Approach Considerations
The objectives of laboratory testing and imaging include the following:
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To determine the presence or absence of myocardial infarction for diagnosis and differential diagnosis (point–of-care testing and testing in central laboratory of cardiac biomarkers)
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To characterize the locus, nature (STEMI or NSTEMI), and extent of myocardial infarction (ie, to estimate infarct size)
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To detect recurrent ischemia or myocardial infarction (extension of myocardial infarction)
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To detect early and late complications of myocardial infarction
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To estimate the patient's prognosis
Laboratory evaluation is particularly helpful in the presence of comorbid conditions that may affect the patient's prognosis and influence his or her care. Such comorbidities include the following:
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Diabetes
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Renal or hepatic failure
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Anemia
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Bleeding disorders
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Respiratory failure
Cardiac imaging
The role of imaging in ACSs is broad, but the procedures are primarily used to confirm or rule out coronary disease. Furthermore, it may help define the anatomy and degree of myocardial perfusion abnormalities. In lower-risk individuals in whom ACS is suspected and who do not have serial ECG changes or positive serial cardiac biomarker findings, the ACC/AHA guidelines recommend some form of stress testing to help confirm the diagnosis and guide therapy. [28]
For individuals with highly probable or confirmed ACS, consultation with a cardiologist is carried out so that coronary angiography can be performed; this procedure can be used to definitively diagnose or rule out coronary artery disease. 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 grafting (CABG) surgery.
High-risk coronary plaque may independently predict ACS in patients with acute chest pain in the emergency department (ED). [32, 33, 34] Coronary computed-tomography angiography (CCTA) may detect high-risk coronary plaque features in patients with acute chest pain and a negative initial ECG or troponin test in the ED; such plaques may predict which patients are at higher risk of imminent ACS (MI or unstable angina). [32, 33]
In addition, high-risk plaque appears to be an independent risk factor for an increased risk of ACS. The data were derived from 472 patients in the CCTA arm of the Rule Out Myocardial Infarction With Computer Assisted Tomography II (ROMICAT II) study which showed that, after adjustment for stenosis (>50%) and other cardiovascular risk factors, patients with high-risk plaques were significantly more likely to have ACS during their index hospitalization. [32, 33]
In a separate study, automated software that quantified plaque features in 56 coronary lesions improved the ability to predict lesion-specific ischemia. [33, 34] The investigators believe that this technique has the potential to noninvasively identify hemodynamically significant coronary lesions. [34]
Cardiac Biomarkers/Enzymes
The American College of Cardiology/American Heart Association (ACC/AHA) guidelines on unstable angina/NSTEMI recommend that in patients with suspected myocardial infarction, cardiac biomarkers should be measured at presentation. The guidelines recommend a total turnaround time of less than 1 hour and preferably less than 30 minutes for the cardiac biomarker measurements.
Several studies have shown that implementation of point-of-care testing (POCT) for cardiac biomarkers may improve early diagnosis as well as decrease patient length of stay. [35] Additional studies are needed to determine the relative analytic performance of different POCT assays for troponins, creatine phosphokinase–myocardial band (CPK-MB) and myoglobin alone or in combination in the current state of analytical technologies.
If initial markers are negative and have been measured within 6 hours of symptom onset, the biomarkers should be remeasured within 8-12 hours after symptom onset. Remeasuring cardiac enzyme levels at regular intervals for the first 24 hours is a reasonable approach to improving the sensitivity of detection of myocardial necrosis, and the degree of positivity can be important for prognostication. Note the graph below. [28]
Timing of release of various cardiac biomarker peaks after the onset of myocardial infarction
In addition, biomarkers alone or as part of accelerated diagnostic protocols (ADP) can reduce the number of patients with a missed diagnosis of NSTEMI who are at increased risk of major adverse cardiac events. Furthermore, such approaches can facilitate early discharge from the ED in patients who a have a low short-term risk of a major cardiac event as reported in The Asia-Pacific Evaluation of Chest Pain Trial (ASPECT). [36]
Troponin Levels
Troponin is a contractile protein that normally is not found in serum. It is released only when myocardial necrosis occurs.
Troponin levels are now considered to be the criterion standard for defining and diagnosing myocardial infarction, according to the American College of Cardiology (ACC)/American Heart Association (AHA) consensus statement on myocardial infarction. [37, 38]
Positive troponin levels are considered virtually diagnostic of myocardial infarction, according to a revised version of the ACC/AHA consensus statement, as they are without equal in combined specificity and sensitivity in this diagnosis. Reichlan et al suggest that absolute changes in troponin levels have a significantly higher diagnostic accuracy for acute myocardial infarction than relative changes. [39]
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.
Improved cardiac troponin assays offer even greater diagnostic accuracy than the standard assays do, according to a study by Reichlin et al. This is especially true for the early diagnosis of acute myocardial infarction, particularly in patients with a recent onset of chest pain, according to the investigators. [40]
Keller et al suggest that among patients with suspected acute coronary syndrome, highly sensitive troponin I assay (hsTnI) or contemporary troponin I assay (cTnI) determination 3 hours after admission for chest pain may facilitate early rule-out of acute myocardial infarction. A serial change in hsTnI or cTnI levels from admission (using the 99th percentile diagnostic cutoff value) to 3 hours postadmission may aid in early diagnosis of acute myocardial infarction. [41]
According to Hubbard et al, in patients without heart failure with marginally increased troponin levels, a low BNP level (BNP ≤80 pg/mL) cannot identify patients at low-risk for 30-day acute MI or death. [42]
MI is a strong trigger of N-terminal pro-B-type natriuretic peptide (NT-proBNP) release, and checking these levels may improve the early diagnosis and risk stratification of patients with suspected acute MI. [43]
For more information, see Use of Cardiac Markers in the Emergency Department.
Creatine Kinase Levels
The 3 CK isoenzymes are as follows:
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CK with muscle subunits (CK-MM), which is found mainly in skeletal muscle
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CK with brain subunits (CK-BB), which is found predominantly in the brain
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CK-MB, which is found mainly in the heart
Serial measurements of CK-MB isoenzyme levels were previously the standard criterion for the diagnosis 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. levels peak earlier (wash out) if reperfusion occurs. Sensitivity is approximately 95%, with high specificity. However, sensitivity and specificity are not as high as they are for troponin levels, and, as mentioned above, the trend has favored using troponins for the diagnosis of myocardial infarction.
Myoglobin levels
Myoglobin, a low-molecular-weight heme protein found in cardiac and skeletal muscle, is released more rapidly from infarcted myocardium than is troponin. Urine myoglobin levels rise within 1-4 hours from the onset of chest pain. Myoglobin levels are highly sensitive but not specific; they may be useful within the context of other studies and in the early detection of myocardial infarction in the emergency department (ED).
Other Significant 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.
Electrocardiogram
As recommended by the most recent ACC/AHA guidelines for the management of unstable angina/NSTEMI, last updated in 2007, patients with active ongoing symptoms suggestive of an acute coronary syndrome should have early risk stratification by checking cardiac enzyme levels and undergoing a 12-lead ECG within 10 minutes of presentation of the emergency department. For patients with ongoing symptoms, serial ECGs should be performed to look for dynamic changes in the ST segment. [28]
The ECG is the most important tool in the initial evaluation and triage of patients in whom an ACS is suspected. It is confirmatory of the diagnosis in approximately 80% of cases. The electrocardiographic evidence of myocardial infarction is seen in the images below.
Obtain an ECG immediately if myocardial infarction is considered or suspected. In patients with inferior myocardial infarction, record a right-sided ECG to rule out right ventricular infarct. Qualified personnel should review the ECG as soon as possible.
Electrocardiography should be performed serially upon presentation to evaluate progression and assess changes with and without pain. Obtain daily serial ECGs for the first 2-3 days and additionally as needed.
Because the symptoms of acute myocardial infarction can be subtle or protean, electrocardiography 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.
Electrocardiographic abnormalities
The diagnosis may be established with certainty when 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 myocardial infarction is difficult to differentiate from that seen in the presence of ischemia without myocardial infarction or in unrelated conditions.
ST-segment depression followed by T-wave inversion without the evolution of Q waves may result from non–Q-wave myocardial infarction or from subendocardial ischemia without myocardial infarction. True posterior-wall myocardial infarctions may cause precordial ST depression, 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.
High probability of myocardial infarction is indicated either by ST-segment elevation greater than 1 mm in 2 anatomically contiguous leads or by the presence of new Q waves. Results that indicate intermediate probability of myocardial infarction are ST-segment depression, T-wave inversion, and other nonspecific ST-T wave abnormalities. Results that indicate low probability of myocardial infarction are normal findings on ECGs; however, normal or nonspecific findings on ECGs do not exclude the possibility of myocardial infarction.
Localization based on distribution of electrocardiographic abnormalities is as follows:
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Inferior wall - II, III, aVF (See the image below.)
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.
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Lateral wall - I, aVL, V4 through V6
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Anteroseptal - V1 through V3
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Anterolateral - V1 through V6
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Right ventricular - RV4, RV5
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Posterior wall - R/S ratio greater than 1 in V1 and V2; T-wave changes (ie, upright) in V1, V8, and V9
Right ventricular myocardial infarction commonly is manifested by ST-segment elevation or Q waves detectable in right-sided precordial leads. The appearance of abnormalities in a large number of ECG leads often indicates extensive injury or concomitant pericarditis.
Anterior and anterolateral myocardial infarctions tend to involve more left ventricular myocardium than do inferior or true posterior myocardial infarctions. Hyperacute (symmetrical and often but not necessarily pointed) T waves are frequently an early sign of myocardial infarction at any locus. The characteristic electrocardiographic changes may be seen in conditions other than acute myocardial infarction. For example, patients with previous myocardial infarction and left ventricular aneurysm may have persistent ST elevation resulting from dyskinetic wall motion, rather than from acute ischemic injury. ST-segment changes may also be the result of misplaced precordial leads, hypothermia (elevated J point or Osborne waves), or hypothyroidism.
False q waves may be seen in septal leads in hypertrophic-obstructive cardiomyopathy (HOCM). They may also result from cardiac rotation.
Substantial T-wave inversion may be seen in some forms of left ventricular hypertrophy with secondary changes. The Q-T segment may be prolonged because of ischemia or hypomagnesemia. 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 myocardial infarction. Brugada electrocardiographic changes may be seen during the administration of procainamide or a beta-blocker in patients whose ECG was previously normal. Brain injuries also may trigger changes in T waves.
Convex ST-segment elevation with upright or inverted T waves is generally indicative of myocardial infarction in the appropriate clinical setting. ST depression and T-wave changes may also indicate evolution of NSTEMI.
Unfortunately, in a series of missed myocardial infarction, the failure to recognize ischemic changes is frequent. The inferior leads, in particular, must be scrutinized carefully for any evidence of ST-segment elevation by using a straight edge across the T-P segments.
Another common error is to recognize ischemic changes and then discharge the patient without definitively proving that the changes were preexistent.
Nonischemic causes of ST-segment elevation include left ventricular hypertrophy, pericarditis, ventricular-paced rhythms, hypothermia, hyperkalemia, and left ventricular aneurysm. Nonischemic causes may lead to overtreatment.
Patients with a permanent pacemaker in place may confound recognition of STEMI by 12-lead ECG due to the presence of paced ventricular contractions.
Cardiac Imaging
The roles and appropriateness of imaging in acute coronary syndromes (ACSs) are broad but primarily are used to confirm or rule out coronary disease. Furthermore, it may help define the anatomy and degree of myocardial perfusion abnormalities.
In lower-risk individuals in whom ACS is suspected, serial ECG changes are not present, and serial cardiac biomarkers are negative, the ACC/AHA guidelines recommend for some form of stress testing to help confirm diagnosis and guide therapy. [28] In individuals with highly probable or confirmed ACS, consultation to a cardiologist is made to perform a coronary angiogram to definitively diagnose or rule out coronary artery disease. Based on the angiographic result and patient comorbidities, subsequent treatment recommendations can be made: medical therapy, percutaneous coronary intervention (PCI), or coronary artery bypass grafting (CABG) surgery.
High-risk coronary plaque may independently predict ACS in patients with acute chest pain in the emergency department (ED). [32, 33, 34] Coronary computed-tomography angiography (CCTA) may detect high-risk coronary plaque features in patients with acute chest pain and a negative initial ECG or troponin test in the ED; such plaques may predict which patients are at higher risk of imminent ACS (MI or unstable angina). [32, 33]
In addition, high-risk plaque appears to be an independent risk factor for an increased risk of ACS. The data were derived from 472 patients in the CCTA arm of the Rule Out Myocardial Infarction With Computer Assisted Tomography II (ROMICAT II) study which showed that, after adjustment for stenosis (>50%) and other cardiovascular risk factors, patients with high-risk plaques were significantly more likely to have ACS during their index hospitalization. [32, 33]
In a separate study, automated software that quantified plaque features in 56 coronary lesions improved the ability to predict lesion-specific ischemia. [33, 34] The investigators believe that this technique has the potential to noninvasively identify hemodynamically significant coronary lesions. [34]
Please see Acute Myocardial Infarct Imaging for more detailed information.
Stress echocardiography
Stress echocardiography can be used to rule out myocardial ischemia in patients who come to the emergency department with chest pain, according to a retrospective study of 474 unselected consecutive patients who presented with spontaneous chest pain, a nondiagnostic ECG, and negative cardiac enzymes at baseline and after 6 and 12 hours. [44, 45]
Exercise stress echocardiography was performed in 270 patients, showing inducible ischemia in 41; dobutamine stress echocardiography was performed in 218, showing inducible ischemia in 72. Of the 113 patients with inducible ischemia, 98 underwent angiography, which revealed significant coronary artery disease in 78. [45] The 2 types of stress echocardiography yielded statistically similar sensitivities (88% and 90%, respectively), positive predictive values (90% and 70%), and negative predictive values (98% and 95%); exercise stress echocardiography was significantly more specific (98% vs 83%).
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. However, in high-risk patients or in those who have established coronary artery disease, the test does not appear to be helpful at this time. [37, 38]
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Acute anterior myocardial infarction.
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Acute inferior myocardial infarction.
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Acute posterolateral myocardial infarction.
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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.
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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.
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Timing of release of various cardiac biomarker peaks after the onset of myocardial infarction
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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.
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Apical 2-chamber view depicts a large left ventricular apical thrombus with mobile extensions.
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Parasternal long-axis view of the left ventricle demonstrates a large inferobasal aneurysm. Note the wide neck and base of the aneurysm.
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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.
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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 posterior left ventricular transmural infarct. The mechanism of death was hemopericardium.
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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.
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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.
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Healed myocardial infarction, anterior left ventricle. There is diffuse scarring (white) with marked thinning of the ventricle (aneurysm).
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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.
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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.
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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.
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Healing myocardial infarct. At 10 days to 2 weeks, there is chronic inflammation, hemosiderin-laden macrophages, and early fibroblasts without significant collagen deposition.
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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.
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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.
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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.
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- Overview
- Presentation
- DDx
- Workup
- Treatment
- Approach Considerations
- Prehospital Care
- Emergency Department Care
- In-Hospital Treatment
- Thrombolytic Therapy
- Antithrombotic Agents
- Aspirin and Antiplatelet Therapy
- Additional Medical Therapy
- Percutaneous Coronary Intervention
- Coronary Artery Bypass Graft Surgery
- No-Reflow Phenomenon
- New Treatment Strategies
- Special Concerns for Elderly Patients
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