Chest pain is the second most common complaint in emergency departments, with 6.4 million visits annually in the United States. A quarter of these patients will be diagnosed with acute coronary syndromes, but among those, nearly half will have nondiagnostic electrocardiograms. Non–ST-segment elevation myocardial infarction (NSTEMI) is twice as common as ST-segment elevation myocardial infarction (STEMI), and lack of clarity surrounding the best management of this condition can contribute to adverse outcomes. In this review, current national management guidelines for NSTEMI are summarized as they pertain to the ED, and the evidence base supporting them is considered. Issues surrounding special patient populations are addressed, and new diagnostic and therapeutic modalities are discussed.
A 76-year-old woman presents to the ED with chest pain. She said that for the past month she has been getting short of breath more easily on her daily walks, with occasional discomfort in her chest, requiring her to stop and rest. Two hours prior to ED arrival, she was doing yard work and developed chest pain that was much more severe. The pain is located in the center of her chest, and she describes it as a “pressure” sensation. Her only past medical history is hypertension. In the ED, her vital signs are within normal limits and her exam is unremarkable. Her ECG shows nonspecific ST-segment flattening, and her initial troponin is 0.09 ng/mL (reference range, 0-0.04 ng/mL). Your intern asks if she can go home since her troponin is low and she looks well...
A 69-year-old man presents to the ED with chest pain that began an hour prior to presentation, while he was walking home from the store. Initially, it felt similar to his usual episodes of angina, with left-sided pressure radiating to his left arm. However, the pain didn’t resolve with rest and has been worsening since onset, and is currently 9/10 in severity. He also notes dyspnea and lightheadedness. He has a history of hypertension, diabetes, and coronary artery disease, with baseline stable angina. His heart rate is 110 bpm and blood pressure is 90/40 mm Hg. He has bibasilar crackles and visibly increased work of breathing. Chest x-ray confirms your clinical suspicion of pulmonary edema. His ECG shows 4-mm anterior ST-segment depressions. His initial troponin is still pending. You wonder if you should activate the cath lab, or if a bedside echo might help...
An 82-year-old woman presents to the ED with chest pain. It started 3 hours prior to presentation during an argument with her husband, and she describes it as “squeezing,” localized to her left chest, with radiation to the neck and jaw. She has had several episodes of similar pain in the past, typically associated with emotional distress or exertion. She has never been evaluated by a doctor for it, as it typically resolves within 10 to 15 minutes with rest and relaxation techniques. Today, however, it has been more persistent and severe than usual. She has a past medical history of hypertension, diabetes, end-stage renal disease, and heart failure with reduced ejection fraction. Her vital signs are stable, and her exam is benign. Her ECG shows 3-mm ST-segment depressions in the lateral leads, and her troponin is 1.22 ng/mL. You start dual antiplatelet therapy and heparin, and her pain resolves. You admit her to the hospital, but wonder whether the inpatient team will take her to the cath lab or just manage her medically…
In the United States, 6.3% of adults have coronary artery disease, and 3% have had a myocardial infarction (MI). This year, more than a million Americans will suffer MIs, meaning that an MI occurs approximately every 40 seconds.1 There are approximately 6.4 million emergency department (ED) visits for chest pain annually in the United States, representing 5.3% of total visits, making chest pain the second most common reason for seeking ED care.2 Among ED patients with chest pain, up to 25% will be diagnosed with an acute coronary syndrome (ACS), which includes STEMI (ST-segment elevation myocardial infarction), NSTEMI (non–ST-segment elevation myocardial infarction), and unstable angina.3 Effective management of patients with ACS is essential to minimize their risk for a major adverse cardiac event (MACE), including re-infarction, stroke, dysrhythmia, heart failure, cardiogenic shock, and death.
Emergency clinicians must be able to differentiate patients with cardiac ischemia from those with more benign causes of chest pain. Nonetheless, approximately 2% of patients presenting to EDs with ACS are misdiagnosed and inappropriately discharged.3 Misdiagnosis is most common among women younger than 55 years; other important risk factors for misdiagnosis include nonwhite race, presenting complaint of dyspnea, and normal or nondiagnostic electrocardiogram (ECG).4 Failure to hospitalize patients with ACS nearly doubles their mortality risk and is associated with significant legal liability.4
Myocardial infarction is defined as clinical evidence of acute myocardial ischemia in the setting of cardiac biomarker elevation above the 99th percentile.5 Biomarker elevations in the absence of clinical ischemia are termed myocardial injury. Clinical evidence of ischemia may include any of the following:
In patients with MI, it is essential to differentiate between STEMI and NSTEMI, as those with STEMI require emergent coronary intervention. STEMI is defined by ECG criteria in the presence of symptoms compatible with myocardial ischemia:5
Patients with MI who do not meet STEMI criteria are considered to have NSTEMI. NSTEMI is more common than STEMI, representing 60% to 70% of MIs.6 The incidence of STEMI has decreased in recent years, while the incidence of NSTEMI has remained stable or risen slightly.1 In-hospital mortality rates are comparable between patients with STEMI and NSTEMI, at approximately 10%; however, the 1-year case fatality rate for patients with NSTEMI is more than double that for STEMI, at nearly 25%.6
This issue of Emergency Medicine Practice provides a comprehensive review of the literature on NSTEMI, the key diagnostic findings, and best-practice recommendations for management.
A PubMed search using the terms myocardial infarction [MeSH]) AND emergency service, hospital [MeSH] yielded 1905 articles, all of which were screened for relevance for this review. Because the majority of important literature addressing the diagnosis and management of MI is not specific to the ED setting, a broader strategy was needed. It was not feasible to conduct a comprehensive review using the term myocardial infarction [MeSH] alone, as this yielded 168,567 articles. We therefore augmented our ED-based search by reviewing national/international expert consensus guidelines, along with the literature cited by these guidelines, with additional targeted searches as needed.
In 2014, the American Heart Association (AHA) and the American College of Cardiology (ACC) released guidelines for NSTEMI management.7 It should be noted that the AHA/ACC have been criticized for possible conflict of interest due to extensive pharmaceutical industry funding of both the organizations themselves and their individual leaders.8 The European Society of Cardiology (ESC) released NSTEMI guidelines in 2015,9 and the American College of Emergency Physicians (ACEP) published a Clinical Policy on NSTEMI in 2018.10
The AHA/ACC and the ESC use a common system for grading the strength of recommendations and the supporting evidence. (See Table 1.) The ACEP policy translates levels of evidence into recommendation levels, wherein level A represents a high degree of clinical certainty, level B represents a moderate degree of clinical certainty, and level C represents a lack of clinical certainty. Recommendation classes cited in this article are from AHA/ACC, except where noted.
4. “I was taking care of an NSTEMI patient with a heart rate of 120 and blood pressure of 110/62 mm Hg. Pulmonary edema was noted on chest x-ray. I was worried about the heart rate, so I gave metoprolol 5 mg IV. Now the blood pressure is down to 80/40 mm Hg and he is in respiratory distress.”
Beta blockers should never be given to NSTE-ACS patients who have evidence of heart failure or shock. While beta blockers may be considered for stable patients, they should always be given orally. Furthermore, although patients with coronary artery disease benefit in the long term from being on a beta blocker, no benefit has been shown with administration in the first 24 hours.
5. “My chest pain patient is 68 years old and has a history of hypertension, diabetes, hypercholesterolemia, and morbid obesity. Her ECG is nonischemic, but she has left ventricular hypertrophy. Her pain has a ‘burning’ quality, and she associates it with indigestion. Her initial troponin is negative, and I really think this is just gastroesophageal reflux disease. I’m going to give her a GI cocktail and discharge her.”
Even with an unconvincing story, this patient has a HEART score of 4 (ECG, +1; age, +1; risk, +2), which puts her in a high-risk category. Serial troponin measurement is mandatory, and observation versus admission for further workup should be pursued.
6. “The NSTE-ACS patient had a history of heparin-induced thrombocytopenia, so I withheld anticoagulation and gave just aspirin.”
While most emergency clinicians have limited experience and comfort with alternate parenteral anticoagulants, agents such as fondaparinux and bivalirudin have been shown to be safe and effective in NSTE-ACS. These medications should be considered for patients with proven NSTE-ACS who have significant contraindications to heparins, and failure to administer them is not consistent with standard of care.
Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are equally robust. The findings of a large, prospective, randomized, and blinded trial should carry more weight than a case report.
To help the reader judge the strength of each reference, pertinent information about the study, such as the type of study and the number of patients in the study is included in bold type following the references, where available. In addition, the most informative references cited in this paper, as determined by the author, are highlighted.
Emergency Department management of Non-St Segment Elevation Myocardial Infarction, by Drs Julianna Jung and Sharon Bord.
Guidelines reviewed include those from:
STEMI definition from the European Society of cardiology:
MACE= Major Adverse Cardiovascular Event: including re-infarction, stroke, dysrhythmia, heart failure, cardiogenic shock, and death.
Immediate/urgent revascularization is recommended for all patients with NSTEMI who show signs of clinical instability, including refractory angina, sustained ventricular dysrhythmias, new or worsening heart failure, or shock (AHA class Ia recommendation; ESC class Ic recommendation). Otherwise, there is no clear benefit to immediate revascularization on all NSTEMI patients.
Dr. Ashoo is a practicing emergency physician, board-certified in emergency medicine and clinical informatics. Join him as he takes you through the January 2020 issue of Pediatric Emergency Medicine Practice: Emergency Department Management of Non–ST-Segment Elevation Myocardial Infarction.
The HEART score for major cardiac events predicts the 6-week risk of major adverse cardiac events.
Why to Use
The HEART score objectively risk-stratifies patients into low-, moderate-, and high-risk categories. This helps guide management, leading to better resource utilization, shorter hospital and ED stays for low-risk patients, and earlier interventions for moderate- and high-risk patients.
When to Use
The HEART score can be applied to any patient presenting to the ED with chest pain who the physician deems appropriate to evaluate for possible ACS.
Carlos Rodriguez, MD
Hyunjoo Lee, MD
The HEART score should be used in patients aged ≥ 21 years who present with symptoms suggestive of ACS. Do not use the HEART score if there is new ST-segment elevation ≥ 1 mm, or if there are other new ECG changes, hypotension, life expectancy < 1 year, or if the clinician identifies noncardiac medical, surgical, or psychiatric illness requiring admission.
Do not use the HEART score if the ECG shows new ST-segment elevation requiring immediate intervention, or with clinically unstable patients.
The HEART score was originally developed by Backus et al (2008) in a cohort of 122 patients with chest pain in an ED setting. The study included any patients admitted to the ED due to chest pain, irrespective of age, prehospital assumptions, and previous medical treatments. It excluded patients with chest pain and significant ST-segment elevations. End points in this study were acute myocardial infarction, percutaneous coronary intervention, coronary artery bypass graft, and death. HEART scores of 0 to 3 points confer a risk of 2.5% for any end point, and were therefore used to support discharge from the ED. Conversely, HEART scores of 4 to 6 points confer a risk of 20.3% for any end point, implying admission for clinical observation is necessary. HEART scores of ≥ 7 points have a risk of 72.7% for any end point and support early invasive strategies.
In a retrospective multicenter validation study also by Backus et al (2010), 880 patients presenting with chest pain were evaluated. The primary end points studied were the same as in the original study. In this study, 158 patients (17.95%) reached a primary end point. Of the 303 patients with HEART scores of 0 to 3 points, 3 (0.99%) had a MACE. Among 413 patients with HEART scores of 4 to 6 points, 48 cases (11.6%) resulted in a MACE, and among patients with HEART scores of 7 to 10 points, a MACE was identified in 107 of 164 cases (65.2%).
Backus et al (2013) externally validated HEART with a prospective multicenter study. The study evaluated 2440 patients presenting with chest pain to 10 EDs in the Netherlands. The primary end point was the occurrence of any MACE within 6 weeks. The performance of HEART was also compared to TIMI and GRACE. In the low-risk group (HEART scores of 0-3 points), 15 of 870 patients (1.7%) were found to have a MACE. In the group with HEART scores of 4 to 6 points, 183 of 1101 patients (16.6%) were diagnosed with a MACE. A MACE occurred in 50.1% of patients with HEART scores of 7 to 10 points. The C-statistic of the HEART score (0.83) was significantly higher than the C-statistic of the TIMI score (0.75) and the GRACE score (0.70), respectively (P < .0001).
Poldervaart et al (2017) studied the HEART score in a stepped-wedge, cluster-randomized trial, with the objective of measuring both outcomes and use of healthcare resources. The 9 Dutch hospitals included in the study were instructed to start usual care when assessing patients with chest pain. Every 6 weeks, one of the hospitals was randomly assigned to use HEART to assess patients with chest pain. A total of 3648 patients were included (1827 receiving usual care and 1821 receiving HEART care). The study found that the 6-week MACE incidence while using HEART was 1.3% lower than with usual care, but there were no statistically significant differences in early discharge, readmissions, recurrent ED visits, outpatient visits, or visits to general practitioners.
Recent studies have compared HEART head-to-head with other clinical decision rules for the ability to safely identify low-risk patients. A study by Poldervaart et al (2017) comparing HEART to TIMI and GRACE showed that HEART outperformed the others when identifying low-risk patients, with only 0.8% incidence of MACE in the low-risk group. In addition, Nieuwets et al (2016) compared HEART with TIMI for identifying low-risk patients without compromising safety, while also evaluating expected cost reductions. The study found that the HEART score identified more patients as low-risk than the TIMI score did, which would have led to potential cost savings of €64,107 (~USD $76,000) by using the HEART score cutoffs versus cost savings of €14,670 (~USD $17,000) using the TIMI score cutoffs.
The HEART pathway developed by Mahler et al (2015) combined the HEART score with 0- and 3-hour cardiac troponin tests in a decision aid designed to identify ED patients who are safe for early discharge. The study found that the HEART pathway decreased length of stay by 12 hours, decreased objective cardiac testing by 12%, and increased early discharges by 21%. No MACE was seen within 30 days in patients who were identified for early discharge. Of note, this study (and the original HEART studies) used regular-sensitivity cardiac troponin testing.
Barbra Backus, MD
The HEART pathway was designed to aid in efficiently evaluating patients with acute chest pain, using the previously validated HEART score.
Why to Use
Chest pain is one of the most common and potentially life-threatening chief complaints in emergency medicine. Many patients presenting with chest pain undergo unnecessarily extensive and costly evaluations to rule out ACS. The HEART pathway can reduce the number of prolonged and invasive evaluations while maintaining high sensitivity and negative predictive value for ACS.
Unlike other scoring systems such as the TIMI risk score or the GRACE risk score, the HEART pathway is designed to predict the likelihood of ACS in the patient presenting to the ED with acute chest pain. TIMI and GRACE risk scores are used to risk stratify patients who have been diagnosed with ACS.
When to Use The HEART pathway can be used in patients aged ≥ 21 years presenting with symptoms suggestive of ACS. It should not be used in patients with new ST-segment elevation ≥ 1 mm, or if there are other new ECG changes, hypotension, life expectancy < 1 year, or if the clinician identifies noncardiac medical, surgical, or psychiatric illness requiring admission.
Cullen Clark, MD
The HEART pathway is an accelerated diagnostic pathway. It is not designed to replace clinical judgment. Any patient with a concerning presentation or clinical progression should receive workup and treatment based on the clinician’s discretion, regardless of the risk predeicted by the HEART pathway.
Shared decision-making is a crucial part of further management after ACS risk has been determined, especially in patients with moderate risk who are recommended for observation and comprehensive cardiac evaluation. There is notable risk involved with hospitalization as well as risks for false-positive or nondiagnostic testing that would result in invasive procedures such as cardiac catheterization. The patient should be presented with the risks of both missed ACS and hospitalization for further workup.
Any patient who presents with chest pain and is subsequently discharged should be informed that, even with a negative workup, there is still a small risk of ACS. Patients should have close follow-up arranged and be given extensive return precautions prior to discharge.
Clinician judgment should prevail, even if patients are deemed to be at low risk by the HEART pathway. If there is some other cause for concern for an acute cardiac event, workup should be individualized to the patient.
All patients presenting to the ED with chest pain concerning for ACS should receive aspirin unless there is an absolute contraindication, such as known allergy, active bleeding, or if the patient has received a therapeutic aspirin dose prior to arrival.
The HEART pathway was developed by Mahler et al in 2015 in a randomized controlled single-center trial. The control arm was managed at the discretion of care providers encouraged to follow American College of Cardiology/American Heart Association guidelines for acute chest pain. The use of the HEART pathway in this study was designed to mimic the real world in that it was used as an accelerated diagnostic pathway. Patient care was at the discretion of the clinician and not mandated by the outcome of the HEART pathway.
There were 282 patients studied, with 141 patients in each treatment group. The primary outcome was the rate of objective cardiac testing (stress test, coronary computed tomography angiogram, or invasive coronary angiography) within 30 days of presentation. Secondary outcomes were early discharge rate, index length of stay, cardiac-related recurrent ED visits, and nonindex hospitalization at 30 days.
The rate of objective cardiac testing in the HEART pathway group was 12% less than in the usual care group. The rate of early discharge in the HEART pathway group was 21% higher than in the usual care group. The index length of stay was 12 hours shorter using the HEART pathway. There was no significant difference between the 2 groups for cardiac-related recurrent ED visits or nonindex hospitalization at 30 days. No patients identified for early discharge in either group had a missed major adverse cardiac event (MACE) during the first 30-day follow-up period. The study was not designed to adequately detect differences in MACE between the 2 study groups.
Riley et al in 2017 published a cost analysis of the HEART pathway compared to usual care, using the same data set as the original HEART pathway trial. There were 270 patients studied. Billing data were missing for 12 patients from the original study. Cost metrics considered in each group were index visit cost, total cost at 30 days, cardiac-related healthcare cost at 30 days, cardiac and noncardiac diagnostic testing cost, ED cost, inpatient cost for index visit, and outpatient cost. HEART pathway patients had a significantly lower mean and median cost for both index visit and 30-day follow-up. There was no significant difference between the median and mean costs of the other metrics. Average savings per patient was $216 when using the HEART pathway. On a larger scale, this would mean approximately $2 billion in savings per year for undifferentiated chest pain.
Mahler et al in 2017 also published a secondary analysis looking at high-sensitivity cardiac troponin I (hs-cTnI) and high-sensitivity cardiac troponin T (hs-cTnT). The study compared risk stratification using cardiac troponin I (cTnI) versus hs-cTnI and hs-cTnT in calculating the HEART pathway score. Blood samples were sent for cTnI, hs-cTnI, and hs-cTnT for 133 patients.
All of the troponin assays had poor sensitivity for predicting MACE when used separately from the HEART score. There was no difference in the pre-dicted risk of MACE between the use of serial cTnI and 3-hour hs-cTnI in the HEART pathway. Using hs-cTnT in the HEART pathway led to 1 patient with an NSTEMI (non–ST-segment elevation myocardial
infarction) being misclassified as low risk. The study found the HEART pathway using serial cTnI or 3-hour hs-cTnI to have sensitivity and negative predictive value of 100% for 30-day MACE. Although hs-cTnT use in the HEART pathway caused an NSTEMI to be misclassified as low risk, the reduction in sensitivity was not statistically significant, given the small study population. The authors recommend further appropriately powered studies to determine small differences in the accuracy of the high-sensitivity troponin assays.
Simon A. Mahler, MD
The GRACE risk score estimates in-hospital and 6-month mortality for patients with acute coronary syndromes.
Why to Use
Many guidelines recommend more aggressive medical management, or even early-invasive management, for patients with a high mortality risk. Knowing a patient’s risk may help with management and with discussions about the goals of care with patients and their families. A patient with some nonspecific features in the workup (eg, history, ECG, troponin) can be more objectively risk-stratified for chest pain by quantifying the risk; this can potentially lead to shorter hospital stays, fewer inappropriate interventions, and more appropriate interventions.
When to Use
The GRACE risk score can be used in patients with known STEMI or UA/NSTEMI to determine mortality risk.
The GRACE Research Group provides information about risk levels based on the GRACE risk score.
Graham Walker, MD
GRACE is a large international database from 94 hospitals in 14 countries, which gives it excellent external validity a priori. The original GRACE risk score study conducted by Fox et al (2006) looked at the cumulative 6-month risk of death, and death or myocardial infarction, in patients who had suspected ACS that was not secondary to trauma, surgery, or other significant comorbidity (n = 43,810; 21,688 in derivation set, 22,122 in validation set).
Patients included in the study presented with signs or symptoms of acute cardiac ischemia and also had ECG findings consistent with ACS, cardiac biomarker serial increases consistent with ACS, or documented coronary artery disease. The in-hospital mortality status was available in 98.1% of the 11,389 ACS patients studied. Twenty-two percent of the in-hospital deaths occurred within 24 hours of admission, which suggests that this registry contains a very sick cohort of patients.
In 2014, Fox et al updated the GRACE risk score to GRACE 2.0. This new version of the GRACE risk score for 1-year outcomes was derived in the more recent data set of 32,037 patients from the GRACE registry who were enrolled between January 2002 and December 2007. Of note, GRACE 2.0 evalu-ated variables for nonlinear mortality associations, providing a more accurate estimate of outcome. GRACE 2.0 also includes mortality estimates up to 3 years after the ACS event via several other data sets with longer follow-up windows.
Joel Gore, MD and Keith A. A. Fox, MBBS, FRCP
The TIMI risk score for UA/NSTEMI estimates mortality in patients with unstable angina and non-ST-segment elevation myocardial infarction.
Why to Use
Chest pain is one of the most common complaints bringing patients to the ED for evaluation. The identification and acute management of STEMI is rarely a conundrum. However, UA/ NSTEMI can go missed. Traditionally, the TIMI risk score for UA/NSTEMI can correlate the risk of adverse outcome in chest pain patients.
When to Use
The TIMI risk score for UA/NSTEMI can be used to help risk stratify patients with presumed ischemic chest pain. However, it was originally derived in patients with confirmed UA or NSTEMI.
Hyunjoo Lee, MD
Carlos Rodriguez, MD
Patients in the 0 to 1 point group should be further risk stratified using another risk score or institutional practices, as their risk is not low enough to safely discharge them from the hospital. Many guidelines recommend aggressive medical intervention and/or early-invasive management for higher-risk patients.
Antman et al (2000) used a merged database of 7081 UA/NSTEMI patients in the TIMI 11B and ESSENCE trials for the original derivation and validation of this TIMI risk score. The TIMI risk score was originally derived from 1957 UA/NSTEMI patients receiving unfractionated heparin in the TIMI 11B trial, and was internally validated in 3 cohorts of patients from the rest of the merged data: 1953 patients receiving enoxaparin in the TIMI 11B trial; 1564 patient receiving unfractionated heparin in the ESSENCE trial; and 1607 patients receiving enoxaparin in the ESSENCE trial. The study included UA/NSTEMI patients with chest pain at rest who presented within 24 hours of symptoms, and who had ST-segment deviation on their presenting ECG, history of coronary artery disease, and a measured cardiac enzyme that was elevated. Patients were excluded if revascularization was performed within 24 hours or if the patient had a contraindication for anticoagulation. The primary end points were composite all-cause mortality, myocardial infarction (MI), or urgent revascularization within 14 days.
By the end of the 14 days, 16.7% of the derivation group had died, had an MI, or needed urgent revascularization. An increase in the TIMI risk score correlated with an increase in all-cause mortality, MI, or urgent revascularization. The same pattern was seen in the internally validated groups. There have been many external validation studies since the original derivation.
Scirica et al (2002) externally validated the TIMI risk score in patients from 9 sites in the TIMI III registry. This study included UA/NSTEMI patients with ischemic chest pain lasting more than 5 minutes who presented within 96 hours of symptom onset. Patients were excluded if they had a STEMI, chest pain of other origin, planned revascularization, or if the patient was in a prior TIMI trial. Primary end points were death, MI, and recurrent ischemia within 6 weeks and at 1 year.
As in the original derivation study and internal validation studies, there was an increase in mortality, MI, and recurrent ischemia with each increase in the TIMI risk score. However, this study modified the TIMI risk score definitions to some degree by substituting a patient’s history of MI or revascularization history for “known coronary artery stenosis > 50%,” and assigning 1 point for aspirin use in the past 24 hours, not the past 7 days as in the original trial by Antman et al. Still, this population was in a registry for patients with known UA/NSTEMI. This validation is less useful for patients with undifferentiated chest pain seen in the acute care setting of the emergency department (ED).
Pollack et al (2006) externally validated the TIMI risk score in a prospective observational cohort study of 3929 adult patients with chest pain in the ED. The study included adult chest pain patients aged > 24 years who were evaluated with ECG. Adults aged < 24 years were included if the chest pain was preceded by cocaine use within the previous week. Patients were excluded if they had a STEMI. Whereas the original derivation study looked at adverse outcomes within 14 days, and Scirica et al (2002) validated the risk score looking up to 6 weeks and even 1 year, Pollack et al followed up with patients for up to 30 days from presentation for adverse outcomes of death, MI, or revascularization. As in prior studies, the higher the TIMI risk score, the higher the likelihood of adverse outcome within the measured time period, which was 30 days in this study. However, the patient population was different in that there were more black patients and more female patients. Also, if no cardiac markers were ordered, a score of 0 was assumed and assigned to the category of cardiac enzymes.
Chase et al (2006) externally validated the TIMI risk score in a prospective observational study of 1458 patient visits in the ED. The study included patients aged > 30 years with nontraumatic chest pain who had an ECG performed in the ED. Whereas Pollack et al included patients with cocaine use, Chase et al excluded patients if cocaine was used in the 7 days prior to presentation. Like Pollack et al, Chase et al assigned a score of 0 to cardiac enzymes if they were not drawn. Chase et al also followed patients for up to 30 days. Within 30 days, 12.8% of patients had an adverse outcome of death, MI, or revascularization. In patients with a TIMI risk score of 0, 1.7% had an adverse outcome.
Although there was a general correlation of an increase in adverse outcome with higher TIMI risk score, this study did not show a similar stepwise increase. This is likely secondary to having a study population that was dissimilar to the original derivation group or other validation studies, as this study had patients with mostly low TIMI scores and included STEMI patients in the study population.
Elliot M. Antman, MD
Julianna Jung, MD, MEd, FACEP; Sharon Bord, MD, FACEP
Michael Gottlieb, MD; Bradley Shy, MD
January 1, 2020
January 31, 2023
4 AMA PRA Category 1 Credits™, 4 ACEP Category I Credits, 4 AAFP Prescribed Credits, 4 AOA Category 2-A or 2-B Credits.
Date of Original Release: January 1, 2020. Date of most recent review: December 10, 2019. Termination date: January 1, 2023.
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