Myocardial Infarction Workup

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

Approach Considerations

The objectives of laboratory testing and imaging include the following:

  • To determine the presence or absence of myocardial infarction (MI) for diagnosis and differential diagnosis (point–of-care testing and testing in central laboratory of cardiac biomarkers)
  • To characterize the locus, nature (ST-elevation MI [STEMI] or non–ST-elevation MI [NSTEMI]), and extent of MI (ie, to estimate infarct size)
  • To detect recurrent ischemia or MI (extension of MI)
  • To detect early and late complications of MI
  • To estimate the patient's prognosis

The electrocardiograph (ECG) is the most important tool in the initial evaluation and triage of patients in whom an acute coronary syndrome (ACS) is suspected. 

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Electrocardiography

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 electrocardiogram (ECG) in a timely fashion in their recommendations for management of acute coronary syndrome (ACS) and ST-elevation myocardial infarction (MI) (STEMI). The latest guidelines from the ACC/AHA and the ESC in this regard recommend obtaining a 12-lead ECG in patients with active ongoing symptoms suggestive of acute MI within 10 minutes of presentation, with interpretation by an experienced physician.[8, 30]

The ECG is the most important tool in the initial evaluation and triage of patients in whom an ACS is suspected. According to recommendations from the AHA/ACC and the ESC, obtaining an ECG by emergency medical services (EMS) personnel at the site of first medical contact in patients with symptoms consistent with 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.[9, 44]  

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

Acute anterior myocardial infarction. Acute anterior myocardial infarction.
Acute inferior myocardial infarction. Acute inferior myocardial infarction.
Acute posterolateral myocardial infarction. Acute posterolateral myocardial infarction.
The right-sided leads indicate ST-segment elevatio 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 or protean, 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.[9, 38, 44]

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, V 4 through V 6
  • Anteroseptal - V 1 through V 3
  • Anterolateral - V 1 through V 6
  • Right ventricular - RV 4, RV 5
  • Posterior wall - R/S ratio greater than 1 in V 1 and V 2, and T-wave changes in V 1, V 8, and V 9

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.

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Laboratory Studies

Laboratory tests used in the diagnosis of myocardial infarction 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 myocardial infarction
  • Troponin levels: Troponin is a contractile protein that normally is not found in serum; it is released only when myocardial necrosis occurs.
  • Creatine kinase (CK) levels: CK-MB levels increase within 3-12 hours of the onset of chest pain, reach peak values within 24 hours, and return to baseline after 48-72 hours
  • Myoglobin levels: Myoglobin is released more rapidly from infarcted myocardium than is troponin; urine myoglobin levels rise within 1-4 hours from the onset of chest pain
  • Complete blood count
  • Chemistry profile
  • Lipid profile
  • C-reactive protein (CRP) and other inflammation markers
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Cardiac Biomarkers

The American College of Cardiology/American Heart Association (ACC/AHA) and the European Society of Cardiology (ESC) guidelines on the management of acute coronary syndrome (ACS) have stated that measurement of biomarkers of myocardial necrosis complement both the clinical assessment and 12-lead electrocardiography (ECG) in the diagnosis, risk stratification and treatment in patients with ACS and ST-elevation myocardial infarction (MI) STEMI.[8, 30]

Different cardiac biomarkers have been used to evaluate patients with suspected acute MI (ACS and STEMI). The cardiac-specific troponins I and T, creatine kinase (CK), the MB isoenzyme of creatine kinase (CK-MB), and myoglobin have been used as surrogates for myocardial necrosis.

The ACC/AHA and ESC guidelines mandate the measurement of cardiac biomarkers in all patients with suspected acute MI at presentation.[8, 30] Most recently, both guidelines have recommended the preference of measuring high-sensitivity cardiac troponin, as cardiac troponins are more sensitive and specific markers of myocardial injury than CK-MB and myoglobin. Furthermore, the AHA/ACC guidelines recommend against measuring CK-MB and myoglobin if cardiac troponins can be obtained.[8]

Cardiac troponin detection and quantification has improved dramatically over the years as advanced technology allows obtaining cardiac troponin assays running on automated platforms with a high degree of sensitivity. Although implementation of point-of-care testing (POCT) for cardiac biomarkers may seem to improve early diagnosis,[45, 46]  with an advantage of having a shorter turnaround time, this comes at the expense of substantial lower sensitivity and accuracy compared to results obtained from central laboratory testing.[47, 48, 49]

Serial measurement of cardiac troponins after the initial level is obtained at presentation, 3 to 6 hours after symptom onset, is recommended. If initial levels are negative, additional measurements beyond the 6-hour mark should be obtained.

The graph below demonstrates the timing of release of various cardiac biomarker peaks after the onset of MI.[50]

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

Troponin is a contractile protein that normally is not found in serum. It is released only when myocardial necrosis occurs. Of the three troponin subunits, two (troponin I and troponin T) are derived from the myocardium.

Highly sensitive assays can now detect cardiac troponin in patients with acute myocardial infarction (MI) with a high degree of certainty. This has led to the change in clinical practice guidelines to recommend relying solely on the results of sensitive or high-sensitive troponin I or troponin T assays for diagnostic and prognostication purposes in patients with symptoms suggestive of acute MI.[8, 51]  

Serum levels increase within 3-12 hours from the onset of chest pain, peak at 24-48 hours, and return to baseline over 5-14 days.

Measurement of troponin levels for patients with chest pain in the emergency setting has been studied extensively. Baseline measurement of troponin levels followed by serial measurements of troponin 3 hours afterward should be performed; both the absolute value of the troponin level as well as the degree of change in the troponin level should be considered. This has been associated with better performance in an accurate diagnosis of acute MI.[52, 53, 54]

For more information, see Cardiac Markers.

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Creatine Kinase-MB Isoenzyme

Although the MB isoenzyme of creatine kinase (CK-MB) is mainly found in the heart muscle, and it is released in the serum if myocardial necrosis occurs, it can be found in other tissues in the body as well. Because of this, CK-MB is less sensitive for detection of myocardial injury than troponin, and substantially more tissue injury is required for its detection. CK-MB levels may, however, be used to estimate the size/extent of myocardial infarction. 

CK-MB levels increase within 3-12 hours of the onset of chest pain, reach peak values within 24 hours, and return to baseline after 48-72 hours.

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Myoglobin

Myoglobin is a low molecular weight protein derived from the heme compound of blood. It is found in cardiac and skeletal muscle and released more rapidly from infarcted myocardium than troponin.

Urine myoglobin levels rise within 1-4 hours from the onset of chest pain.

Myoglobin levels are highly sensitive, but  they are not specific; hence, they are not commonly used currently in the work-up of acute myocardial infarction, especially if more sensitive cardiac troponin assays are available.

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B-Type Natriuretic Peptide

B-type natriuretic peptide (BNP) is a 32-amino acid polypeptide secreted by the ventricles of the heart in response to excessive stretching of cardiomyocytes.

Current practice guidelines do not recommend measurement of BNP or N-terminal pro-B-type natriuretic peptide (NT-pro-BNP) for the diagnosis of acute MI, but they do emphasize the utility of these biomarkers in risk stratification and prognostication of patients with acute MI.[35, 55]

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Other Laboratory Studies

Complete blood cell count

Obtain a complete blood cell (CBC) count if myocardial infarction is suspected in order to rule out anemia as a cause of decreased oxygen supply and prior to giving thrombolytic agents. Leukocytosis is also common, but not universal, in the setting of acute myocardial infarction.

A platelet count is necessary if a IIb/IIIa agent is considered; furthermore, the patient's white blood cell (WBC) count may be modestly elevated in the setting of myocardial infarction, signifying an acute inflammatory state. The platelet count may become dangerously low after the use of heparin because of heparin-induced thrombocytopenia (HIT). The leukocyte count may be normal initially, but it generally increases within 2 hours and peaks in 2-4 days, with predominance of polymorphonuclear leukocytes and a shift to the left. Elevations generally persist for 1-2 weeks.

Chemistry profile

In the setting of myocardial infarction, closely monitor potassium and magnesium levels. The creatinine level is also needed, prior to initiating treatment with an ACE inhibitor.

The erythrocyte sedimentation rate (ESR) rises above reference range values within 3 days and may remain elevated for weeks.

The serum lactate dehydrogenase (LDH) level rises above the reference range within 24 hours of myocardial infarction, reaches a peak within 3-6 days, and returns to the baseline within 8-12 days.

Blood oxygenation should be checked and repeatedly corrected if any clinical findings suggest hypoxemia; hypoxemia may result from pulmonary congestion, atelectasis, or ventilatory impairment secondary to complications of myocardial infarction or excessive sedation or analgesia. Fingertip oximetry may be adequate in the absence of carbon dioxide retention and may obviate puncture to assess arterial blood gases (ABGs). Such puncturing may lead to bleeding in patients being treated with thrombolytic drugs. However, normal oxygen saturation does not exclude impending respiratory failure.

Lipid profile

This may be helpful if obtained upon presentation, because levels can change after 12-24 hours of an acute illness.

C-reactive protein and other inflammation markers

Consider measuring C-reactive protein (CRP) levels and other inflammation markers upon presentation if an ACS is suspected.

Coronary artery calcium scoring 

Coronary artery calcium scoring is an emerging technique that appears to add some predictive value in identifying patients at low risk for coronary artery disease (CAD). However, in high-risk patients or in those who have established CAD, the test does not appear to be helpful at this time.[56, 57]

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Cardiac Imaging

The role of imaging in the work-up of acute myocardial infarction (MI) is broad, but the procedures are primarily used to confirm or rule out coronary artery disease (CAD). Furthermore, imaging may help to define the anatomy and degree of myocardial perfusion abnormalities. In lower-risk individuals in whom acute coronary syndrome (ACS) is suspected and who do not have serial electrocardiographic (ECG) changes or positive serial cardiac biomarker findings, current practice guidelines from the ACC/AHA and the ESC recommend some form of stress testing to help confirm the diagnosis and guide therapy.[8, 30]

For individuals with highly probable or confirmed ACS, consult with a cardiologist so that coronary angiography can be performed; this procedure can be used to definitively diagnose or rule out CAD. Based on the angiographic result and patient comorbidities, subsequent treatment recommendations can be made, which may include medical therapy, percutaneous coronary intervention (PCI), or coronary artery bypass graft (CABG) surgery.

Multidetector computed tomography (MDCT) coronary angiography should be considered as an alternative to invasive angiography to exclude ACS when there is a low to intermediate likelihood of CAD and when cardiac troponin and/or ECG results are inconclusive.[58]  This imaging modality can be used in the emergency department for triage of patients with chest pain.[59]

Alternatively, the use of myocardial perfusion imaging (MPI) with single-photon emission CT (SPECT) or positron emission tomography (PET) scanning in the emergency department for low-risk patients has a low yield for detecting ischemia. Therefore, use of SPECT or PET scanning to diagnose MI in patients with negative serial troponin results and nondiagnostic ECGs is not routinely performed.[60]

Echocardiography is highly recommended and is required to evaluate ventricular function and wall-motion abnormalities. It is also used to identify pericardial effusion, ischemic mitral regurgitation, and cardiac tamponade that may complicate acute MI.

See Acute Myocardial Infarct Imaging for more detailed information.

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Coronary Artery Calcium Scoring

Coronary artery calcium scoring is an emerging technique that appears to add some predictive value in identifying patients at low risk for coronary artery disease (CAD). However, in high-risk patients or in those who have established CAD, the test does not appear to be helpful at this time.[56, 57]

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Contributor Information and Disclosures
Author

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

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

Disclosure: Nothing to disclose.

Coauthor(s)

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

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

Disclosure: Nothing to disclose.

Specialty Editor Board

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

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

Chief Editor

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

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

Disclosure: Nothing to disclose.

Additional Contributors

Samer M Garas, MD, FACC, FSCAI Interventional Cardiologist, President, St Vincent's Health System Executive Council

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

Disclosure: Nothing to disclose.

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

Disclosure: Nothing to disclose.

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

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

Disclosure: Nothing to disclose.

Acknowledgements

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

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

Disclosure: Nothing to disclose.

Drew Evan Fenton, MD, FAAEM Private Practice

Disclosure: Nothing to disclose.

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

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

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

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

Disclosure: Medscape Salary Employment

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

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

Disclosure: Nothing to disclose.

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



 



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



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



(TNK-tPA)



30 mg for weight <60 kg



35 mg for 60–69 kg



40 mg for 70–79 kg



45 mg for 80–89 kg



50 mg for >90 kg



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



 



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



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