulting in fewer unplanned revascularization procedures and earlier hospital discharge with similar or lower cost.19Download figureDownload PowerPointFigure 1. Pooled analysis of the short-term results from 23 randomized trials comparing primary PCI and fibrinolytic therapy in 7739 total patients. Data from Reference 13. Data vary slightly from Reference 13 because of presentation of relative risks (RRs) rather than ORs.A major mechanism underlying the reduction in mortality and infarct size with primary PCI compared with fibrinolytic reperfusion is the greater rate of successful recanalization of the epicardial infarct-related artery (IRA) with the catheter-based approach. Normal antegrade (Thrombolysis in Myocardial Infarction [TIMI] grade 3) flow in the IRA is restored in ≈90% to 95% of patients after primary PCI compared with ≈30% to 40% after streptokinase and ≈50% to 60% after fibrin-specific agents and strongly correlates with early and late survival (Figure 2).19–21 In addition, reinfarction is the second-most-common cause of death after reperfusion therapy in STEMI and may result in infarct extension, life-threatening arrhythmias, and mechanical complications such as rupture of a papillary muscle, the left ventricular septum, or the free wall.22,23 By treating the underlying fissured plaque, primary PCI also reduces recurrent ischemia and reinfarction compared with both fibrin-specific and -nonspecific agents.13 Moreover, reperfusion injury and hemorrhagic transformation of a bland infarction, which occurs after fibrinolytic therapy but rarely after primary PCI,24,25 also may result in increased myonecrosis and the mechanical complications of transmural infarction.26 Finally, despite exclusion of patients at high risk for major bleeding and neurological events in the randomized comparative trials, hemorrhagic stroke occurred in 1.1% of patients after fibrinolysis compared with 0.05% after primary PCI.13 Because most patients die or are severely disabled after hemorrhagic stroke in STEMI,27,28 avoiding this iatrogenic complication of fibrinolysis contributes to the improved outcomes with primary PCI. Download figureDownload PowerPointFigure 2. Impact of postprocedure TIMI flow on 6-month survival after primary angioplasty in 2507 patients from the Primary Angioplasty in Myocardial Infarction-1, -2, and stent pilot and randomized trials (unpublished data). Postprocedure TIMI grade 3 flow (present in 92.5% of patients) was strongly correlated with long-term survival. Postprocedure TIMI grade 2 flow (present in 6.0% of patients) was associated with a 3-fold increase in mortality, whereas mortality was increased 8-fold in the 1.5% of patients with postprocedure TIMI grade 0/1 flow.Time Issues in Catheter-Based Reperfusion TherapyThe favorable outcomes achieved with primary PCI in the comparative randomized trials represent the collective results from hundreds of academic and community-based urban and rural hospitals despite variable delays to PCI. Nonetheless, most studies have found that excessive delays to angioplasty impair survival and myocardial recovery after primary PCI. From a pooled analysis of 1199 patients from 4 contemporary primary PCI trials, infarcts measured by technetium-99m sestamibi single-photon-emission computed tomography imaging were smallest when total symptom-to-balloon time was 3 hours (median infarct size, 4%, 8%, and 11%, respectively).29 Of note, catheter-based reperfusion within 2 and 3 hours in this series was attained in only 7% and 30% of patients, respectively. Prolonged door-to-balloon30–33 or symptom-to-balloon34–37 times have been correlated with increased mortality after primary PCI. Registry studies linking PCI delays to adverse outcomes may be confounded by associated patient comorbidities and complications before catheterization that can prolong reperfusion times and other concomitant suboptimal treatment processes, although survivor bias also may play a role in patients recanalized late after symptom onset. Nonetheless, reducing delays from symptom onset to presentation and treatment should improve the prognosis of patients undergoing primary PCI, justifying the current emphasis and resource expenditure toward this goal.The threshold at which delays to PCI become excessive so that mortality may favor fibrinolysis is unknown. The current ACC/AHA guidelines strongly recommend that all hospital systems achieve a median door-to-balloon time for primary PCI of 90 minutes).38 A limitation of this analysis, however, was that only 1 data point was available to examine PCI-related time delays of >60 minutes, and that study reported lower mortality with primary PCI. In contrast, using institution-based randomized trial data from these same trials from several hundred hospitals, Boersma et al39 determined that the mortality benefit of PCI may persist even with incremental PCI-related delays of up to 2 hours. In that study, the 30-day mortality among all 6763 randomized patients was 7.9% with fibrinolytic therapy and 5.3% with primary PCI (OR, 0.63). Among the 1349 randomized patients with the greatest incremental PCI delay (>79 to 120 minutes), 30-day mortality was 9.6% with fibrinolytic therapy and 6.6% with primary PCI (OR, 0.62). These findings persisted when only accelerated tissue plasminogen activator trials were considered. Considering time delays from symptom onset to hospital presentation, primary PCI was associated with reduced mortality for all presentation intervals, although the absolute survival benefit of primary PCI compared with fibrinolytic therapy widened in patients with increasing presentation delays, consistent with the fact that older thrombi are more resistant to fibrinolytic reperfusion, whereas primary PCI recanalization rates are independent of time to reperfusion. The reductions in reinfarction and stroke with catheter-based therapy compared with fibrinolytic reperfusion were time independent. These conclusions, however, cannot be considered definitive because subgroup analysis is inherently underpowered and prone to selection bias. Schomig et al40 also found that myocardial salvage was greater with primary PCI than fibrinolysis at all time intervals, although more so with greater presentation delays.The acceptable degree of PCI-related delay appears to depend on the time to presentation and the risk profile of the patient. Subset analysis from the Comparison of Angioplasty and Prehospital Thrombolysis in Acute Myocardial Infarction (CAPTIM) trial of prehospital thrombolysis versus primary PCI suggested that delays to PCI in patients randomized within the first 2 hours of infarct onset might favor the pharmacological approach.41 Similarly, in the 2082-patient randomized Controlled Abciximab and Device Investigation to Lower Late Angioplasty Complications (CADILLAC) trial, door-to-balloon times were independently correlated with mortality in patients presenting within 2 hours after symptom onset but not later.36 Brodie et al33 also reported from a large single-center database of 2322 STEMI patients undergoing primary PCI that prolonged door-to-balloon times (>2 versus <2 hours) were associated with higher mortality at 83 months in patients presenting early (<3 hours) (24.7% versus 15.0%; P 3 hours) (21.1% versus 18.5%; P=0.80) after symptom onset. In both studies, delays to treatment affected mortality only in high-risk patients (the elderly, patients with anterior infarcts, and patients with heart failure or renal insufficiency).33,36 Pinto et al42 examined outcomes from 192 509 STEMI patients at 645 hospitals participating in the National Registry of Myocardial Infarction (NRMI) treated with either primary PCI or fibrinolysis. Similar to other studies, the less the incremental PCI-related delay was, the greater the survival advantage of catheter-based reperfusion compared with fibrinolysis was; after multivariate adjustment for baseline differences, mortality remained lower with primary PCI until a PCI-related delay of 114 minutes (which notably applied to only ≈5% of patients). This threshold varied, however, from 179 minutes in patients >65 years of age with nonanterior infarction presenting >2 hours after symptom onset to 40 minutes in patients <65 years of age with anterior infarction presenting within 2 hours of symptom onset.Finally, the Register of Information and Knowledge About Swedish Heart Intensive Care Admissions (RIKS-HIA) investigators reported outcomes from 26 205 consecutive patients with STEMI treated with reperfusion therapy between 1999 and 2005 at 75 hospitals in Sweden.43 The median symptom-to-needle and symptom-to-balloon times were 120 minutes for patients receiving prehospital fibrinolysis (n=3078), 167 minutes for those receiving in-hospital fibrinolysis (n=16 043), and 210 minutes for patients receiving primary PCI (n=7084). Despite these incremental delays to angioplasty, primary PCI was associated with significantly lower early and late mortality than either prehospital or in-hospital fibrinolysis after multivariable adjustment for 24 baseline covariates and treatment propensity (Figure 3). Primary PCI also resulted in significantly lower rates of both early and late reinfarction and reduced hospital length of stay compared with fibrinolytic therapy. The study investigators concluded that the mortality benefits of primary PCI are ≈20% in the early hours after STEMI symptom onset and increase to 30% to 35% in the later hours and that not until a delay to PCI of 6 to 7 hours does the mortality of primary PCI become comparable with fibrinolysis administered within the first hours.43 The conclusions from any observational study must be considered exploratory, given the possibility of unmeasured confounders. Nonetheless, the results from this carefully conducted nationwide registry, in concert with the Boersma et al39 and Pinto et al42 analyses, suggest that mortality could be reduced and event-free survival enhanced by withholding fibrinolytic therapy for the preferential performance of primary PCI in most patients. Download figureDownload PowerPointFigure 3. Mortality at different time periods in Sweden between 1999 and 2005 in 26 206 patients with STEMI treated with in-hospital thrombolysis, prehospital thrombolysis, or primary PCI without fibrinolytic therapy. In each case, the adjusted hazard ratio (adj HR; after correction for differences in baseline characteristics and the propensity to receive primary PCI) for patients receiving in-hospital fibrinolysis was set to 1.0. The top box reflects the adjusted HR and 95% CI for the comparison of in-hospital fibrinolysis vs prehospital fibrinolysis; the bottom box reflects the comparison of in-hospital fibrinolysis with primary PCI. Excl SK indicates excluding patients who received streptokinase. Data from Reference 43.Late Infarct Artery InterventionThe studies described above refer to PCI performed within 12 hours of symptom onset. Few studies have examined whether PCI performed later after symptom onset is beneficial. Indeed, reperfusion therapy would be expected to reduce mortality by salvaging myocardium in most cases only if achieved within the first few hours after symptom onset, which is feasible in a minority of patients.44 It has been hypothesized that late IRA recanalization of totally occluded coronary arteries might improve survival by preventing infarct expansion, enhancing electrical stability, or providing collateral supply for other ischemic territories, the "open-artery hypothesis."45 PCI of patent but high-grade residual stenoses also may theoretically reduce rates of recurrent ischemia and reinfarction and enhance myocardial recovery.In the Beyond 12 hours Reperfusion AlternatiVe Evaluation (BRAVE-2) trial, 365 patients with STEMI presenting 12 to 48 hours after symptom onset (mean, 22.5 hours) without ongoing chest pain with both occluded and patent infarct vessels were randomized to either primary PCI or medical therapy.46 Infarct size assessed by technetium-99m sestamibi SPECT imaging between 5 and 10 days, the primary end point of the study, was significantly reduced with the invasive compared with the conservative approach (median, 8% versus 13%; P<0.001), and myocardial salvage was greater (median, 44% versus 23%; P<0.001). This trial, although modest in size and awaiting confirmation, suggests that some patients may have ongoing myocardial injury in the watershed zone or hibernating myocardium late after infarct onset and may benefit from routine PCI within 48 hours of symptom onset.After a series of small to moderate-sized randomized trials that were inconclusive,47–51 the issue of whether occluded infarct vessels should be recanalized days to weeks after STEMI was addressed in the large-scale Occluded Artery Trial (OAT).52 In this study, 2166 stable patients with an occluded IRA identified 3 to 28 days after STEMI were prospectively randomized to PCI or conservative therapy. Stents were implanted in 87% of patients in the invasive arm. At the 4-year follow-up, there were no differences between the 2 groups in either the rate of the primary composite end point of death, reinfarction, or class IV heart failure (17.2% versus 15.6%, respectively; P=0.20) or mortality (9.1% versus 9.4%; P=0.83). Angina occurred less frequently in the invasive group for the first 2 years after revascularization, resulting in a 19% relative reduction in the need for subsequent revascularization procedures (18.4% versus 22.3%; P=0.03), despite the fact that few patients received DES. At the 1-year follow-up angiography (performed in a substudy of 332 patients), left ventricular ejection fraction (LVEF) had increased to the same extent in both groups (mean improvement, 4.2% versus 3.5%, respectively; P=0.47), despite the fact that 83% of PCI versus only 25% of medical therapy patients had a patent IRA.53 Of note, only 20% of the patients enrolled in OAT had received prior fibrinolytic therapy, 67% had Q waves consistent with completed transmural infarction, and 90% of the patients who had a stress test before randomization had absent or mild ischemia. The infarct artery was the left anterior descending artery in only 36% of patients, and severe left ventricular dysfunction was uncommon (mean LVEF, 48%). Thus, routine PCI of totally occluded coronary arteries 3 to 28 days after STEMI cannot be recommended in patients without significant ischemia, although further study is required to determine whether the open-artery hypothesis might still apply to patients with larger infarcts, more extensive coronary artery disease, and moderate or severe ischemia.The importance of ischemia before deferred revascularization was demonstrated in the Swiss Interventional Study on Silent Ischemia Type II (SWISSI-II), in which 201 patients at 3 hospitals with recent STEMI or non-STEMI in whom silent ischemia was confirmed by stress imaging were prospectively randomized to balloon angioplasty (without stents) with intended complete revascularization or optimal medical therapy and were followed up for mean of 10.2 years.54 After multivariable adjustment, those treated with the invasive strategy had a 67% reduction in the primary composite end point of cardiac death, nonfatal MI, or symptom-driven revascularization; an 81% reduction in cardiac mortality; a 69% reduction in nonfatal reinfarction; a 52% reduction in symptom-driven revascularization; and improved functional capacity and LVEF at 4 and 10 years (mean LVEF, 54.4% versus 50.6% [P=0.05] and 55.6% versus 48.8%, respectively [P<0.001]). Limitations of this study include the facts that most patients had well-preserved LVEF and that contemporary PCI modalities and optimal medical therapies were not used. Moreover, as in BRAVE-2, patients enrolled in SWISSI-II had a mixture of both occluded and patent infarct vessels; thus, the results are not directly comparable to OAT. However, as discussed in part 2 of this review, similar benefits of PCI have been demonstrated in patients with ischemia after fibrinolytic therapy.55 These studies thus support an approach of routine stress testing after STEMI to identify ischemia with subsequent revascularization when appropriate.Role of BMS and DESAlthough high rates of TIMI grade 3 flow are achieved, dissection and residual luminal narrowing after balloon angioplasty may result in early or late reocclusion or restenosis of the IRA, occurrences that may be prevented by the mechanical scaffolding properties of coronary stents.56–59 Thirteen prospective, randomized trials have been performed in which 6922 patients with AMI within 24 hours of onset were randomized to balloon angioplasty or BMS.60 Stenting compared with balloon angioplasty resulted in similar rates of early and late mortality and reinfarction, although target vessel revascularization (TVR) was markedly reduced by BMS at both 30 days and 12 months (Figure 4). In the largest such trial, CADILLAC (n=2082), BMS and balloon angioplasty resulted in similar rates of postprocedural TIMI grade 3 flow and myocardial recovery at 7 months, underlying the finding of similar survival, although stents resulted in lower rates of restenosis (22.2% versus 40.8%; P<0.0001) and IRA reocclusion (5.7% versus 11.3%; P=0.01), explaining the dramatically reduced 1-year TVR rates.61 A 206-patient single-center randomized trial suggested that direct stent implantation, when feasible, may decrease embolization and enhance ST-segment resolution compared with balloon predilatation followed by stent implantation.62 A larger trial is warranted to confirm these findings and to determine whether direct stent implantation can further improve event-free survival. Download figureDownload PowerPointFigure 4. Pooled analysis of the 30-day and 6- to 12-month results from 13 randomized trials comparing BMS with balloon angioplasty alone in 6922 total patients with STEMI. Data from Reference 60. Data vary slightly from Reference 60 because of presentation of relative risks (RRs) rather than ORs.Stents eluting the immunosuppressive and antiproliferative agents sirolimus and paclitaxel reduce restenosis and the need for repeat revascularization procedures compared with BMS in stable coronary artery disease63 and have subsequently been investigated in STEMI. To date, 9 prospective, randomized trials (6 with sirolimus-eluting stents [SES], 2 with paclitaxel-eluting stents [PES], and 1 with multiple DES types) have been reported in which 3728 patients with STEMI within 12 hours of onset were randomized to BMS or DES; the pooled results from 7 of these studies have been reported in a recent meta-analysis.64 With follow-up ranging from 8 months to 1 year, DES resulted in a marked reduction in target lesion revascularization (TLR), with similar rates of death, reinfarction, and stent thrombosis (Figure 5). From this analysis, only 13 patients would need to be treated with DES rather than BMS to avoid 1 repeat revascularization procedure. The greater freedom from revascularization with DES may be explained by the further reductions in angiographic restenosis than are achieved with BMS.65–68 Of note, although no heterogeneity in efficacy was noted between PES and SES in this meta-analysis,64 the reported reduction in TLR with PES compared with BMS in the Paclitaxel-Eluting Stent Versus Conventional Stent in ST-Segment Elevation Myocardial Infarction (PASSION) trial did not reach statistical significance (5.3% versus 7.8%, respectively; P=0.23), possibly because of the lack of routine angiographic follow-up resulting in lower-than-anticipated event rates.69 However, in a randomized trial of PES versus BMS during primary PCI in which routine follow-up angiography was performed, PES reduced the occurrence of binary restenosis from 24.0% to 1.4% (P<0.001).68Download figureDownload PowerPointFigure 5. Pooled analysis of 7 randomized trials comparing DES and BMS in 2357 total patients with STEMI. Follow-up rates are at 12 months in 6 trials and 8 months in 1 trial. Mortality data are from 5 trials (1857 patients). MACE indicates major adverse cardiovascular events consisting of death, reinfarction, or TVR (TLR in 1 trial). Data from Reference 64. RR indicates relative risk.The 2 largest DES versus BMS trials completed to date in patients with STEMI have recently been reported. In the Drug Elution and Distal Protection in ST-Elevation Myocardial Infarction (DEDICATION) trial, 626 patients with STEMI were randomized to a mixed group of DES (PES, SES, or zotarolimus-eluting stents) or BMS.70 At 8 months, patients treated with DES compared with BMS had lower rates of angiographic restenosis (6.7% versus 17.9%; P<0.001) and TLR (5.1% versus 13.1%; P<0.001), with nonsignificantly different rates of death (5.1% versus 2.6%; P=0.14), reinfarction (1.6% versus 2.6%; P=0.42), and stent thrombosis (2.2% versus 2.2%; P=1.0). In the Multicentre Evaluation of Single High-Dose Bolus Tirofiban vs Abciximab With Sirolimus-Eluting Stent or Bare Metal Stent in Acute Myocardial Infarction Study (MULTISTRATEGY) trial, 745 patients with STEMI were randomized to SES versus BMS.71 Angiographic follow-up was not performed in this study. At 8 months, patients treated with DES compared with BMS had lower rates of TVR (3.2% versus 10.2%; P<0.001), with nonsignificantly different rates of composite death or reinfarction (5.9% versus 7.5%; P=0.37) and stent thrombosis (2.7% versus 4.0%; P=0.31).Before DES can be recommended routinely in STEMI, further studies are required to allay concerns about their long-term safety and efficacy in this setting. In this regard, all of the small to moderate-sized randomized trials performed to date have been underpowered to address low-frequency safety events, which may be increased with DES implantation in STEMI. In a large registry in which 13 500 patients were treated with DES at 17 Spanish hospitals from 2002 to 2006, STEMI was the most powerful determinant of early and late stent thrombosis.72 Premature thienopyridine discontinuation is a well-documented risk factor for stent thrombosis,73 a situation that may be both more common and hazardous after STEMI. In the multicenter Prospective Registry Evaluating Myocardial Infarction: Events and Recovery (PREMIER), 13.6% of 500 patients receiving DES for STEMI were thienopyridine noncompliant at 30 days, a finding associated with markedly higher 1-year mortality (7
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