INTRODUCTION — Coronary reperfusion with primary percutaneous coronary intervention (PCI) improves outcomes in patients with acute ST elevation myocardial infarction (MI), an MI with a new or presumably new left bundle branch block, or a true posterior MI if performed in a timely fashion. Most procedures are now performed with drug-eluting stents, which are associated with a lower rate of restenosis than bare metal stents. A concern about a somewhat higher rate of very late stent thrombosis relative to bare metal stents exists, but ongoing trials should effectively address this issue. (See "Percutaneous coronary intervention with intracoronary stents: Overview".)

This topic will address some of the technical aspects of PCI, as well as adjunctive medications when used in the periprocedural period. Issues related to the performance of primary PCI will be reviewed here. The determinants of outcome, the clinical trials demonstrating the benefit of primary PCI compared with fibrinolytic therapy, selection of a reperfusion strategy, the possible role of PCI after fibrinolysis, and the role of PCI in non-ST elevation acute coronary syndromes are discussed separately. (See "Primary percutaneous coronary intervention in acute ST elevation myocardial infarction: Determinants of outcome" and "Acute ST-elevation myocardial infarction: Selecting a reperfusion strategy" and "Percutaneous coronary intervention after fibrinolysis for acute ST-elevation myocardial infarction" and "Non-ST-elevation acute coronary syndromes: Revascularization".)

PERCUTANEOUS CORONARY INTERVENTION AFTER FIBRINOLYTIC THERAPY — Percutaneous coronary intervention after fibrinolytic therapy may be indicated in patients who remain unstable or in stable patients who have had incomplete reperfusion or as part of a pharmacoinvasive strategy. This issue is discussed elsewhere. (See "Percutaneous coronary intervention after fibrinolysis for acute ST-elevation myocardial infarction".)

TECHNICAL ISSUES

Radial versus femoral approach — Bleeding complications are common in patients with ST elevation myocardial infarction (STEMI) and they predict a worse prognosis [1]. Many of these major bleeds occur in relation to the access site for percutaneous coronary intervention (PCI), particularly when the femoral artery is used. The risk of bleeding is lower with radial artery access. In patients undergoing primary PCI, we prefer the radial to the femoral approach if performed by skilled operators. This issue is discussed in greater detail separately. (See "Periprocedural complications of percutaneous coronary intervention", section on 'Access site bleeding' and "Periprocedural complications of percutaneous coronary intervention", section on 'Radial artery access'.)

Intravascular imaging — The role of adjunctive intravascular imaging techniques, such as intravascular ultrasound (IVUS) and optical coherence tomography (OCT), has not been established in patients with primary PCI. Several registries have found discordant results. In the ADAPT–DES study in which 813 STEMI patients were enrolled, IVUS use was associated with improved outcomes in STEMI patients [2]. In the CREDO-Kyoto AMI Registry, 3028 patients with STEMI underwent PCI with or without IVUS. Following risk adjustment, there was no difference in target vessel failure between the groups (adjusted hazard ratio =1.14; CI 0.86-1.51) [3]. However, the risk of stent thrombosis was lower with IVUS guidance. Likewise, a randomized, multicenter trial of angiographic compared with OCT-guided drug-eluting stent placement found that OCT-guidance did not reduce the incidence of major adverse cardiac events. OCT guidance led to post-PCI stent optimization in 29 percent of patients [4].

With their superior temporal and spatial resolution compared with angiography, IVUS and OCT may result in additional balloon inflations, and/or stent deployment to treat angiographically silent findings such as minor edge dissections, strut metal apposition, and plaque prolapse. Whether this will translate into improved clinical outcomes await larger, prospective randomized trials.

Direct stenting — We suggest performing direct stenting of the culprit lesion in most cases. Aspiration thrombectomy may be a useful strategy prior to direct stenting. (See "Suboptimal reperfusion after primary percutaneous coronary intervention in acute ST-elevation myocardial infarction".)

The availability of low-profile stent delivery systems has led to the consideration of direct stenting (ie, without predilation). Advantages of direct stenting include less radiation exposure and contrast use, as well as shorter procedural times. (See "Percutaneous coronary intervention with intracoronary stents: Overview".)

In patients with an acute STEMI undergoing primary PCI, direct stenting may also reduce embolization of plaque constituents, lowering the incidence of the no-reflow phenomenon, thereby increasing myocardial perfusion and salvage [5-7]. (See "Suboptimal reperfusion after primary percutaneous coronary intervention in acute ST-elevation myocardial infarction", section on 'No reflow'.)

The efficacy of this approach was best evaluated in a randomized trial of 206 patients with an acute STEMI who underwent primary stenting with or without predilation [5]. Although the incidence of TIMI flow grade 3 and the corrected TIMI frame count were the same with both approaches, the incidence of the composite angiographic end point (slow and no reflow or distal embolization) was significantly lower with direct stenting (12 versus 27 percent with predilation before stenting) and ST segment resolution was more frequent (80 versus 62 percent).

Additional but weak evidence of benefit comes from a (nonrandomized) cohort study of 2528 patients with STEMI enrolled in the HORIZONS-AMI trial who underwent either direct stenting (28 percent) or predilation at the operator’s discretion [8] (see "Anticoagulant therapy in acute ST-elevation myocardial infarction", section on 'Unfractionated heparin compared with bivalirudin'). At one-year follow-up, direct stenting was associated with a significantly lower rate of all-cause death (1.6 versus 3.8 percent).

Direct stenting also may improve myocardial perfusion and the incidence of death, MI, or heart failure compared to conventional stenting in patients who undergo PCI after fibrinolysis. This was illustrated in an observational study in which the choice of procedure was at the discretion of the treating physician [6]. Among patients with occluded infarct-related arteries, the likelihood of achieving TIMI myocardial perfusion grade 3 was significantly greater with direct stenting (54 versus 25 percent with conventional stenting). (See "Diagnosis and management of failed fibrinolysis or threatened reocclusion in acute ST-elevation myocardial infarction", section on 'Rescue PCI' and "Diagnosis and management of failed fibrinolysis or threatened reocclusion in acute ST-elevation myocardial infarction", section on 'Primary failure'.)

Contraindications to direct stenting include heavy calcification of the vessel or poor visualization due to TIMI 0 flow (table 1).

Selection of stent type — Drug-eluting stents (DES) are used in preference to bare-metal stents (BMS) in many PCI procedures because they reduce the incidence of restenosis and target vessel revascularization without causing a significant increase in the cumulative rate of adverse outcomes in many patient groups. (See "Clinical use of intracoronary bare metal stents", section on 'BMS compared with DES'.)

However, rates of stent thrombosis are higher for first generation stents than BMS and there has been a concern that the magnitude of the difference could be greater in patients with STEMI, where the baseline risk of stent thrombosis is higher than in patients with stable disease. (See "Coronary artery stent thrombosis: Incidence and risk factors", section on 'Impact of ACS'.)

Based on the evidence presented below, we prefer second generation DES to first generation DES or BMS for patients undergoing primary PCI who are able to comply with a recommendation for one year of dual antiplatelet therapy.

First-generation drug-eluting stents versus bare metal stents — Similar outcomes between first generation DES and BMS have been shown in patients with acute STEMI undergoing primary PCI. However, since patients with an acute MI (within 48 to 72 hours) were excluded from the pivotal trials, primary PCI has been considered an "off-label" use of DES in the United States. However, first generation stents are rarely being used in practice. (See "Clinical use of intracoronary bare metal stents" and "Drug-eluting intracoronary stents: Stent types".)

Many randomized trials, including TYPHOON, PASSION, SESAMI, DEDICATION, and HORIZONS AMI, have evaluated outcomes at one year or less [9-14]. They suggest that the lower rate of restenosis of sirolimus- or paclitaxel-eluting stents relative to BMS, when used for primary PCI, is similar to that in other settings.

Longer-term outcomes comparing DES to BMS have been evaluated in multiple meta-analyses of the randomized trials. We believe that the best evidence comes from a 2012 meta-analysis that used individual patient data from nearly 6300 patients enrolled in 11 randomized trials of primary PCI that compared either paclitaxel- or sirolimus-eluting stents to BMS [15]. The following findings were noted after follow-up as long as six years (mean of 3.3 years):

●There was no significant difference in mortality, which was the primary end point of the study (8.5 versus 10.2 percent; HR 0.85, 95% CI 0.70-1.04).

●The rate of target vessel revascularization was lower with DES (12.7 versus 20.1 percent; HR 0.57, 95% CI 0.50-0.66).

●There was no significant difference in the cumulative rate of stent thrombosis (5.8 versus 4.3 percent; HR 1.13, 95% CI 0.86-1.47). However, the rate of very late stent thrombosis (events after two years) was higher for DES (HR 2.81, 95% CI 1.28-6.19).

●There was no significant difference in the cumulative rate of reinfarction (9.4 versus 5.9 percent; HR 1.12, 95% CI 0.88-1.41). However, after two years, the rate significantly increased for DES (HR 2.06, 95% CI 1.22-3.49).

This finding of a higher rate of very late stent thrombosis after DES was confirmed in a second meta-analysis [16].  

Limitations of this meta-analysis include possible lack of applicability to sicker real world patients who were not included in the randomized trials.

Current-generation drug-eluting stents versus bare metal stents — In patients with STEMI who are able to comply with a recommendation for a minimum of one year of dual antiplatelet therapy, we prefer second generation DES to BMS. Among the commercially available second generation stents, we prefer everolimus-eluting stents in these patients.  

A 2013 comprehensive network meta-analysis of STEMI patients found the following [17]:

●Comparing CoCr-EES or phosphorylcholine polymer-based zotarolimus-eluting stents (PC-ZES) to BMS, the one-year risk of cardiac death or MI was reduced with the former but not the latter (OR 0.63, 95% CI 0.42-0.92 and 0.86, 95% CI 0.50-1.49).

●Comparing CoCr-EES to BMS and PC-ZES to BMS, the one-year risk of target vessel revascularization was reduced with the former but not the latter (OR 0.45, 95% CI 0.29-0.66 and 0.60, 95% CI 0.34-1.05).

●Comparing CoCr-EES to BMS and PC-ZES to BMS, the one-year risk of definite stent thrombosis was reduced with the former but not the latter (OR 0.32, 95% CI 0.11-0.78 and 0.44, 95% CI 0.12-1.79).

●There were trends toward lower one-year rates of cardiac death or MI, definite stent thrombosis, and target vessel revascularization with CoCr-EES compared to PC-ZES (OR 0.73, 95% CI 0.40-1.30, 0.72, 95% CI 0.17-3.16, and 0.74, 95% CI 0.38-1.42, respectively).

Five-year results from the EXAMINATION trial, which was included in the above meta-analysis, have been reported [18]. The combined patient-oriented outcome of all-cause death, an MI, or any revascularization occurred in 21 percent of patients who received and EES and 26 percent of those who received a BMS (hazard ratio 0.80, 95% CI 0.65-0.98). The difference was driven mainly by an unexplained lower rate of all-cause mortality.

The COMFORTABLE AMI trial randomly assigned 1161 patients to either biolimus-eluting or BMS [19]. The biolimus on this stent was embedded in a biodegradable polymer. The primary end point was the composite rate of cardiac death, target vessel-related reinfarction, and ischemia-driven target-lesion revascularization at one year. The following findings were noted:

●The primary end point occurred less frequently in patients receiving the biolimus-eluting stent (4.3 versus 8.7 percent; HR 0.49, 95% CI 0.30-0.80).

●The difference in the primary end point was driven primarily by a lower risk of target vessel-related reinfarction (0.5 versus 2.7 percent) and ischemia-driven target-lesion revascularization (1.6 versus 5.7 percent).

●There was a lower rate of definite stent thrombosis with the biolimus-eluting stent (0.9 versus 2.1 percent) but the difference was not statistically significant.

These lower rates of stent thrombosis and target vessel-related reinfarction in patients with STEMI are similar to the findings in patients with predominantly stable disease. The biolimus-eluting stent is not approved for use in the United States, but is approved for use in Europe.

Bioresorbable versus durable polymer drug-eluting stents — Bioresorbable (biodegradable) polymer DES have been evaluated in patients in the setting of primary PCI. In those locations where the Orsiro stent is available, we believe it is a reasonable alternative to current-generation stents. (See "Drug-eluting intracoronary stents: Stent types", section on 'Bioresorbable polymer drug-eluting stents' and "Drug-eluting intracoronary stents: Stent types", section on 'Ultra-thin-strut bioresorbable drug-eluting stents'.)

A biolimus-eluting stent with a biodegradable polymer was evaluated in the COMFORTABLE AMI trial, which is discussed above. (See 'Current-generation drug-eluting stents versus bare metal stents' above.)

The BIOSTEMI trial randomly assigned 1300 STEMI patients undergoing primary PCI to biodegradable polymer sirolimus-eluting ultra-thin strut (Orsiro) stents or durable polymer everolimus-eluting stents [20]. The primary composite endpoint of target lesion failure (eg, cardiac death, target vessel MI, and clinically indicated target lesion revascularization) within 12 months occurred in 4 and 6 percent of the two groups, respectively (difference -1.9 percentage points; rate ratio 0.59, 95% Bayesian credibility interval 0.37-0.94). The difference was principally attributable to a lower rate of ischemia-driven target lesion revascularization. The event rate in both groups was lower than expected.

We do not have a preference for the Orsiro stent, as it was compared with only one of many current-generation stents and as this was a moderate-sized trial with fewer endpoints than expected.

Drug-eluting balloons — Due to concerns of an increase in the rate of very late stent thrombosis with DES (see 'First-generation drug-eluting stents versus bare metal stents' above), the efficacy and safety of a drug-eluting balloon (DEB) used in conjunction with a BMS was evaluated in the DEB-AMI trial [21]. In this study, 150 STEMI patients were randomly assigned to BMS, DEB (paclitaxel) plus BMS, or DES (paclitaxel). The primary end point of six-month angiographic in-stent late-luminal loss was not significantly different between the DEB-BMS and BMS groups and neither group performed as well as the DES group. In addition, DEB induced more uncovered and malapposed stent struts than BMS, but less than DES. The results of this study have limited applicability as a first-generation stent was the comparator. (See "Coronary artery stent thrombosis: Incidence and risk factors", section on 'Incomplete stent apposition'.)

In this patient population, one small study found that DEB angioplasty, compared with a current-generation DES, led to a similar fractional flow reserve at nine months [22].

Non-culprit percutaneous coronary intervention — The management of non-culprit lesions found at the time of primary PCI is discussed elsewhere. (See "Primary percutaneous coronary intervention in acute ST-elevation myocardial infarction: Non-culprit lesions".)

Deferred stenting — Despite evidence of benefit in a few early studies, we do not recommend deferred stenting for STEMI patients undergoing primary PCI.

Coronary lesions causing acute STEMI often have substantial thrombus associated with them. This thrombus can embolize spontaneously or be pushed downstream with periprocedural intracoronary artery manipulation. Macro- or microembolization of this material to the distal circulation, which occurs in 5 to 10 percent of cases, is associated with worse clinical outcomes [23,24]. Interventions such as thrombectomy or the use of distal embolic protection devices have not been shown to improve patient important outcomes. (See "Suboptimal reperfusion after primary percutaneous coronary intervention in acute ST-elevation myocardial infarction", section on 'No reflow' and "Suboptimal reperfusion after primary percutaneous coronary intervention in acute ST-elevation myocardial infarction", section on 'Prevention'.)

A few observational studies and one small randomized trial raised the possibility that deferred (at a second procedure) placement of a stent might reduce the impact of thrombus-related impairment of distal flow [25-27]. The DANAMI 3-DEFER trial randomly assigned 1215 STEMI patients to either standard PCI with stenting or to deferred stent implantation 48 hours after the index procedure [28]. At a median follow-up of 42 months, there was no difference in the rate of the primary end point, a composite of all-cause mortality, hospital admission for heart failure, recurrent infarction, and any unplanned revascularization of the target vessel within two-year follow-up (18 versus 17 percent; hazard ratio 0.99, 95% CI 0.76-1.29).

Our recommendation to not perform deferred stenting in most cases is based an absence of clear benefit and the increased costs (eg, longer hospital stay and greater radiation and contrast exposure) associated with performing two procedures.

Intraaortic balloon counterpulsation — For patients who undergo primary PCI and receive aggressive antithrombotic therapy, we do not use an intraaortic balloon pump (IABP) for those without cardiac shock, acute mitral regurgitation, or acute ventricular septal rupture.

Studies performed before the routine use of stenting and aggressive antithrombotic therapy came to differing conclusions regarding the benefit from prophylactic IABP after primary PCI [29,30].

One observational study suggested benefit from the use of prophylactic IABP before primary PCI [31]. This issue was directly addressed in the CRISP AMI trial, which randomly assigned 337 patients who presented within six hours of acute anterior STEMI but without cardiogenic shock, to either IABP or no IABP prior to primary PCI [32]. There was no significant difference in the primary outcome of mean infarct size (expressed as a percentage of left ventricular mass and measured by cardiac magnetic resonance imaging at three to five days) between the IABP and no IABP groups (42.1 and 37.5 percent, respectively). At six months, there was no difference in the rate of all-cause death.

IABP use in cardiogenic shock is discussed elsewhere in detail. (See "Prognosis and treatment of cardiogenic shock complicating acute myocardial infarction", section on 'Intraaortic balloon pump'.)

Ischemic postconditioning — Ischemic postconditioning refers to the ability of a series of brief occlusions of either the coronary or a remote arterial circulation after a severe ischemic insult to protect against ischemic-reperfusion injury. An initial clinical trial of intermittent coronary artery occlusion in primary PCI suggested smaller infarct size and a higher myocardial blush grade. Before postconditioning can be recommended in patients who undergo primary PCI, additional studies are needed to confirm efficacy in a larger number of patients, to determine the optimal protocol, to assess treatment effect using a more accepted measure of infarct size after reperfusion (eg, SPECT imaging), and to determine long-term outcomes. (See "Myocardial ischemic conditioning: Clinical implications", section on 'Therapeutic applications'.)

Intracoronary hyperoxemic reperfusion therapy — Based upon success in the reduction of infarct size in animal models, an infusion of blood mixed with aqueous oxygen into the coronary arteries after primary PCI has been shown to be safe and feasible in humans [33].

However, benefit was not confirmed in the first outcome trial of this technology (AMIHOT) in which 269 patients with STEMI were randomly assigned after successful primary or rescue PCI to receive intracoronary hyperoxemic reperfusion or normoxemic blood autoreperfusion over 90 minutes [34]. There was no difference between the two groups in any of the primary efficacy end points (final infarct size at 14 days, ST-segment resolution, or change in regional wall motion score index at three months). At 30 days, the incidence of major adverse cardiac events was not different between the two groups.

Thrombectomy devices — The role of thrombectomy in patients with STEMI is discussed separately. (See "Suboptimal reperfusion after primary percutaneous coronary intervention in acute ST-elevation myocardial infarction", section on 'Thrombectomy'.)

ADJUNCTIVE THERAPY — Adjunctive therapy with primary percutaneous coronary intervention (PCI) primarily consists of antiplatelet and antithrombotic therapy to reduce thrombotic complications and beta blockers. Other nonpharmacologic adjunctive therapies will be discussed here as well.

The role of intracoronary agents during PCI to prevent no reflow is discussed separately. (See "Suboptimal reperfusion after primary percutaneous coronary intervention in acute ST-elevation myocardial infarction", section on 'Prevention'.)

Antithrombotic therapy — The role and duration of antiplatelet and anticoagulant therapy in patients undergoing primary PCI are discussed in detail separately. (See "Acute ST-elevation myocardial infarction: Antiplatelet therapy" and "Antithrombotic therapy for elective percutaneous coronary intervention: General use" and "Anticoagulant therapy in acute ST-elevation myocardial infarction", section on 'Primary PCI'.)

Summarized briefly, we recommend the following approach, which is in general agreement with the 2013 American College of Cardiology Foundation/American Heart Association ST elevation myocardial infarction (STEMI) guideline [35,36]:

●Aspirin – Nonenteric coated aspirin is given as soon as possible after the onset of symptoms in patients thought to have an acute MI. Therapy is begun with a loading dose of 162 to 325 mg of uncoated aspirin. The first tablet should be chewed or crushed to rapidly establish a high blood level.

●A platelet P2Y₁₂ receptor blocker is given to all patients undergoing primary PCI.

•Clopidogrel – We suggest a clopidogrel loading dose of 600 mg, to be given as soon as possible after presentation, followed by a maintenance dose of 75 mg/day. (See "Acute ST-elevation myocardial infarction: Antiplatelet therapy", section on 'Patients receiving primary PCI' and "Antithrombotic therapy for elective percutaneous coronary intervention: Clinical studies", section on 'Timing and dose'.)

•Prasugrel or ticagrelor – Prasugrel and ticagrelor are newer oral antiplatelet agents that inhibit platelet aggregation more quickly than clopidogrel. We suggest a loading dose of 60 mg of prasugrel or a loading dose of 180 mg of ticagrelor to be given as soon as possible after presentation or at the time of PCI. (See "Acute ST-elevation myocardial infarction: Antiplatelet therapy", section on 'Patients receiving primary PCI'.)

●Glycoprotein (GP) IIb/IIIa inhibitor – Among patients with an STEMI, published trials have showed significant reductions in mortality and reinfarction with GP IIb/IIIa inhibitor therapy prior to primary PCI. Early administration of thienopyridine derivatives may attenuate this benefit. The role of GP IIb/IIIa inhibitor therapy, either early after the diagnosis of STEMI is made or later in the catheterization laboratory during primary PCI, is discussed separately.

●Anticoagulant therapy – Patients undergoing primary PCI typically receive intravenous unfractionated heparin during the procedure to prevent acute vessel closure due to thrombosis. Heparin monitoring is usually performed via serial monitoring of the activated clotting time (ACT). Careful monitoring of the ACT is important because some patients have persistent thrombin activity despite heparin therapy.

•A target ACT of 250 to 350 seconds seems to be most often used in interventional practice. However, the heparin regimen should probably be less aggressive (target ACT 200 to 250 seconds) when GP IIb/IIIa inhibitors are used. Careful monitoring of the ACT is important because some patients have persistent thrombin activity despite heparin therapy. (See "Anticoagulant therapy in acute ST-elevation myocardial infarction", section on 'Anticoagulant compared with placebo' and "Antithrombotic therapy for elective percutaneous coronary intervention: Clinical studies", section on 'Heparin'.)

•Postprocedural heparin is not recommended in patients with an uncomplicated procedure, since it is associated with increased bleeding and vascular complications without added benefit [37]. Sheath removal should be accomplished when the ACT falls to less than 150 to 180 seconds to reduce the incidence of complications at the access site.

•The potential use of bivalirudin in patients with STEMI undergoing PCI is discussed separately. (See "Anticoagulant therapy in acute ST-elevation myocardial infarction", section on 'Primary PCI'.)

Beta blockers — Beta blockers significantly reduce morbidity and mortality in patients with an acute MI. They are also beneficial in patients undergoing primary PCI and should be started intravenously or orally as soon as practical after diagnosis based on hemodynamic and electrical stability [38]. Administration should not delay the process of getting the patient to the catheterization laboratory as quickly as possible. (See "Acute myocardial infarction: Role of beta blocker therapy".)

A randomized trial demonstrated a higher left ventricular ejection fraction at six months and lower rate of major adverse cardiac events (defined as death, reinfarction, heart failure readmission, and malignant arrhythmia) at two years for patients pretreated with intravenous beta blockers [39].

A possible benefit from preprocedural intravenous administration of a beta blocker was shown in a retrospective analysis from the CADILLAC trial of 2082 patients [40]. At 30 days, patients who had received a preprocedural beta blocker had a significantly lower mortality than those who had not (1.5 versus 2.8 percent); the reduction in mortality was limited to patients who had not been receiving an oral beta blocker before admission. Although preprocedural use is preferred, lower mortality has also been seen in retrospective analyses when beta blocker therapy is begun after primary PCI [41].

CORONARY ARTERY BYPASS GRAFT SURGERY — If coronary artery bypass surgery is necessary, mortality is increased in the first three to seven days after the infarction. This risk must be weighed against the estimated benefit from early surgery; surgery should be delayed in patients who are stable but should be performed during the initial hospitalization in those with critical anatomy [42]. (See "Coronary artery bypass graft surgery in patients with acute ST-elevation myocardial infarction".)

EARLY DISCHARGE IN LOW-RISK PATIENTS — Discharge at 72 hours is suggested for stable ST elevation myocardial infarction patients, based in part on the following two studies:

●In one study that used the Zwolle risk index, more than two-thirds of patients undergoing primary percutaneous coronary intervention (PCI) were classified as low risk (risk score ≤3) [43]. For these patients, the mortality rate was 0.1 percent at two days and 0.2 percent between 2 and 10 days post-myocardial infarction. It was suggested that such low-risk patients could safely be discharged early (48 hours after PCI). (See "Risk stratification after acute ST-elevation myocardial infarction", section on 'Zwolle primary PCI index'.)

●The potential safety of early discharge was evaluated in the PAMI-2 trial, which included 471 patients who were deemed to be at low risk after successful primary PCI (age ≤70, no malignant arrhythmias, native vessel being the infarct-related artery, one or two vessel disease, and left ventricular ejection fraction >45 percent) [44]. These patients were randomly assigned to traditional care or to accelerated care on a telemetry unit followed by hospital discharge on day three. Patients receiving accelerated care were discharged three days earlier (4.2 versus 7.1 days for traditional care) with a significant reduction in cost. At six months, there was no significant difference between the two groups in terms of mortality (0.8 versus 0.4 percent), unstable angina, reinfarction, stroke, heart failure, or their combined occurrence (15.2 versus 17.5 percent).

Despite scant randomized trials regarding early discharge, observational data have not identified a risk to early discharge. In a study linking the National Cardiovascular Data Registry CathPCI Registry to the United States Center for Medicare and Medicaid Services claims, 33,920 patients were examined [45]. There was no difference in 30-day mortality and major adverse cardiovascular events between short (≤3 days) and medium (4 to 5 days) length of stay (adjusted hazard ratio 1.00; 95% CI 0.74-1.34).

RECOMMENDATIONS OF OTHERS — Our recommendations are generally in agreement with those made in the 2014 guideline on myocardial revascularization from the European Society of Cardiology/European Association for Cardio-Thoracic Surgery [46].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: ST-elevation myocardial infarction (STEMI)".)

SUMMARY AND RECOMMENDATIONS

●Pretreatment with fibrinolysis is limited to patients in whom primary percutaneous coronary intervention (PCI) is likely to be excessively delayed because of local logistic problems or interhospital transfer. Fibrinolytic therapy given just before planned PCI (previously called “facilitated PCI”) is not recommended because outcomes may be worse. (See 'Percutaneous coronary intervention after fibrinolytic therapy' above and "Percutaneous coronary intervention after fibrinolysis for acute ST-elevation myocardial infarction".)

●For patients undergoing primary PCI, we prefer the radial, as opposed to the femoral, approach if performed by operators skilled in radial technique and if the anticipated impact on door-to-balloon time is negligible. 

●For most patients undergoing primary PCI, we suggest performing non-culprit vessel PCI of significant lesions rather than culprit vessel only PCI (Grade 1B). Patients for whom this recommendation may not be appropriate are discussed above. (See 'Non-culprit percutaneous coronary intervention' above.)

●Direct stenting after aspiration thrombectomy should be performed in most patients. (See 'Direct stenting' above and 'Thrombectomy devices' above.)

●For patients who are likely to comply with one year of dual antiplatelet therapy, we prefer cobalt-chromium everolimus-eluting stents to bare metal stents or zotarolimus-eluting stents. (See 'Selection of stent type' above.) We prefer second to first generation drug-eluting stents.

●All patients should receive aspirin (initial dose 162 to 325 mg followed by 75 to 162 mg once a day; the first tablet should be chewed or crushed). (See 'Antithrombotic therapy' above.)

●All patients should receive a P2Y₁₂ receptor blocker as soon as possible after presentation. We suggest ticagrelor or prasugrel in preference to clopidogrel.

●Intravenous therapy with either heparin or bivalirudin should be given as soon as possible after presentation. (See 'Antithrombotic therapy' above and "Anticoagulant therapy in acute ST-elevation myocardial infarction", section on 'Summary and recommendations'.)

●Beta blockers reduce mortality in patients with ST-elevation myocardial infarction undergoing primary PCI, and should be administered either intravenously or orally as soon as practical after diagnosis based on hemodynamic and electrical stability. (See 'Beta blockers' above.)

●Discharge at 72 hours is suggested for stable ST-elevation myocardial infarction patients. (See 'Early discharge in low-risk patients' above.)