INTRODUCTION — The first step in the management of the patient with an acute ST-elevation myocardial infarction (STEMI) is prompt recognition, since the beneficial effects of therapy with reperfusion are greatest when performed soon after presentation. For patients presenting to the emergency department with chest pain suspicious for an acute coronary syndrome, the diagnosis of STEMI can be confirmed by the electrocardiogram. Biomarkers may be normal early. (See "Diagnosis of acute myocardial infarction" and "Initial evaluation and management of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department".)

This topic will summarize emergent/early management issues for patients with acute STEMI and then direct the reader to a more detailed discussion in other topics. The management of the patient after a reperfusion strategy has been chosen and carried out is discussed separately. (See "Overview of the non-acute management of ST elevation myocardial infarction".)

The management of the patient with a non-ST elevation MI or with a complication of an acute MI (eg, cardiogenic shock, mitral regurgitation, ventricular septal defect) is discussed separately. (See "Overview of the acute management of non-ST elevation acute coronary syndromes" and "Prognosis and treatment of cardiogenic shock complicating acute myocardial infarction" and "Acute myocardial infarction: Mechanical complications".)

STEMI AFTER NONCARDIAC HOSPITAL ADMISSION — A minority of patients who sustain an acute ST-elevation myocardial infarction (STEMI) do so while hospitalized for another reason. The approach to such patients, which is discussed below in this topic, is generally similar to that for patients who present to emergency departments. However, patients with STEMI after hospital admission have different baseline characteristics and have worse outcomes than those who present to the emergency department.

Three observational studies highlight these differences [1-3]:

●Inpatients are older and more likely female. They have higher rates of hypertension, chronic kidney disease, and prior cerebrovascular events, as well as more complex STEMI presentations (including cardiac arrest and cardiogenic shock).

●The time from healthcare provider recognition of the onset of the ischemic event to first electrocardiogram is significantly longer in inpatients. The percent of patients who are within 90 minutes is less with STEMI after hospital admission (68 versus 91 percent) [2].

●Common reasons for the initial hospital admission in patients with STEMI after hospital admission include non-ST elevation acute coronary syndrome, surgery, respiratory failure, and percutaneous coronary intervention (complicated by stent thrombosis).

●Coronary angiography and percutaneous coronary intervention are performed in fewer individuals with inpatient STEMI.

●In-hospital patients have a significantly prolonged length of stay and are less likely to be discharged directly to home.

●Two of three studies found that survival to discharge is significantly lower for inpatient STEMI (approximately 65 compared to 95 percent), despite similar sized infarcts [1,3]. The third study found no difference [2].

●Patients with STEMI after hospital admission have a higher one-year mortality (16.9 versus 9.4 percent) compared to patients who presented to the emergency department [2].

GENERAL PRINCIPLES — Once the diagnosis of an acute STEMI is made, the early management of the patient involves the simultaneous achievement of several goals:

●Relief of ischemic pain

●Assessment of the hemodynamic state and correction of abnormalities that are present

●Initiation of reperfusion therapy with primary percutaneous coronary intervention (PCI) or fibrinolysis

●Antithrombotic therapy to prevent rethrombosis or acute stent thrombosis

●Beta blocker therapy to prevent recurrent ischemia and life-threatening ventricular arrhythmias

This is then followed by the in-hospital initiation of different drugs that may improve the long-term prognosis:

●Antiplatelet therapy to reduce the risk of recurrent coronary artery thrombosis or, with PCI, coronary artery stent thrombosis.

●Angiotensin converting enzyme inhibitor therapy to prevent remodeling of the left ventricle.

●Statin therapy.

●Anticoagulation in the presence of left ventricular thrombus or chronic atrial fibrillation to prevent embolization.

SELECTED PATIENT GROUPS

Transient ST-segment elevation — Studies have found that 5 to 25 percent of patients who present with symptoms and electrocardiographic (ECG) changes consistent with STEMI have resolution of symptoms and complete normalization of the ST-segment (elevation) prior to receiving reperfusion therapy [4,5] (see 'Reperfusion' below). These individuals are referred to as having transient STEMI, and there is some evidence that the size of the infarct is small in most [6]. The optimal timing of reperfusion, and even the decision to reperfuse, has not been well studied.

In the TRANSIENT trial, 142 patients with transient STEMI were randomly assigned to an immediate or delayed (within 24 hours for high risk or within 72 hours for lower risk) invasive strategy [6]. There was no difference in the primary outcome of infarct size as a percentage of the left ventricular myocardial mass measured by cardiac magnetic resonance imaging on day four. In addition, major adverse cardiac outcomes and left ventricular ejection fraction were similar between groups. Although these data are intriguing, the study size is small. Pending the results of larger studies, we treat these patients with early intervention, similar to the broad group of patients with STEMI.

Elderly patients — The majority of MIs in older patients with ECGs are nondiagnostic or have ST-segment depression, but STEMI is not uncommon [7]. It is estimated that 60 to 65 percent of STEMIs occur in patients ≥65 years of age and 28 to 33 percent occur in patients ≥75 years of age [7-9]. In addition, as many as 80 percent of all deaths related to MI occur in persons ≥65 years of age. (See "Overview of the acute management of non-ST elevation acute coronary syndromes", section on 'Elderly patients'.)

Although patients age 75 and older have been underrepresented in clinical trials of ACS, the following observations concerning acute MI in older compared to younger patients are generally accepted [7]:

●Older patients more frequently have an atypical presentation, including silent or unrecognized MI [7,10]. As an example, chest pain is present in 57 percent of patients ≥85 years of age compared to 90 percent for those under age 65. Left bundle branch block and Killip class ≥2 acute heart failure are much more common in patients ≥85 years of age (34 and 45 percent, respectively). Delays in diagnosis have been well documented and often lead to delays in therapy.

●Patients ≥75 years of age have a higher in-hospital mortality, which often occurs in those with electrical and mechanical complications [7].

●Outcomes in older patients, as in younger patients, appear to be better with primary PCI than fibrinolysis [7]. (See 'Percutaneous coronary intervention' below.)

●Older patients are more likely to have frequent and severe bleeding as a consequence of antithrombotic therapy [7]. As an example, the risk of stroke as a consequence of fibrinolysis is approximately 2.9 percent in patients ≥85 years of age [7]. Nevertheless, patients ≥85 years of age who have no contraindications to fibrinolysis, including a high risk for intracranial hemorrhage, can be treated with fibrinolysis. (See 'Fibrinolysis' below and "Acute ST-elevation myocardial infarction: The use of fibrinolytic therapy", section on 'Stroke'.)

Women — The approach to women and men should be the same, despite the fact that women have more atypical symptoms, are older, have greater delays to presentation, and have higher prevalence of hypertension. In addition, they are at higher risk of bleeding.

Most women who present with an ACS will have acute plaque rupture as the cause; however, coronary artery dissection may be the cause in young or peripartum individuals. (See "Clinical features and diagnosis of coronary heart disease in women", section on 'Role of coronary angiography'.)

Other entities such as myocarditis, aortic dissection, or stress-induced cardiomyopathy should be considered. (See 'MI with no obstructive coronary artery disease' below and "Clinical manifestations and diagnosis of stress (takotsubo) cardiomyopathy", section on 'Clinical manifestations' and "Clinical features and diagnosis of acute aortic dissection", section on 'Clinical features' and "Clinical manifestations and diagnosis of myocarditis in adults", section on 'Clinical manifestations'.)

Cocaine-associated MI — MI is a well-described complication among patients presenting with cocaine-induced ischemic symptoms. (See "Clinical manifestations, diagnosis, and management of the cardiovascular complications of cocaine abuse", section on 'Myocardial ischemia/infarction'.)

We agree with the 2008 American Heart Association scientific statement on the management of cocaine-associated chest pain and MI, which states that these patients should be managed in a manner similar to other ACS patients [11]. The following two points were also made:

●Benzodiazepines should be administered early

●Beta blockers should not be used in the setting of acute cocaine intoxication with chest pain due to the possibility of exacerbation of coronary artery vasoconstriction.

Possible stent thrombosis — The in-hospital mortality of STEMI is higher in patients with coronary artery stent thrombosis as the cause, as opposed to a ruptured plaque. Immediate PCI is the treatment of choice, similar to spontaneous MI. Fibrinolysis has also been used for patients with STEMI due to coronary artery stent thrombosis. (See "Coronary artery stent thrombosis: Incidence and risk factors" and "Long-term antiplatelet therapy after coronary artery stenting in stable patients".)

INITIAL ASSESSMENT — Clinical assessment of the patient with a possible acute coronary syndrome (ACS) begins as soon as the patient arrives in the emergency department and continues in the coronary care unit. Initial assessment consists of acute triage and early risk stratification. An electrocardiogram (ECG) should be obtained within 10 minutes of arrival, if it has not been obtained already by emergency medical service providers in the prehospital arena. A detailed approach to the evaluation and management of patients with an ACS in the emergency department is found separately.

Acute triage — A focused evaluation on presentation should address, in order of importance, those findings that permit rapid triage and initial diagnosis and management:

●Responsiveness, airway, breathing, and circulation – In patients who present with respiratory or cardiorespiratory arrest, the appropriate resuscitation algorithms should be followed. (See "Advanced cardiac life support (ACLS) in adults" and "Supportive data for advanced cardiac life support in adults with sudden cardiac arrest" and "Adult basic life support (BLS) for health care providers".)

●Evidence of systemic hypoperfusion (hypotension; tachycardia; impaired cognition; cool, clammy, pale, ashen skin) – Cardiogenic shock complicating acute myocardial infarction (MI) requires aggressive evaluation and management. This issue is discussed in detail separately. (See "Clinical manifestations and diagnosis of cardiogenic shock in acute myocardial infarction" and "Prognosis and treatment of cardiogenic shock complicating acute myocardial infarction".)

●Left heart failure with hypoxia – Patients who present with dyspnea, hypoxia, pulmonary edema, and/or impending respiratory compromise require aggressive oxygenation, airway stabilization, diuretic therapy, and afterload reduction in addition to the standard treatments. (See "Treatment of acute decompensated heart failure: General considerations".)

●Ventricular arrhythmias – Sustained ventricular tachyarrhythmias in the peri-infarction period must be treated immediately because of their deleterious effect on cardiac output, possible exacerbation of myocardial ischemia, and the risk of deterioration into ventricular fibrillation. (See "Ventricular arrhythmias during acute myocardial infarction: Incidence, mechanisms, and clinical features" and 'Arrhythmia prevention and management' below.)

Early risk stratification — Analyses from several large clinical trials and registries have established a number of clinical predictors of adverse outcomes among patients with acute ST elevation MI (STEMI). There are many clinical prognostic factors that are immediately available to the physician based upon the initial history, physical examination, ECG, and chest radiograph. Given the speed with which reperfusion therapy is administered in patients with STEMI, their clinical utility in early medical decision-making in the emergency department is often limited. They do provide good prognostic information that has utility in the post-reperfusion period, however, and may provide guidance regarding the optimum method of reperfusion.

High-risk features include advanced age, low blood pressure, tachycardia, heart failure, and an anterior MI. Specific scoring systems, such as the TIMI risk score, permit a fairly precise determination of the risk of in-hospital mortality (calculator 1) [12,13].

Patients at high risk require an aggressive management strategy in addition to standard medical management. Direct prehospital transport or, less optimally, prompt interhospital transfer to a facility with revascularization capabilities is recommended for such patients.

INITIAL THERAPY — The patient with acute ST elevation myocardial infarction (STEMI) should have continuous cardiac monitoring, oxygen, and intravenous access. Therapy should be started to relieve ischemic pain, stabilize hemodynamic status, and reduce ischemia while the patient is being assessed as a candidate for fibrinolysis or primary percutaneous coronary intervention (PCI). Other routine hospital measures include anxiolytics, serial electrocardiograms, and blood pressure monitoring. The following sections summarize acute therapy.

Oxygen — We give supplemental oxygen to patients with an arterial saturation less than 90 percent, patients in respiratory distress, including those with heart failure, or those with other high-risk features for hypoxia [14]. Supplemental oxygen in patients without hypoxia has not been shown to lead to benefit or harm and has the disadvantages of discomfort of use and cost.

The best evidence regarding the possible benefits and harms of supplemental oxygen therapy comes from the Determination of the Role of Oxygen in Suspected Acute Myocardial Infarction (DETO2X-AMI) registry-based, open-label trial published in 2017 [15]. In this study, 6629 patients with suspected MI and an oxygen saturation of 90 percent or higher were randomly assigned to receive either supplemental oxygen (6 liters per minute for 6 to 12 hours, delivered through an open face mask) or ambient air. There was no difference in the rate of the primary end point of death from any cause within one year (5.0 versus 5.1 percent; hazard ratio [HR] 0.97, 95% CI 0.79-1.21). In addition, there was no difference in the rate of rehospitalization with MI within one year (3.8 versus 3.3 percent; HR 1.13, 95% CI 0.88-1.46). During a median follow-up of 2.1 years, there was no difference in the rate of the composite end point of all-cause death, rehospitalization for MI, or hospitalization for heart failure (11.2 versus 10.8 percent; HR 1.02, 95% CI 0.88-1.17) [16].

A 2018 meta-analysis of seven studies (n = 7702), in which most of the patients came from DETO2X-AMI, found that the routine use of oxygen did not decrease the individual risks of all-cause death, recurrent ischemia or MI, heart failure, or occurrence of arrhythmia events [17]. These findings in this meta-analysis were consistent with those in a 2016 Cochrane review [18].

In the 2015 AVOID study, 441 normoxic (oxygen saturation ≥94 percent on pulse oximeter) patients with confirmed STEMI were randomly assigned, at the time of electrocardiographic diagnosis made by paramedics, to either oxygen (8 L/min) or no supplemental oxygen [19]. AVOID showed no improvement in the primary end point of a diminution in infarct size as measured by cardiac enzymes cTnI and creatinine kinase (CK); in fact, there was a significant increase in mean peak CK in the oxygen group (1949 versus 1543 U/L; means ratio 1.27, 95% CI 1.04-1.52). At six months, the oxygen group had a larger MI size as measured with cardiac magnetic resonance.

A pathophysiologic basis for the potential of harm with supplemental oxygen in patients with normoxia has been articulated [20-22]. Hyperoxia, which might occur with the administration of oxygen to normoxic individuals, has been shown to have a direct vasoconstrictor effect on the coronary arteries [20].

The potential benefit from the use of hyperbaric oxygen therapy was evaluated in a 2015 meta-analysis of six small studies with 665 participants with MI or severe angina. While a reduction in the risk of death was found (relative risk 0.58, 95% CI 0.36-0.92), methodologic limitations of the studies prevent us from having confidence in the use of such therapy [23].

Reperfusion — Prompt restoration of myocardial blood flow is essential to optimize myocardial salvage and to reduce mortality (figure 1) [24]. A decision must be made as soon as possible as to whether reperfusion will be achieved with fibrinolytic agents or primary (direct) PCI. (See "Acute ST-elevation myocardial infarction: Selecting a reperfusion strategy".)

We suggest the following approach for patients with STEMI at hospitals without on-site PCI capability:

●For patients who present within two hours of the onset of symptoms, we suggest full-dose fibrinolytic therapy and transferral to a PCI center. This assumes that primary PCI cannot be performed in less than 90 minutes at a local PCI center.

●For patients who present with symptoms that last longer than two to three hours, we suggest transferral for primary PCI. However, there are times when the patient presents after two hours, and PCI cannot be accomplished in less than 120 minutes. In this setting, clinical judgement needs to be exercised; fibrinolytic therapy may be appropriate in patients with up to 12 hours of symptoms.

As noted above, all patients who undergo primary PCI should be pretreated at diagnosis with anticoagulant and antiplatelet therapy. (See 'Antiplatelet therapy' below and 'Anticoagulant therapy' below.)

Percutaneous coronary intervention — If high-quality PCI is available, multiple randomized trials have shown enhanced survival and a lower rate of intracranial hemorrhage and recurrent MI compared to fibrinolysis [25]. The use of primary PCI is discussed separately. (See "Primary percutaneous coronary intervention in acute ST elevation myocardial infarction: Periprocedural management".)

If primary PCI is not available on site, rapid transfer to a PCI center can produce better outcomes than fibrinolysis, as long as the door-to-balloon time, including interhospital transport time, is less than 90 minutes. This door-to-balloon time is difficult to obtain unless rapid transport protocols and relatively short transport distances are in place. (See "Primary percutaneous coronary intervention in acute ST elevation myocardial infarction: Determinants of outcome".)

Fibrinolysis — The use of fibrinolytic therapy is discussed separately. (See "Acute ST-elevation myocardial infarction: The use of fibrinolytic therapy".)

Angiography after fibrinolysis — Fibrinolysis immediately before primary PCI, previously called facilitated PCI, is not recommended. (See "Percutaneous coronary intervention after fibrinolysis for acute ST-elevation myocardial infarction", section on 'Facilitated PCI (with fibrinolytic therapy)'.)

The data evaluating the role of elective coronary angiography, which might include adjunctive and early elective PCI, are discussed in detail elsewhere. (See "Acute ST-elevation myocardial infarction: Selecting a reperfusion strategy", section on 'Fibrinolysis'.)

The use of "rescue PCI" for patients with recurrent ischemia or infarction is better established. (See "Diagnosis and management of failed fibrinolysis or threatened reocclusion in acute ST-elevation myocardial infarction", section on 'Primary failure'.)

Bypass surgery — Coronary artery bypass graft surgery (CABG) is infrequently performed in patients with STEMI. The main indications are for emergent or urgent CABG related to failure of fibrinolysis or PCI, or hemodynamically important mechanical complications. (See "Coronary artery bypass graft surgery in patients with acute ST-elevation myocardial infarction".)

The benefit of revascularization must be weighed against the increase in mortality associated with CABG in the first three to seven days after STEMI. Thus, if the patient has stabilized, surgery should be delayed to allow myocardial recovery. Patients with critical anatomy should undergo CABG during the initial hospitalization.

Medications — A summary of the specific agents listed below and their usual dosing regimens is found elsewhere. (See "Initial evaluation and management of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department", section on 'ST elevation'.)

Antiplatelet therapy — Antiplatelet therapy including aspirin, a P2Y₁₂ receptor blocker, and, in patients undergoing primary PCI, a GP IIb/IIIa inhibitor improves outcomes. These agents are discussed in detail elsewhere. (See "Acute ST-elevation myocardial infarction: Antiplatelet therapy".)

Anticoagulant therapy — The evidence to support parenteral anticoagulant therapy in most cases of STEMI is strong. However, the evidence to recommend one agent over another is less robust, in part because it is derived from many studies that were performed before the current era of aggressive antiplatelet therapy or studies that conflict with each other. The choice of agent depends upon the overall treatment strategy designed for each patient: fibrinolytic therapy with either fibrin specific or non-fibrin specific agents, primary PCI, or no reperfusion. (See "Anticoagulant therapy in acute ST-elevation myocardial infarction".)

Nitrates — Intravenous nitroglycerin is useful in patients with persistent chest pain after three sublingual nitroglycerin tablets, as well as in patients with hypertension or heart failure. (See "Nitrates in the management of acute coronary syndrome".)

However, nitrates must be used with caution or avoided in settings in which hypotension is likely or could result in serious hemodynamic decompensation, such as right ventricular infarction or severe aortic stenosis. In addition, nitrates are contraindicated in patients who have taken a phosphodiesterase inhibitor for erectile dysfunction (or pulmonary hypertension) within the previous 24 hours. (See "Sexual activity in patients with cardiovascular disease" and "Right ventricular myocardial infarction", section on 'Optimization of right ventricular preload'.)

Morphine — In the setting of acute myocardial infarction, intravenous morphine should be avoided if possible and reserved for patients with an unacceptable level of pain since a large but retrospective study suggests its use is associated with an adverse effect on outcome. We give intravenous morphine sulfate at an initial dose of 2 to 4 mg, with increments of 2 to 8 mg repeated at 5- to 15-minute intervals.

In a study of 57,039 patients enrolled in the CRUSADE Initiative, a nonrandomized, retrospective observational registry of patients with non ST-elevation acute coronary syndrome, those treated with morphine (29.8 percent) had a higher adjusted risk of death than those not (odds ratio 1.48, 95% CI 1.33-1.64) [26].

While the mechanism(s) by which morphine might be associated with decreased survival is not known, at least two studies have raised the possibility that it acts by interfering with the antiplatelet effect of the P2Y₁₂ receptor blockers (see "Acute ST-elevation myocardial infarction: Antiplatelet therapy", section on 'Our approach to early DAPT'):

●In the IMPRESSION trial, 70 acute MI patients treated with ticagrelor were randomly assigned to receive intravenous morphine (5 mg) or placebo [27]. Morphine lowered (active) ticagrelor plasma concentration and impaired its antiplatelet effect.

●In a study of 24 healthy subjects who received a loading dose of 600 mg of clopidogrel and either 5 mg of intravenous morphine or placebo, morphine significantly delayed clopidogrel absorption and reduced the area under the curve levels of its active metabolite by 34 percent [28]. Platelet inhibition, as measured by multiple tests, was less pronounced in those given morphine.

●In a study of 50 patients with STEMI undergoing primary PCI who were randomly assigned to either prasugrel or ticagrelor, morphine was an independent predictor of high residual platelet reactivity at two hours (odds ratio 5.29, 95% CI 1.44-19.49) [29].

Beta blockers — Oral beta blockers are administered universally to all patients without contraindications who experience an acute STEMI [30,31]. Contraindications include heart failure, evidence of a low output state, high risk for cardiogenic shock, bradycardia, heart block, or reactive airway disease. (See "Acute myocardial infarction: Role of beta blocker therapy".)

Statin therapy — Intensive statin therapy should be initiated as early as possible in all patients with STEMI. This issue is discussed in detail elsewhere. (See "Low density lipoprotein-cholesterol (LDL-C) lowering after an acute coronary syndrome", section on 'Our approach to in-hospital therapy'.)

Other

Arrhythmia prevention and management — Both atrial and ventricular arrhythmias can be seen during and after the acute phase of STEMI. These include atrial fibrillation or flutter, which can cause symptomatic hypoperfusion due to a rapid rate, and life-threatening ventricular tachycardia or ventricular fibrillation. (See "Supraventricular arrhythmias after myocardial infarction" and "Ventricular arrhythmias during acute myocardial infarction: Incidence, mechanisms, and clinical features".)

Prophylactic intravenous or intramuscular lidocaine to prevent ventricular tachycardia/ventricular fibrillation in the acute MI patient is NOT recommended [32]. Recommended prophylactic measures include early administration of an intravenous beta blocker and treatment of hypokalemia and hypomagnesemia. Treatment of ventricular tachyarrhythmias in the setting of acute MI is discussed separately. (See "Ventricular arrhythmias during acute myocardial infarction: Incidence, mechanisms, and clinical features".)

Sinus bradycardia can occur in patients with STEMI, especially when the inferior wall is involved. If the patient is symptomatic, therapy with atropine is indicated. Persistent sinus bradycardia may require temporary pacing. (See "Supraventricular arrhythmias after myocardial infarction", section on 'Sinus bradycardia'.)

Atrioventricular nodal and intraventricular conduction abnormalities also may be seen in STEMI, particularly of the anterior wall. If the patient is symptomatic, temporary pacing is indicated. Asymptomatic patients with certain types of conduction abnormalities may also require prophylactic temporary pacemaker therapy, and some may require permanent pacemaker implantation. (See "Conduction abnormalities after myocardial infarction".)

Nonsteroidal anti-inflammatory drugs — Nonsteroidal anti-inflammatory drugs (except aspirin) should be discontinued immediately due to an increased risk of cardiovascular events associated with their use. (See "NSAIDs: Adverse cardiovascular effects".)

Potassium and magnesium — Although there are no clinical trials documenting the benefits of electrolyte replacement in acute MI, the American College of Cardiology/American Heart Association guidelines recommend maintaining the serum potassium concentration above 4.0 meq/L and a serum magnesium concentration above 2.0 meq/L (2.4 mg/dL or 1 mmol/L) [33]. Much of the evidence for this recommendation was derived from studies before the routine use of beta blocker and the use of reperfusion in many patients. (See "Ventricular arrhythmias during acute myocardial infarction: Incidence, mechanisms, and clinical features", section on 'Ventricular fibrillation'.)

A 2012 retrospective cohort study of almost 39,000 individuals found that for patients with acute MI, the lowest mortality was observed in those with post-admission serum potassium values between 3.5 and <4.5 meq/L [34]. (See "Risk factors for adverse outcomes after ST-elevation myocardial infarction", section on 'Serum potassium'.)

We suggest that the serum potassium fall within the range of 3.5 to 4.5 meq/L. It may be difficult to lower the potassium below 4.5 meq/L in some patients, such as those with chronic kidney disease.

Transfusions — Red blood cell transfusion is generally reserved for severe or symptomatic anemia, such as hemoglobin <8 g/dL or hemoglobin 8 to 10 g/dL with hemodynamic instability or ongoing ischemia. Clinical judgment is required to determine if transfusion is likely to improve oxygen delivery or if there are other reasons to consider transfusion such as active bleeding or trauma. (See 'Initial assessment' above.)

The rationale for using a restrictive transfusion strategy (limiting transfusions, transfusing for a lower rather than a higher hemoglobin level) includes avoiding risks of transfusion reactions or transfusion-transmitted infection and limiting burdens and costs while using evidence-based thresholds for optimal outcomes. While anemia correlates with worse outcomes, this is likely to be an association rather than causation. (See "Indications and hemoglobin thresholds for red blood cell transfusion in the adult", section on 'Overview of our approach'.)

Supporting data for the thresholds used in acute MI are presented separately. (See "Indications and hemoglobin thresholds for red blood cell transfusion in the adult", section on 'Acute coronary syndrome (including MI)'.)

Intravenous glucose-insulin-potassium — Based on the available evidence, we do not recommend the use of intravenous glucose-insulin-potassium (GIK) to improve outcomes in patients with suspected or diagnosed acute MI. Reviews of the potential mechanism of action and potential benefits have been published [35].

Experimental and early clinical evidence suggested that metabolic support of the ischemic myocardium may limit the extent of myocardial injury and decrease the frequency of potentially lethal arrhythmias after MI. GIK was thought to be a possible approach to improving myocardial energy metabolism [36]. A 1997 meta-analysis of early trials of GIK found a significant reduction in in-hospital mortality [37].

More trials, in which patients received current therapies for acute coronary syndromes such as urgent PCI, aggressive antithrombotic therapy, and a statin drug, have not provided conclusive evidence of benefit [38-43]. The CREATE-ECLA and IMMEDIATE trials provide the best evidence against a benefit from GIK:

●The CREATE-ECLA trial evaluated 20,201 patients with an acute STEMI who presented within 12 hours of symptom onset [38]. The patients were randomly assigned to a GIK infusion or placebo for 24 hours. Reperfusion was performed in 83 percent of patients (74 percent with thrombolytic therapy and 9 percent with primary PCI). The GIK infusion was begun at the time of randomization.

At 30 days, there was no difference between the two groups in mortality (10 versus 9.7 percent with usual care), cardiac arrest (1.5 versus 1.4 percent), cardiogenic shock (6.3 versus 6.6 percent), or reinfarction (2.4 versus 2.3 percent). A potential limitation of this trial was the relatively late use of GIK: The median time from symptom onset to treatment was approximately six hours.

●The IMMEDIATE trial randomly assigned 871 patients with suspected acute coronary syndromes (approximately 40 percent with ST-elevation on the presenting electrocardiogram) to intravenous GIK or identical-appearing 5 percent glucose placebo, which was administered by paramedics in the out-of-hospital setting and continued for 12 hours [39]. There was no difference in the rate of progression to MI (as measured by biomarkers and ECG evidence) at 24 hours or the rate of death at 30 days among patients who received GIK compared to those who received placebo (48.7 versus 52.6 percent; odds ratio 0.88, 95% CI 0.66-1.13 and 4.4 versus 6.1 percent; odds ratio 0.72, 95% CI 0.40-1.29, respectively).

MI WITH NO OBSTRUCTIVE CORONARY ARTERY DISEASE — At the time of coronary angiography, as many as 7 percent of patients with acute ST-elevation myocardial infarction (MI) do not have a critical coronary artery lesion [44], including approximately 3 percent who have normal epicardial coronary arteries [45-47]. The prevalence is greater in younger patients and in women [44]. Potential mechanisms that can be identified in some of these patients include coronary spasm, acquired or inherited coagulation disorders, toxins such as cocaine, collagen vascular disease, embolism, myocarditis, and microvascular disease [46]. The prevalence of lack of a critical lesion or normal epicardial coronary arteries may also be higher in referral populations, due in part to misinterpretation of the presenting electrocardiogram (respective values 14 and 9.5 percent, respectively, in a review of 1335 referred patients) [48]. (See "Coronary heart disease and myocardial infarction in young men and women" and "Vasospastic angina" and "Clinical manifestations, diagnosis, and management of the cardiovascular complications of cocaine abuse" and "Microvascular angina: Angina pectoris with normal coronary arteries", section on 'Clinical presentation' and "Clinical manifestations and diagnosis of myocarditis in adults", section on 'Electrocardiogram' and "Myocardial infarction with no obstructive coronary atherosclerosis".)

Stress-induced cardiomyopathy (takotsubo cardiomyopathy) is an increasingly reported syndrome, generally characterized by transient systolic dysfunction of the apical and/or mid segments of the left ventricle that mimics MI, but in the absence of significant coronary artery disease. This issue is discussed elsewhere. (See "Clinical manifestations and diagnosis of stress (takotsubo) cardiomyopathy".)

In a study of 323 women 45 years or older who presented to a community hospital over one year and who were diagnosed with an acute MI (including an elevated troponin), 5.9 percent met criteria for stress-induced cardiomyopathy [49].

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)" and "Society guideline links: Secondary prevention of cardiovascular disease".)

SUMMARY AND RECOMMENDATIONS

●Acute ST-elevation myocardial infarction (STEMI) is a medical emergency requiring the simultaneous application of multiple therapies. After the emergent period, other therapies may need to be started. (See "Overview of the non-acute management of ST elevation myocardial infarction".)

●Women and men should be managed similarly. Other patients with acute STEMI, such as older individuals and those with either cocaine-associated MI or possible stent thrombosis, are managed somewhat differently. (See 'General principles' above.)

●The initial assessment and therapy of STEMI is summarized in table form (table 1).

●For patients suspected of acute MI who have an oxygen saturation on room air of 90 percent or greater, we recommend not administering supplemental oxygen (Grade 1B). (See "Overview of the acute management of non-ST elevation acute coronary syndromes", section on 'Oxygen'.)

However, for patients with a history of heart failure with this level of oxygen saturation, we consider administration reasonable.

ACKNOWLEDGMENT — The UpToDate editorial staff thank Dr. Robert S. Rosenson for his past contributions as an author to this topic review.