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Myocardial Infarction Treatment & Management

  • Author: A Maziar Zafari, MD, PhD; Chief Editor: Eric H Yang, MD  more...
 
Updated: Mar 28, 2016
 

Approach Considerations

The first goal for healthcare professionals in management of acute myocardial infarction (MI) is to diagnose the condition in a very rapid manner.

As a general rule, initial therapy for acute MI is directed toward restoration of perfusion as soon as possible to salvage as much of the jeopardized myocardium as possible. This may be accomplished through medical or mechanical means, such as percutaneous coronary intervention (PCI), or coronary artery bypass graft (CABG) surgery.

Although the initial treatment of the different types of acute coronary syndrome (ACS) may appear to be similar, it is very important to distinguish between whether the patient is having an ST-elevation MI (STEMI) or a non–STEMI (NSTEMI), because definitive therapies differ between these two types of MI. Particular considerations and differences involve the urgency of therapy and the degree of evidence regarding different pharmacologic options.

Morbidity and mortality from MI are significantly reduced if patients and bystanders recognize symptoms early, activate the emergency medical service (EMS) system, and thereby shorten the time to definitive treatment. Trained prehospital personnel can provide life-saving interventions if the patient develops cardiac arrest. The key to improved survival is the availability of early defibrillation. Approximately 1 in every 300 patients with chest pain transported to the emergency department by private vehicle goes into cardiac arrest en route.[61]  In the United States, several studies have confirmed that patients with STEMI usually do not call 911, and only about 40% of patients with a confirmed coronary event used EMS.[62]

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Prehospital Care and Initial Management

All patients being transported for chest pain should be managed as if the pain is ischemic in origin, unless clear evidence to the contrary is established. If available, an advanced cardiac life support (ACLS)–trained unit should transport patients with hemodynamic instability or respiratory difficulty.

Prehospital notification by emergency medical services (EMS) personnel should alert emergency department staff to the possibility of a patient with myocardial infarction (MI). EMS personnel should receive online medical advice for a patient with high-risk features; this allows for early and prompt delivery of medical treatment and, most importantly, facilitates the transportation of patients to facilities with the appropriate level of care.

Specific prehospital care includes the following:

  • Intravenous access, supplemental oxygen, pulse oximetry
  • Immediate administration of aspirin en route
  • Nitroglycerin for active chest pain, given sublingually or by spray
  • Telemetry and prehospital electrocardiography (ECG), if available

Most deaths caused by MI occur early and are attributable to primary ventricular fibrillation (VF). Therefore, initial objectives are immediate ECG monitoring; electric cardioversion in cases of VF; and rapid transfer of the patient to facilitate prompt coronary assessment.

Prehospital integration of ECG interpretation has been shown to decrease "door-to-balloon time,” allow paramedics to bypass non–percutaneous coronary intervation (PCI)–capable hospitals in favor of PCI-capable facilities, and to expedite care by allowing an emergency department physician to activate the catheterization laboratory before the patient's arrival.

Additional objectives of prehospital care by paramedical and emergency personnel include adequate analgesia (generally achieved with morphine); pharmacologic reduction of excessive sympathoadrenal and vagal stimulation; treatment of hemodynamically significant or symptomatic ventricular arrhythmias (generally with amiodarone and lidocaine); and support of cardiac output, systemic blood pressure, and respiration.

Prehospital fibrinolytic therapy by the administration of tissue-type plasminogen activator (t-PA), aspirin, and heparin may be given to patients with bona fide MI by paramedics, as guided by electrocardiographic findings, within 90 minutes of the onset of symptoms. This treatment improves outcomes, as compared with thrombolysis begun after the patient arrives at the hospital. Prehospital fibrinolytic therapy is not used widely in the United States due to the lack of resources to train EMS personnel or the lack of funding for necessary equipment. However, it is more widespread in some regions in Europe and the United Kingdom.

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Emergency Department Care and In-Hospital Management

Triage and evaluation

Because acute coronary syndrome (ACS) is a spectrum of conditions, initial evaluation to establish a working diagnosis is crucial, as this will dictate management owing to some differences in management steps and timelines for each component of the ACS spectrum.

All patients presenting to the the emergency department with symptoms suggestive of acute myocardial infarction (MI) should be evaluated with a targeted history and focused physical examination (see Presentation). A 12-lead electrocardiogram (ECG) interpreted by an experienced physician should be completed within 10 minutes of arrival, in addition to establishing intravenous (IV) access.

Initial management

The initial management of the overall management plan for patients with acute MI has the following aims:

  • Restoration of the balance between oxygen supply and demand to prevent further ischemia
  • Pain relief
  • Prevention and treatment of complications

Oxygen

Continuous oxygen saturation monitoring by pulse oximetry is needed for all patients.

Supplemental oxygen by a mask or nasal cannula is indicated only for patients who are breathless, hypoxic (oxygen saturation <90%), or who present with heart failure. The use of oxygen in patients with acute MI who don’t fall into one of the three above-mentioned categories remains uncertain, with some studies suggesting possible harm in such patients.[63]

Aspirin

All patients presenting with ACS should receive aspirin in a dose of at least 162 to 325 mg, unless there is a clear history of aspirin allergy. Patients with aspirin intolerance still should receive aspirin at presentation.

Chewed aspirin is preferred, as this promotes rapid absorption into the bloodstream to achieve faster therapeutic levels.

Reduction of cardiac pain

Nitrates

Nitrates are potent vasodilators, and they act mainly to relax the venous system. Systemic venodilation results in reduction of venous blood return to the heart (ie, reducing the ventricular preload); this will lead to reduction of the workload of the heart, less oxygen demand, and reduction in ischemic pain. Nitrates are also the most commonly used agents to reduce cardiac chest pain related to ischemia via coronary vasodilation; however, their use is not associated with reduction in ACS-associated mortality.

Nitrates are usually given as a 0.4 mg dose in a sublingual tablet, followed by close observation of the effect on chest pain and the hemodynamic response. If the initial dose is well tolerated, further nitrates can be administered. The most common side effect of nitrates are hypotension and headache.

When chest pain persists or recurs, IV nitrates are indicated, usually started at a dose of 5 to 10 µg/min and gradually increased until relief of chest pain is achieved.

Nitrates should not be used in patients presenting with marked hypotension or bradycardia, or if there is suspicion of right ventricular infarction.

Special attention should be made in taking the history of whether concomitant use of phosphodiesterase (PDE) inhibitors (eg, sildenafil) has occurred within the last 24 hours, because this drug combination may lead to life-threatening hypotension.

Analgesia

Refractory or severe pain should be treated symptomatically with IV morphine.

The initial dose of morphine of 2 to 4 mg as an IV bolus can be given, with increments of 2 to 4 mg repeated every 5 to 10 minutes until the pain is relieved or intolerance is manifested by hypotension, vomiting, or depressed respiration. Should toxicity occur, a morphine antagonist such as naloxone is used for reversal. The patient's blood pressure and pulse must be monitored; the systolic blood pressure must be maintained above 100 mm Hg and, optimally, below 140 mm Hg.

The use of other analgesic agents, such as nonsteroidal anti-inflammatory drugs (NSAIDs) should be avoided if at all possible, as the use of these agents has been associated with adverse cardiovascular events.[64]

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ST-Elevation Myocardial Infarction

Management of ST-elevation myocardial infarction (MI) (STEMI) relies on two essential and key components: rapid recognition and timely reperfusion. Therefore, systems must be placed and implemented to prevent delay in management of patients who develop STEMI. Minimizing delays has been associated with improved overall outcomes as well as reduced mortality and long-term morbidity.[65, 66]  Current clinical practice guidelines have emphasized adopting institutional quality improvement measures to reduce total ischemic time, which is the principal determinant of outcome,[67, 68]  greatest emphasis is to be placed on the appropriate and timely use of some form of reperfusion therapy which is likely more important than the choice of therapy.[9]

Some factors that may lead to shortening total ischemic time include the following:

  • Prehospital electrocardiography (ECG) to diagnose STEMI to activate the percutaneous coronary intervention (PCI) team while the patient is en route to the hospital
  • Emergency department physicians activate the PCI team
  • A single call to a central page operator who activates the PCI team
  • The goal is set for the PCI team to arrive in the catheterization laboratory within 20 minutes after being paged
  • Timely data feedback and analysis are provided to members of the STEMI care team

Reperfusion

Early mechanical intervention (primary PCI) or pharmacologic reperfusion should be performed as soon as possible for patients with clinical presentation of STEMI within 12 hours of symptom onset and who have persistent ST-segment elevation or new or presumed new left bundle branch block (LBBB). In addition, it is reasonable to consider an early reperfusion strategy for patients presenting after more than 12 hours, provided there is clinical and/or ECG evidence of ongoing ischemia, with primary PCI being the preferred method in this population.

In the United States, only a minority of hospitals have the capability of performing primary PCI; therefore, a multifaceted community-wide approach that involves patient education, improvements in emergency medical services (EMS) and emergency department care, establishment of networks of STEMI-referral (non–PCI-capable) and STEMI-receiving (PCI-capable) hospitals, has been implemented to overcome this limitation.[69]

For patients presenting to a PCI-capable hospital, primary PCI should be accomplished within 90 minutes. For patients presenting to a non–PCI-capable hospital, it is very important to rapidly assess the following to reach a decision about administration of fibrinolytic therapy:

  1. The time from onset of symptoms
  2. The risk of complications related to STEMI
  3. The risk of bleeding with fibrinolysis therapy
  4. The presence of shock or severe heart failure
  5. The time required for transfer to a PCI-capable hospital

Even when interhospital transfer times are short, there may be relative advantages to a strategy of immediate fibrinolytic therapy versus any delay to primary PCI for eligible patients who present within the first 1 to 2 hours after symptom onset.[9]

Primary percutaneous intervention

PCI is defined as an emergent percutaneous coronary intervention in the setting of STEMI, without previous fibrinolytic treatment. It is the preferred reperfusion strategy in patients with STEMI, provided it can be performed expeditiously within clinical practice guidelines–mandated times and in high-volume centers with experienced interventional cardiology teams and skilled support staff.

PCI achieves superior reperfusion outcomes and is associated with less complications, death, and long-term complications of STEMI when compared to fibrinolytic therapy.[9, 44, 69, 70, 71]

Current guidelines strongly recommend performing primary PCI in patients presenting with symptoms of less than 12 hours' duration, or those who present with cardiogenic shock or who develop acute severe heart failure, irrespective of time of delay from onset of symptoms. Guidelines also recommend considering primary PCI for patients who present between 12 and 24 hours after onset of symptoms, provided there is ongoing clinical or ECG evidence of myocardial ischemia. Currently, PCI of the noninfarct related artery (nonculprit artery) at the time of primary PCI of the culprit lesion is under active investigation.

This method of reperfusion entails performing emergent coronary angiography, after establishing arterial access, which can be achieved via the radial or femoral artery. After identifying the anatomy of the coronary circulation and determining the culprit vessel, coronary stents are placed to establish reperfusion.

Drug-eluting stents (DES) or bare-metal stents (BMS) are used. However, if there are financial or social barriers that may limit patient compliance, an increased risk of bleeding, or an anticipated invasive or surgical procedure, the use of DES is not recommended.[9]

Placement of coronary stents requires dual antiplatelet therapy for an extended time period (see the subsection "Antiplatelet agents," below). The duration of therapy is dependent of the type of stent used.

Fibrinolysis

Fibrinolysis is an important reperfusion strategy, particularly in settings where primary PCI cannot be offered to STEMI patients within the recommended timelines. The benefit of fibrinolytic therapy in patients with STEMI is well established, with the largest benefit seen when administered early (within 12 hours after symptomatic onset) and in patients with the highest cardiovascular risk, including patients older than 75 years.[72, 73]

Fibrinolytic therapy may not be beneficial in patients who present more than 12 hours after symptom onset, although current practice guidelines recommend consideration of fibrinolysis in symptomatic patients with a large area of myocardium at risk (based on ECG or cardiovascular imaging) or hemodynamic instability if PCI is unavailable. See absolute and relative contraindications to fibrinolytic therapy in table 1, below.

Table 1. Absolute and Relative Contraindications to Fibrinolytic Therapy in Patients with STEMI (Open Table in a new window)

Absolute Contraindications Relative Contraindications
  • Any prior intracranial hemorrhage
  • Known structural cerebral vascular lesion
  • Known intracranial neoplasm (primary or metastatic)
  • Ischemic stroke within the past 3 months (except for acute stroke within 4.5 hours)
  • Suspected aortic dissection
  • Active bleeding or bleeding diathesis (excluding menses)
  • Significant closed-head or facial trauma within 3 months
  • Intracranial or intraspinal surgery within 2 months
  • Severe uncontrolled hypertension (unresponsive to emergency therapy)
  • For streptokinase (no longer marketed in the US): Prior treatment within previous 6 months
  • History of chronic, severe, poorly controlled hypertension
  • Systolic pressure >180 mm Hg or diastolic pressure >110 mm Hg
  • History of prior ischemic stroke >3 months
  • Dementia
  • Known intracranial pathology not covered in absolute contraindications
  • Traumatic or prolonged CPR (>10 minutes)
  • Recent (within 2-4 weeks) internal bleeding
  • Noncompressible vascular punctures
  • Pregnancy
  • Active peptic ulcer disease
  • Current use of anticoagulants: The higher the INR, the higher the risk of bleeding
  • For streptokinase (no longer marketed in the US): Prior exposure (>5 days previously) or prior allergic reaction to these agents
CPR = cardiopulmonary resuscitation; INR = international normalized ratio; STEMI = ST-elevation myocardial infarction; US = United States of America.



 



Table modified from 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.[9]



Fibrinolytic therapy is associated with an excess of strokes, mainly due to cerebral hemorrhage, which is more commonly seen in patients with advanced age, lower weight, female sex, prior cerebrovascular disease, and hypertension on admission.[74]

Different fibrinolytic agents are available, and table 2, below, lists different fibrinolytic agents with some of their key characteristics. In general, fibrin-specific agents are preferred when available. Note: Streptokinase is no longer marketed in the United States.

Table 2. Fibrinolytic Agents Used in Management of STEMI. (Open Table in a new window)

Fibrinolytic Agent Dose Fibrin Specificity Antigenic Patency Rate
Non-fibrin specific        
Streptokinase (no longer marketed in the US) 1.5 million units IV given over 30–60 min No Yes 60%–68%
Fibrin specific        
Tenecteplase



(TNK-tPA)



30 mg for weight <60 kg



35 mg for 60–69 kg



40 mg for 70–79 kg



45 mg for 80–89 kg



50 mg for >90 kg



++++ No 85%
Reteplase (rPA) 10-U IV boluses given 30 min apart ++ No 84%
Alteplase (tPA) Bolus 15 mg followed by infusion 0.75 mg/kg for 30 min (maximum 50 mg), then 0.5 mg/kg (maximum 35 mg) over the next 60 min; total dose not to exceed 100 mg. ++ No 73%-84%
IV = intravenous; rPA = recombinant human tissue plasminogen activator; STEMI = ST-elevation myocardial infarction; tPA = tissue plasminogen activator; US = United States of America.



 



Table modified from 2013 ACCF/AHA guidelines for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.[9]



 

Coronary artery bypass grafting (CABG)

Despite great improvement of intraoperative myocardial preservation, CABG has a limited role in the acute management of STEMI. However, CABG remains indicated for cardiogenic shock, failed PCI, high-risk anatomy, surgical repair of a mechanical complication of STEMI (eg, ventricular septal rupture, free-wall rupture, or severe mitral regurgitation from papillary muscle dysfunction or rupture).

Anticoagulation

Anticoagulant agents are an important adjunctive therapy for reperfusion therapy regardless of the strategy chosen (ie, whether it is primary PCI or fibrinolysis therapy). Different anticoagulation agents are available; the utility of each agent depends on the clinical context, taking into account the method of reperfusion.

For primary PCI, unfractionated heparin (UFH), bivalirudin,[9, 44]  and low molecular weight heparin (LMWH) (eg, enoxaparin[44] ) are the available options. Fondaparinux is not used in this setting because of the increased risk of catheter thrombosis.[75]

In patients receiving fibrinolytic therapy, anticoagulation should be given until revascularization is performed; if reperfusion is not feasible anticoagulants should be given for at least 48 hours or for the duration of hospital stay up to 8 days.[44]  UFH or LMWH may be used, with LMWH (enoxaparin) being preferred.[76, 77, 78]  Use caution with the administration of enoxaparin in patients older than 75 years as well as those with impaired renal function, because the use of enoxaparin is associated with a higher risk of intracranial bleeding. Bivalirudin may be used for patients who develop or have a history of heparin-induced thrombocytopenia (HIT) and require anticoagulation.[79]

Antiplatelet agents

All patients with STEMI should receive an empiric loading dose of aspirin (150.5 to 325 mg) as early as possible and prior to reperfusion, regardless of the reperfusion method. A lifelong maintenance dose of (75 to 81 mg) daily should be prescribed to all patients after STEMI.

Other antiplatelet agents used for dual antiplatelet therapy are the P2Y12 receptor inhibitors (eg, clopidogrel, ticagrelor, prasugrel); a loading dose of these agents is given before or at the time of reperfusion and an extended duration maintenance dose is administered thereafter, depending on the method of reperfusion.

For patients undergoing primary PCI, a loading dose of 600 mg of clopidogrel, 180 mg of ticagrelor, or 60 mg of prasugrel should be given as early as possible or at the time of primary PCI. A maintenance dose of P2Y12 receptor inhibitors should be continued for at least 1 year for patients who receive a stent, either a BMS or a DES. A daily dose of 75 mg clopidogrel, 90 mg ticagrelor (twice daily), or 10 mg prasugrel is recommended. It is reasonable to discontinue P2Y12 receptor inhibitor agents prior to 1 year for patients who receive a BMS if there is evidence of increased bleeding.

The use of prasugrel is not recommended for patients with a history of stroke or transient ischemic attack (TIA).[80, 81, 82]

For patients who receive fibrinolytic therapy, a loading dose of clopidogrel 300 mg followed by a daily maintenance dose of 75 mg should be given, preferably for 1 year or a minimum of 14 days. The use of other P2Y12 receptor inhibitor agents in patients treated with fibrinolysis has not been prospectively studied.[9]

Other antiplatelet agents that may be used in STEMI management are the intravenous (IV) glycoprotein (GP) IIb/IIIa receptor antagonists. The adjunctive use of GP IIb/IIIa agents at the time of PCI can be considered on an individual basis for a large thrombus burden or inadequate P2Y12 receptor antagonist loading. For patients receiving bivalirudin as the primary anticoagulant, routine adjunctive use of GP IIb/IIIa inhibitors is not recommended but may be considered in selected cases.[9, 44]

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Non-ST-Elevation (NSTE) ACS

Key points in the management of patients with non–ST-elevation acute coronary syndrome (NSTE-ACS) (unstable angina and non-STE myocardial infarction [NSTEMI]) is early evaluation and assessment of hemodynamic and electrical stability, estimatation of the overall risk in these patients, and guidance of therapy.

There are two alternative management strategies, either an early invasive strategy with angiography, with intent for revascularization with percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG), or a conservative strategy with initial medical therapy and noninvasive cardiovascular imaging. Regardless of the strategy, both entail aggressive utility of medications such as anticoagulants, antiplatelet agents, beta blockers, statins, and possible use of angiotensin-converting enzyme (ACE) inhibitors for appropriate patient populations.

Patients with refractory angina, clinical evidence of heart failure, or hemodynamic or electrical instability who do not have serious comorbidities or contraindications to angiography/PCI should undergo an early invasive strategy.

An immediate early invasive strategy is also recommended for patient who are stable but at a high risk for clinical events. It is reasonable to consider an early invasive strategy within 24 hours of admission in patients with intermediate/high risk. For patients who fall outside this category, a delayed invasive strategy within 25 to 72 hours of admission versus a conservative (ischemia-guided) strategy may be considered.[8]

Beta blockers

Beta blockers work by reduction of oxygen consumption of the myocardium by lowering the heart rate, blood pressure, and myocardial contractility. They also play an important role in reduction of reinfarction and complex ventricular arrhythmias.[27, 83] These agents are recommended to be given orally within the first 24 hours, preferably using one of the three drugs proven to reduce mortality in heart failure patients: metoprolol, carvedilol, or bisoprolol.

Beta blockers should not be given intravenously in patients with evidence of low cardiac output state (heart rate >110 beats/min or systolic blood pressure <100 mmHg), and used with caution in elderly patients or in individuals with an unknown left ventricular ejection fraction.[83]  These agents should also not be given to patients who have a contraindication to beta blockers (eg, first-degree heart block with a PR interval >240 ms, second- or third-degree heart block without a cardiac pacemaker, recent cocaine use, severe/advanced active reactive airway disease).

In patients with chronic obstructive lung disease or chronic asthma, beta-1 selective beta blockers are preferred and should be initiated at low doses.

Calcium channel blockers

Non-dihydropyridine calcium channel blockers (eg, verapamil or diltiazem) should be given for recurrent myocardial ischemia only if there are contraindications to using beta blockers. Similar to beta blockers, use of non-dihydropyridine calcium channel blockers can also increase the likelihood of developing cardiogenic shock, thus, similar caution should be used when considering the use of these drugs.[83]

Avoid short-acting nifedipine in patients who are not receiving beta blockers, as this may result in increased mortality in patients with ACS.[83]

Antiplatelet agents

Aspirin

Nonenteric-coated chewable aspirin 150 to 325 mg should be given to all patients with NSTE-ACS as soon as possible after presentation.

A maintenance dose of aspirin 75-100 mg daily should be continued indefinitely.[8, 30]

Some clinical data suggest that maintenance dose of aspirin higher than 160 mg daily is associated with increased risk of bleeding with no clear improvement in outcomes.[84, 85]

P2Y12 receptor inhibitors

The use of P2Y12 receptor inhibitors in addition to aspirin has resulted in better outcomes, with a reduction of the incidence of cardiovascular death, MI, and stroke. The three P2Y12 receptor inhibitors most commonly used in the treatment of NSTE-ACS are described in this section, as follows:

  • Clopidogrel
  • Ticagrelor
  • Prasugrel

All three agents are given with an initial loading dose, followed by a daily maintenance dose up to 12 months for all patients treated for NSTE ACS with either early invasive or conservative strategies.

With the wider use of new generation drug-eluting stents (DES), a shorter duration of P2Y12 receptor inhibitors of 3-6 months can be considered in patients who are at high bleeding risk.

Clopidogrel

A oading dose of clopidogrel 300-600 mg is recommended, followed by a maintenance dose of 75 mg daily.

Extrapolated results from the Clopidogrel versus Aspirin in Patients at Risk of Ischemic Events (CAPRIE) trial demonstrated that clopidogrel can be used in patients with NSTE-ACS who are intolerant to aspirin.[86]

Ticagrelor

Ticagrelor is a reversible inhibitor of the P2Y12 receptor that has a more rapid onset of action and a shorter half-life than clopidogrel; therefore, it is administered twice daily for maintenance. A loading dose of ticagrelor 180 mg is recommended, followed by a maintenance dose of 90 mg twice daily. 

The Platelet Inhibition and Patient Outcomes (PLATO) trial compared clopidogrel to ticagrelor in patients with NSTE-ACS and concluded that patients receiving ticagrelor had lower events of MI, stroke, and overall mortality.[87]

A unique side effect observed in patients taking ticagrelor is dyspnea, but this is rarely severe enough to cause termination of treatment.[88]

Ticagrelor should not be used concomitantly with higher doses of aspirin (>100 mg daily).

Prasugrel

A loading dose of prasugrel 60 mg is recommended, followed by a maintenance dose of 10 mg daily.

Because of the unique metabolic conversion pathways of prasugrel, it has a more rapid and more consistent platelet inhibition than clopidogrel, which was demonstrated in the Therapeutic Outcomes by Optimizing Platelet Inhibition with Prasugrel–Thrombolysis in Myocardial Infarction (TRITON–TIMI) 38 trial. However, there was a concern of an increased bleeding risk in individuals treated with prasugrel.[80, 81, 82] Therefore, major contraindication to the use of prasugrel are a previous history of stroke or transient ischemic attack (TIA), age over 75 years, and low body weight (<60 kg).[80]

Current clinical practice guidelines have different recommendations with regard to the use of prasugrel upfront in patients with NSTE-ACS. The American College of Cardiology/American Heart Association (ACC/AHA) guidelines do not recommend the use of prasugrel in this setting; however, its use can be considered for those undergoing PCI.[83]  The ESC guidelines, however, recommend the use of prasugrel upfront in patients treated for NSTE-ACS—provided there is no contraindication to its use.[30]

Glycoprotein (GP) IIb/IIIa receptor inhibitors

The Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy (PURSUIT) trial[89] and the Randomized Efficacy Study of Tirofiban for Outcomes and Restenosis (RESTORE) trial[90] demonstrated the efficacy of these agents in the treatment of NSTE-ACS.

The preferred GP IIb/IIIa receptor inhibitors are eptifibatide or tirofiban. Patients undergoing an early invasive strategy who received dual antiplatelet therapy with high-risk features are considered candidates to receive either of these two agents.[8, 30]

However, GP IIb/IIIa agents are associated with an increased risk of bleeding complications, and most of the clinical trials studying these drugs were completed prior to the release of the P2Y12 receptor inhibitors. Thus, their use in NSTE-ACS is limited currently.

Anticoagulant therapy

Anticoagulant agents are recommended to be given to all patients with NSTE-ACS, regardless of the initial treatment strategy, in addition to antiplatelet therapy. The following agents may be considered as treatment options from this group of medications.

Unfractionated heparin (UH)

An initial loading dose of 60 IU/kg (maximum 4,000 IU) with an initial infusion of 12 IU/kg per hour (maximum 1,000 IU/h) adjusted per activated partial thromboplastin time (PTT) is recommended to maintain therapeutic anticoagulation according to the specific hospital protocol. This regimen is continued for 48 hours or until PCI is performed.

A major disadvantage of the use of unfractionated heparin is the large interindividual variability and narrow therapeutic window.

Low molecular weight heparin (LMWH)

Enoxaparin is given at a dose of 1 mg/kg subcutaneously (SC) every 12 hours. It should be continued for the duration of hospitalization or until PCI is performed. A dose reduction is required for patients with impaired kidney function.

Enoxaparin results in a more predictable and efficient anticoagulation compared to unfractionated heparin, leading to reduction in recurrent MI events[91, 92] ; however, there is possibly a higher bleeding risk in patients undergoing PCI.[93] These findings were demonstrated in the Efficacy and Safety of Subcutaneous Enoxaparin in Non–Q wave Coronary Events (ESSENCE) trial.[91, 92, 93]

Bivalirudin

Bivalirudin is direct thrombin inhibitor that is given as 0.1 mg/kg loading dose, followed by 0.25 mg/kg per hour only in patients managed with an early invasive strategy. This regimen is continued until diagnostic angiography or PCI.[94] In the Acute Catheterization and Urgent Intervention Triage Strategy (ACUITY) Trial, the efficacy of bivalirudin was noninferior to the use of heparin plus GP IIb/IIIa.[95]

Fondaparinux

Fondaparinux is a selective factor X inhibitor. This agent is given as a once-daily SC injection of 2.5 mg, which is continued for the duration of hospitalization or until PCI is performed.

Note that fondarparinux is contraindicated in patients with impaired kidney function. In addition, in patients undergoing PCI, administer another anticoagulant agent (eg, unfractionated heparin or bivalirudin), as fondaparinux is associated with a higher risk of catheter thrombosis; this was demonstrated in the Fifth Organization to Assess Strategies in Ischemic Syndromes (OASIS-5) trial.[75, 96, 97]

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Additional Aspects of Management and Late Hospital Care

After the initial management and stabilization of the patient in the early and critical phase of acute myocardial infarction (MI), the goals of care for these patients is to restore normal activities, prevent long-term complications, as well as aggressively modify lifestyle and risk factors. This multifaceted goal is achieved with the implementation of important key elements, including the use of cardioprotective medications and cardiac rehabilitation, as well as physical activity, diet, and patient education.

Cardioprotective medications

Inhibitors of the renin-angiotensin-aldosterone (RAA) system

Initiate angiotensin-converting enzyme (ACE) inhibitors and continue administration indefinitely in all patients with a left ventricular ejection fraction that is less than 40% and in those with hypertension, diabetes mellitus, or stable chronic kidney disease, unless contraindicated.[98, 99]

Angiotensin-receptor blockers (ARBs) are recommended in patients who are intolerant of ACE inhibitors.[100]

Aldosterone blockers are recommended in addition to beta blockers and ACE inhibitors in patient who have had an MI with a reduced left ventricular ejection fraction of less than 40%, provided they have no renal impairment and have normal blood potassium levels (<5 mEq/L). This was emphasized in the Eplerenone Post-acute myocardial infarction Heart failure Efficacy and Survival Study (EPHESUS).[101]  

Beta blockers

After an MI, all patients should be maintained on a beta blocker. Current clinical practice guidelines recommend use of one of three beta blocker agents proven to reduce mortality in patients with heart failure: metoprolol, carvedilol, or bisoprolol.

See the discussion on beta blockers in the previous section, "Non-ST-Elevation (NSTE) ACS."

Statins

All patients with an acute MI should be started on high-potency statin therapy and continued indefinitely.

Current clinical practice guidelines, high potency statins such as atorvastatin 40 mg or 80 mg, or rosuvastatin 20 mg are recommended.[8, 9, 102]

The Effects of Atorvastatin on Early Recurrent Ischemic Events In Acute Coronary Syndromes (MIRACL) trial[103] and the Atorvastatin for Reduction of Myocardial Damage During Angioplasty-Acute Coronary Syndromes (ARMYDA-ACS) trial[104] demonstrated a reduction in mortality rates in patients who received high-potency statins after acute MI as compared to placebo.

Lifestyle modifications and cardiac rehabilitation

Much emphasis has been placed on postdischarge care for patients after MI.

The American College of Cardiology/American Heart Association (ACC/AHA) guidelines highly recommend extensive patient education that includes providing easily understood and culturally sensitive written and verbal instructions about symptoms of MI, as well as how and when to seek emergency care, in addition to providing instructions about medication types, purposes, doses, frequency, and side effects.[8, 9, 105]

Several lifestyle modifications have been strongly linked to a reduction in recurrent MI and prevention of further progression of cardiovascular disease. These modification include dietary changes that adopt a low-fat and low-salt diet with dietary counseling, smoking cessation, up-to-date vaccination, and an increase in physical activity and exercise.

Referral to a well-structured cardiac rehabilitation program after MI should be considered for all patients, as this will promote patient compliance with the medical regimen and enhance lifestyle changes. In addition, aerobic exercise training within a cardiac rehabilitation program should be offered to patients after MI, with the need for an evaluation of both exercise capacity and exercise-associated risk.

The recommended frequency of regular exercise training is three or more times a week, for at least 30 minutes per session.[8, 9, 105]

Special considerations for elderly patients

Elderly patients should be treated aggressively. However, this patient population with MI is at an increased risk for developing complications, such as a greater risk of bleeding with thrombolytic therapy, but they also have the most to gain from this treatment. 

Very elderly patients should undergo primary angioplasty if available, but they should receive thrombolytic agents if excessive delay is anticipated before angioplasty can be performed.

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Complications

Complications of myocardial infarction (MI) include arrhythmic complications, mechanical complications, left ventricular aneurysm formation, ventricular septal rupture, associated right ventricular infarction, ventricular pseudoaneurysm, and other issues. See Complications of Myocardial Infarction.

Arrhythmic complications

Cardiac arrhythmias are not uncommon during and immediately after an acute MI. The incidence increases with ST-elevation MI STEMI and decreases with non-STEMI (NSTEMI). Of all patients who have an acute MI, about 90% develop some form of cardiac arrhythmias. In 25% of patients, such rhythm abnormalities occur within the first 24 hours. The risk of serious arrhythmias, such as ventricular fibrillation (VF), is greatest in the first hour and then declines thereafter. 

Most peri-infarction arrhythmias are benign and self-limited. However, aggressively monitor and treat arrhythmias that result in hypotension, increase myocardial oxygen requirements, and/or predispose the patient to malignant ventricular arrhythmias.

Mechanical complications

The three major mechanical complications of MI, each of which can cause cardiogenic shock, are as follows:

Left ventricular aneurysm formation

Left ventricular aneurysm is defined as a localized area of myocardium with abnormal outward bulging and deformation during systole and diastole. The rate of left ventricular aneurysm formation after acute MI is approximately 3-15%. Risk factors for these aneurysms after acute MI include the following:

  • Female sex
  • Total occlusion of the left anterior descending (LAD) coronary artery
  • Single-vessel coronary artery disease (CAD)
  • Absence of previous angina pectoris

Clinically, ventricular aneurysms may be recognized late, with symptoms and signs of heart failure, recurrent ventricular arrhythmias, or recurrent embolization.

Ventricular septal rupture

Ventricular septal rupture is a rare but critical complication of MI. It occurs 2-8 days after an infarction and often precipitates cardiogenic shock. The differential diagnosis of postinfarction cardiogenic shock should exclude free ventricular wall rupture and rupture of the papillary muscles.

Ventricular rupture is more common in women, patients with hypertension, and those receiving nonsteroidal anti-inflammatory drugs (NSAIDs) or steroids.

To avoid the high morbidity and mortality associated with ventricular septal rupture, patients should undergo emergent surgery.[106, 107]

Concomitant coronary artery bypass grafting (CABG) may be required. Developments in myocardial protection and improved prosthetic materials have contributed greatly to successful management of ventricular septal rupture.[108] Long-term survival can be achieved in patients who undergo prompt surgery.

Ventricular rupture occurs in the interventricular septum or the left ventricular free wall. Rupture in either location is a catastrophic event, with a greater than 90% mortality. Prompt recognition, stabilization, and surgical repair are crucial for patient survival. An echocardiogram can usually define the abnormality, and a right heart catheterization can show an oxygen saturation step-up in the case of a septal rupture.

Associated right ventricular infarction

Approximately one third of patients with inferior MI develop right ventricular infarction, which presents a special challenge because the adjunctive therapy, other than reperfusion, is somewhat different.

A right-sided electrocardiogram (ECG) with a more than 1-mm ST elevation in lead V3 R or V4 R describes a right ventricular infarction. An echocardiogram may be helpful in confirming the diagnosis.

On physical examination, signs of right-sided heart failure may be present, such as elevated jugular venous pulsation, right-sided S3, Kussmaul sign, or hypotension, but the patient may have clear lung fields.

The patient becomes volume dependent to maintain adequate left and right ventricular filling. Occasionally, dobutamine may be needed, or even an intraaortic balloon pump for hemodynamic support.

Avoid nitrates or any medications that lower preload in this setting. A pulmonary artery catheter can be helpful in guiding therapy.

For more information, see Right Ventricular Infarction.

Ventricular pseudoaneurysm

Complications of MI, such as ventricular pseudoaneurysms, are confirmed by means of echocardiography,magnetic resonance imaging (MRI), or contrast-enhanced computed tomography (CT) scanning. Imaging of a pseudoaneurysm typically shows a relatively narrow neck and a complete absence of muscle in the wall of the pseudoaneurysm—unlike a true aneurysm, which has a rim of myocardial wall that may be identified on angiography by the presence of mural vessels.

Miscellaneous complications

Left ventricular mural thrombus 

Left ventricular mural thrombus Is a well-known complication of acute anterior MI and frequently develops after left anterior wall infarction. The incidence of left ventricular mural thrombus as a complication of acute MI ranges from 20% to 40% but may reach 60% in patients with large, anterior-wall acute MIs who are not treated with anticoagulant therapy.

Left ventricular mural thrombus is associated with high risk of systemic embolization. Anticoagulant therapy may substantially decrease the rate of embolic events by 33% compared with no anticoagulation.

Pericarditis

The incidence of early pericarditis after MI is approximately 10%, and this complication usually develops within 24-96 hours after MI. Pericarditis is caused by inflammation of pericardial tissue overlying the infarcted myocardium. The clinical presentation may include severe chest pain, usually pleuritic, and pericardial friction rub.

Before the era of reperfusion, the incidence of post-MI pericarditis (Dressler syndrome) ranged from 1% to 5% after acute MI, but this rate has dramatically declined with the advent of thrombolysis and percutaneous coronary intervention (PCI).

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Future and Emerging Therapies

Local injection of progenitor cells, growth factors, or stem cells may stimulate vascular development. Investigators in the Reinfusion of Enriched Progenitor Cells And Infarct Remodeling in Acute Myocardial Infarction (REPAIR-AMI) study examined 204 patients with acute STEMI and reported greater improvement in left ventricular ejection fraction (LVEF) among patients who received intracoronary progenitor cell infusion than among those given placebo.[109]

Several smaller clinical trials have suggested that intracoronary delivery of autologous bone marrow mononuclear cells (BMCs) have improved left ventricular function when administered within the first week following MI. However, results from the LateTIME Randomized Trial that evaluated whether intracoronary delivery of autologous BMCs delivered 2-3 weeks following first MI improved global and regional left ventricular function when compared with placebo suggested little improvement with this strategy in patients with MI and left ventricular dysfunction following reperfusion with percutaenous coronary intervention (PCI).[110]

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Contributor Information and Disclosures
Author

A Maziar Zafari, MD, PhD Professor of Medicine, Emory University School of Medicine; Chief, Section of Cardiology, Atlanta Veterans Affairs Medical Center

A Maziar Zafari, MD, PhD is a member of the following medical societies: American Association for the Advancement of Science, American College of Cardiology, American Heart Association, American Society of Echocardiography, Association of Professors of Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Mahmoud H Abdou, MD Fellow, Division of Cardiology, Emory University School of Medicine

Mahmoud H Abdou, MD is a member of the following medical societies: American College of Cardiology, American College of Physicians, Libyan Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

Eric H Yang, MD Associate Professor of Medicine, Director of Cardiac Catherization Laboratory and Interventional Cardiology, Mayo Clinic Arizona

Eric H Yang, MD is a member of the following medical societies: Alpha Omega Alpha

Disclosure: Nothing to disclose.

Additional Contributors

Samer M Garas, MD, FACC Interventional Cardiologist, Administrative Physician, Diagnostic Cardiology Associates, St Vincent’s Healthcare

Samer M Garas, MD, FACC is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.

Ahmad M Jeroudi, MD Fellow in Cardiovascular Disease, Division of Cardiology, Emory University School of Medicine

Disclosure: Nothing to disclose.

Shilpa V Reddy, MD Fellow in Cardiovascular Disease, Division of Cardiology, Emory University School of Medicine

Shilpa V Reddy, MD is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.

Acknowledgements

David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital

David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Drew Evan Fenton, MD, FAAEM Private Practice

Disclosure: Nothing to disclose.

Gary Setnik, MD Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School

Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; ProceduresConsult.com Royalty Other

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Eric Vanderbush, MD, FACC Chief, Department of Internal Medicine, Division of Cardiology, Harlem Hospital Center; Clinical Assistant Professor of Cardiology, Columbia University College of Physicians and Surgeons

Eric Vanderbush, MD, FACC is a member of the following medical societies: American College of Cardiology and American Heart Association

Disclosure: Nothing to disclose.

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Acute anterior myocardial infarction.
Acute inferior myocardial infarction.
Acute posterolateral myocardial infarction.
A 53-year-old patient who had experienced 3 hours of chest pain had a 12-lead electrocardiogram performed, and the results are as shown. He was given sublingual nitroglycerin and developed severe symptomatic hypotension. His blood pressure normalized with volume resuscitation.
The right-sided leads indicate ST-segment elevations in RV<inf>3</inf> to RV<inf>5</inf>, which are consistent with a right ventricular infarct.
Timing of release of various cardiac biomarker peaks after the onset of myocardial infarction
Modified 2-dimensional (top) echocardiogram and color flow Doppler image (bottom). Apical 4-chamber views show a breach in the interventricular septum and free communication between ventricles through a large apical septum ventricular septal defect in a patient who recently had an anterior myocardial infarction.
Apical 2-chamber view depicts a large left ventricular apical thrombus with mobile extensions.
Parasternal long-axis view of the left ventricle demonstrates a large inferobasal aneurysm. Note the wide neck and base of the aneurysm.
Acute myocardial infarct. At 3 days, there is a zone of yellow necrosis surrounded by darker hyperemic borders. The arrow points to a transmural infarct in the posterior wall of the left ventricle, in this short axis slice through the left and right ventricular chambers.
Acute myocardial infarction, reperfusion type. In this case, the infarct is diffusely hemorrhagic. There is a rupture track through the center of this posterior left ventricular transmural infarct. The mechanism of death was hemopericardium.
Healing myocardial infarction, lateral left ventricle. In this heart, there is a variegated or mottled appearance to the lateral left ventricle (left). This infarct began 19 days prior to death.
Early healed myocardial infarction, anterior septum. There is a glistening gelatinous appearance to this infarction, which occurred 6 weeks prior to death, from embolization during valve surgery.
Healed myocardial infarction, anterior left ventricle. There is diffuse scarring (white) with marked thinning of the ventricle (aneurysm).
Acute myocardial infarct. The earliest change is hypereosinophilia (above) with an intense pink cytoplasm. There is no inflammation at border between the necrotic myocardium and the viable myocardium (left and below), indicating that the necrosis is about 12-24 hours in age.
Acute myocardial infarct. After 24 hours, there is a neutrophilic infiltrate at the border of the infarct. Viable myocardium is at the left, and neutrophils with apoptosis (karyorrhexis) are seen infiltrating the necrotic muscle. This patient experienced abdominal pain 35 hours prior to death.
Healing myocardial infarct. This patient died 8 days after experiencing sudden chest pain at rest. There is a large area of necrosis with hypereosinophilia of myocytes, with a rim of viable myocardium at the very bottom. At the border, there is chronic inflammation with early granulation tissue, with ingrowth of endothelial cells.
Healing myocardial infarct. At 10 days to 2 weeks, there is chronic inflammation, hemosiderin-laden macrophages, and early fibroblasts without significant collagen deposition.
Healed myocardial infarct. At 3 months, there is dense scar, which is blue on this Masson trichrome stain. This infarct was subendocardial, in the posterior left ventricle near the ventricular septum.
This is a posteroanterior view of a right ventricular endocardial activation map during ventricular tachycardia in a patient with a previous septal myocardial infarction. Earliest activation is recorded in red; late activation shows as blue to magenta. Fragmented low-amplitude diastolic local electrocardiograms were recorded adjacent to the earliest (red) breakout area, and local ablation in this scarred zone (red dots) resulted in termination and noninducibility of this previously incessant arrhythmia.
A color-enhanced angiogram of the heart left shows a plaque-induced obstruction (top center) in a major artery, which can lead to myocardial infarction (MI). MIs can precipitate heart failure.
Table 1. Absolute and Relative Contraindications to Fibrinolytic Therapy in Patients with STEMI
Absolute Contraindications Relative Contraindications
  • Any prior intracranial hemorrhage
  • Known structural cerebral vascular lesion
  • Known intracranial neoplasm (primary or metastatic)
  • Ischemic stroke within the past 3 months (except for acute stroke within 4.5 hours)
  • Suspected aortic dissection
  • Active bleeding or bleeding diathesis (excluding menses)
  • Significant closed-head or facial trauma within 3 months
  • Intracranial or intraspinal surgery within 2 months
  • Severe uncontrolled hypertension (unresponsive to emergency therapy)
  • For streptokinase (no longer marketed in the US): Prior treatment within previous 6 months
  • History of chronic, severe, poorly controlled hypertension
  • Systolic pressure >180 mm Hg or diastolic pressure >110 mm Hg
  • History of prior ischemic stroke >3 months
  • Dementia
  • Known intracranial pathology not covered in absolute contraindications
  • Traumatic or prolonged CPR (>10 minutes)
  • Recent (within 2-4 weeks) internal bleeding
  • Noncompressible vascular punctures
  • Pregnancy
  • Active peptic ulcer disease
  • Current use of anticoagulants: The higher the INR, the higher the risk of bleeding
  • For streptokinase (no longer marketed in the US): Prior exposure (>5 days previously) or prior allergic reaction to these agents
CPR = cardiopulmonary resuscitation; INR = international normalized ratio; STEMI = ST-elevation myocardial infarction; US = United States of America.



 



Table modified from 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.[9]



Table 2. Fibrinolytic Agents Used in Management of STEMI.
Fibrinolytic Agent Dose Fibrin Specificity Antigenic Patency Rate
Non-fibrin specific        
Streptokinase (no longer marketed in the US) 1.5 million units IV given over 30–60 min No Yes 60%–68%
Fibrin specific        
Tenecteplase



(TNK-tPA)



30 mg for weight <60 kg



35 mg for 60–69 kg



40 mg for 70–79 kg



45 mg for 80–89 kg



50 mg for >90 kg



++++ No 85%
Reteplase (rPA) 10-U IV boluses given 30 min apart ++ No 84%
Alteplase (tPA) Bolus 15 mg followed by infusion 0.75 mg/kg for 30 min (maximum 50 mg), then 0.5 mg/kg (maximum 35 mg) over the next 60 min; total dose not to exceed 100 mg. ++ No 73%-84%
IV = intravenous; rPA = recombinant human tissue plasminogen activator; STEMI = ST-elevation myocardial infarction; tPA = tissue plasminogen activator; US = United States of America.



 



Table modified from 2013 ACCF/AHA guidelines for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines.[9]



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