Posted by American Heart Association, Inc. on Dec 4th 2019
2019 AHA Focused Updates Released November 14, 2019 Part 9: Acute Coronary Syndromes
2019 AHA Focused Updates Released November 14, 2019
Part 9: Acute Coronary Syndromes
Web-based Integrated 2010 & 2015 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Expand Collapse Accessible Version
The 2015 Guidelines Update marks a change in the scope of the AHA guidelines for the evaluation and management of ACS. Starting with this update, recommendations will be limited to the prehospital and emergency department phases of care. In-hospital care is addressed by guidelines for the management of myocardial infarction published jointly by the AHA and the American College of Cardiology Foundation.
Summary of Key Issues and Major Changes
Key issues with major changes in the 2015 Guidelines Update recommendations for ACS include the following:
- Prehospital ECG acquisition and interpretation
- Choosing a reperfusion strategy when prehospital
fibrinolysis is
available - Choosing a reperfusion strategy at a non–PCI-capable hospital
- Troponin to identify patients who can be safely
discharged from the
emergency department - Interventions that may or may not be of benefit if
given before
hospital arrival
Prehospital ECG Acquisition and Interpretation
2015 (New): Prehospital 12-lead ECG should be acquired early for patients with possible ACS.
2015 (New): Trained non physicians may perform ECG interpretation to determine whether or not the tracing shows evidence of STEMI.
2015 (Updated): Computer-assisted ECG interpretation may be used in conjunction with interpretation by a physician or trained provider to recognize STEMI.
2015 (Updated): Prehospital notification of the receiving hospital and/or prehospital activation of the catheterization laboratory should occur for all patients with a STEMI identified on prehospital ECG.
2010 (Old): If providers are not trained to interpret the 12-lead ECG, field transmission of the ECG or a computer report to the receiving hospital was recommended.
2010 (Old): Advance notification should be provided to the receiving hospital for patients identified as having STEMI.
Why: A 12-lead ECG is inexpensive, is easy to perform, and can rapidly provide evidence of acute ST elevation. Concern that nonphysician interpretation of ECGs could lead to either overdiagnosis with a resulting overuse of resources or, alternately, underdiagnosis, which could result in a delay to treatment, has inhibited expansion of ECG programs to EMS systems. Similar concerns existed with computer interpretation of ECGs. A review of the literature shows that when fibrinolysis is not given in the prehospital setting, early hospital notification of the impending arrival of a patient with ST elevation or prehospital activation of the catheterization laboratory reduces time to reperfusion and reduces morbidity and mortality. Because it may take time for the inexperienced provider to develop skill with 12-lead ECG interpretation, computer interpretation can be expected to increase the accuracy of interpretation when used in conjunction with trained nonphysician interpretation.
Reperfusion
2015 (New): Where prehospital fibrinolysis is available as part of the STEMI system of care and direct transport to a PCI center is available, prehospital triage and transport directly to a PCI center may be preferred because it results in a small relative decrease in the incidence of intracranial hemorrhage. There is, however, no evidence of mortality benefit of one therapy over the other.
2015 (New): In adult patients presenting with STEMI in the emergency department of a non–PCI-capable hospital, we recommend immediate transfer without fibrinolysis from the initial facility to a PCI center, instead of immediate fibrinolysis at the initial hospital with transfer only for ischemia-driven PCI.
2015 (New): When STEMI patients cannot be transferred to a PCI-capable hospital in a timely manner, fibrinolytic therapy with routine transfer for angiography (see below) may be an acceptable alternative to immediate transfer to primary PCI.
2015 (New): When fibrinolytic therapy is administered to a STEMI patient in a non–PCI-capable hospital, it may be reasonable to transport all postfibrinolysis patients for early routine angiography in the first 3 to 6 hours and up to 24 hours rather than transport postfibrinolysis patients only when they require ischemia-guided angiography.
2010 (Old): Transfer of high-risk patients who have received primary reperfusion with fibrinolytic therapy is reasonable.
Why: Fibrinolysis has been the standard of care for STEMI for more than 30 years. In the past 15 years, PPCI has become more readily available in most parts of North America and has been shown to modestly improve outcomes, compared with fibrinolysis, when PPCI can be provided in a timely manner by experienced practitioners. However, when there is a delay to PPCI, depending on the length of that delay, immediate fibrinolysis may overcome any additional benefits of PCI. Direct transfer to a PCI-capable hospital compared with prehospital fibrinolysis does not produce any difference in mortality, but transfer for PPCI does result in a small relative decrease in the incidence of intracranial hemorrhage. A fresh look at the evidence has allowed stratification of treatment recommendations according to time from symptom onset and anticipated delay to PPCI, and has enabled recommendations specifically for clinicians at non–PCI-capable hospitals. Immediate PCI after treating with fibrinolysis provides no added benefit, but routine angiography within the first 24 hours after giving fibrinolysis does reduce the incidence of reinfarction.
Troponin to Identify Patients Who Can Be Safely Discharged From the Emergency Department
2015 (New): High-sensitivity troponin T and troponin I alone measured at 0 and 2 hours (without performing clinical risk stratification) should not be used to exclude the diagnosis of ACS, but high-sensitivity troponin I measurements that are less than the 99th percentile, measured at 0 and 2 hours, may be used together with low-risk stratification (Thrombolysis in Myocardial Infarction [TIMI] score of 0 or 1, or low risk per Vancouver rule) to predict a less than 1% chance of 30-day major adverse cardiac event (MACE). Also, negative troponin I or troponin T measurements at 0 and between 3 and 6 hours may be used together with very low-risk stratification (TIMI score of 0, low risk score per Vancouver rule, North American Chest Pain score of 0 and age less than 50 years, or low-risk HEART score) to predict a less than 1% chance of 30-day MACE.
2010 (Old): If biomarkers are initially negative
within 6 hours of symptom onset, it was recommended that biomarkers should be
remeasured between 6 to 12 hours after
symptom onset.
Why: Relying on a negative troponin test result, either alone or in combination with unstructured risk assessment, results in an unacceptably high rate of MACE at 30 days. However, predictions based on negative troponin test results, combined with structured risk assessment, carry a risk of less than 1% of MACE at 30 days.
Other Interventions
When a medication reduces morbidity or mortality, prehospital compared with hospital administration of that medication allows the drug to begin its work sooner and may further decrease morbidity or mortality. However, when urban EMS response and transport times are short, the opportunity for beneficial drug effect may not be great. Moreover, adding medications increases the complexity of prehospital care, which may in turn produce negative effects.
- Adenosine diphosphate inhibition for hospital patients with suspected STEMI has been recommended for many years. Administration of an adenosine diphosphate inhibitor in the prehospital setting provides neither additional benefit nor harm compared with waiting to administer it in the hospital.
- Unfractionated heparin (UFH) administered to patients with STEMI in the prehospital setting has not been shown to provide additional benefits to giving it in the hospital. In systems where prehospital administration of UFH already occurs, it is reasonable to continue to use it. Where it is not already used in the prehospital setting, it is just as reasonable to wait to give UFH until hospital arrival.
- Before the 2010 recommendations, oxygen was routinely administered to all patients with suspected ACS regardless of oxygen saturation or respiratory condition. In 2010, weak evidence of no benefit and possible harm prompted a recommendation that supplementary oxygen was not needed for patients with ACS who had an oxyhemoglobin saturation of 94% or greater (i.e., no hypoxemia) and no evidence of respiratory distress. Further evidence that the routine administration of supplementary oxygen may be harmful, supported by a multicenter randomized controlled trial published since the 2015 systematic review,1 strengthens the recommendation that oxygen be withheld from patients with possible ACS who have a normal oxygen saturation (ie, who are without hypoxemia).
- For STEMI patients, prehospital administration of UFH or bivalirudin is reasonable.
- For suspected STEMI patients who are being transferred for PPCI, enoxaparin is a reasonable alternative to UFH.
These Web-based Integrated Guidelines incorporate the relevant recommendations from 2010 and the new or updated recommendations from 2015.
Clinicians often struggle with uncertainty and complexity in deciding which course of treatment will likely lead to an optimal outcome for an individual patient. Scientific research provides information on how patient populations have responded to treatment regimens, and this information, combined with a knowledge of the individual patient, can help guide the clinician’s decisions.
The recommendations in the 2015 American Heart Association (AHA) Guidelines Update for Cardiopulmonary Resuscitation (CPR) and Emergency Cardiovascular Care (ECC) are based on an extensive evidence review process that was begun by the International Liaison Committee on Resuscitation (ILCOR) after the publication of the ILCOR 2010 International Consensus on Cardiopulmonary Resuscitation and Emergency Cardiovascular Care Science With Treatment Recommendations2,3 and was completed in February 2015.4,5
In this in-depth evidence review process, ILCOR examined topics and then generated a prioritized list of questions for systematic review. Questions were first formulated in PICO (population, intervention, comparator, outcome) format,6 and then a search for relevant articles was performed. The evidence was evaluated by the ILCOR task forces by using the standardized methodologic approach proposed by the Grading of Recommendations Assessment, Development and Evaluation (GRADE) Working Group.7
The quality of the evidence was categorized based on the study methodologies and the 5 core GRADE domains of risk of bias, inconsistency, indirectness, imprecision, and other considerations (including publication bias). Then, where possible, consensus-based treatment recommendations were created.
To create this 2015 AHA Guidelines Update for CPR and ECC, the AHA formed 15 writing groups, with careful attention to avoid conflicts of interest, to assess the ILCOR treatment recommendations, and to write AHA treatment recommendations by using the AHA Class of Recommendation and Level of Evidence (LOE) system. The recommendations made in the 2015 Guidelines Update for CPR and ECC are informed by the ILCOR recommendations and GRADE classification, in the context of the delivery of medical care in North America. In the online version of this publication, live links are provided so the reader can connect directly to the systematic reviews on the Scientific Evidence Evaluation and Review System (SEERS) website. These links are indicated by a superscript combination of letters and numbers (eg, ACS 873).
This 2015 Guidelines Update offers recommendations for the care of patients with acute coronary syndromes (ACS). The recommendations in this Web-based Integrated Guidelines include issues that were reviewed in 2015 as well as the recommendations from the the 2010 Guidelines that are still relevant.
The ILCOR ACS Task Force did not review areas in which it found a paucity of new evidence between 2010 and 2015; therefore, the 2010 Guidelines for these unreviewed areas remain current. For example, acetylsalicylic acid administration has been shown to be of benefit in ACS and was recommended by the 2010 Guidelines.8 Acetylsalicylic acid was not reviewed by the ACS Task Force in 2015, so the recommendations from 2010 should be used. (Note: The First Aid section of this 2015 Guidelines Update makes recommendations on acetylsalicylic acid administration by nonmedical personnel—see “Part 15: First Aid”). The recommendations that were not reviewed in 2015 will either be reviewed and included in future AHA Guidelines for CPR and ECC or will be in the most recent ACC/AHA Guidelines.9-11
A table of recommendations made in this update, as well as the recommendations made in “Part 10: Acute Coronary Syndromes” of the 2010 Guidelines,8 can be found in the Appendix.
The 2015 Guidelines for ACS are directed toward practitioners who provide care for patients with suspected ACS from the time of first medical contact until disposition from the emergency department (ED). Care providers during this time may include emergency medical service (EMS) dispatchers, first responders, EMT-Bs, paramedics, nurses, physicians, and other independent practitioners.
ILCOR performed 18 systematic reviews (14 based on meta-analyses) on more than 110 relevant studies that span 40 years. Based on these reviews, the ACS Writing Group assessed the evidence and assigned an LOE by using AHA definitions. The LOE for a given intervention supports the class or “strength” of recommendation that the writing group assigned. This update uses the newest AHA Class of Recommendation and LOE classification system, which contains modifications to the Class III recommendation and introduces LOE B-R (randomized studies) and B-NR (nonrandomized studies), as well as LOE C-LD (limited data) and LOE C-EO (consensus of expert opinion). For further information, see “Part 2: Evidence Evaluation and Management of Conflicts of Interest.”
Patient and Healthcare Provider Recognition of ACS
Prompt diagnosis and treatment offers the greatest potential benefit for myocardial salvage in the first hours of STEMI; and early, focused management of unstable angina and NSTEMI reduces adverse events and improves outcome.12 Thus, it is imperative that healthcare providers recognize patients with potential ACS in order to initiate the evaluation, appropriate triage, and management as expeditiously as possible; in the case of STEMI, this recognition also allows for prompt notification of the receiving hospital and preparation for emergent reperfusion therapy. Potential delays to therapy occur during 3 intervals: from onset of symptoms to patient recognition, during prehospital transport, and during emergency department (ED) evaluation.
Patient-based delay in recognition of ACS and activation of the emergency medical services (EMS) system often constitutes the longest period of delay to treatment.13 With respect to the prehospital recognition of ACS, numerous issues have been identified as independent factors for prehospital treatment delay (ie, symptom-to-door time), including older age,14 racial and ethnic minorities,15,16 female gender,17 lower socioeconomic status,18,19 and solitary living arrangements.15,20
Hospital-based delays in ACS recognition range from nonclassical patient presentations and other confounding diagnostic issues to provider misinterpretation of patient data and inefficient in-hospital system of care.17,21-24
Symptoms of ACS may be used in combination with other important information (biomarkers, risk factors, ECG, and other diagnostic tests) in making triage and some treatment decisions in the out-of-hospital and ED settings. The symptoms of AMI may be more intense than angina and most often persist for longer periods of time (eg, longer than 15–20 minutes). The classic symptom associated with ACS is chest discomfort, but symptoms may also include discomfort in other areas of the upper body, shortness of breath, sweating, nausea, vomiting, and dizziness. Most often the patient will note chest or upper body discomfort and dyspnea as the predominant presenting symptoms accompanied by diaphoresis, nausea, vomiting, and dizziness.25-27 Isolated diaphoresis, nausea, vomiting, or dizziness are unusual predominant presenting symptoms.28 Atypical or unusual symptoms are more common in women, the elderly, and diabetic patients.29-31 The physical examination of the patient with ACS is often normal.
Figure 1: Prehospital Fibrinolytic Checklist
(Figure 1). Prehospital Fibrinolytic Checklist. Adapted from Antman EM, et al. ACC/AHA guidelines for the management of patients with ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Committee to Revise the 1999 Guidelines for the Management of Patients with Acute Myocardial Infarction). Circulation. 2004;110:e82-e292, with permission from Lippincott Williams & Wilkins. Copyright 2004, American Heart Association.
Public education campaigns increase patient awareness and knowledge of the symptoms of ACS, yet have only transient effects on time to presentation.32,33 For patients at risk for ACS (and for their families), primary care physicians and other healthcare providers should consider discussing the appropriate use of aspirin and activation of EMS system. Furthermore, an awareness of the location of the nearest hospital that offers 24-hour emergency cardiovascular care can also be included in this discussion. Previous guidelines have recommended that the patient, family member, or companion activate the EMS system rather than call their physician or drive to the hospital if chest discomfort is unimproved or worsening 5 minutes after taking 1 nitroglycerin treatment.34
Half the patients who die of ACS do so before reaching the hospital. VF or pulseless VT is the precipitating cardiac arrest rhythm in most of these deaths,35,36 and it is most likely to develop in the early phase of ACS evolution.37 Communities should develop programs to respond to cardiac emergencies that include the prompt recognition of ACS symptoms by patients and their companions as well as by healthcare and public safety providers and early activation of the EMS system. Additional features of such a program include high-quality CPR for patients in cardiac arrest (see Part 5: “Adult Basic Life Support”) and rapid access to and use of an automated external defibrillator (AED) through community AED programs (see Part 6: “Electrical Therapies”).38 Emergency dispatch center personnel should be educated in the provision of CPR instructions for lay rescuers before the arrival of EMS. EMS providers should be trained to respond to cardiovascular emergencies, including ACS and its acute complications.
Emergency dispatch center personnel can provide instructions to the patient or caller before EMS arrival.
Because aspirin should be administered as soon as possible after symptom onset to patients with suspected ACS, it is reasonable for EMS dispatchers to instruct patients with no history of aspirin allergy and without signs of active or recent gastrointestinal bleeding to chew an aspirin (160 to 325 mg) while awaiting the arrival of EMS providers.39-44 (Class IIa, LOE C)
Last Updated: Oct 2010
EMS providers should be familiar with the presentation of ACS and trained to determine the time of symptom onset. EMS providers should monitor vital signs and cardiac rhythm and be prepared to provide CPR and defibrillation if needed.
EMS providers administer oxygen during the initial assessment of patients with suspected ACS. However, there is insufficient evidence to support its routine use in uncomplicated ACS.
If the patient is dyspneic, hypoxemic, or has obvious signs of heart failure, providers should titrate therapy, based on monitoring of oxyhemoglobin saturation, to ≥94%.45 (Class I, LOE C)
Last Updated: Oct 2010
EMS providers should administer nonenteric aspirin (160* to 325* mg). (Class I, LOE BClass I, LOE C)
Last Updated: Oct 2010
The patient should chew the aspirin tablet to hasten absorption.39,46-48EMS providers should administer up to 3 nitroglycerin doses (tablets or spray) at intervals of 3 to 5 minutes. Nitrates in all forms are contraindicated in patients with initial systoloic blood pressure <90 mm Hg or ≥30 mm Hg below baseline and in patients with right ventricular infarction.49-51 Caution is advised in patients with known inferior wall STEMI, and a right-sided ECG should be performed to evaluate RV infarction. Administer nitrates with extreme caution, if at all, to patients with inferior STEMI and suspected right ventricular (RV) involvement because these patients require adequate RV preload. Nitrates are contraindicated when patients have taken a phosphodiesterase-5 (PDE-5) inhibitor within 24 hours (48 hours for tadalafil).52
Morphine is indicated in STEMI when chest discomfort is unresponsive to nitrates. (Class I, LOE C)
Last Updated: Oct 2010
Morphine should be used with caution in unstable angina (UA)/NSTEMI due to an association with increased mortality in a large registry.53 (Class IIa, LOE C)
Last Updated: Oct 2010
The efficacy of other analgesics is unknown.
Diagnostic Interventions in ACS - Updated
Prehospital 12-lead ECGs speed the diagnosis, shorten the time to reperfusion (fibrinolytics 54-61 or primary percutaneous coronary intervention [PPCI]62-69). EMS personnel should routinely acquire a 12-lead electrocardiogram (ECG) as soon as possible for all patients exhibiting signs and symptoms of ACS. The ECG may be transmitted for remote interpretation by a physician or screened for STEMI by properly trained paramedics, with or without the assistance of computer-interpretation.
Prehospital acquisition of 12-lead electrocardiograms (ECGs) has been recommended by the AHA Guidelines for CPR and Emergency Cardiovascular Care since 2000. The 2015 ILCOR systematic review examined whether acquisition of a prehospital ECG with transmission of the ECG to the hospital, notification of the hospital of the need for fibrinolysis, or activation of the catheterization laboratory changes any major outcome.
Obtaining an ECG early in the assessment of patients with possible ACS ensures that dynamic ECG changes suggestive of cardiac ischemia and ACS will be identified, even if they normalize before initial treatment.70
An early ECG may also enable ST elevation myocardial infarction (STEMI) to be recognized earlier. Acquiring a prehospital ECG and determining the presence of STEMI effectively makes the prehospital provider the first medical contact. The prehospital ECG can reliably enable identification of STEMI before arrival at the hospital,71 but if notification of the receiving facility does not occur, any benefit to prehospital STEMI recognition is lost.
Prehospital ECG acquisition coupled with hospital notification if STEMI is identified consistently reduces the time to reperfusion in-hospital (first medical contact–to–balloon time, first medical contact–to–needle time, door-to-balloon time, door-to-needle time).72To reduce time to STEMI reperfusion in-hospital, rapid transport and early treatment must occur in parallel with hospital preparation for the arriving patient.
Prehospital ECGs reduce the time to reperfusion with fibrinolytic therapy and also reduce the time to primary percutaneous coronary intervention (PPCI) and facilitate triage of STEMI patients to specific hospitals.5 Prehospital activation of the catheterization laboratory (as opposed to delaying cardiac catheterization laboratory activation until the patient arrives at the hospital) is independently associated with improved times to PPCI and reduced mortality.5
Prehospital ECG acquisition and hospital notification reduce mortality by 32% when PPCI is the reperfusion strategy (benefit is accentuated when prehospital activation occurs) and by 24% when ED fibrinolysis is the reperfusion strategy.5
2015 Recommendations - Updated
Prehospital 12-lead ECG should be acquired early for patients with possible ACS. (Class I, LOE B-NR)
Last Updated: Oct 2015
Prehospital notification of the receiving hospital (if fibrinolysis is the likely reperfusion strategy) and/or prehospital activation of the catheterization laboratory should occur for all patients with a recognized STEMI on prehospital ECG. (Class I, LOE B-NR)
Last Updated: Oct 2015Previous Versions
Implementation of 12-lead ECG diagnostic programs with concurrent medically-directed quality assurance is recommended. (Class I, LOE B)
Last Updated: Oct 2010
Prehospital personnel can accurately identify ST-segment elevation from the 12-lead ECG.56,59,73-86
If providers are not trained to interpret the 12-lead ECG, field transmission of the ECG or a computer report to the receiving hospital is recommended. (Class I, LOE B)
Last Updated: Oct 2010
ED Evaluation and Risk Stratification (Figure 1, Boxes 3 and 4)
Focused Assessment and ECG Risk Stratification
ED providers should quickly assess patients with possible ACS. Ideally within 10 minutes of ED arrival providers should obtain a targeted history while a monitor is attached to the patient and a 12-lead ECG is obtained (if not done in the prehospital setting).87 The evaluation should focus on chest discomfort, associated signs and symptoms, prior cardiac history, risk factors for ACS, and historical features that may preclude the use of fibrinolytics or other therapies.
This initial evaluation must be efficient because if the patient has STEMI, the goals of reperfusion are to administer fibrinolytics within 30 minutes of arrival (30-minute interval “door-to-drug”) or to provide PCI within 90 minutes of arrival (90-minute interval “door-to-balloon”). (Class I, LOE A)
Last Updated: Oct 2010
Potential delay during the in-hospital evaluation period may occur from door to data, from data (ECG) to decision, and from decision to drug (or PCI). These 4 major points of in-hospital therapy are commonly referred to as the “4 D’s.”88 All providers must focus on minimizing delays at each of these points. Prehospital transport time constitutes only 5% of delay to treatment time; ED evaluation constitutes 25% to 33% of this delay.89,88-91
The physical examination is performed to aid diagnosis, rule out other causes of the patient’s symptoms, and evaluate the patient for complications related to ACS. Although the presence of clinical signs and symptoms may increase suspicion of ACS, evidence does not support the use of any single sign or combination of clinical signs and symptoms alone to confirm the diagnosis.25-27,92
When the patient presents with symptoms and signs of potential ACS, the clinician uses ECG findings (Figure 2: Acute Coronary Syndromes, Box 4) to classify the patient into 1 of 3 groups:
Figure 2: Acute Coronary Syndromes Algorithm
1. ST-segment elevation or presumed new LBBB (Box 5) is characterized by ST-segment elevation in 2 or more contiguous leads and is classified as ST-segment elevation MI (STEMI). Threshold values for ST-segment elevation consistent with STEMI are J-point elevation 0.2 mV (2 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads (men ≥40 years old); J-point elevation 0.25 mV (2.5 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads (men <40 years old); J-point elevation 0.15 mV (1.5 mm) in leads V2 and V3 and 0.1 mV (1 mm) in all other leads (women).93
2. Ischemic ST-segment depression >0.5 mm (0.05 mV) or dynamic T-wave inversion with pain or discomfort (Box 9) is classified as UA/NSTEMI. Nonpersistent or transient ST-segment elevation ≥0.5 mm for <20 minutes is also included in this category. Threshold values for ST-segment depression consistent with ischemia are J-point depression 0.05 mV (-.5 mm) in leads V2 and V3 and -0.1 mV (-1 mm) in all other leads (men and women).93
3. The nondiagnostic ECG with either normal or minimally abnormal (ie, nonspecific ST-segment or T-wave changes, Box 13). This ECG is nondiagnostic and inconclusive for ischemia, requiring further risk stratification. This classification includes patients with normal ECGs and those with ST-segment deviation of <0.5 mm (0.05 mV) or T-wave inversion of ≤0.2 mV. This category of ECG is termed nondiagnostic.
The interpretation of the 12-lead ECG is a key step in this process, allowing not only for this classification but also the selection of the most appropriate diagnostic and management strategies.
Serial cardiac biomarkers are often obtained during evaluation of patients suspected of ACS. Cardiac troponin is the preferred biomarker and is more sensitive than creatine kinase isoenzyme (CK-MB). Cardiac troponins are useful in diagnosis, risk stratification, and determination of prognosis. An elevated level of troponin correlates with an increased risk of death, and greater elevations predict greater risk of adverse outcome.94
Clinicians should take into account the timing of symptom onset and the sensitivity, precision, and institutional norms of the assay, as well as the release kinetics and clearance of the measured biomarker.
A diagnosis of myocardial infarction can be made when clinical symptoms or new ECG abnormalities are consistent with ischemia and one biomarker is elevated above the 99th percentile of the upper reference limit (URL) using a test with optimal precision defined as a CV ≤10%.
There is insufficient evidence to support the use of troponin point-of-care testing (POCT) either in or out of hospital. There is also insufficient evidence to support the use of myoglobin, β-natriuretic peptide (BNP), NT-proBNP, D-dimer, C-reactive protein, ischemia-modified albumin pregnancy-associated plasma protein A (PAPP-A) or interleukin-6 in isolation.
STEMI (Figure 1, Boxes 5 Through 8)
Patients with STEMI usually have complete occlusion of an epicardial coronary artery. The primary goal of initial treatment is early reperfusion therapy through administration of fibrinolytics (pharmacological reperfusion) or PPCI (mechanical reperfusion). Providers should rapidly identify patients with STEMI and quickly screen them for indications and contraindications to fibrinolytic therapy and PCI. Patients who are ineligible for fibrinolytic therapy should be considered for transfer to a PCI facility regardless of delay.
Within a STEMI system of care, the first physician who encounters a patient with STEMI determines the need and strategy (fibrinolytic or PPCI) for reperfusion therapy (see Table 1: ST-Segment Elevation or New or Presumably New LBBB: Evaluation for Reperfusion).
If the patient meets the criteria for fibrinolytic therapy, a door-to-needle time (initiation of fibrinolytic agent) <30 minutes is recommended—the earlier the better. (Class I, LOE A)
Last Updated: Oct 2010
Routine consultation with a cardiologist or another physician is not recommended except in equivocal or uncertain cases.95,96
Consultation delays therapy and is associated with increased hospital mortality rates. (Class III, LOE B)
Last Updated: Oct 2010
Table 1: 2010 - ST-Segment Elevation or New or Presumably New LBBB: Evaluation for Reperfusion
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UA and NSTEMI (Figure 1, Boxes 9 Through 12)
Unstable angina (UA) and NSTEMI are difficult to distinguish initially. These patients usually have a partially or intermittently occluding thrombus. Both ACS syndromes may present with similar symptoms and ECG. Clinical features can correlate with the dynamic nature of clot formation and degradation (eg, waxing and waning clinical symptoms). The ECG will demonstrate a range of findings short of diagnostic ST-segment deviation; these ECG presentations include normal, minimal nonspecific ST-segment/T-wave changes, and significant ST-segment depression and T-wave inversions.
An elevated biomarker separates NSTEMI from UA and has incremental value in addition to the ECG. Elevation of cardiac troponin indicates increased risk for major adverse cardiac events and benefit from an invasive strategy. Cardiac troponins indicate myocardial necrosis, although numerous conditions other than ACS may cause elevated biomarkers (eg, myocarditis, heart failure, and pulmonary embolism).
Management strategies for UA/NSTEMI include antiplatelet, antithrombin, and antianginal therapy and are based on risk stratification. Fibrinolysis is contraindicated in this heterogenous group of patients and may be harmful; an invasive strategy is indicated in patients with positive biomarkers or unstable clinical features.
The Process of Risk Stratification
Diagnosis of ACS and risk stratification become an integrated process in patients presenting to an acute care setting with possible ACS and an initially nondiagostic evaluation. This nondiagnostic evaluation includes a normal or nondiagnostic 12-lead ECG and normal serum cardiac biomarker concentrations. The majority of these patients will not be experiencing an ACS, but many may have underlying CAD or other clinical features putting them at subsequent risk for major adverse cardiac events over the course of a few days to several months.
A major goal of the risk stratification process is to identify those patients who do not appear to have high-risk features on initial assessment but are found, through the course of the diagnostic process, to have ACS and clinically significant CAD. This strategy allows physicians to target patients who would benefit from guidelines-based ACS therapies while avoiding unnecessary procedural and pharmacological risks (eg, anticoagulation therapy and invasive cardiac catheterization) in patients with low risk for major adverse cardiac events.
Although the diagnosis of ACS is important and will help to guide immediate therapy, the estimation of risk for major adverse cardiac events in the immediate, short-term, and long-term time frames helps the physician determine the urgency in completing the diagnostic workup not just for ACS but also for CAD. Many patients can be managed in the outpatient setting once it is determined that they are at very low risk for short-term (30 days) major adverse cardiac events.
ACC/AHA Guidelines recommend that all patients be risk stratified for the selection of an initial management strategy and site of care.89 A well-recognized approach is the one initially proposed and later refined by Braunwald and colleagues and published in ACC/AHA Guidelines on the Management of Patients With Unstable Angina and Non-ST Segment Elevation MI.97-101 This approach is based on a combination of historical, clinical, laboratory, and ECG variables and answers two questions: what is the likelihood that signs and symptoms represent ACS secondary to obstructive CAD, and what is the likelihood of an adverse clinical outcome?
Table 2102 is a modified version of Braunwald and colleagues’ approach updated over several publications.99,101,103 Patients are initially risk-stratified according to the likelihood that symptoms are due to unstable CAD. Patients at intermediate or high risk for CAD are further classified by their risk of major adverse cardiac events. This second classification is useful for prospectively identifying patients at intermediate or high risk who can benefit from an invasive strategy and more aggressive pharmacology with antiplatelet and antithrombin agents. Other risk stratification schemes include the TIMI, GRACE, and PURSUIT risk scores developed for short- and longer-term risk assessment.104-108 Stratification tools cannot be used to determine discharge from the ED.
Table 2: 2010 - Likelihood That Signs and Symptoms Represent ACS Secondary to CAD
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Recommendations concerning TIMI Risk Scores were not reviewed in 2015. Please refer to the 2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromes or the 2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction for information on this topic.
Indicators for Early Invasive Strategies
Risk stratification (Figure 2, Boxes 9, 13, 14, 15) helps the clinician identify patients with non–ST-elevation ACS who should be managed with an early invasive strategy versus a selectively invasive one. Early coronary angiography may allow the clinician to determine whether patients are appropriate candidates for revascularization with PCI or coronary artery bypass grafting (CABG).
The 2007 Focused Update of the ACC/AHA/SCAI 2005 Guideline Update for Percutaneous Coronary Intervention contains the following recommendations related to the selection of early invasive PCI versus conservative strategies.
1. An early invasive PCI strategy is indicated for patients with non–ST-elevation ACS who have no serious comorbidity and who have coronary lesions amenable to PCI and an elevated risk for clinical events. (Class I, LOE A)
Last Updated: Oct 2010
(See Table 3 and Section 3.3 of the ACC/AHA 2007 UA/NSTEMI Guidelines).
2. An early invasive strategy (ie, diagnostic angiography with intent to perform revascularization) is indicated in non–ST-elevation ACS patients who have refractory angina or hemodynamic or electric instability (without serious comorbidities or contraindications to such procedures). (Class I, LOE B)
Last Updated: Oct 2010
3. In initially stabilized patients, an initially conservative (ie, a selectively invasive) strategy may be considered as a treatment strategy for non–ST-elevation ACS patients (without serious comorbidities or contraindications to such procedures) who have an elevated risk for clinical events including those with abnormal troponin elevations. (Class IIb, LOE B)
Last Updated: Oct 2010
4. The decision to implement an initial conservative (versus initial invasive) strategy in these patients may be made by considering physician and patient preference. (Class IIb, LOE C)
Last Updated: Oct 2010
Table 3: 2010 - Selection of Initial Treatment Strategy for Patients With Non-ST-Elevation ACS: Invasive Versus Conservative Strategy
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Normal or Nondiagnostic ECG Changes (Figure 1, Boxes 13 Through 17)
The majority of patients with normal or nondiagnostic ECGs do not have ACS. Patients in this category with ACS are most often at low or intermediate risk. The physician’s goal involves risk stratification (see above) to provide appropriate diagnostic or treatment strategies for an individual patient. These strategies then target patients at increased risk for benefit while avoiding risk (eg, anticoagulation therapy and invasive cardiac catheterization) in patients with low or minimal risk.
Chest pain observation protocols may be employed in a dedicated space (ie, a physical chest pain unit [CPU]) or throughout an ED/hospital (ie, virtual CPU). These chest pain observation protocols are a rapid system of patient assessment that should generally include a history and physical examination, a period of observation, serial electrocardiography, and serial measurement of serum cardiac markers. In selected patients, an evaluation for inducible myocardial ischemia or anatomic coronary disease after AMI is excluded when indicated. Eleven randomized trials109-119 suggest that these protocols may be used to improve accuracy in identifying patients requiring inpatient admission or further diagnostic testing and, thereby, reduce length of stay, rate of hospital admission, and health care costs while improving quality of life measures.
In patients with suspicion for ACS, normal initial biomarkers, and nonischemic ECG, chest pain observation protocols may be recommended as a safe and effective strategy for evaluating patients in the ED. (Class I, LOE A)
Last Updated: Oct 2010
There is no direct evidence demonstrating that CPUs/observation protocols reduce adverse cardiovascular outcomes, including mortality for patients presenting with possible ACS, normal serum cardiac biomarkers, and a nondiagnostic ECG.
Advanced Testing to Detect Coronary Ischemia and CAD
For ED/CPU patients who are suspected of having ACS, have nonischemic ECG’s and negative biomarkers, a noninvasive test for inducible myocardial ischemia or anatomic evaluation of the coronary arteries (eg, computed tomography [CT] angiography, cardiac magnetic resonance, myocardial perfusion imaging, stress echocardiography) can be useful in identifying patients suitable for discharge from the ED. (Class IIa, LOE B)
Last Updated: Oct 2010
This strategy may be considered to increase diagnostic accuracy for ACS thereby decreasing costs, length of stay, time to diagnosis, and can provide valuable short-term and long-term prognostic information of future major cardiac events.
Myocardial perfusion scintigraphy (MPS) has a high negative predictive value (NPV) for ruling out ACS; 99% in patients presenting to the ED with acute chest pain, nondiagnostic ECG, and negative cardiac markers.
MPS can also be used for risk stratification, especially in low- to intermediate-likelihood of cardiac events according to traditional cardiac markers.120-123 (Class IIa, LOE B)
Last Updated: Oct 2010
MPS is best utilized in patients with an intermediate probability or LOE of risk stratification.
The use of multidetector computed tomography (MDCT) angiography (64-slice scanner) after presentation to the ED with chest discomfort, a nondiagnostic ECG, and negative cardiac biomarkers has also been demonstrated to have high sensitivity and specificity for CAD and ACS.124,125
The use of MDCT angiography for selected low-risk patients can be useful to allow for safe early discharge from the ED.126-128 (Class IIa, LOE B)
Last Updated: Oct 2010
It is reasonable to consider both the exposure to radiation and iodinated contrast agents when using MDCT angiography and myocardial perfusion imaging. Little evidence is available to support the use of MRI in this patient population.
Safety of Discharge and Risk of Major Adverse Cardiac Events After Discharge From the ED/CPU
The final step in the CPU risk-stratification process is the decision to discharge or admit the patient. No simple clinical decision rule is adequate and appropriate to identify ED chest discomfort patients with suspected ACS who can be safely discharged from the ED.129
The use of inpatient-derived risk scoring systems are useful for prognosis* but are not recommended to identify patients who may be safely discharged from the ED. (*Class I, LOE A; **Class III, LOE C)
Last Updated: Oct 2010
The Bayesian process of serial assignment of pretest risk, diagnostic testing, and reclassification into post-test risk levels based on the test results is the most reliable method to identify patients at the lowest risk for short term major adverse cardiac events and those patients in need of further evaluation for underlying CAD.
Patients at low and intermediate clinical risk for ACS who have remained stable in the CPU and have negative serial ECGs, serial cardiac biomarker measurements, and noninvasive physiological or anatomic testing for ACS have very low rates of major adverse cardiac events at 30 days from ED discharge.130-134 Patients younger than 40 years-of-age with nonclassical presentations and no significant past medical history have very low short-term rates of major adverse cardiac events when serial biomarkers and 12-lead ECGs are normal. These patients may be discharged directly from the ED/CPU if appropriate outpatient testing can be arranged within 72 hours.89,130-132,134-136 Any system that attempts to facilitate outpatient testing should include mechanisms to ensure patient access to outpatient clinics and testing facilities and should consider nonmedical barriers to discharge from the ED that may require inpatient admission.
Computer-Assisted ECG STEMI Interpretation - Updated ACS 559
The identification of STEMI in patients with suspected STEMI is often made on clinical grounds in combination with ECG findings as interpreted by a physician. The 2015 ILCOR systematic review addressed whether computer-assisted ECG interpretation improves identification of STEMI while minimizing unnecessary intervention.
Studies examined both underdiagnosis (false-negative results) and overdiagnosis (false-positive results)137,138 or overdiagnosis alone139-143 by computer ECG interpretation. There was wide variation in the proportion of false-positive results (0% to 42%) and of false-negative results (22% to 42%).
These variations in accuracy seemed to occur because different ECG machines use different algorithms and because the computer interpretations are compared variously with interpretation by cardiologists, emergency physicians, and discharge diagnosis of STEMI. Moreover, the sensitivity and specificity of the test will differ depending on the prevalence of STEMI.
Both studies that examined false-negative results suggest that computer interpretation of ECG tracing produces unacceptably high rates of false-negative results in the identification of STEMI. A few studies show that computer interpretation can produce an unacceptably high rate of false-positive diagnoses. Interpretation by trained personnel in conjunction with computer interpretation may lower the rate of false results obtained when using computer interpretation alone.
Because of high false-negative rates, we recommend that computer-assisted ECG interpretation not be used as a sole means to diagnose STEMI. (Class III: Harm, LOE B-NR)
Last Updated: Oct 2015
We recommend that computer-assisted ECG interpretation may be used in conjunction with physician or trained provider interpretation to recognize STEMI . (Class IIb, LOE C-LD)
Last Updated: Oct 2015
Nonphysician STEMI ECG Interpretation - Updated ACS 884
When physicians are not present or not available to interpret an ECG, other methods for interpretation must be used so that timely patient care is not adversely affected. The 2015 ILCOR systematic review examined whether nonphysicians such as paramedics and nurses could identify STEMI on an ECG so that earlier identification of STEMI could be made with acceptable rates of either underdiagnosis (false-negative results) or overdiagnosis (false-positive results).
Three observational studies compared the diagnostic accuracy of the interpretation of ECGs as either STEMI or No STEMIby physicians and paramedics.144-146 While the studies used different methods to adjudicate the diagnosis, including World Health Organization criteria,144 discharge diagnosis,145 and catheterization laboratory activation,146 all 3 studies showed a fairly high rate of agreement between physician and paramedic rates of distinguishing STEMI from No STEMI.
Overidentification of STEMI may have a significant adverse effect on resource utilization. An additional 6 studies examined the accuracy of paramedic identification of STEMI and reported false-positive rates (patients incorrectly diagnosed with STEMI by paramedics when no STEMI was present) ranging from 8% to 40%.140,147-151 One study reported that transmission of the ECG to the ED for emergency physician interpretation, compared with paramedic interpretation alone, improves the positive predictive value of the prehospital 12-lead ECG for triage and therapeutic decision making.147 The time from hospital arrival to percutaneous coronary intervention (PCI) with balloon inflation was significantly shorter if EMS activated the catheterization laboratory than if the laboratory was activated by hospital staff148,149,151 or if the patient was directly admitted to the catheterization laboratory.150
While transmission of the prehospital ECG to the ED physician may improve positive predictive value (PPV) and therapeutic decision-making regarding adult patients with suspected STEMI, if transmission is not performed, it may be reasonable for trained nonphysician ECG interpretation to be used as the basis for decision-making, including activation of the catheterization laboratory, administration of fibrinolysis, and selection of destination hospital. (Class IIa, LOE B-NR)
Last Updated: Oct 2015