Posted by American Heart Association, Inc. on Dec 5th 2019
2019 AHA Focused Updates Released November 14, 2019 Part 9: Acute Coronary Syndromes - Continued
Biomarkers in ACS - Updated ACS 737
Cardiac troponin measurement, along with the ECG, is an integral part of the evaluation of patients with signs and symptoms suspicious for ACS. The detection of an elevated troponin (Tn) above the 99th percentile upper reference limit is highly sensitive and specific for myocardial necrosis, and is required in the universal definition of myocardial infarction (MI).152
Contemporary troponin assays are termed “high-sensitivity” (hs) if they are able to detect measurable troponin levels even in healthy individuals, with a threshold of detection of 0.006 ng/ml for hs-cTnI and 0.005 for hs-cTnT. Positive results are an order of magnitude higher than the threshold for detection and are usually defined as exceeding the 99th percentile of values with a coefficient of variation of less than 10%.153
More than 8 million patients are evaluated for potential ischemic chest pain in US EDs each year, with troponin measurement serving as one of the crucial diagnostic tests.154 Because of this vast number of patients with potential ischemic chest pain, it is highly desirable to find some combination of diagnostic testing that can reliably identify patients who are not experiencing ischemia and can be safely discharged from the ED.
The 2015 ILCOR systematic review examined whether a negative troponin test could be used to identify patients at low risk for ACS when they did not have signs of STEMI,ischemia, or changes on the ECG that could mask signs of acute ischemia or MI.
The clinician should bear in mind that unstable angina can present without any objective data of myocardial ischemic injury (ie, with normal ECG and normal troponin), in which case the initial diagnosis depends solely on the patient’s clinical history and the clinician’s interpretation and judgment.
Two observational studies used troponin (cTnI, cTnT, or hscTnT) measured at 0 and 2 hours to assess whether patients could be safely discharged from the ED.155,156 In these studies, 2.5% to 7.8% of patients with ACS had (false-) negative tests. That is, ACS would have been missed in 2.5% to 7.8% of the patients studied. With an unstructured risk assessment used in addition to the troponin testing, 2.3% of patients identified as being at low risk have a major adverse cardiac event (MACE) on 30-day follow-up. A formal risk assessment instrument was not used in either of these 2 studies.
Six additional observational studies combined troponin testing (using cTnI, cTnT, hs-cTnI, or hs-cTnT) with use of clinical decision rules such as TIMI, Vancouver, North American, or HEART. The proportion of false-negative results among patients with 30-day MACE ranged from 0% to 1.2%.157-162 When the age cutoff for low-risk patients was increased from 50 years to 60 years for the North American Chest Pain Rule, the proportion of false-negative results rose from 0% to 1.1%.160 Because the rules were used in combination with different troponin measurements, and each test identified 99% of patients with ACS as defined by 30-day MACE, it was difficult to directly compare rule or assay performance. One study159 identified 1 additional ACS patient by using the Vancouver rule when the hs-cTnI was used instead of the cTnI.
We recommend against using hs-cTnT and cTnI alone measured at 0 and 2 hours (without performing clinical risk stratification) to identify patients at low risk for ACS.
Last Updated: Oct 2015
We recommend that hs-cTnI measurements that are less than the 99th percentile, measured at 0 and 2 hours, may be used together with low-risk stratification (TIMI score of 0 or 1 or low risk per Vancouver rule) to predict a less than 1% chance of 30-day MACE.
Last Updated: Oct 2015
We recommend that negative cTnI or cTnT 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.
Last Updated: Oct 2015
Therapeutic Interventions in ACS - Updated
Several initial therapeutic measures are appropriate for all patients with suspected ACS in the ED setting. These include continuous cardiac monitoring, establishment of intravenous (IV) access, and consideration of several medications discussed below.
ADP Inhibition: Adjunctive Therapy in Patients With Suspected STEMI—ADP Inhibitors - Updated ACS 335
The 2015 ILCOR systematic review addressed the clinical impact of the timing of administration of adenosine diphosphate (ADP) inhibition in the treatment of patients with suspected STEMI. The relative merit of early prehospital as compared with hospital administration of ADP inhibition as ageneral treatment strategy was assessed. Differences between individual ADP inhibitors were not examined.
The preferred reperfusion strategy for patients with STEMI is identification and restoration of normal flow in the infarct-related artery using primary percutaneous intervention. The use of potent dual antiplatelet therapy in STEMI patients undergoing PPCI is associated with improved clinical outcomes as well as lower rates of acute stent thrombosis.163,164 Given the short time from first medical contact to balloon inflation, treatment with oral ADP inhibitors in a prehospital setting has the potential to enhance platelet inhibition and improve procedural and clinical outcomes after PCI.
Three randomized controlled trials (RCTs)165-167 showed no additional benefit to the outcome of 30-day mortality and no additional benefit or harm with respect to major bleeding with prehospital administration compared with in-hospital administration of an ADP-receptor antagonist.
In patients with suspected STEMI intending to undergo PPCI, initiation of ADP inhibition may be reasonable in either the prehospital or in-hospital setting.
Last Updated: Oct 2015
Prehospital Anticoagulants Versus None in STEMI - Updated ACS 562
In patients with suspected STEMI, anticoagulation is standard treatment recommended by the American College of Cardiology Foundation/AHA Guidelines.10,11 The 2015 ILCOR systematic review sought to determine if any important outcome measure was affected if an anticoagulant was administered prehospital compared with whether that same anticoagulant was administered in-hospital.
A single nonrandomized, case-control study found that while flow rates were higher in an infarct-related artery when heparin and aspirin were administered in the prehospital setting versus the ED, there was no significant difference in death, PCI success rate, major bleeding, or stroke.168
While there seems to be neither benefit nor harm to administering heparin to patients with suspected STEMI before their arrival at the hospital, prehospital administration of medication adds complexity to patient care.
We recommend that EMS systems that do not currently administer heparin to suspected STEMI patients do not add this treatment, whereas those that do administer it may continue their current practice.
Last Updated: Oct 2015
In suspected STEMI patients for whom there is a planned PCI reperfusion strategy, administration of unfractionated heparin (UFH) can occur either in the prehospital or in-hospital setting.
Last Updated: Oct 2015
Prehospital Anticoagulation for STEMI - Updated ACS 568
The 2015 ILCOR systematic review examined whether the prehospital administration of an anticoagulant such as bivalirudin, dalteparin, enoxaparin, or fondaparinux instead of UFH, in suspected STEMI patients who are transferred for PPCI, changes any major outcome.
One RCT provided evidence in patients transferred for PCI for STEMI that there was no significant difference between prehospital bivalirudin compared with prehospital UFH with respect to 30-day mortality, stroke, or reinfarction. However, this same study did demonstrate a decreased incidence of major bleeding with bivalirudin.169 Another study (this one a non-RCT) also demonstrated no difference between prehospital bivalirudin compared with prehospital UFH with respect to 30-day mortality, stroke, and reinfarction. In contrast to the RCT, this study did not find a difference in major bleeding.170
Although stent thrombosis was not considered as an a priori outcome, bivalirudin was strongly associated with the risk of acute stent thrombosis (relative risk, 6.11; 95% confidence interval, 1.37–27.24).169 Such association is also consistently reported in other published in-hospital studies and meta-analyses of this agent in patients undergoing PCI.171-173 While the benefit of bivalirudin over UFH alone in reducing bleeding complications has been shown, this benefit may be offset by the risk of stent thrombosis.
We have identified 1 RCT174 enrolling 910 patients transferred for PPCI for STEMI that showed no significant difference between prehospital enoxaparin compared with prehospital UFH with respect to 30-day mortality, stroke, reinfarction, or major bleeding.
It is important to consider the results of the comparison between anticoagulants given in prehospital versus in-hospital settings in STEMI patients. Only UFH has been evaluated directly in this setting, and because there is no clear evidence of benefit, we are not recommending that EMS systems implement anticoagulant administration in the prehospital setting.
It may be reasonable to consider the prehospital administration of UFH in STEMI patients or the prehospital administration of bivalirudin in STEMI patients who are at increased risk of bleeding.
Last Updated: Oct 2015
In systems in which UFH is currently administered in the prehospital setting for patients with suspected STEMI who are being transferred for PPCI, it is reasonable to consider prehospital administration of enoxaparin as an alternative to UFH.
Last Updated: Oct 2015
Routine Supplementary Oxygen Therapy in Patients Suspected of ACS - Updated ACS 887
The 2010 AHA Guidelines for CPR and ECC noted that there was insufficient evidence to recommend the routine use of oxygen therapy in patients who had an uncomplicated ACS without signs of hypoxemia or heart failure and that older literature suggested harm with supplementary oxygen administration in uncomplicated ACS without demonstrated need for supplementary oxygen.175,176 The 2010 Guidelines, however, did recommend that oxygen be administered to patients with breathlessness, signs of heart failure, shock, or an oxygen saturation less than 94%.8
In 2015, the ILCOR systematic review specifically addressed the use of oxygen as an adjunctive medication in thetreatment of patients who had normal oxygen saturation but had suspected ACS. The 2 treatment approaches (either providing or withholding oxygen) were compared with respect to outcomes: rate of death, infarction size, resolution of chest pain, and ECG abnormality resolution. The new recommendation in this 2015 Guidelines Update applies only to the use of oxygen for patients suspected of ACS who have normal oxygen saturations.
Adjunctive Therapy in Patients Suspected of ACS: Oxygen - Updated
Respiratory compromise, manifested by oxygen desaturation, can occur during ACS, most often as a result of either acute pulmonary edema or chronic pulmonary disease. Supplementary oxygen has previously been considered standard therapy for the patient suspected of ACS, even in patients with normal oxygen saturation. The rationale for oxygen therapy was a belief that maximization of oxygen saturation may improve delivery of oxygen to the tissues and thus reduce the ischemic process and related negative outcomes. In other patient groups, such as resuscitated cardiac arrest patients, hyperoxia has been associated with worse outcomes as compared with normoxia.177-179
There is limited evidence regarding the use of supplementary oxygen therapy in suspected ACS patients with normal oxygen saturation. The practice of administering oxygen to all patients regardless of their oxygen saturation is based on both rational conjecture and research performed before the current reperfusion era in acute cardiac care.175 More recent study of this issue is also limited,180,181although 2 trials addressing this question are in progress or are recently completed. The AVOID trial,182 a multicentered prospective RCT published since the 2015 ILCOR systematic review, compared oxygen administration with no oxygen administration in suspected STEMI patients without respiratory compromise. When oxygen was administered, the patients experienced increased myocardial injury at presentation and larger infarction size at 6 months. Reinfarction and the incidence of cardiac arrhythmias were also increased in the oxygen therapy group.182 Because this study was published after the ILCOR systematic review, it was not considered in our treatment recommendation.
There is no evidence that withholding supplementary oxygen therapy in normoxic patients suspected of ACS affects the rate of death and/or resolution of chest pain; there is only a very low level of evidence that withholding supplementary oxygen reduces infarction size, and there is no evidence that withholding supplementary oxygen therapy affects the resolution of ECG abnormality.175,176,180,181
The provision of supplementary oxygen to patients with suspected ACS who are normoxic has not been shown to reduce mortality or hasten the resolution of chest pain. Withholding supplementary oxygen in these patients has been shown to minimally reduce infarct size.
The usefulness of supplementary oxygen therapy has not been established in normoxic patients. In the prehospital, ED, and hospital settings, the withholding of supplementary oxygen therapy in normoxic patients with suspected or confirmed acute coronary syndrome may be considered.
Last Updated: Oct 2015Previous Versions
Aspirin and Nonsteroidal Anti-Inflammatory Drugs
Early administration of aspirin (acetylsalicylic acid [ASA]), has been associated with decreased mortality rates in several clinical trials.39,41,183,184 Multiple studies support the safety of aspirin administration.
Therefore, unless the patient has a known aspirin allergy or active gastrointestinal hemorrhage, nonenteric aspirin should be given as soon as possible to all patients with suspected ACS.
Last Updated: Oct 2010
Aspirin produces a rapid clinical antiplatelet effect with near-total inhibition of thromboxane A2 production. It reduces coronary reocclusion and recurrent ischemic events after fibrinolytic therapy. Aspirin alone reduced death from AMI in the Second International Study of Infarct Survival (ISIS-2), and its effect was additive to that of streptokinase.41 Aspirin was found to substantially reduce vascular events in all patients with AMI, and in high-risk patients it reduced nonfatal AMI and vascular death.185 Aspirin is also effective in patients with NSTEMI. The recommended dose is 160 to 325 mg. Chewable or soluble aspirin is absorbed more quickly than swallowed tablets.186,187
Aspirin suppositories (300 mg) are safe and can be considered for patients with severe nausea, vomiting, or disorders of the upper gastrointestinal tract.
Other nonsteroidal anti-inflammatory medications (NSAIDS) are contraindicated and should be discontinued in patients who are taking these medications. NSAIDs (except for aspirin), both nonselective as well as COX-2 selective agents, should not be administered during hospitalization for STEMI because of the increased risk of mortality, reinfarction, hypertension, heart failure, and myocardial rupture associated with their use.
Last Updated: Oct 2010
(Research related to this recommendation statements can be found in the linked references.188-190)
Nitroglycerin (or Glyceryl Trinitrate)
Nitroglycerin has beneficial hemodynamic effects, including dilation of the coronary arteries (particularly in the region of plaque disruption), the peripheral arterial bed, and venous capacitance vessels. The treatment benefits of nitroglycerin are limited, however, and no conclusive evidence has been shown to support the routine use of IV, oral, or topical nitrate therapy in patients with AMI.191 With this in mind, these agents should be carefully considered, especially in the patient with low blood pressure and when their use would preclude the use of other agents known to be beneficial, such as angiotensin-converting enzyme (ACE) inhibitors.
Patients with ischemic discomfort should receive up to 3 doses of sublingual or aerosol nitroglycerin at 3- to 5-minute intervals until pain is relieved or low blood pressure limits its use.
Last Updated: Oct 2010
Topical nitrates are acceptable alternatives for patients who require anti-anginal therapy but who are hemodynamically stable and do not have ongoing refractory ischemic symptoms. Parenteral formulations, rather than long acting oral preparations, can be used acutely to enable titration in patients with obvious ACS, objective test abnormality, and ongoing discomfort. In patients with recurrent ischemia, nitrates are indicated in the first 24 to 48 hours.
The use of nitrates in patients with hypotension (SBP <90 mm Hg or ≥30 mm Hg below baseline), extreme bradycardia (<50 bpm), or tachycardia in the absence of heart failure (>100 bpm) and in patients with right ventricular infarction is contraindicated.
Last Updated: Oct 2010
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-wall MI and suspected right ventricular (RV) involvement because these patients require adequate RV preload. Nitroglycerin should not be administered to patients who had taken a phosphodiesterase inhibitor (eg, sildenafil) for erectile dysfunction within 24 hours (48 hours if tadalafil use).
Relief of chest discomfort with nitroglycerin is neither sensitive nor specific for ACS; gastrointestinal etiologies as well as other causes of chest discomfort can “respond” to nitroglycerin administration.26,192-194
Providers should administer analgesics, such as intravenous morphine, for chest discomfort unresponsive to nitrates. Morphine is the preferred analgesic for patients with STEMI.
Last Updated: Oct 2010
However, analysis of retrospective registry data raised a question about the potentially adverse effects of morphine in patients with UA/NSTEMI.53 As a result, the ACC AHA UA/NSTEMI writing group reduced morphine use to a Class IIa recommendation for that patient population.89
Reperfusion Decisions in STEMI Patients - Updated
Acute reperfusion therapy using PPCI or fibrinolytic therapy in patients with STEMI restores flow in the infarct-related artery, limits infarct size, and translates into early mortality benefit that is sustained over the next decade.195,196 While optimal fibrinolysis restores normal coronary flow (TIMI 3) in 50% to 60% of subjects, PPCI is able to achieve restored flow in >90% of subjects. The patency rates achieved with PPCI translates into reduced mortality and reinfarction rates as compared to fibrinolytic therapy.197 This benefit is even greater in patients presenting with cardiogenic shock. PPCI also results in a decreased risk of intracranial hemorrhage and stroke, making it the reperfusion strategy of choice in the elderly and those at risk for bleeding complications.
The 2010 ILCOR systematic review addressed the use of reperfusion therapy, including fibrinolysis and PPCI, in patients with STEMI who present initially to non–PCI-capable hospitals. The 2015 AHA Guidelines Update for CPR and ECC examines the most appropriate reperfusion therapy in STEMI patients presenting to non–PCI-capable hospitals as well as the need for hospital transfer for PCI, or ischemiaguided (ie, rescue) coronary angiography and/or PCI.
In summary, for patients presenting within 12 hours of symptom onset and electrocardiographic findings consistent with STEMI, reperfusion should be initiated as soon as possible – independent of the method chosen.
Last Updated: Oct 2010
Fibrinolytics & Percutaneous Coronary Intervention (PCI) Overview
A cooperative and interdisciplinary effort between emergency medicine and cardiology, as well as among the EMS agencies, the catheterization laboratory, and the CCU, has the potential to reduce markedly the door-to-therapy time in STEMI patients and therefore limit delays in providing this time-sensitive treatment. Prior agreement between the ED and cardiovascular physicians at institutions with invasive capability must be obtained so that consideration of PCI does not introduce further delays in fibrinolytic drug administration; such cooperation can limit additional delays in the administration of fibrinolytic agents in patients who are considered for PCI in AMI.
A systems of care approach involving a reperfusion team or “STEMI alert” system mobilizes hospital-based resources, optimizing the approach to the patient. This system, whether activated by data gathered in the ED or prehospital-based information, has the potential to offer time-sensitive therapies in a rapid fashion to these ill patients.
Early fibrinolytic therapy is a well-established treatment modality for patients with STEMI who present within 12 hours of the onset of symptoms and who lack contraindications to its use.196,198-201 Patients are evaluated for risk and benefit; for absolute and relative contraindications to therapy (see Table 4).
Table 4: 2010 - Fibrinolytic Therapy
Open table in a new window
If fibrinolysis is chosen for reperfusion, the ED physician should administer fibrinolytics to eligible patients as early as possible according to a predetermined process of care developed by the ED and cardiology staff.
Last Updated: Oct 2010
Patients with STEMI presenting at later times in the myocardial infarction evolution are much less likely to benefit from fibrinolysis.
In fact, fibrinolytic therapy is generally not recommended for patients presenting between 12 and 24 hours after onset of symptoms based on the results of the LATE and EMERAS trials,202,203 unless continuing ischemic pain is present with continuing ST-segment elevation.
Last Updated: Oct 2010
Fibrinolytic therapy should not be administered* to patients who present greater than 24 hours after the onset of symptoms.
Last Updated: Oct 2010
Physicians who administer fibrinolytic agents must be aware of the indications, contraindications, benefits, and major risks of administration so that they are able to weigh the net clinical benefit for each patient (see Table 4).204,203 This net clinical benefit requires integration of relative and absolute contraindications versus overall potential clinical gain.
Patients who present early after symptom onset with extensive ECG changes (consistent with a large AMI) and a low risk of intracranial bleeding receive the greatest benefit from fibrinolytic therapy.198 Patients who have symptoms highly suggestive of ACS and ECG findings consistent with LBBB are also appropriate candidates for intervention because they have the highest mortality rate when LBBB is due to extensive AMI. Inferior wall STEMI also benefits from fibrinolysis, yet the magnitude of this outcome improvement is markedly less robust. More extensive inferior STEMI presentations, of course, demonstrate more robust benefit when undergoing fibrinolysis; inferior wall STEMI with RV involement is such an example. Fibrinolytics have been shown to be beneficial across a spectrum of patient subgroups with comorbidities such as previous MI, diabetes, tachycardia, and hypotension.198 Although superior to placebo, the lack of efficacy in the setting of cardiogenic shock makes referral for PPCI an optimal strategy in this setting.
Although older patients (>75 years) have a higher risk of death, their absolute benefit appears to be similar to that of younger patients. The incidence of stroke does increase with advancing age,205,206 reducing the relative benefit of fibrinolytic therapy. Older age is the most important baseline variable predicting nonhemorrhagic stroke.206 Although 1 large trial reported lower early and 1-year mortality rates with accelerated administration of tissue plasminogen activator (rtPA) in patients <85 years of age,207 a retrospective analysis found no specific survival advantage and possible risk for patients >75 years of age.208
Fibrinolytic therapy is associated with a small but definite increase in the risk of hemorrhagic stroke, which contributes to increased mortality.198 More intensive fibrinolytic regimens using rtPA (alteplase) and heparin pose a greater risk than streptokinase and aspirin.209,210 Clinical factors that may help risk-stratify patients at the time of presentation are age (≥65 years), low body weight (<70 kg), hypertension on presentation (>180/110 mm Hg), and use of rtPA. The number of risk factors can be used to estimate the frequency of stroke, which ranges from 0.25% with no risk factors to 2.5% with 3 risk factors.203Several risk factor estimates are available for use by clinicians, including Simoons,203 the Co-Operative Cardiovascular Project,211 and the In-Time 2 trial.212
Percutaneous Coronary Intervention (PCI)
Coronary angioplasty with or without stent placement is the treatment of choice for the management of STEMI when it can be performed effectively with a door-to-balloon time 75 PCIs per year) at a skilled PCI facility (performing >200 PCIs annually, of which at least 36 are primary PCI for STEMI).34,213,214
Last Updated: Oct 2010
Primary PCI (PPCI) may also be offered to patients presenting to non-PCI centers when prompt transfer can result in an effective ballon time of <90 minutes from first medical contact as a systems goal.215 The TRANSFER AMI trial supports the transfer of high-risk patients who receive fibrinolysis in a non-PCI center to a PCI center within 6 hours of presentation to receive routine early PCI.216
Primary PCI performed at a high-volume center within 90 minutes of first medical contact by an experienced operator that maintains an appropriate expert status is reasonable, as it improves morbidity and mortality as compared with immediate fibrinolysis (<30 minutes door-to-needle).
Last Updated: Oct 2010
For those patients with a contraindication to fibrinolysis, PCI is recommended despite the delay, rather than foregoing reperfusion therapy.
Last Updated: Oct 2010
For those STEMI patients presenting in shock, PCI (or CABG) is the preferred reperfusion treatment. Fibrinolysis should only be considered in consultation with the cardiologist if there is a substantial delay to PCI.
Prehospital fibrinolysis requires a sophisticated system of provider expertise, well-established protocols, comprehensive training programs, medical oversight, and quality assurance.5 In many European systems, a physician provides prehospital fibrinolysis, but nonphysicians can also safely administer fibrinolytics.217 The 2015 ILCOR systematic review evaluated whether prehospital fibrinolysis is preferred to reperfusion inhospital where the prehospital fibrinolysis expertise, education, and system support exists.
Prehospital fibrinolysis will achieve earlier treatment as compared with ED fibrinolysis. Where transport times are more than 30 to 60 minutes, the time advantage conferred by prehospital fibrinolysis provides a mortality benefit.5 This benefit from prehospital fibrinolysis was found consistently by 3 RCTs performed more than 20 years ago.218-220 However, these studies were performed at a time when hospital fibrinolytic administration typically took well in excess of 60 minutes. It is not clear the extent to which that mortality benefit would be maintained today when the hospital time to fibrinolytic treatment is typically considerably shorter than it was 20 years ago. The only recent evidence for this therapy comes from a non-RCT that confirms a small mortality benefit to prehospital fibrinolysis.221 When transport times are shorter than 30 to 60 minutes, the mortality benefit from administering fibrinolytics before hospital arrival may be lost and may no longer outweigh the relative complexity of providing this therapy outside of a hospital.
However, PPCI is generally preferred to in-hospital fibrinolysis for STEMI reperfusion.222 Prehospital providers can transport STEMI patients directly to PCI centers, and activation of the team before arrival allows the team to assemble and prepare in parallel with transport. Several studies in the past 15 years have compared transport directly for PPCI with prehospital fibrinolysis and found no mortality benefit of either therapy, although the relatively rare harm from intracranial hemorrhage is greater with fibrinolysis.223-226
2015 Recommendations - Updated
Where prehospital fibrinolysis is available as part of a STEMI system of care, and in-hospital fibrinolysis is the alternative treatment strategy, it is reasonable to administer prehospital fibrinolysis when transport times are more than 30 minutes.
Last Updated: Oct 2015Previous Versions
It is strongly recommended that systems which administer fibrinolytics in the prehospital setting include the following features: protocols using fibrinolytic checklists, 12-lead ECG acquisition and interpretation, experience in advanced life support, communication with the receiving institution, medical director with training and experience in STEMI management, and continuous quality improvement.
Last Updated: Oct 2010
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 of the small relative decrease in the incidence of intracranial hemorrhage without evidence of mortality benefit to either therapy.
Last Updated: Oct 2015
If PCI is the chosen method of reperfusion for the prehospital STEMI patient, it is reasonable to transport patients directly to the nearest PCI facility, bypassing closer EDs as necessary, in systems where time intervals between first medical contact and balloon times are <90 minutes and transport times are relatively short (ie, <30 minutes).
Last Updated: Oct 2010
ED Fibrinolysis and Immediate PCI Versus Immediate PCI Alone - Updated ACS 882
Delays in the performance of PPCI are commonly observed in clinical practice. In many regions, the delay arises because of the relative paucity of dedicated PPCI centers, resulting in the need for prolonged transfer times. In this context, combining the availability and ease of administration of fibrinolytic with the downstream certainty of mechanical reperfusion with facilitated PCI was an attractive concept, with its promise of both restoring early flow to the infarct-related artery while addressing the concerns of pharmacologic failure and need for rescue. This was counterbalanced by the concern for a heightened risk of bleeding complications and detrimental procedural outcomes in this prothrombotic milieu.
The 2015 ILCOR systematic review addressed the merits for reperfusion in STEMI patients with a strategy of initial fibrinolysis followed by immediate PCI versus immediate PCI alone.
A number of randomized clinical trials have addressed clinical outcomes after initial treatment with a half- or full-dose fibrinolytic agent followed by dedicated immediate PCI compared with immediate PCI alone.
The studies showed no benefit to mortality,227-231 nonfatal MI,227-231 or target vessel revascularization227-230 when fibrinolytic administration is combined with immediate PCI as compared with immediate PCI alone.
The studies did, however, identify harm from intracranial hemorrhage227-229 or major bleeding227-231 when fibrinolytic administration is combined with immediate PCI versus immediate PCI alone.
In the treatment of patients with suspected STEMI, the combined application of fibrinolytic therapy followed by immediate PCI (as contrasted with immediate PCI alone) is not recommended.
Last Updated: Oct 2015
Delayed PCI Versus Fibrinolysis Stratified by Time From Symptom Onset - Updated ACS 337
Although the overall survivability benefits of reperfusion therapy are time dependent, the loss of efficacy caused by delay is more pronounced with fibrinolysis than with PCI.232 The success of PCI in achieving TIMI-3 flow in the early hours after STEMI does not change with time, whereas the ability of fibrinolytic therapy to achieve TIMI-3 flow decreases significantly with increasing ischemic time.233 In this context, the choice of reperfusion therapy for a STEMI patient when access to PCI is delayed is a challenging one. The clinician has to weigh the advantages of immediate fibrinolysis, which includes ease of administration and potential to open the infarct-related artery in a timely manner versus the limitations of fibrinolysis, which include the risk of intracranial hemorrhage and bleeding and the time sensitivity of the intervention’s efficacy to open the infarct-related artery. Thus, total ischemic time is an important variable in weighing the merits of delayed PCI versus immediate fibrinolysis.
In the 2010 AHA Guidelines for CPR and ECC,8 the recommendations were directed at patients in whom PCI could not be accomplished within 90 minutes of first medical contact.
The 2015 ILCOR systematic review compared the relative benefits of immediate fibrinolysis versus primary but delayed PCI in treating STEMI patients, stratifying patients by time from initial medical contact.
In STEMI patients presenting less than 2 hours after symptom onset in whom immediate PPCI will delay treatment 60 to 160 minutes compared with fibrinolysis, 2 RCTs (combined into a single analysis) using an outcome of 30-day mortality234 and 1 RCT using an outcome of 5-year mortality showed greater harm with delayed PPCI compared with fibrinolysis.235 No differences were found to incidence of reinfarction234 or severe bleeding.236
For STEMI patients presenting 2 to 6 hours after symptom onset in whom PPCI will delay treatment 60 to 160 minutes compared with fibrinolysis, 2 RCTs using an outcome of 1-year mortality234 and 1 RCT using an outcome of 5-year mortality showed no benefit of delayed PPCI over fibrinolysis.235 There was also no difference in the incidence of reinfarction,234 but 1 RCT236 showed more severe bleeding with fibrinolysis as compared with delayed PPCI.
In STEMI patients presenting 3 to 12 hours after symptom onset in whom PPCI will delay treatment 60 to 120 minutes as compared with fibrinolysis, 1 RCT237 using a 30-day mortality outcome showed that delayed PPCI conferred a benefit as compared with immediate fibrinolysis.
A reanalysis of the raw data from 16 RCTs238 has suggested that the acceptable fibrinolysis to PPCI delay varies depending on the patient’s baseline risk and delay to presentation. A pragmatic simplification of the formula derived in the analysis has been suggested in an editorial239 associated with the publication of the analysis: Patients older than 65 years and all patients in Killip class greater than 1 should be treated with PPCI. Patients older than 65 years in Killip class 1 should have PPCI unless delay is greater than 35 minutes.
2015 Recommendations - Updated
The following recommendations are not in conflict with, and do not replace, the 2013 ACC/AHA STEMI Guidelines, which are endorsed by this ACS Writing Group. These 2015 Guidelines Update recommendations are derived from a different set of studies that examined the interval between symptom onset and reperfusion, rather than the interval between first medical contact and reperfusion. The symptom onset interval is appropriate to consider when time of symptom onset is known. However, time from symptom onset may be difficult to ascertain or may be unreliable. When time from symptom onset is uncertain, it is appropriate to follow the ACC/AHA STEMI Guidelines recommendation that PPCI is the preferred reperfusion strategy when time from symptom onset is less than 12 hours and time to PPCI from first medical contact in these patients is anticipated to be less than 120 minutes.
Regardless of whether time of symptom onset is known, the interval between first medical contact and reperfusion should not exceed 120 minutes.
Last Updated: Oct 2015
In STEMI patients presenting within 2 hours of symptom onset, immediate fibrinolysis rather than PPCI may be considered when the expected delay to PPCI is more than 60 minutes.
Last Updated: Oct 2015Previous Versions
In STEMI patients presenting within 2 to 3 hours after symptom onset, either immediate fibrinolysis or PPCI involving a possible delay of 60 to 120 minutes might be reasonable.
Last Updated: Oct 2015Previous Versions
In STEMI patients presenting within 3 to 12 hours after symptom onset, performance of PPCI involving a possible delay of up to 120 minutes may be considered rather than initial fibrinolysis.
Last Updated: Oct 2015Previous Versions
It is acknowledged that fibrinolysis becomes significantly less effective more than 6 hours after symptom onset, and thus a longer delay to PPCI may be the better option for patients more than 6 hours after symptom onset.
In STEMI patients, when delay from first medical contact to PPCI is anticipated to exceed 120 minutes, a strategy of immediate fibrinolysis followed by routine early (within 3 to 24 hours) angiography and PCI if indicated may be reasonable for patients with STEMI.
Last Updated: Oct 2015Previous Versions
Hospital and ED protocols should clearly identify criteria for expeditious transfer of patients to PCI facilities.
These include patients who are ineligible for fibrinolytic therapy or who are in cardiogenic shock.
Last Updated: Oct 2010
(Research related to this recommendation statements can be found in the linked references.240)
A door-to-departure time <30 minutes is recommended by ACC/AHA Guidelines.34
Transfer of high-risk patients who have received primary reperfusion with fibrinolytic therapy is reasonable.
Last Updated: Oct 2010
(Research related to this recommendation statements can be found in the linked references.216,241)
Reperfusion Therapy for STEMI in Non–PCI-Capable Hospitals - Updated ACS 332 ACS 334 ACS 779
The rapid restoration of perfusion in the infarct-related coronary artery, using either fibrinolytic therapy or PPCI, provides the opportunity for an optimal outcome.
Fibrinolytic therapy unequivocally improves survival in patients presenting with STEMI and has widespread availability.242 STEMI patients with contraindications to fibrinolytic therapy and who are in cardiogenic shock are not appropriate candidates for this form of reperfusion therapy.243 PPCI is superior to fibrinolytic therapy in the management of STEMI,244 because PPCI also improves survival rates and enhances other important outcomes in the STEMI patient. However, this form of reperfusion therapy is not widely available.
The superiority of PPCI over fibrinolytic therapy is not absolute. For STEMI patients presenting to a non–PCIcapable hospital, the decision to administer fibrinolytic therapy at the initial facility as compared with immediate-transfer PPCI requires consideration of several factors, including the location of the MI, patient age, the duration of STEMI at time of initial ED presentation, time required to complete transfer for and performance of PPCI, and the abilities of the PPCI cardiologist and hospital.244 Furthermore, the hemodynamic status of the patient is important; specifically, patients in cardiogenic shock are most appropriately managed with PPCI.243
Fibrinolysis Versus Transfer for PPCI - Updated
In a non–PCI-capable hospital, the choice of reperfusion therapy in the STEMI patient is either immediate fibrinolytic therapy or transfer for PPCI; the time required for transfer of the patient to a PCI-capable hospital must be considered in making the choice. Comparison studies showed benefit of immediate transfer to a PCI center with respect to 30-day mortality, stroke, and/or reinfarction.237,245-251 There was no difference in major hemorrhage.247,250
Fibrinolysis and Routine Transfer for Angiography Versus Immediate Transfer for PPCI - Updated
When immediate fibrinolysis in a non–PCI-capable hospital followed by routine transfer for angiography was compared with immediate transfer to a PCI center for PPCI, 3 studies showed no benefit to 30-day mortality, stroke, and/or reinfarction and no difference in the rates of intracranial hemorrhage or major bleeding.224,252,253
In patients who received a fibrinolytic agent for STEMI in a non–PCI-capable hospital, studies comparing either routine transfer for angiography at 3 to 6 hours and up to 24 hours or no transfer except for ischemia-driven PCI (rescue PCI) in the first 24 hours showed no benefit with respect to 30-day mortality224,251,254-258 or 1-year mortality.224,254,255,258-260
In patients who received a fibrinolytic agent for STEMI in a non–PCI-capable hospital, studies comparing either routine transfer for angiography at 3 to 6 hours and up to 24 hours or no transfer except for ischemia-driven PCI (rescue PCI) in the first 24 hours demonstrated no difference in incidence of intracranial hemorrhage,224,254-258 major bleeding,224,254-258 or stroke.251,254,256,258
Fibrinolysis and Routine Transfer for Angiography Versus No Routine Transfer: Reinfarction - Updated
When immediate fibrinolysis for STEMI was followed by routine transfer for angiography at 3 to 6 hours and up to 24 hours as compared with no transfer except for ischemia-driven PCI (rescue PCI) in the first 24 hours, a decrease in the rate of reinfarction was demonstrated.224,251,254-258
In adult patients presenting with STEMI in the ED 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.
Last Updated: Oct 2015
When STEMI patients cannot be transferred to a PCI-capable hospital in a timely manner, fibrinolytic therapy with routine transfer for angiography may be an acceptable alternative to immediate transfer to PCI.
Last Updated: Oct 2015
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.
Last Updated: Oct 2015
It is recognized that there may be practical and logistical circumstances, including geographic limitations, where transfer for angiography within 24 hours is difficult or impossible. In these cases, the small but measurable decrease in reinfarction rates may not justify a prolonged or difficult transfer.
Hospital Reperfusion Decisions After ROSC - Updated
PCI After ROSC With and Without ST Elevation - Updated ACS 340 ACS 885
In 2010, the ILCOR systematic review combined ST-elevation and non–ST-elevation patients after ROSC. However, the 2010 AHA Guidelines for CPR and ECC did make separate recommendations for each of these distinct groups of patients, recommending emergency coronary angiography for ST-elevation patients after ROSC, while supporting the consideration of coronary angiography for non–ST-elevation patients after ROSC.
The 2015 ILCOR systematic review examined whether immediate coronary angiography (angiography performed within 24 hours after ROSC) for patients with and without ST elevation after cardiac arrest improved outcomes.
Evidence regarding the timing of coronary angiography immediately after cardiac arrest (defined variously, but within 24 hours) is limited to observational studies.
Aggregated data from 15 studies of 3800 patients having ST elevation on ECG after ROSC after cardiac arrest demonstrated a benefit of immediate coronary angiography, favoring survival to hospital discharge,261-275 while 9 of these studies enrolling a total of 2819 patients also demonstrated a benefit favoring neurologically favorable outcomes.261-263,266,268-270,273,276
In patients without ST elevation on initial postarrest ECG, 2 studies demonstrated a benefit favoring improved survival to hospital discharge and improved neurologically favorable outcome when patients received immediate coronary angiography.261,266
In these studies, the decision to undertake the intervention was influenced by a variety of factors such as patient age, duration of CPR, hemodynamic instability, presenting cardiac rhythm, neurologic status upon hospital arrival, and perceived likelihood of cardiac etiology.
2015 Recommendations - Updated
Coronary angiography should be performed emergently (rather than later in the hospital stay or not at all) for OHCA patients with suspected cardiac etiology of arrest and ST elevation on ECG).
Last Updated: Oct 2015Previous Versions
Emergency coronary angiography is reasonable for select (eg, electrically or hemodynamically unstable) adult patients who are comatose after OHCA of suspected cardiac origin but without ST elevation on ECG.
Last Updated: Oct 2015Previous Versions
It is reasonable to include cardiac catheterization and coronary angiography in standardized post–cardiac arrest protocols as part of an overall strategy to improve neurologically intact survival in this patient group (Class IIa, LOE B) and appropriate treatment of ACS or STEMI, including PCI or fibrinolysis, should be initiated regardless of coma.
Last Updated: Oct 2010
Angiography and/or PCI need not preclude or delay other therapeutic strategies including therapeutic hypothermia.
Last Updated: Oct 2010
Coronary angiography is reasonable in post–cardiac arrest patients where coronary angiography is indicated regardless of whether the patient is comatose or awake.
Last Updated: Oct 2015Previous Versions
A 12-lead ECG should be performed as soon as possible after ROSC.
Last Updated: Oct 2010
Complicated Acute Myocardial Infarction (AMI)
Cardiogenic Shock, LV Failure, and Congestive Heart Failure
Infarction of ≥40% of the LV myocardium usually results in cardiogenic shock and carries a high mortality rate. Of those who developed shock,277 patients with ST-segment elevation developed shock significantly earlier than patients without ST-segment elevation. Cardiogenic shock and congestive heart failure are not contraindications to fibrinolysis, but PCI is preferred if the patient is at a facility with PCI capabilities. Based on the results of the SHOCK trial ACC/AHA guidelines note that PPCI is reasonable in those who develop shock within 36 hours of symptom onset and who are suitable candidates for revascularization that can be performed within 18 hours of the onset of shock.89 Although the benefits in the SHOCK trial were observed only in patients ≤75 years of age, selected elderly patients also appear to benefit from this strategy. The guidelines also support the use of hemodynamic support with intra-aortic balloon counterpulsation (IABP) in this setting as part of aggressive medical treatment. The IABP works synergistically with fibrinolytic agents in this setting, and the benefits observed with early revascularization strategy in the SHOCK trial were also obtained in the setting of IABP support. The use of PPCI for patients with cardiogenic shock has increased over time and contributes to the observed decrease in hospital mortality.278,279 The majority of survivors following cardiogenic shock experience a good quality of life, and the early mortality benefit with revascularization is sustained over time.280-282 In hospitals without PCI facilities, fibrinolytic administration needs to be considered with prompt transfer to a tertiary care facility where adjunct PCI can be performed if cardiogenic shock or ongoing ischemia ensues.283 The ACC/AHA STEMI guidelines recommend a door-to-departure time of ≤30 minutes for transfer to a PCI-capable center.89
Right Ventricular (RV) Infarction
RV infarction or ischemia may occur in up to 50% of patients with inferior wall MI. The clinician should suspect RV infarction in patients with inferior wall infarction, hypotension, and clear lung fields. In patients with inferior wall infarction, obtain an ECG with right-sided leads. ST-segment elevation (>1 mm) in lead V4R is sensitive (sensitivity, 88%; specificity, 78%; diagnostic accuracy, 83%) for RV infarction and is a strong predictor of increased in-hospital complications and mortality.284
The in-hospital mortality rate of patients with RV dysfunction is 25% to 30%, and these patients should be routinely considered for reperfusion therapy. Fibrinolytic therapy reduces the incidence of RV dysfunction.285 Similarly PCI is an alternative for patients with RV infarction and is preferred for patients in shock. Patients with shock caused by RV failure have a mortality rate similar to that for patients with shock due to LV failure.
Patients with RV dysfunction and acute infarction are dependent on maintenance of RV “filling” pressure (RV end-diastolic pressure) to maintain cardiac output.286 Thus, nitrates, diuretics, and other vasodilators (ACE inhibitors) should be avoided because severe hypotension may result. Hypotension is initially treated with an IV fluid bolus.
ACE Inhibitors in the Prehospital Setting
Despite multiple studies that have shown a benefit of ACE inhibitors and ARBs in patients with a myocardial infarction when therapy is started during the first 24 hours of the index hospitalization, no trial specifically evaluates patients in the ED or prehospital settings. An older randomized trial showed a reduction in mortality with an increased risk of hypotension in patients treated soon after presentation in the inpatient setting.191 Several trials showed a reduction in the rate of heart failure and mortality in patients treated soon after fibrinolysis,287-289 and several others showed no benefit with the early or prehospital use of angiotensin converting enzyme.288,290,291
In conclusion, although ACE inhibitors and ARBs have been shown to reduce long-term risk of mortality in patients suffering an AMI, there is insufficient evidence to support the routine initiation of ACE inhibitors and ARBs in the prehospital or ED setting. (Class IIb, LOE C)
Last Updated: Oct 2010
Other recommendations concerning ACE Inhibitors in the hospital setting were not reviewed in 2015. Please refer to the 2014 AHA/ACC Guideline for the Management of Patients With Non–ST-Elevation Acute Coronary Syndromesor the2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction for information on this topic.
This section discusses management of arrhythmias during acute ischemia and infarction.
Ventricular Rhythm Disturbances
Treatment of ventricular arrhythmias during and after AMI has been a controversial topic for three decades. Primary VF accounts for the majority of early deaths during AMI.292-294 The incidence of primary VF is highest during the first 4 hours after onset of symptoms 37,295-297 but remains an important contributor to mortality during the first 24 hours. Secondary VF occurring in the setting of CHF or cardiogenic shock can also contribute to death from AMI. VF is a less common cause of death in the hospital setting with the use of fibrinolytics and percutaneous revascularization as early reperfusion strategies. Broad use of β-blockers also contributes significantly in the reduction of VF incidence in the after AMI.
Although prophylaxis with lidocaine reduces the incidence of VF, an analysis of data from ISIS-3 and a meta-analysis suggest that lidocaine increased all-cause mortality rates.298
Thus, the practice of prophylactic administration of lidocaine is not recommended.
Last Updated: Oct 2010
Sotalol has not been adequately studied.
Last Updated: Oct 2010
Amiodarone in a single RCT did not appear to improve survival in low doses and may increase mortality in high doses when used early in patients with suspected myocardial infarction.299
Last Updated: Oct 2010
Twenty published studies including 14 RCTs and 4 meta-analyses/reviews provide no good evidence that prophylactic antiarrhythmics improve outcomes (survival to discharge, 30/60 day mortality) and despite a documented decrease in the incidence of malignant ventricular arrhythmias, they may cause harm.
Therefore prophylactic antiarrhythmics are not recommended for patients with suspected ACS or myocardial infarction in the prehospital or ED.
Last Updated: Oct 2010
Routine IV administration of β-blockers to patients without hemodynamic or electric contraindications is associated with a reduced incidence of primary VF.
Last Updated: Oct 2010
Low serum potassium, but not magnesium, has been associated with ventricular arrhythmias.
It is prudent clinical practice to maintain serum potassium >4 mEq/L and magnesium >2 mEq/L.
Last Updated: Oct 2010
Routine administration of magnesium to patients with MI has no significant clinical mortality benefit, particularly in patients receiving fibrinolytic therapy.191 ISIS-4 enrolled >58 000 patients and showed a trend toward increased mortality rates when magnesium was given in-hospital for primary prophylaxis to patients within the first 4 hours of known or suspected AMI.
Following an episode of VF, there is no conclusive data to support the use of lidocaine or any particular strategy for preventing VF recurrence. Further management of ventricular rhythm disturbances is discussed in Part 7: Adult Advanced Cardiovascular Life Support.
Robert E. O’Connor, Chair; Abdulaziz S. Alali; William J. Brady; Chris A. Ghaemmaghami; Venu Menon; Michelle Welsford; Michael Shuster
Table 5: 2015 - Part 9: Acute Coronary Syndromes: 2015 Guidelines Update Writing Group Disclosures
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Robert E. O’Connor, Chair; William Brady; Steven C. Brooks; Deborah Diercks; Jonathan Egan; Chris Ghaemmaghami; Venu Menon; Brian J. O’Neil; Andrew H. Travers; Demetris Yannopoulos
Table 6: 2010 - Guidelines Part 10: ACS Writing Group Disclosures
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The American Heart Association requests that this document be cited as follows:
American Heart Association. Web-based Integrated Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care – Part 9: Acute Coronary Syndromes. ECCguidelines.heart.org.
© Copyright 2015 American Heart Association, Inc.