Overview of the acute management of ST-elevation myocardial infarction

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 "Mechanical complications of acute myocardial infarction".)

STEMI AFTER NONCARDIAC HOSPITAL ADMISSIONA 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 PRINCIPLESOnce 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 — Although the majority of MIs in the elderly population present with
ECGs that are nondiagnostic or have ST-segment depression, 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 elderly compared to younger patients are
generally accepted [7]:

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

●Elderly 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 "Fibrinolysis for acute ST elevation myocardial infarction: Initiation of 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 normal coronary arteries' 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 ASSESSMENTClinical 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 "Basic life support
(BLS) in adults".)

●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 THERAPYThe 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]. As a result, 2013 American
College of Cardiology Foundation/American Heart Association guideline for the
management of STEMI recommends use of primary PCI for any patient with an acute
STEMI who can undergo the procedure in a timely manner by persons skilled in the
procedure [26,27]. Timely is defined as an ideal first medical contact to PCI time of 90
minutes or less for patients transported to PCI-capable hospital or 120 minutes or less for
patients who initially arrive at or are transported to a non-PCI capable hospital and are then
taken to a PCI-capable hospital.

Patients with typical and persistent symptoms in the presence of a new or presumably new
left bundle branch block are also considered eligible. (See "Primary percutaneous coronary
intervention in acute ST elevation myocardial infarction: Determinants of outcome".)

For patients presenting 12 to 24 hours after symptom onset, the performance of primary
PCI is reasonable if the patient has severe heart failure, hemodynamic or electrical
instability, or persistent ischemic symptoms. Randomized trials of routine late PCI have
shown an improvement in left ventricular function but not in hard clinical end points. This
approach is not recommended. (See "Coronary artery patency and outcome after
myocardial infarction", section on 'Late PCI to open an occluded artery'.)

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 2013 American College of Cardiology Foundation/American Heart

Association guideline for the management of STEMI recommends the use of fibrinolytic
therapy in patients with symptom onset within 12 hours who cannot receive primary
percutaneous coronary intervention within 120 minutes of first medical contact (table 1A-
B) [26,27]. The time interval from hospital arrival to initiation of fibrinolytic drug infusion
should be less than 30 minutes [26-29]. (See "Acute ST elevation myocardial infarction:
Selecting a reperfusion strategy" and "Fibrinolysis for acute ST elevation myocardial
infarction: Initiation of therapy", section on 'Timing'.)

Fibrinolytic therapy has generally not improved outcomes in patients presenting at 12 hours
or later and is therefore not indicated in those who are stable and asymptomatic. However,
fibrinolysis can be considered up to 24 hours after symptom onset if the patient has ongoing
or stuttering chest pain and PCI is not available. (See "Fibrinolysis for acute ST elevation
myocardial infarction: Initiation of therapy", section on 'Timing'.)

A number of different fibrinolytic regimens have been evaluated and each agent has its own
preferred dosing regimen (table 2). (See "Characteristics of fibrinolytic (thrombolytic)
agents and clinical trials in acute ST elevation myocardial infarction".)

Patients receiving fibrinolytic therapy benefit from pretreatment with clopidogrel but not a
glycoprotein (GP) IIb/IIIa inhibitor [29]. (See "Antiplatelet agents in acute ST elevation
myocardial infarction".)

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'.)

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
followed by PCI'.)

The use of "rescue PCI" for patients with recurrent ischemia or infarction is better
established. (See "Management of failed fibrinolysis (thrombolysis) 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 "Antiplatelet agents in acute ST elevation
myocardial infarction".)

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) [30].

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 "Antiplatelet agents in acute ST
elevation myocardial infarction", section on 'Choosing antiplatelet therapy'):

●In the IMPRESSION trial, 70 acute MI patients treated with ticagrelor were randomly
assigned to receive intravenous morphine (5 mg) or placebo [31]. 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 resorption and reduced the area under the curve levels of its active metabolite
by 52 percent [32]. 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) [33].

Beta blockers — Oral beta blockers are administered universally to all patients without
contraindications who experience an acute STEMI [26,27]. 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'.)

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 [34].
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) [35]. 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 [36]. (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.

Erythropoietin — Clinical interest in the use of erythropoietin as a cardioprotective agent

emanated from a growing body of experimental evidence showing that erythropoietin’s
non-erythropoietic effects include anti-inflammatory, antiapoptotic, and angiogenic
properties. Preclinical studies suggested that erythropoietin may be cardioprotective in
patients with acute STEMI, based on improvement in infarct size attributed to its
antiapoptotic and angiogenic properties. However, in the REVEAL trial, which randomly
assigned 222 patients who underwent successful PCI to either intravenous erythropoietin or
placebo within four hours of the procedure, there was no significant difference between the
groups in infarct size, expressed as percentage of left ventricular mass as assessed by
cardiac magnetic resonance imaging performed at baseline and at 10 to 14 weeks [37]. In
addition, a significantly increased risk of death, recurrent MI, stroke, or stent thrombosis in
erythropoietin-treated patients suggested an increased thrombotic risk due to erythropoietin
in patients with STEMI. This observation of adverse events has been noted in other studies
of noncardiac populations [38-40].

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 [41].

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 [42]. A 1997 meta-analysis of early trials of GIK
found a significant reduction in in-hospital mortality [43].

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 [44-49]. 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 [44]. 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 [45]. 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 NORMAL CORONARY ARTERIESAt 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 [50], including approximately 3 percent who have
normal epicardial coronary arteries [51-53]. The prevalence is greater in younger patients
and in women [50]. 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 [52]. 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) [54]. (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'.)

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 [55].

SOCIETY GUIDELINE LINKSLinks 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 coronary heart 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 should be managed similarly to men. Other patients with acute STEMI, such as
the elderly 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 3).

●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.

ACKNOWLEDGMENTThe UpToDate editorial staff would like to thank Dr. Robert S.

Rosenson for his past contributions as an author to this topic review.