Myocardial Infarction

Practice Essentials

Myocardial infarction (MI) (ie, heart attack) is the irreversible death (necrosis) of heart muscle secondary to prolonged lack of oxygen supply (ischemia). Approximately 1.5 million cases of MI occur annually in the United States. See the images below.

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Acute myocardial infarction, reperfusion type. In this case, the infarct is diffusely hemorrhagic. There is a rupture track through the center of this....

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Acute anterior myocardial infarction.

See Are You Missing Subtle MI Clues on ECGs? Test Your Skills, a Critical Images slideshow, to help identify a variety of electrocardiographic abnormalities.

Signs and symptoms

Patients with typical MI may have the following symptoms in the days or even weeks preceding the event (although typical STEMI may occur suddenly, without warning):

Fatigue
Chest discomfort
Malaise

Typical chest pain in acute MI has the following characteristics:

Intense and unremitting for 30-60 minutes
Substernal, and often radiates up to the neck, shoulder, and jaw, and down the left arm
Usually described as a substernal pressure sensation that also may be characterized as squeezing, aching, burning, or even sharp
In some patients, the symptom is epigastric, with a feeling of indigestion or of fullness and gas

The patient’s vital signs may demonstrate the following in MI:

The patient’s heart rate is often increased (tachycardic) secondary to a high sympathoadrenal discharge
The pulse may be irregular because of ventricular ectopy, an accelerated idioventricular rhythm, ventricular tachycardia, atrial fibrillation or flutter, or other supraventricular arrhythmias; bradyarrhythmias may be present
In general, the patient's blood pressure is initially elevated because of peripheral arterial vasoconstriction resulting from an adrenergic response to pain and ventricular dysfunction
However, with right ventricular MI or severe left ventricular dysfunction, hypotension and cardiogenic shock can be seen
The respiratory rate may be increased in response to pulmonary congestion or anxiety
Coughing, wheezing, and the production of frothy sputum may occur

See Clinical Presentation for more detail.

Diagnosis

Laboratory studies

Laboratory tests used in the diagnosis of MI include the following:

Cardiac biomarkers/enzymes: The American College of Cardiology/American Heart Association (ACC/AHA) and the European Society of Cardiology (ESC) guidelines recommend that cardiac biomarkers should be measured at presentation in patients with suspected MI, and that the only biomarker that is recommended to be used for the diagnosis of acute MI at this time is cardiac troponin due to its superior sensitivity and accuracy.^{[1, 2, 3, 4]}
Troponin levels: Troponin is a contractile protein that normally is not found in serum; it is released only when myocardial necrosis occurs
Complete blood cell count
Comprehensive metabolic panel
Lipid profile

Electrocardiography

The ECG is the most important tool in the initial evaluation and triage of patients in whom an acute coronary syndrome (ACS), such as MI, is suspected. It is confirmatory of the diagnosis in approximately 80% of cases.

Cardiac imaging

For individuals with highly probable or confirmed acute MI, coronary angiography can be used to definitively diagnose or rule out coronary artery disease.

See Workup for more detail.

Management

Prehospital care

For patients with chest pain, prehospital care includes the following:

Intravenous access, supplemental oxygen if SaO₂ is less than 90%, pulse oximetry
Immediate administration of nonenteric-coated chewable aspirin
Nitroglycerin for active chest pain, given sublingually or by spray
Telemetry and prehospital ECG, if available

Emergency department and inpatient care

Initial stabilization of patients with suspected MI and ongoing acute chest pain should include administration of sublingual nitroglycerin if patients have no contraindications to it.

The American Heart Association (AHA) recommends the initiation of beta blockers to all patients with STEMI (unless beta blockers are contraindicated).^{[1, 2]}

If STEMI is present and the patient is within 90 minutes of a PCI-capable facility, the patient should undergo emergent coronary angiography and primary PCI. If the patient is longer than 120 minutes from a PCI-capable facility, fibrinolysis should be considered.^[2]

Although patients presenting without ST-segment elevation (non-STE-ACS) are not candidates for immediate administration of thrombolytic agents, they should receive anti-ischemic therapy and may be candidates for PCI urgently or during admission.

Coronary care units have reduced early mortality rates from acute MI by approximately 50% by providing immediate defibrillation and by facilitating the implementation of beneficial interventions. These interventions include the administration of intravenous (IV) medications and therapy designed to do the following:

Limit the extent of MI
Salvage jeopardized ischemic myocardium
Recanalize infarct-related arteries

See Treatment and Medication for more detail.

References

Definitions

The third universal definition of myocardial infarction

Myocardial infarction (MI), commonly known as a heart attack, is defined pathologically as the irreversible death of myocardial cells caused by ischemia. Clinically, MI is a syndrome that can be recognized by a set of symptoms, chest pain being the hallmark of these symptoms in most cases, supported by biochemical laboratory changes, electrocardiographic (ECG) changes, or findings on imaging modalities able to detect myocardial injury and necrosis.

According to the third universal definition of MI, implemented by a joint task force from the European Society of Cardiology (ESC), American College of Cardiology (ACC) Foundation, American Heart Association (AHA), and the World Heart Federation (WHF), MI is diagnosed when either of the following two criteria are met.^[9]

1. Detection of an increase or decrease in cardiac biomarker values (preferably using cardiac troponin [cTn]) with at least one value above the 99^th percentile of the upper reference limit (URL) and with at least one of the following findings:

Symptoms of ischemia
New or presumed new significant ST-segment-T wave (ST-T) changes or new left bundle branch block (LBBB)
Development of pathologic Q waves on the ECG
Imaging evidence of new loss of viable myocardium or a new regional wall motion abnormality
Identification of an intracoronary thrombus by angiography or autopsy

2. Cardiac death with symptoms suggestive of myocardial ischemia and presumed new ischemic changes or injury or new BBB on ECG, but death occurred before cardiac biomarker levles were obtained, or before cardiac biomarker values would be increased.

Types of MI

The Joint ESC/ACCF/AHA/WHF Task Force further classified MI into 5 types on the basis of the underlying cause^[7]:

Type 1 (spontaneous MI): Related to atherosclerotic plaque rupture, ulceration, fissuring, erosion, or dissection with intraluminal thrombus in one or more of the coronary arteries, leading to decreased myocardial blood flow or distal platelet emboli and thereby resulting in myocyte necrosis. The patient may or may not have underlying obstructive coronary artery disease (CAD).
Type 2 (MI secondary to an ischemic imbalance): MI consequent to increased oxygen demand or a decreased supply (eg, coronary endothelial dysfunction, coronary artery spasm, coronary artery embolus, tachyarryhthmias/bradyarrhythmias, anemia, respiratory failure, hypertension, or hypotension).
Type 3 (MI resulting in death when biomarker values are unavailable): Sudden, unexpected cardiac death before blood samples for biomarkers could be drawn or before their appearance in the circulation.
Type 4a (MI related to percutaneous coronary intervention [PCI]): Elevation of biomarker values (cTn is preferred) to more than 5 times the 99^th percentile of the URL in patients with normal baseline values (< 99^th percentile URL) or a rise of values over 20% if the baseline values are elevated but stable or falling. In addition, any of the following are required: (1) symptoms suggestive of myocardial ischemia; (2) new ischemic ECG changes or new BBB; (3) angiographic loss of patency of a major coronary artery or a side branch or persistent slow flow or no flow or embolization; or (4) demonstration of the new loss of viable myocardium or new regional wall motion abnormality by cardiac imaging.
Type 4b (MI related to stent thrombosis): MI associated with stent thrombosis as detected by coronary angiography or autopsy in the setting of myocardial ischemia in combination with a rise and/or fall of cardiac biomarkers with at least one value above the 99^th percentile URL.
Type 5 (MI related to coronary artery bypass grafting [CABG]): Elevation of cardiac biomarker values more than 10 times the 99^th percentile URL in patients with normal baseline cTn values. In addition, either (1) new pathologic Q waves or new BBB, (2) angiographic-documented new graft or native coronary artery occlusion, or (3) evidence of new loss of viable myocardium or new regional wall motion abnormality by cardiac imaging is required.

Acute coronary syndrome

The term "acute coronary syndrome" (ACS) refers to a spectrum of conditions that occur due to acute myocardial ischemia and/or infarction as a result of an abrupt reduction in blood flow through the coronary artery circulation.

ACS is divided into two main categories, non–ST elevation (NSTE) ACS and ST-elevation MI (STEMI)

NSTE ACS

NSTE ACS is further divided into unstable angina (UA) and non–ST-elevation myocardial infraction (NSTEMI). These two conditions resemble each other very closely. UA is distinguished from NSTEMI by the absence of an elevation of cardiac biomarker levels.^[1]

STEMI

The major discriminating feature of STEMI is the presence of symptoms of myocardial ischemia/injury along with persistent ECG ST-segment elevation in addition to the presence of cardiac biomarkers.^[2]

References

Pathophysiology

Cellular effects of myocardial infarction (MI)

Myocardial injury and myocardial cell death

For the normal heart to continue to function and to steadily pump blood efficiently to meet the demands of the body, it needs to have a constant supply of oxygen and nutrients provided mainly by the coronary circulation. A condition called myocardial ischemia happens if blood supply to the myocardium does not meet the demand. If this imbalance persists, it triggers a cascade of cellular, inflammatory and biochemical events, leading eventually to the irreversible death of heart muscle cells, resulting in MI.

Evolution of MI and ventricular remodeling

The spectrum of myocardial injury depends not only on the intensity of impaired myocardial perfusion but also on the duration and the level of metabolic demand at the time of the event. Severe loss of the ability of the heart muscle cell to contract can be observed as early as within 60 seconds. Persistence of oxygen deprivation to the myocardium through the cessation of blood supply will lead to irreversible myocardial injury within 20 to 40 minutes and up to several hours, depending on several factors including the existing metabolic state of the body and presence of coronary collateral blood flow.^[10]

Typical MI initially manifests as coagulation necrosis that is ultimately followed by a healing process characterized by formation of myocardial scarring, known as myocardial fibrosis. This mechanism allows significant architectural changes to the composition, shape and contractile function of the myocardium, especially in the left ventricle, which is the major contributor to the contractile function of the heart. Eventually the left ventricle dilates and changes to a more spherical shape, in a process known as ventricular remodeling. Despite being an irreversible process, ventricular remodeling is a regulated process, therefore, specific treatment strategies and agents should be used in acute MI management in order to reduce the occurrence and severity of ventricular remodeling.^[11]

Reperfusion injury

In some occasions, restoration of blood flow to the damaged myocardium triggers further ischemic cellular damage, this paradoxical effect is known as reperfusion injury. This process involves a complex interaction between oxygen free radicals and intracellular calcium, leading to acceleration of myocardial damage and death, microvascular dysfunction and fatal arrhythmias. The role of nitric oxide (an endothelium-derived relaxing factor) as a cardioprotective agent against reperfusion injury, has been demonstrated, as nitric oxide works to inactivate oxygen free radicals, therefore, ameliorating the process of reperfusion injury.^[12]Despite the improved understanding of the process of reperfusion injury, there are no specific therapies to prevent it.

Stunned and hibernating myocardium

Stunned myocardium is a condition of transient left ventricular dysfunction following an ischemic event to the myocardium. It occurs if coronary blood flow was impaired for a brief period of time (5 to 15 minutes). Usually, stunned myocardium persists for hours or days following the re-establishment of coronary blood flow.

However, prolonged exposure of the myocardium to an ischemic state, results in an impairment of its contractile function, which can be partial or complete, this is known as myocardial hibernation, and is reversible with revascularization.

Both myocardial stunning and hibernation occur because of loss of essential metabolites required for normal myocardial contractility, such as adenosine, which is needed for adenosine triphosphate (ATP)-dependent contraction.^[13]

Plaque

The atheromatous plaque responsible for acute MI develops in a dynamic process in multiple stages. Starting with arterial intimal thickening, which consists of vascular smooth muscles with very minimal or no inflammatory cells, this process can be observed soon after birth. Subsequently, the formation of fibrous cap atheroma occurs, which has a lipid-rich necrotic core that is surrounded by fibrous tissue. Eventually, a thin-cap fibroatheroma develops, this is also known as a vulnerable plaque which is composed mainly of a large necrotic core separated from the vascular lumen by a thin fibrous cap that is infiltrated by inflammatory cells and is deficient of smooth muscle cells, making it vulnerable to rupture.^{[14, 15]}

The process of acute coronary thrombosis leading to ACS involves the pathogenic mechanism of plaque rupture, and less frequently plaque erosion.

The Brasilia Heart Study Group indicates that changes in high-density lipoprotein (HDL) during an MI may alter the antiatherogenic function of HDL to transport lipids from arterial walls.^[16] The investigators noted a simultaneous decrease in lipid transfer to HDL and in the capacity of HDL to efflux cholesterol from cells occurs in the acute period after an MI.

In a nested case-control study that evaluated the associations of plasma metabolic markers with the risks of incident MI, ischemic stroke, and intracerebral hemorrhage, investigators found positive associations of lipoproteins and lipids with MI and ischemic stroke but not with intracerebral hemorrohage, as well as positive associations between triglyceride concentrations and MI.^[17]Except for small HDL, there was also an inverse association of HDL particles with MI, and an inverse association of cholesterol in large HDL with MI and ischemic stroke. The study cohort included 912 patients with MI, 1146 with ischemic stroke, 1138 with intracerebral hemorrhage, and 1466 control subjects.^[17]

References

History

The patient’s history is critical in diagnosing myocardial infarction (MI) and sometimes may provide the only clues that lead to the diagnosis in the initial phases of the patient presentation.

Patients with typical acute MI usually present with chest pain and may have prodromal symptoms of fatigue, chest discomfort, or malaise in the days preceding the event; alternatively, typical ST-elevation MI (STEMI) may occur suddenly without warning.

The typical chest pain of acute MI usually is intense and unremitting for 30-60 minutes. It is retrosternal and often radiates up to the neck, shoulder, and jaws, and down to the left arm. The chest pain is usually described as a substernal pressure sensation that is also perceived as squeezing, aching, burning, or even sharp. In some patients, the symptom is epigastric, with a feeling of indigestion or of fullness and gas.

In some cases, patients do not recognize the chest pain, have an unusually high pain threshold, or have a disorder that impairs pain perception and results in a defective anginal warning system (eg, diabetes mellitus). In addition, some patients may have an altered mental status caused by medications or impaired cerebral perfusion. Elderly patients with preexisting altered mental status or dementia may have no recollection of recent symptoms and may have no complaints whatsoever.

MI occurs most often in the early morning hours. Mechanisms that may explain this circadian variation include the morning increase in sympathetic tone leading to increases in blood pressure, heart rate, coronary vascular tone, and myocardial contractility; the morning increase in blood viscosity, coagulability, and platelet aggregability; and the increased morning levels of serum cortisol and plasma catecholamines leading to sympathetic overactivity, thereby resulting in increased myocardial demand.^{[44, 45]}

Initial rapid evaluation should include obtaining a brief history and performing a focused physical examination. Important elements of the history, such as characteristics of the pain and important associated symptoms, and past history of or risk factors for cardiovascular disease, are used to determine the likelihood that these symptoms represent acute coronary syndrome (ACS) and to predict the likelihood of clinical outcomes.^[1]

Several risk assessment scores and clinical prediction algorithms are used to help identify patients with ACS at increased risk of adverse outcomes, such as TIMI (Thrombolysis In Myocardial Infarction) risk score, the GRACE (Global Registry of Acute Coronary Events) risk score, and the NCDR-ACTION (National Cardiovascular Data Registry-Acute Coronary Treatment and Intervention Outcomes Network) registry.^{[1, 3]}

Investigators have also proposed a novel risk scoring system that may have the potential to predict cardiovascular death in patients with acute MI; the CHA2DS2-VASc-CF takes into account cigarette smoking and a family history of coronary artery disease as risk factors.^[46] In a retrospective study (2009-2016) comprising 4373 patients with acute MI (STEMI: n = 1427; NSTEMI: n = 2946) who presented to an emergency department and underwent cardiac catherization proceures, patients who experienced cardiac death in the follow-up period had significantly higher CHA2DS2-VASc and CHA2DS2-VASc-CF scores, and were more likely to have had major adverse cardiac events and hypertension, were older and current smokers, and have a family history of coronary artery disease; this group also had a significantly lower left ventricular ejection fraction and glomerular filtration rate than those who did not experience cardiovascular death. When the cutoff score for the CHA2DS2-VASc-CF was defined as greater than 3, there was a 78.4% sensitivity and 76.4% specificity for predicting long-term cardiovascular death.^[46]

A high index of suspicion for MI should be maintained, especially when evaluating women, patients with diabetes, older patients, patients with dementia, patients with a history of heart failure, cocaine users, patients with hypercholesterolemia, and patients with a positive family history for early coronary disease (see Etiology). A positive family history includes any first-degree male relative aged 45 years or younger or any first-degree female relative aged 55 years or younger who experienced an MI or the need for coronary revascularization.

Other symptoms of myocardial infarction include the following:

Anxiety, commonly described as a sense of impending doom
Pain or discomfort in areas of the body, including the arms, left shoulder, back, neck, jaw, or stomach
Lightheadedness, with or without syncope
Cough
Nausea, with or without vomiting
Profuse sweating
Shortness of breath
Wheezing
Rapid or irregular heart rate
Fullness, indigestion, or choking feeling

The patient may recall only an episode of indigestion as an indication of myocardial infarction (see Physical Examination). In some cases, patients do not recognize chest pain, possibly because they have a stoic outlook, have an unusually high pain threshold, have a disorder that impairs function of the nervous system and that results in a defective anginal warning system (eg, diabetes mellitus), or have obtundation caused by medication or impaired cerebral perfusion. Elderly patients with preexisting altered mental status or dementia may have no recollection of recent symptoms and may have no complaints whatsoever.

References

Physical Examination

Physical examination findings for myocardial infarction (MI) can vary; one patient may be comfortable in bed, with normal examination results, whereas another patient may be in severe pain, with significant respiratory distress and a need for ventilatory support.

Patients with ongoing symptoms usually lie quietly in bed and appear pale and diaphoretic.

Vital signs

Heart rate

The patient's heart rate is often increased (tachycardia secondary to sympathoadrenal discharge). The pulse may be irregular because of ventricular ectopy, an accelerated idioventricular rhythm, ventricular tachycardia, atrial fibrillation or flutter, or other supraventricular arrhythmias.

Depressed heart rate may also be present in some cases. Bradyarrhythmias may be attributable to impaired function of the sinus node. An atrioventricular (AV) nodal block or infranodal block may also be present.

Unequal palpable pulses can be suggestive of the presence of aortic dissection, which commonly presents with chest pain radiating to the back, accompanied by a blood pressure difference of 15 mm Hg or greater between both arms and an aortic regurgitation murmur.

Blood pressure

In general, the patient's blood pressure is initially elevated (hypertension because of peripheral arterial vasoconstriction resulting from an adrenergic response to pain, anxiety, and ventricular dysfunction). However, it is not uncommon to have increased blood pressure as the precipitant of acute MI.

Alternatively, hypotension can also be seen. Usually this indicates either right ventricular MI or severe left ventricular dysfunction due to a large infarct area or impaired global cardiac contractility.

Respiratory rate

The respiratory rate may be increased in response to pulmonary congestion or anxiety.

Temperature

Fever is usually present within 24-48 hours, with the temperature curve generally parallel to the time course of elevations of creatine kinase (CK) levels in the blood. Body temperature may occasionally exceed 102°F.^{[47, 48, 49]}

Neck veins

In patients with acute inferior-wall MI with right ventricular involvement, distention of neck veins is commonly described as a sign of failure of the right ventricle. Impaired right ventricular function also leads to systemic venous hypertension, edema, and hepatomegaly.

Heart

On palpation, lateral displacement of the apical impulse, dyskinesis, a palpable S₄ gallop, and a soft S₁ sound may be found. These signs indicate diminished contractility of the compromised left ventricle.

Paradoxical splitting of S₂ may reflect the presence of left bundle-branch block or prolongation of the pre-ejection period with delayed closure of the aortic valve, despite decreased stroke volume.

A new mitral regurgitation murmur (typically holosystolic near the apex) indicates papillary muscle dysfunction or rupture, or mitral annular dilatation; it may be audible even when cardiac output is substantially decreased.

A holosystolic murmur that radiates to the midsternal border and not to the back, possibly with a palpable thrill, suggests a ventricular septal rupture; such a rupture may occur as a complication in some patients with full-thickness MIs. With resistive flow and an enlarged pressure difference, the ventricular septal defect murmur becomes harsher, louder, and higher in pitch than before.

A pericardial friction rub may be audible as a to-and-fro rasping sound; it is produced through sliding contact of inflammation-roughened surfaces.

Chest

Rales or wheezes may be auscultated; these occur secondary to pulmonary venous hypertension, which is associated with extensive acute left ventricular MI. Unilateral or bilateral pleural effusions may produce egophony at the lung bases.

Abdomen

Patients frequently develop tricuspid incompetence; hepatojugular reflux may be elicited even when hepatomegaly is not marked.

A pulsatile abdominal mass may suggest an abdominal aortic aneurysm.

Extremities

Peripheral cyanosis, edema, pallor, diminished pulse volume, delayed rise, and delayed capillary refill may indicate vasoconstriction, diminished cardiac output, and right ventricular dysfunction or failure. Pulse and neck-vein patterns may reveal other associated abnormalities, as previously discussed.

References

Electrocardiography

The electrocardiogram (ECG) is the most important tool in the initial evaluation and triage of patients in whom an acute coronary syndrome (ACS) is suspected. Obtaining an ECG by emergency medical services (EMS) personnel at the site of first medical contact in patients with symptoms consistent with ST-elevation myocardial infarction (STEMI) not only confirms the diagnosis in more than 80% of cases, but also helps to detect life-threatening arrhythmias and allows early and prompt defibrillation therapy, if indicated.^{[2, 4]}

Expert medical societies and organizations including the American College of Cardiology (ACC), the American Heart Association (AHA), and the European Society of Cardiology (ESC) have implemented the importance of obtaining a 12-lead ECG in a timely fashion (≤10 mins of presentation) in their recommendations for management of ACS and STEMI, with interpretation by an experience physician.^{[1, 3]}

Examples of ECGs showing MI are seen in the images below.

View Image

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.

ECGs should be performed serially upon presentation to evaluate progression and assess changes with and without pain.

Because the symptoms of acute MI can be subtle, an ECG should be performed on any patient who is older than age 45 years and is experiencing any form of thoracoabdominal discomfort, including new epigastric pain or nausea.

In younger patients, an ECG should be considered when suggestive symptoms are present or when risk factors exist for early coronary artery disease. Younger patients are disproportionately represented in missed cases. An ECG is a rapid, low-risk, relatively low-cost measure.

Different ECG abnormalities

ECG is an effective tool to distinguish between acute MI and the myocardial ischemia that usually precedes it, as not all patients with myocardial ischemia will develop MI.

Transitioning from ischemia to infarction results in precise sequential electrical abnormalities captured on ECG. Moreover, these changes are localized, which helps in detection of the involved region of the myocardium in most cases.

In STEMI, typical ST-segment elevation persists for hours and is followed by inversion of T waves during the first few days and by the development of Q waves. However, initial ST depression or T-wave inversion associated with MI is difficult to differentiate from that seen in the presence of ischemia without MI or other unrelated conditions. ST-segment depression followed by T-wave inversion without the evolution of Q waves may result from non–ST-elevation MI (NSTEMI) or from subendocardial ischemia without MI.

High-probability ECG features of MI are the following:

ST-segment elevation greater than 1 mm in two anatomically contiguous leads
The presence of new Q waves

Intermediate-probability ECG features of MI are the following:

ST-segment depression
T-wave inversion
Other nonspecific ST-T wave abnormalities

Low-probability ECG features of MI are normal ECG findings. However, normal or nonspecific findings on ECGs do not exclude the possibility of MI.

Special attention should be made if there is diffuse ST depression in the precordial and extremity leads associated with more than 1 mm ST elevation in lead aVR, as this may indicate stenosis of the left main coronary artery or the proximal section of the left anterior descending coronary artery.^{[2, 4, 41]}

Localization of the involved myocardium based on distribution of ECG abnormalities in MI is as follows:

Inferior wall - II, III, aVF
Lateral wall - I, aVL, V₄ through V₆
Anteroseptal - V₁ through V₃
Anterolateral - V₁ through V₆
Right ventricular - RV₄, RV₅
Posterior wall - R/S ratio greater than 1 in V₁ and V₂, and T-wave changes in V₁, V₈, and V₉

True posterior-wall MIs may cause precordial ST depressions, inverted and hyperacute T waves, or both. ST-segment elevation and upright hyperacute T waves may be evident with the use of right-sided chest leads.

Hyperacute (symmetrical and, often, but not necessarily pointed) T waves are frequently an early sign of MI at any locus.

The appearance of abnormalities in a large number of ECG leads often indicates extensive injury or concomitant pericarditis.

The characteristic ECG changes may be seen in conditions other than acute MI. For example, patients with previous MI and left ventricular aneurysm may have persistent ST elevations resulting from dyskinetic wall motion, rather than from acute myocardial injury. ST-segment changes may also be the result of misplaced precordial leads, early repolarization abnormalities, hypothermia (elevated J point or Osborne waves), or hypothyroidism.

False Q waves may be seen in septal leads in hypertrophic cardiomyopathy (HCM). They may also result from cardiac rotation.

Substantial T-wave inversion may be seen in left ventricular hypertrophy with secondary repolarization changes.

The QT segment may be prolonged because of ischemia or electrolyte disturbances.

Saddleback ST-segment elevation (Brugada epsilon waves) may be seen in leads V₁-V₃ in patients with a congenital predisposition to life-threatening arrhythmias. This elevation may be confused with that observed in acute anterior MI.

Diffuse brain injuries and hemorrhagic stroke may also trigger changes in T waves, which are usually widespread and global, involving all leads.

Convex ST-segment elevation with upright or inverted T waves is generally indicative of MI in the appropriate clinical setting. ST depression and T-wave changes may also indicate evolution of NSTEMI.

Patients with a permanent pacemaker may confound recognition of STEMI by 12-lead ECG due to the presence of paced ventricular contractions.

To summarize, non-ischemic causes of ST-segment elevation include left ventricular hypertrophy, pericarditis, ventricular-paced rhythms, hypothermia, hyperkalemia and other electrolyte imbalances, and left ventricular aneurysm.

References

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 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.

Over the last decade, inhibition of proprotein convertase subtilisin/kexin type 9 (PCSK9) has emerged as a promising target to reduce residual cardiovascular disease risk. PCSK9 is a protein that binds to low-density lipoprotein (LDL) receptors (LDLR) to promote their degradation. Monoclonal antibodies inhibit PCSK9 and thus prevent LDLR degradation. This action will increase the number of LDLRs and subsequently increase the clearance of LDL, ultimately lowering LDL-C levels.

In December 2017, the FDA approved the first PCSK9 inhibitor, evolocumab (Repatha), for the prevention of strokes, heart attacks, and coronary revascularizations.^[64]The approval was based on data from the evolocumab cardiovascular outcomes study (FOURIER). In the FOURIER clinical trial, evolocumab demonstrated significant benefits for 27,564 patients with established cardiovascular disease. The study revealed that when used in addition to optimized statin therapy, evolocumab reduced the risk of heart attack by 27%, the risk of stroke by 21%, and the risk of coronary revascularization by 22%. In addition, evolocumab showed a statistically significant 15% reduction in the risk of the primary composite endpoint, which included hospitalization for unstable angina, coronary revascularization, heart attack, stroke, or cardiovascular death.^[65]

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.^[66] 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.^[67]

2017 American Heart Association/American College of Cardiology (AHA/ACC) clinical performance and quality measures for adults with STEMI and NSTEMI

Revised STEMI and NSTEMI measures ^{[68, 69]}

Statin use for patients with AMI (acute myocardial infarction)

Evaluation of LVEF (left ventricular ejection fraction)

P2Y₁₂receptor (clopidogrel, ticagrelor, prasugret) inhibitor prescribed at discharge. All 3 medications are inhibitors of the P2Y₁₂ receptor and are recommended in addition to aspirin (as part of a dual antiplatelet regimen) to reduce recurrent ischemic events after AMI.

New STEMI/NSTEMI measures ^{[68, 69]}

Immediate angiography for resuscitated out-of-hospital cardiac arrest in STEMI patients.

Noninvasive stress testing before discharge in conservatively treated patients to detect inducible ischemia in medically treated STEMI and NSTEMI patients.

Early cardiac troponin measurement (within 6 hours of arrival).

Participation in regional or national acute myocardial infarction registry to help track and assess the outcomes, complications, and quality of care for patients with AMI.

Risk score stratification for NSTEMI patients to dictate the appropriate strategy (invasive versus ischemic-guided) and the timing of the strategy (early versus late invasive) in patients with NSTEMI.

Early invasive strategy (within 24 hours) in high-risk NSTEMI patients.

Therapeutic hypothermia for comatose STEMI patients with out-of-hospital cardiac arrest.

Aldosterone antagonist at discharge.

Inappropriate in-hospital use of nonsteroidal antiinflammatory drugs (NSAIDs) (caution against the use of these drugs after AMI).

Inappropriate prescription of prasugrel at discharge in patients with a history of prior stroke or transient ischemic attack (TIA) (caution against the use of prasugrel in patients with prior TIA/stroke, because of net clinical harm in these patients. The FDA also issued a black box warning on this.)

Inappropriate prescription of high-dose aspirin with ticagrelor at discharge (caution against the use of high-dose aspirin >100 mg among patients receiving ticagrelor. The FDA also issued a black box warning on this.)

References

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.^{[73, 74]} Current clinical practice guidelines have emphasized adopting institutional quality improvement measures to reduce total ischemic time, which is the principal determinant of outcome,^{[75, 76]} 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.^[2]

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.^[77]

For patients presenting to a PCI-capable hospital, emergent coronary angiography and primary PCI should be accomplished within 90 minutes. For patients presenting to a non–PCI-capable hospital, if they cannot be transferred to a PCI-capable hospital within 120 minutes, it is very important to rapidly assess the following to reach a decision about administration of fibrinolytic therapy:

The time from onset of symptoms
The risk of complications related to STEMI
The risk of bleeding with fibrinolysis therapy
The presence of shock or severe heart failure
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.^[2]

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.^{[2, 4, 77, 78, 79]}

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.

PCI of the noninfarct related artery (nonculprit artery) at the time of primary PCI of the culprit lesion is under active investigation. In a meta-analysis of 9 trials comprising 2991 patients with STEMI that compared complete multivessel PCI (revacularization of infarct-related and noninfarct-related arteries) to culprit-infarct-artery-only PCI, Vaidya et al noted their findings suggested complete revascularization is safe in patients with STEMI and multivessel disease.^[80]Although complete vascularization appeared to be associated with lowered rates of major adverse cardiac events, cardiac death, and repeat revascularization in this population, no reduction in all-cause mortality and nonfatal MI was observed.^[80]

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.

In patients with STEMI, the evaluation of 70% ST-segment resolution following primary PCI appears to be a 5-year independent predictor of patient-oriented composite endpoint, particularly all-cause death and any revascularization.^[81]The investigators suggested it may be used to identify those at high risk of very long-term cardiovascular events.

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.^[2]

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.

Cardiac rupture is a major lethal complication of primary PCI for treatment of patients with STEMI. In a study comprising 1663 STEMI patients who underwent PCI of whom 33 (1.98%) developed cardiac rupture, investigators noted that the SYNTAX (Synergy between percutaneous coronary intervention with Taxus and Cardiac Surgery) Score II (SSII), which is used to assess anatomic and clinical risk in patients with stable coronary artery disease, is an independent predictor for cardiac rupture, which in itself has a poor prognosis.^[82] Increasing SSII tertiles were noted to be associated with a gradual rise in cardiac rupture occurrence.

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.^{[83, 84]}

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

View Table

See Table

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.^[85]

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.

View Table

See Table

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). CABG is also the preferred revascularization strategy for patients with unprotected left main disease, but PCI with DES is a reasonable alternative treatment option in those with favorable anatomy and high surgical risk.^[86]

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,^{[2, 4]} and low molecular weight heparin (LMWH) (eg, enoxaparin^[4]) are the available options. Fondaparinux is not used in this setting because of the increased risk of catheter thrombosis.^[87]

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.^[4] UFH or LMWH may be used, with LMWH (enoxaparin) being preferred.^{[88, 89, 90]} 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.^[91]

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.

Introducing ticagrelor after myocardial infarction in patients with previous ischemic stroke is associated with lower rates of recurrent ischemic stroke, without an increase in intracranial bleeding.^[92]

The use of prasugrel is not recommended for patients with a history of stroke or transient ischemic attack (TIA).^{[93, 94, 95]}

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.^[2]

Other antiplatelet agents that may be used in STEMI management are the intravenous (IV) glycoprotein (GP) II_b/III_a receptor antagonists. The adjunctive use of GP II_b/III_a 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 II_b/III_a inhibitors is not recommended but may be considered in selected cases.^{[2, 4]}

References

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.^[1]

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.^{[31, 96]}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.^[96] 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.^[96]

Avoid short-acting nifedipine in patients who are not receiving beta blockers, as this may result in increased mortality in patients with ACS.^[96]

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.^{[1, 3]}

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.^{[97, 98]}

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.^[99]

Ticagrelor

Ticagrelor is a reversible inhibitor of the P2Y₁₂receptor 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.^[100]

A unique side effect observed in patients taking ticagrelor is dyspnea, but this is rarely severe enough to cause termination of treatment.^[101]

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.^{[93, 94, 95]}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).^[93]

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.^[96] The ESC guidelines, however, recommend the use of prasugrel upfront in patients treated for NSTE-ACS—provided there is no contraindication to its use.^[3]

Glycoprotein (GP) II_b/III_a receptor inhibitors

The Platelet Glycoprotein IIb/IIIa in Unstable Angina: Receptor Suppression Using Integrilin Therapy (PURSUIT) trial^[102]and the Randomized Efficacy Study of Tirofiban for Outcomes and Restenosis (RESTORE) trial^[103]demonstrated the efficacy of these agents in the treatment of NSTE-ACS.

The preferred GP II_b/III_a 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.^{[1, 3]}

However, GP II_b/III_a 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^{[104, 105]}; however, there is possibly a higher bleeding risk in patients undergoing PCI.^[106]These findings were demonstrated in the Efficacy and Safety of Subcutaneous Enoxaparin in Non–Q wave Coronary Events (ESSENCE) trial.^{[104, 105, 106]}

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.^[107]In the Acute Catheterization and Urgent Intervention Triage Strategy (ACUITY) Trial, the efficacy of bivalirudin was noninferior to the use of heparin plus GP II_b/III_a.^[108]

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.^{[87, 109, 110]}

References

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.^{[111, 112]}

Angiotensin-receptor blockers (ARBs) are recommended in patients who are intolerant of ACE inhibitors.^[113]

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).^[114]

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.^{[1, 2, 115]}

The Effects of Atorvastatin on Early Recurrent Ischemic Events In Acute Coronary Syndromes (MIRACL) trial^[116]and the Atorvastatin for Reduction of Myocardial Damage During Angioplasty-Acute Coronary Syndromes (ARMYDA-ACS) trial^[117]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.

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.^{[1, 2, 118]}

2019 ACC/AHA primary CVD prevention recommendations

The American College of Cardiology (ACC) and the American Heart Association (AHA) published recommendations on the primary prevention of cardiovascular disease (CVD) in March 2019.^{[119, 120]}Ten key messages and a few recommendations from the guidelines are summarized below, including an emphasis on lifestyle choices/modifications and a major shift away from the broad use of aspirin in primary prevention.

◊ Key messages

A healthy lifestyle over a lifetime is the most important way to prevent atherosclerotic vascular disease, heart failure, and atrial fibrillation.

A team-based care approach is an effective strategy for CVD prevention. Clinicians should evaluate the social determinants of health that affect individuals to inform treatment decisions.

Adults aged 40-75 years being evaluated for CVD prevention should undergo 10-year atherosclerotic CVD (ASCVD) risk estimation and have a clinician–patient risk discussion before being started on pharmacotherapy (eg, antihypertensive therapy, a statin, or aspirin). The presence or absence of additional risk factors and/or the use of coronary artery calcium (CAC) scanning can help guide decisions about preventive interventions in select individuals.

All adults should consume a healthy diet that emphasizes consumption of vegetables, fruits, nuts, whole grains, lean vegetable or animal protein, and fish, and minimizes the intake of trans fats, processed meats, refined carbohydrates, and sweetened beverages. In the setting of overweight and obesity, counseling and caloric restriction are recommended to achieve and maintain weight loss.

Adults, including those with type 2 diabetes mellitus (T2DM), should engage in at least 150 minutes per week of accumulated moderate-intensity physical activity or 75 minutes per week of vigorous-intensity physical activity.

For adults with T2DM, lifestyle changes (eg, improving dietary habits, achieving exercise recommendations) are crucial. If medication is indicated, metformin is first-line therapy, followed by consideration of a sodium-glucose cotransporter 2 inhibitor (SGLT2) or a glucagon-like peptide-1 receptor agonist (GLP-1).

At every healthcare visit, assess all adults for tobacco use. Assist tobacco users and strongly advise them to quit.

Aspirin should be used infrequently in the routine primary prevention of ASCVD because of a lack of net benefit.

Statin therapy is first-line treatment for the primary prevention of ASCVD in patients with elevated low-density lipoprotein cholesterol (LDL-C) levels (≥190 mg/dL), those with diabetes mellitus who are aged 40-75 years, and those determined to be at sufficient ASCVD risk after a clinician-patient risk discussion.

Nonpharmacologic interventions are recommended for all adults with elevated blood pressure or hypertension. When pharmacologic therapy is required, target the blood pressure to generally be below 130/80 mmHg.

◊ Select recommendations

For adults aged 40-75 years, routinely assess traditional CV risk factors and calculate their 10-year ASCVD risk with the pooled cohort equations (PCE). For those aged 20-39 years, it is reasonable to assess traditional ASCVD risk factors at least every 4-6 years.

In adults at borderline risk (5% to < 7.5% 10-year ASCVD risk) or intermediate risk (≥7.5% to < 20% 10-year ASCVD risk), using additional risk-enhancing factors is reasonable to guide decisions about preventive interventions (eg, statin therapy).

In adults at intermediate risk (≥7.5% to < 20% 10-year ASCVD risk) or selected adults at borderline risk (5% to < 7.5% 10-year ASCVD risk), if risk-based decisions for preventive interventions (eg, statin therapy) remain uncertain, measuring a CAC score to guide the clinician-patient risk discussion is reasonable, as follows:

CAC = 0: Withholding statin therapy is reasonable; reassess in 5-10 years if higher risk conditions are absent (eg, diabetes, family history of premature coronary heart disease, tobacco use).
CAC = 1-99: Initiating statin therapy is reasonable for those aged 55 years or older.
CAC is ≥100, or is in ≥75th percentile: Initiating statin therapy is reasonable.

For adults aged 20-39 years and for those aged 40-59 years whose 10-year ASCVD risk is below 7.5%, consider estimating their lifetime or 30-year ASCVD risk.

In adults at intermediate risk (≥7.5% to < 20% 10-year ASCVD risk):

If statin therapy is decided upon, use a moderate-intensity agent.
Reduce LDL-C levels by ≥30%; for optimal ASCVD risk reduction, particularly in high-risk patients (≥20% 10-year ASCVD risk), reduce LDL-C levels by ≥50%.
In the setting of risk-enhancing factors, initiating or intensifying statin therapy is favored.

In diabetic adults aged 40-75 years, regardless of the estimated 10-year ASCVD risk, moderate-intensity statin therapy is indicated. High-intensity statin therapy is reasonable for diabetic adults with multiple ASCVD risk factors to reduce LDL-C levels by 50% or more.

The maximally tolerated statin therapy is recommended in patients aged 20-75 years with LDL-C levels of 190 mg/dL (≥4.9 mmol/L) or higher.

Blood pressure (BP)-lowering agents are recommended for the following patients:

Adults with an estimated 10-year ASCVD risk of ≥10% and an average BP of ≥130/80 mmHg (for primary CVD prevention)
Adults with an estimated 10-year ASCVD risk < 10% and a BP of ≥140/90 mmHg

Low-dose aspirin (75-100 mg orally daily) guidance includes the following:

Consider for primary ASCVD prevention in select adults aged 40-70 years who have higher ASCVD risk but not an increased bleeding risk.
Do not routinely administer for primary ASCVD prevention in adults >70 years as well as in adults of any age who have a higher bleeding risk.

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.

References

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:

Ventricular free wall rupture
Ventricular septal defect
Papillary muscle rupture with severe mitral regurgitation

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 defect

Ventricular septal rupture (acute ventricular septal defect) 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 patients with anterior MI, individuals 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.^{[121, 122]}

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.^[123]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).

References

Percutaneous Coronary Intervention

Recommendations for percutaneous coronary intervention (PCI) from the 2013 update of the American College of Cardiology/American Heart Association (ACC/AHA) guidelines for management of ST-elevation myocardial infarction (STEMI),^[2] the 2014 European Society of Cardiology/European Association for Cardio-Thoracic Surgery (ESC/EACTS),^[127]and 2017 ESC guidelines for myocardial revascularization,^[70] include the following:

Primary PCI is indicated in patients with ischemic symptoms shorter than 12 hours and contraindications to thrombolytic therapy (irrespective of the time delay from FMC); and in patients with cardiogenic shock or acute severe heart failure, irrespective of the time delay from MI onset (Class I, level of evidence: A)
Primary PCI is reasonable in patients with ongoing ischemia 12-24 hours after symptom onset (Class IIb)

2015 ACC/AHA/SCAI guidelines

In 2015 the ACC/AHA and Society for Cardiovascular Angiography and Interventions (ACC/AHA/SCAI) issued revised recommendations for PCI in STEMI patients, as indicated below.^[128]

Class IIb

PCI of a noninfarct artery may be considered in selected hemodynamically stable STEMI patients with multivessel disease, either at the time of primary PCI or as a planned staged procedure. (Level of evidence: B-R)

The efficacy of selective and bailout aspiration thrombectomy in patients undergoing primary PCI remains to be established. (Level of evidence: C-LD)

Class III

PCI should not be performed in a noninfarct artery at the time of primary PCI in hemodynamically stable STEMI patients. (Level of evidence: B)

Routine aspiration thrombectomy before primary PCI is not useful. (Level of evidence: A)

The 2017 ESC guidelines recommend primary PCI of the infarct-related artery (class I, level of evidence: A), as well as new coronary angiography with PCI in patients with symptoms/signs or recurrent or remaining ischemia following primary PCI (class I, level of evidence: C).^[70] Note that in patients with coronary artery occlusion/global ischemia in the absence of characteristic ST elevation (eg, bundle branch block, ventricular pacing, hyperacute T-waves, isolated ST-depression in the anterior leads, and/or universal ST depression with ST-elevation in lead aVR) who have a clinical presentation compatible with ongoing myocardial ischemia, a primary PCI strategy (ie, urgent angiography and PCI, if indicated) is recommended.^[70]

The 2017 ESC guidelines also indicate that the following should be considered for noninfarct arteries (all class IIa)^[70]:

Routine revascularization of noninfarct arteries in those with STEMI and multivessel disease before hospital discharge (Level of evidence: A)
PCI of the noninfarct artery during the index procedure in those with cardiogenic shock (Level of evidence: C)
CABG in patients with ongoing ischemia and large areas of at-risk myocardium if the infarct artery is not amenable to PCI (Level of evidence: C)

2011 ACCF/AHA/SCAI guidelines

The 2011 ACCF/AHA/SCAI guidelines for PCI provides the following guidance with regard to the selection of bare-metal stents (BMS) or drug-eluting stents (DES)^[129]:

Before DES implantation, the need for, and duration of, dual antiplatelet therapy (DAPT) and the ability of the patient to comply with and tolerate DAPT should be discussed with the patient. (Class I, level of evidence: C)
DES are useful alternatives to bare-metal stents (BMS) to reduce the risk of restenosis in cases in which there is an elevated risk of restenosis and the patient is likely to be able to tolerate and comply with prolonged DAPT. (Class I, level of evidence: A)
BMS should be used in patients with high bleeding risk, an inability to comply with 1 year of DAPT, or anticipated invasive or surgical procedures in the next 1 year. (Class I, level of evidence: B)
DES implantation should not be performed in patients who are probably unable to tolerate or comply with a prolonged course of DAPT. (Class III, level of evidence: B)

2014 ESC/EACTS and 2017 ESC recommendations

In its 2014 update, the ESC/EACTS significantly diverged from its previous recommendations and those of ACC/AHA above. It recommends unrestricted use of new-generation DES, finding that previous concerns regarding the duration of DAPT, and the risks associated with DAPT cessation were unsubstantiated.^[127] Based on evidence of increased efficacy and safety, ESC/EACTS considers new-generation DES the default in all clinical conditions and lesion subsets where PCI is indicated.^[127]

In the 2017 ESC guidelines, the recommendations for primary PCI reiterate that stenting is preferred over balloon angioplasty and that new-generation DES are preferred over baremetal stents (both class I, level of evidence: A).^[70]In addition, if performed by an experienced radial operator, radial access is preferred over femoral access (class I, level of evidence: A).

2013 ACC/AHA guidelines

In the 2013 ACC/AHA guidelines for management of STEMI, recommendations for antithrombotic therapy in patients undergoing primary PCI include those below^[2]:

Class I

For supportive anticoagulant therapy: Unfractionated heparin (UFH), with additional boluses as needed to maintain therapeutic activated clotting time levels, accounting for whether a GP IIb/IIIa receptor antagonist has been administered (level of evidence: C); or bivalirudin with/without UFH prior therapy. (Level of evidence: B)

Class IIa

For STEMI patients at high risk of bleeding, bivalirudin monotherapy may be preferred over the combination of UFH and a GP IIb/IIIa receptor antagonist. (Level of evidence: B)

Class III

PCI should not be performed with fondaparinux as the sole antithrombin agent. (Level of evidence: B)

The 2014 ESC/EACTS and the 2017 ESC guidelines vary from ACC/AHA in that use of both bivalirudin and enoxaparin (with/without GP IIb/IIIa receptor antagonist) are given a class IIa recommendation.^{[127, 70]}

For patients undergoing PCI after receiving fibrinolytic therapy, ACC/AHA recommends the following^[2]:

Class I

For STEMI patients treated with IV UFH: Additional boluses of UFH as needed during PCI, taking into account whether a GP IIb/IIIa receptor antagonist has been administered
For STEMI patients treated with enoxaparin: If the last subcutaneous dose was administered within the previous 8 hours, no additional enoxaparin should be given; if the last subcutaneous dose was received 8-12 hours prior to the procedure, an additional dose of enoxaparin 0.3 mg/kg IV should be administered at the time of PCI.

Class III

PCI should not be performed with fondaparinux as the sole antithrombin agent. An additional anticoagulant with anti-IIa activity should be administered because of the risk of catheter thrombosis.

For patients undergoing PCI after receiving fibrinolytic therapy, ACC/AHA recommends the following^[2]:

Class I

Aspirin should be continued indefinitely. (Level of evidence: A)
Clopidogrel 300 mg loading dose should be given before or at the time of PCI to patients who did not receive a previous loading dose and who are undergoing PCI within 24 hours of receiving fibrinolytic therapy. (Level of evidence: C)
Clopidogrel 600 mg loading dose should be given before or at the time of PCI to patients who did not receive a previous loading dose and who are undergoing PCI more than 24 hours after receiving fibrinolytic therapy (Level of evidence: C)
Administer a 75-mg dose of clopidogrel after PCI (Level of evidence: C)

Class IIa

After PCI, aspirin 81 mg per day is preferable to higher maintenance doses. (Level of evidence: B)
Prasugrel 60 mg loading dose is reasonable in patients who did not receive a previous loading dose of clopidogrel at the time of administration of a fibrinolytic agent, but it should not be given sooner than 24 hours after administration of a fibrin-specific agent or 48 hours after administration of a non–fibrin-specific agent. (Level of evidence: B)
A 10-mg daily maintenance dose of prasugrel is reasonable after PCI. (Level of evidence: B)

Class III

Prasugrel is contraindicated in patients with a previous history of stroke or transient ischemic attack. (Level of evidence: B)

References

Coronary Artery Bypass Grafting

2014 ACC/AHA guidelines

The 2014 American College of Cardiology/American Heart Association (ACC/AHA) guidelines view coronary artery bypass grafting (CABG) as having a limited role in the acute phase of ST-elevation myocardial infarction (STEMI), but they provide a class I recommendation for CABG in patients whose coronary anatomy is not amenable to percutaneous coronary intervention (PCI) and who have ongoing or recurrent ischemia or cardiogenic shock.^[2]

CABG is also recommended (class I) in patients with STEMI at time of operative repair of mechanical defects such as^[2]:

Ventricular septal defect related to myocardial infarction (MI)
Papillary muscle rupture
Free wall rupture

Emergency CABG is not recommended in patients with the following conditions^[130]:

Persistent angina, a small area of viable myocardium, and hemodynamically stable
No-reflow state (successful epicardial reperfusion with unsuccessful microvascular reperfusion)

In addition, CABG is not advised for patients with ventricular tachycardia with scar and no evidence of ischemia.^[130]

The 2017 European Society of Cardiology guidelines indicate emergent CABG should be considered in patients with a patent infarct-related artery whose anatomy is unsuitable for PCI, and either a large at-risk myocardial area or with cardiogenic shock.^[70]The benefits of surgical revascularization are unclear in the setting of emergent CABG in patients who have experienced a failed PCI or have a coronary occlusion not amenable to PCI. CABG is recommended at the time of repair for those with mechanical complications associated with MI who require coronary revascularization.^[70]

ACC/AHA recommendations for emergency CABG after failed PCI include the following^[130]:

Ongoing ischemia or threatened occlusion with substantial myocardium at risk (Class I)
Hemodynamic compromise without impairment of coagulation and without a previous sternotomy (Class I)
Hemodynamic compromise with impairment of coagulation and without a previous sternotomy (Class IIa)
Hemodynamic compromise and previous sternotomy (Class IIb)
Retrieval of a foreign body (eg, fractured guidewire or stent) in a crucial location (Class IIa)

2015 AHA scientific statement

In 2015, the AHA published a scientific statement on secondary prevention after CABG with the following recommendations^[131]:

Administer aspirin within 6 hours after CABG in doses of 81 to 325 mg daily. Continue aspirin indefinitely to reduce graft occlusion and adverse cardiac events. (Class I, level of evidence: A)
After off-pump CABG, administer dual antiplatelet therapy (DAPT) for 1 year with combined aspirin (81-162 mg daily) and clopidogrel (75 mg daily) to reduce graft occlusion. (Class I, level of evidence: A)
After CABG, clopidogrel 75 mg daily is a reasonable alternative for patients who cannot take aspirin. (Class IIa, level of evidence: C)
In patients who present with acute coronary syndrome (ACS), it is reasonable to administer combination antiplatelet therapy with aspirin and either prasugrel or ticagrelor (preferred over clopidogrel) (Class IIa, level of evidence: B)
After on-pump CABG, combination therapy with aspirin and clopidogrel for 1 year may be considered in patients without recent ACS, but the benefits are not well established. (Class IIb, level of evidence: A)
Warfarin should not be routinely prescribed after CABG for graft patency unless patients have other indications for long-term antithrombotic therapy (such as atrial fibrillation [AF], venous thromboembolism, or a mechanical prosthetic valve). (Class III, level of evidence: A)
Antithrombotic alternatives to warfarin (dabigatran, apixaban, rivaroxaban) should not be routinely administered after CABG. (Class III, level of evidence: C)
CABG patients should receive statin therapy, starting in the preoperative period and restarting early after surgery. (Class I, level of evidence: A)
Administer postoperative high-intensity statin therapy (atorvastatin 40-80 mg, rosuvastatin 20-40 mg) to all CABG patients younger than 75 years. (Class I, level of evidence: A)
Administer moderate-intensity statin therapy for those patients who are intolerant of high-intensity statin therapy and for those at greater risk for drug-drug interactions (ie, patients aged >75 years). (Class I, level of evidence: A)
Pre- or post-CABG discontinuation of statin therapy is not recommended unless patients have adverse reactions to therapy. (Class III, level of evidence: B)
Administer beta-blockers as soon as possible around the time of CABG, in the absence of contraindications, to reduce the risk of postoperative AF and to facilitate blood pressure (BP) control early after surgery. (Class I, level of evidence: A)
Administer angiotensin-converting enzyme (ACE) inhibitor therapy after CABG for patients with recent MI, left ventricular (LV) dysfunction, diabetes mellitus, and chronic kidney disease. Carefully consider the patient's renal function in determining the timing of postoperative ACE inhibitor initiation and dose selection. (Class I, level of evidence: B)
Routine ACE inhibitor therapy is not recommended early after CABG among patients without a history of recent MI, LV dysfunction, diabetes mellitus, or chronic kidney disease, because it may lead to more harm than benefit and an unpredictable BP response. (Class III, level of evidence: B)
Cardiac rehabilitation is recommended for all patients after CABG, with the referral ideally performed early during the surgical hospital stay. (Class I, level of evidence: A)

References

What are the irregular vital signs that may be observed in myocardial infarction (MI, heart attack)?What is myocardial infarction (MI, heart attack), and what is the annual incidence in the US?Which symptoms are recognized as common warning signs preceding a myocardial infarction (MI, heart attack)?What are the characteristics of typical chest pain in acute myocardial infarction (MI, heart attack)?Which lab tests are useful in the diagnosis of myocardial infarction (MI, heart attack)?What is the most important diagnostic tool in the initial evaluation of suspected myocardial infarction (MI, heart attack)?What is the role of coronary angiography in suspected myocardial infarction (MI, heart attack)?What prehospital care is indicated in chest pain and suspected myocardial infarction (MI, heart attack)?Which medications should be used to stabilize patients with ongoing acute chest pain and suspected myocardial infarction (MI, heart attack)?When is emergent coronary angiography and primary PCI indicated in STEMI (heart attack), and which treatment should be considered if PCI is not available?What is the initial treatment approach in non-ST-segment elevation acute coronary syndrome (non-STE-ACS, NSTEMI, MI, heart attack)?What is the role of coronary care units, and how beneficial are they in the treatment of myocardial infarction (MI, heart attack)?What is the etiology of myocardial infarction (MI, heart attack)?What is the role of cardiac biomarkers in the evaluation of myocardial infarction (MI, heart attack)?How is myocardial infarction (MI, heart attack) associated with acute coronary syndrome (ACS)?What are the potential long-term complications of myocardial infarction (MI, heart attack)?What is the role of coronary thrombolysis and mechanical revascularization in acute myocardial infarction (MI, heart attack)?What are the benefits of late recanalization of an infarct-related artery in acute myocardial infarction (MI, heart attack)?What are the treatment options that can be used to supplement coronary thrombolysis and mechanical revascularization in the treatment of myocardial infarction (MI, heart attack)?What is a myocardial infarction (MI, heart attack), and what is the most common symptom?What are the criteria used to diagnose myocardial infarction (MI, heart attack)?What are the types of myocardial infarction (MI, heart attack), and how is each defined?What is acute coronary syndrome (ACS), and what are the two main categories of ACS?What is myocardial ischemia, and how does it ultimately lead to myocardial infarction (MI, heart attack)?What are the factors that contribute to myocardial injury, and what is the result of persistent oxygen deprivation to the myocardium?What is the role of coagulation necrosis in myocardial infarction (MI, heart attack), and how does myocardial fibrosis contribute to ventricular remodeling?What is reperfusion injury, and how might it be prevented?What are stunned myocardium and myocardial hibernation, and how do they occur?How does the atheromatous plaque responsible for acute myocardial infarction (MI, heart attack) develop, and what is its role in acute coronary syndrome (ACS)?What is the etiology of acute coronary syndrome (ACS)?What are the nonmodifiable risk factors and the modifiable risk factors for atherosclerosis?What are the causes of myocardial infarction (MI, heart attack) other than atherosclerosis?What conditions are associated with pediatric coronary artery disease, and what are the factors that contribute to acute myocardial infarction (MI, heart attack) in childhood and adolescence?What is the mortality rate associated with coronary artery disease (CAD) in the US?Which risk factors for coronary artery disease (CAD) were identified in the INTERHEART study?What is the incidence of myocardial infarction (MI, heart attack) in the US?Which groups are at highest risk of mortality due to acute myocardial infarction (MI, heart attack)?How have the mortality rates of coronary artery disease (CAD) and myocardial infarction (MI, heart attack) changed outside the US?What is the prognosis of acute myocardial infarction (MI, heart attack)?Which factors are associated with a better prognosis of myocardial infarction (MI, heart attack)?Which factors are associated with a worse prognosis of myocardial infarction (MI, heart attack)?Which baseline parameters are prognostic predictors of 30-day mortality due to acute myocardial infarction (MI, heart attack)?What is the Killip classification system and how is it used in acute myocardial infarction (MI, heart attack)?What should patients do when they experience active symptoms of acute coronary syndrome (ACS) (MI, heart attack)?How is nitroglycerin used in patients at risk for acute coronary syndrome (ACS) when they experience symptoms?What is the role of diet and exercise in the treatment of a cardiovascular event (MI, heart attack)?What educational resources are available for patients with coronary artery disease (CAD) or myocardial infarction (MI, heart attack)?What is the role of patient history in diagnosing myocardial infarction (MI, heart attack), and what are the typical presenting symptoms?When time of day does myocardial infarction (MI, heart attack) most often occur, and what mechanisms are involved?What should initial rapid evaluation for myocardial infarction (MI, heart attack) include?What is the role of risk assessments in the evaluation of acute coronary syndrome (ACS) symptoms?Which patients require a high index of suspicion of myocardial infarction (MI, heart attack)?In addition to chest pain, what other symptoms of myocardial infarction (MI, heart attack) should be considered when evaluating a patient for MI?What is the role of heart rate in the evaluation of symptoms of myocardial infarction (MI, heart attack)?How can physical exam findings vary in myocardial infarction (MI, heart attack)?What is the role of blood pressure in the evaluation of symptoms of myocardial infarction (MI, heart attack)?Why might respiratory rate be elevated in myocardial infarction (MI, heart attack)?How is body temperature associated with myocardial infarction (MI, heart attack)?What do distended neck veins indicate in the setting of myocardial infarction (MI, heart attack)?Which heart exam findings are associated with heart damage in the setting of myocardial infarction (MI, heart attack)?Which chest exam findings are associated with myocardial infarction (MI, heart attack)?Which abdominal exam findings are associated with myocardial infarction (MI, heart attack)?Which findings on physical exam of the extremities are associated with myocardial infarction (MI, heart attack)?Which GI symptoms are associated with myocardial ischemia and myocardial infarction (MI, heart attack)?Which musculoskeletal symptoms are associated with myocardial ischemia and myocardial infarction (MI, heart attack)?Why is myocardial infarction misdiagnosed more often in younger patients?How can ischemic changes be more readily recognized in myocardial infarction (MI, heart attack), and what are common nonischemic causes of ST-segment elevation?What are the differential diagnoses for Myocardial Infarction?What are the objectives of lab testing and imaging studies in myocardial infarction (MI, heart attack)?What is the most important tool in the initial evaluation of suspected acute coronary syndrome (ACS) or myocardial infarction (MI, heart attack)?Which lab tests do guidelines recommend in the workup of myocardial infarction (MI, heart attack)?What is the role of ECG in the initial evaluation of patients with suspected acute coronary syndrome (ACS) or myocardial infarction (MI, heart attack)?What are the criteria for using ECG in the workup of suspected myocardial infarction (MI, heart attack), and how often should it be performed?Why is ECG an effective tool in detecting myocardial ischemia and acute myocardial infarction (MI, heart attack)?What are the ECG features in ST-elevation 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and quantification changed over the years, and when should serial measurements of cardiac troponins be obtained?How often should cardiac troponins be measured after the initial level is obtained at presentation?What is troponin and when is it found in serum?According to guidelines, what is the role of cardiac troponin testing in the diagnosis and prognosis of acute myocardial infarction (MI, heart attack)?How long are troponin serum levels elevated in myocardial infarction (MI, heart attack), and what is the role of troponin testing in chest pain?What is B-type natriuretic peptide (BNP), and what is its role in the workup of myocardial infarction (MI, heart attack)?When should a CBC count be obtained in suspected myocardial infarction (MI, heart attack), and which conditions should be excluded prior to thrombolytic therapy?When is a platelet count necessary in the workup of suspected myocardial infarction (MI, heart attack), and what may abnormal results indicate?Which lab values should be closely monitored in patients with myocardial infarction (MI, heart attack)?What are the causes of hypoxemia in patients with myocardial infarction (MI, heart attack), and how are oxygen levels monitored?What is the role of a lipid profile in the workup of myocardial infarction (MI, heart attack)?What is the role of imaging in the work-up of acute myocardial infarction (MI, heart attack)?What is the role of coronary angiography in the workup of acute coronary syndrome (ACS), and which treatment options may be indicated by the results?Which imaging study is an alternative to invasive angiography to exclude acute coronary syndrome (ACS) when there is a low to intermediate likelihood of coronary artery disease (CAD)?What is the efficacy of myocardial perfusion imaging (MPI) with SPECT or PET scanning in myocardial infarction (MI, heart attack)?What is the role of ECG in the workup of acute myocardial infarction (MI, heart attack)?What is the first goal in the management of acute myocardial infarction (MI, heart attack), and what is the objective of the initial therapy?Why is it important to distinguish STEMI from non-STEMI in the initial evaluation of acute coronary syndrome (ACS)?What is the role of evolocumab (Repatha) in the prevention of prevention of strokes, myocardial infarction (MI), and coronary revascularization?How can morbidity and mortality from myocardial infarction (MI, heart attack) be significantly reduced, and what is the key to improved survival?Why is effective communication between EMS personnel and emergency department staff important?What prehospital care can be provided by EMS personnel in patients with myocardial infarction (MI, heart attack)?What causes most myocardial infarction-related deaths, and what can prehospital care providers do to improve outcomes?What are the secondary objectives of prehospital care by paramedical and emergency personnel in myocardial infarction (MI, heart attack)?When is prehospital fibrinolytic therapy indicated for myocardial infarction (MI, heart attack), and what is its availability?How is an initial evaluation of acute myocardial infarction (MI, heart attack) performed in the emergency department?What are the goals of the overall management plan for acute myocardial infarction (MI, heart attack)?When are oxygen saturation monitoring via pulse oximetry and supplemental oxygen indicated in acute myocardial infarction (MI, heart attack)?What is the recommended dosage of aspirin in the treatment of acute coronary syndrome (ACS), and which form of aspirin is preferred?What are nitrates, how are they used in the treatment of acute myocardial infarction (MI, heart attack), and what is the recommended dosage?What is the recommended dosage of nitrates when chest pain persists or recurs?When are nitrates contraindicated in patients with symptoms of acute coronary syndrome (ACS)?What is the drug of choice for the treatment of refractory or severe pain associated with myocardial infarction (MI, heart attack), what is the recommended dosage, and which vital signs must be monitored?Which analgesics are contraindicated in the treatment of refractory or severe pain in myocardial infarction (MI, heart attack)?What are the essential components of STEMI management, and which treatment option is emphasized in current clinical guidelines?Which aspects of emergency intervention are key in shortening total ischemic time in ST-elevation myocardial infarction (STEMI) (MI, heart attack)?When are early mechanical intervention (primary PCI) and early reperfusion strategies indicated in the treatment of acute coronary syndrome (ACS)?How readily available are primary PCI services, and how can emergency medical personnel ensure access by patients with myocardial infarction (MI, heart attack)?What is the management approach to ST-elevation myocardial infarction (STEMI) (MI, heart attack) in a hospital with, and a hospital without, primary percutaneous coronary intervention (PCI)?What is percutaneous coronary intervention (PCI), and what is its role in the treatment of ST-elevation myocardial infarction (STEMI) (MI, heart attack)?What are the guidelines for performing PCI in the treatment of ST-elevation myocardial infarction (STEMI) (MI, heart attack)?How does PCI accomplish reperfusion, and what is the role of stents in PCI?How can cardiac rupture be predicted during primary PCI for treatment of ST-segment elevation myocardial infarction (MI) (STEMI)?What is fibrinolysis, and when is it indicated in the treatment of ST-elevation myocardial infarction (STEMI) (MI, heart attack)?What adverse effect is associated with fibrinolytic therapy, and which patients are at greatest risk?Which fibrinolytic agents are available for the management of ST-elevation myocardial infarction (STEMI) (MI, heart attack)?What is the role of coronary artery bypass grafting (CABG) in the acute management of ST-elevation myocardial infarction (STEMI) (MI, heart attack)?What is the role of anticoagulant therapy in the acute management of ST-elevation myocardial infarction (STEMI) (MI, heart attack), and what are the available options?How is anticoagulation used in patients receiving fibrinolytic therapy for the treatment of ST-elevation myocardial infarction (STEMI) (MI, heart attack)?What is the role of aspirin in the treatment of ST-elevation myocardial infarction (STEMI) (MI, heart attack), and which other agents are used for dual antiplatelet therapy?Which antiplatelet agents are used in patients undergoing primary PCI for ST-elevation myocardial infarction (STEMI) (MI, heart attack)?How are antiplatelet agents used in patients receiving fibrinolytic therapy for ST-elevation myocardial infarction (STEMI) (MI, heart attack)?In addition to clopidogrel, which other antiplatelet agents may be used in ST-elevation myocardial infarction (STEMI) (MI, heart attack) management?What is ticagrelor, and what is its role in the treatment of non-ST-elevation acute coronary syndrome (unstable angina and NSTEMI)?What is the role of glycoprotein (GP) IIb/IIIa receptor inhibitors in the treatment of non-ST-elevation acute coronary syndrome (unstable angina and NSTEMI), and which agents are preferred?What is the dosage regimen of bivalirudin in the treatment of non-ST-elevation acute coronary syndrome (unstable angina and NSTEMI)?What are the key points of managing non-ST-elevation acute coronary syndrome (unstable angina and NSTEMI), and what are the alternative management strategies?Which patients with non-ST-elevation acute coronary syndrome (unstable angina and NSTEMI) are candidates for an early invasive management strategy?How do beta blockers work, and how are they used in the treatment of non-ST-elevation acute coronary syndrome (unstable angina and NSTEMI)?When are beta blockers contraindicated in the treatment of non-ST-elevation acute coronary syndrome (unstable angina and NSTEMI)?When are non-dihydropyridine calcium channel blockers indicated in the treatment of non-ST-elevation acute coronary syndrome (unstable angina and NSTEMI)?Which antiplatelet agent is preferred in non-ST-elevation acute coronary syndrome (unstable angina and NSTEMI), and what is the recommended dosage?What are the benefits of P2Y12 receptor inhibitors in the management of myocardial infarction, and which are most commonly used in the treatment of non-ST-elevation acute coronary syndrome (unstable angina and NSTEMI)?What is the treatment regimen for clopidogrel, and when is it indicated in the treatment of non-ST-elevation acute coronary syndrome (unstable angina NSTEMI)?What is the dosage regimen of prasugrel in the treatment of non-ST-elevation acute coronary syndrome (unstable angina and NSTEMI), and when is it contraindicated?Which patients with non-ST-elevation acute coronary syndrome (unstable angina and NSTEMI) should receive anticoagulant therapy?What is the dosage regimen for unfractionated heparin (UH) in the treatment of non-ST-elevation acute coronary syndrome (unstable angina and NSTEMI), and what is its disadvantage?What is the dosage regimen of low molecular weight heparin (LMWH) in the treatment of non-ST-elevation acute coronary syndrome (unstable angina and NSTEM), and what are the benefits and risks of enoxaparin?What is dosage regimen of fondaparinux in the treatment of non-ST-elevation acute coronary syndrome (unstable angina and NSTEMI), and when is it contraindicated?What are the goals of management after the initial treatment and stabilization of acute myocardial infarction (MI, heart attack)?What are the roles of ACE inhibitors, ARBs, and aldosterone blockers in the treatment of acute myocardial infarction (MI, heart attack)?What are the guidelines for the use of beta blockers in long-term treatment after acute myocardial infarction (MI, heart attack)?What are the current clinical practice guidelines for the use of long-term statin therapy in acute myocardial infarction (MI, heart attack)?Which lifestyle modifications are associated with a reduction in recurrent myocardial infarction (MI, heart attack) and prevention of further progression of cardiovascular disease?Which rehabilitation programs should be offered to patients with myocardial infarction (MI, heart attack)?What are the special considerations in treating elderly patients with myocardial infarction (MI, heart attack)?What are the complications of myocardial infarction (MI, heart attack)?What is the incidence of cardiac arrhythmias in patients with acute myocardial infarction (MI, heart attack), and what treatment is indicated?What are the major mechanical complications of myocardial infarction (MI, heart attack)?What is a left ventricular aneurysm, and what are the risk factors for these aneurysms after acute myocardial infarction (MI, heart attack)?When do ventricular septal ruptures occur in the setting of acute myocardial infarction (MI, heart attack), and which patients are at greatest risk for this complication?How can morbidity and mortality associated with ventricular septal rupture be avoided?Where do ventricular ruptures occur, and which interventions are essential to survival?How common does right ventricular infarction complicate inferior myocardial infarction (MI), and how is it diagnosed?What is the presentation of ventricular infarction in patients with myocardial infarction (MI, heart attack), which interventions are indicated, and which medications are contraindicated?How are complications of myocardial infarction (MI, heart attack) diagnosed, and how is pseudoaneurysm differentiated from a true aneurysm on imaging?What is the incidence of left ventricular mural thrombus in the setting of acute anterior myocardial infarction (MI, heart attack), and what are the associated risks and treatment?What are the incidence and clinical presentation of early pericarditis after myocardial infarction (MI, heart attack)?What future and emerging therapies exist for the treatment of myocardial infarction (MI, heart attack)?What are the guidelines for prehospital and emergency care in patients with ST-elevation myocardial infarction (STEMI) (MI, heart attack)?What is the recommended reperfusion strategy for patients with ST-elevation myocardial infarction (STEMI) (MI, heart attack) and symptom onset within the preceding 12-24 hours?What are the 2013 ACC/AHA guidelines for PCI after administration of fibrinolytic therapy in the treatment of ST-elevation myocardial infarction (STEMI) (MI, heart attack)?What are the treatment guidelines for PCI in ST-elevation myocardial infarction (STEMI) (MI, heart attack)?What are the 2015 ACC/AHA/SCAI treatment guidelines for percutaneous coronary intervention (PCI) in ST-elevation myocardial infarction (STEMI) (MI, heart attack)?What are the 2017 ESC treatment guidelines for percutaneous coronary intervention (PCI) in ST-elevation myocardial infarction (STEMI) (MI, heart attack)?What are the 2011 ACC/AHA/SCAI treatment guidelines for percutaneous coronary intervention (PCI) and bare-metal stents (BMS) or drug-eluting stents (DES) for myocardial infarction (MI, heart attack)?What are the 2014 ESC/EACTS and 2017 ESC guidelines regarding the use of drug-eluting stents (DES) in percutaneous coronary intervention (PCI) for the treatment of myocardial infarction (MI, heart attack)?What are the 2013 ACC/AHA guidelines for antithrombotic therapy in patients undergoing primary PCI for ST-elevation myocardial infarction (STEMI) (MI, heart attack)?What are the 2014 ACC/AHA guidelines for coronary artery bypass grafting (CABG) in the treatment of ST-elevation myocardial infarction (STEMI) (MI, heart attack)?What are the 2014 ACC/AHA guidelines for coronary artery bypass grafting (CABG) after failed percutaneous coronary intervention (PCI) in the treatment of myocardial infarction (MI, heart attack)?What are the 2015 AHA guidelines for secondary prevention after coronary artery bypass grafting (CABG)?What are the 2015 SCAI/ACC/HFSA/STS guidelines for mechanical circulatory support (MCS) devices in the treatment of myocardial infarction (MI, heart attack)?According to the 2013 ISHLT guidelines for acute cardiogenic shock, when is mechanical circulatory support (MCS) indicated in the treatment of myocardial infarction (MI, heart attack)?According to the 2016 ACC/AHA guidelines, which medications should be included in a dual antiplatelet therapy (DAPT) regimen in the treatment of myocardial infarction (MI, heart attack)?What are the 2016 ACC/AHA guidelines for the use of dual antiplatelet therapy (DAPT) in non-ST-elevation acute coronary syndrome (NSTE-ACS) or ST-elevation myocardial infarction (STEMI) (MI, heart attack)?Which P2Y12 inhibitor is preferred in non-ST-elevation acute coronary syndrome (NSTE-ACS) or ST-elevation myocardial infarction (STEMI), according to the 2016 ACC/AHA guidelines on duration of dual antiplatelet therapy (DAPT)?According to the 2016 ACC/AHA guidelines on dual antiplatelet therapy (DAPT), when is treatment continued for more than a year, and when is treatment stopped after 6 months in NSTE-ACS or STEMI?According to the 2016 ACC/AHA guidelines on dual antiplatelet therapy (DAPT), when is prasugrel contraindicated in coronary artery disease (CAD)?What are the goals of pharmacotherapy for myocardial infarction (MI, heart attack), and what are the goals of emergency department medical therapy for MI?Which medications in the drug class Antiplatelet Agents are used in the treatment of Myocardial Infarction?Which medications in the drug class Antithrombotic Agents are used in the treatment of Myocardial Infarction?Which medications in the drug class Glycoprotein IIb/IIIa Inhibitors are used in the treatment of Myocardial Infarction?Which medications in the drug class Vasodilators are used in the treatment of Myocardial Infarction?Which medications in the drug class Beta-adrenergic blockers are used in the treatment of Myocardial Infarction?Which medications in the drug class Angiotensin-Converting Enzyme Inhibitors are used in the treatment of Myocardial Infarction?Which medications in the drug class Angiotensin-Receptor Blockers are used in the treatment of Myocardial Infarction?Which medications in the drug class Thrombolytics are used in the treatment of Myocardial Infarction?Which medications in the drug class Analgesics are used in the treatment of Myocardial Infarction?Which medications in the drug class PCSK9 Inhibitors are used in the treatment of Myocardial Infarction?

References

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.^[2]

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.^[2]

Myocardial Infarction

Practice Essentials

Acute myocardial infarction, reperfusion type. In this case, the infarct is diffusely hemorrhagic. There is a rupture track through the center of this....

Acute anterior myocardial infarction.

Signs and symptoms

Diagnosis

Management

Background

Acute inferior myocardial infarction.

Definitions

The third universal definition of myocardial infarction

Acute coronary syndrome

Pathophysiology

Cellular effects of myocardial infarction (MI)

Plaque

Etiology

Epidemiology

United States statistics

European statistics

Cardiovascular disease in other developed countries and in developing nations

Prognosis

Killip classification

Patient Education

History

Physical Examination

Vital signs

Neck veins

Heart

Chest

Abdomen

Extremities

Approach Considerations

Electrocardiography

Acute anterior myocardial infarction.

Acute inferior myocardial infarction.

Acute posterolateral myocardial infarction.

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.

Different ECG abnormalities

Cardiac Biomarkers

Timing of release of various cardiac biomarker peaks after the onset of myocardial infarction

Cardiac Troponin

B-Type Natriuretic Peptide

Other Laboratory Studies

Complete blood cell count

Chemistry profile (comprehensive metabolic panel)

Lipid profile

Cardiac Imaging

Approach Considerations

2017 American Heart Association/American College of Cardiology (AHA/ACC) clinical performance and quality measures for adults with STEMI and NSTEMI

Prehospital Care and Initial Management

Emergency Department Care and In-Hospital Management

Triage and evaluation

Initial management

ST-Elevation Myocardial Infarction

Reperfusion

See Table

See Table

Anticoagulation

Antiplatelet agents

Non-ST-Elevation (NSTE) ACS

Beta blockers

Calcium channel blockers

Antiplatelet agents

Anticoagulant therapy

Additional Aspects of Management and Late Hospital Care

Cardioprotective medications

Lifestyle modifications and cardiac rehabilitation

Special considerations for elderly patients

Complications

Arrhythmic complications

Mechanical complications

Left ventricular aneurysm formation

Ventricular septal defect

Associated right ventricular infarction

Ventricular pseudoaneurysm

Miscellaneous complications

Future and Emerging Therapies

Guidelines Summary

Prehospital and emergency care

Percutaneous Coronary Intervention