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    TIMI Risk Score for UA/NSTEMI

    Estimates mortality for patients with unstable angina and non-ST elevation MI.
    When to Use
    Why Use

    Can be used to help risk stratify patients with presumed ischemic chest pain. However, it was originally derived in patients with confirmed unstable angina or non-ST elevation myocardial infarction.

    • One of the earliest chest pain decision rules that was widely implemented.

    • Originally derived with patients with known unstable angina or NSTEMI.

    • Newer chest pain risk scores such as the HEART Score have been shown to better stratify risk than the TIMI Score, particularly in the undifferentiated chest pain patient.
    • A TIMI risk score of 0 or 1 does not equal zero risk of adverse outcome. The original study showed 4.7% of patients with a score of 0 or 1 had adverse outcomes within 14 days. Validation studies showed 1.7 to 2.1% of patients with a score of 0 still had adverse outcomes within 30 days.

    • Unclear if this risk score can be used in patients with chest pain in the setting of cocaine use.

    • The TIMI Score was further studied as part of an accelerated diagnostic protocol in the ADAPT trial, which includes estimation of pre-test probability using TIMI, plus abnormal EKG and troponin (high-sensitivity cardiac troponin I).

    UA/NSTEMI can sometimes be missed. Traditionally, the TIMI Risk Score for UA/NSTEMI can correlate the risk of adverse outcome in chest pain patients.


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    • Patients with a score of 0 or 1 point are at lower risk of adverse outcome (death, MI, urgent revascularization) compared to patients with a higher risk score. However, the risk is not zero.

    • Patients with a higher risk score may require more aggressive medical or procedural intervention.

    • Newer chest pain risk scores such as the HEART Score have been shown to better stratify risk than the TIMI Score, particularly in the undifferentiated chest pain patient.


    If patients are in the 0 or 1 point group, they should be further risk stratified using another risk score or one’s own institutional practices, as risk is not low enough to safely discharge from the hospital. Many guidelines recommend higher risk levels receiving more aggressive medical intervention and/or receiving early invasive management.

    Critical Actions

    A TIMI Risk Score of 0 does not equate to zero risk of adverse outcome.


    Addition of the selected points:

    Criteria Value
    Age ≥65 +1
    ≥3 CAD risk factors* +1
    Known CAD (stenosis ≥50%) +1
    ASA use in past 7 days +1
    Severe angina (≥2 episodes in 24 hrs) +1
    EKG ST changes ≥0.5mm +1
    Positive cardiac marker +1

    *Risk factors for CAD: Family history of CAD, hypertension, hypercholesterolemia, diabetes, or current smoker (thanks to Jeff Geske at Mayo for this update!)

    Evidence Appraisal

    Antman et al (2000) used a merged database of 7,081 UA/NSTEMI patients in the TIMI 11B and ESSENCE trails for the original derivation and validation of this TIMI risk score for UA/NSTEMI. The risk score was originally derived from 1,957 UA/NSTEMI patients receiving unfractionated heparin in the TIMI 11B trial and internally validated in 3 cohorts of patients from the rest of the merged data: 1,953 patients receiving enoxaparin in the TIMI 11B trial, 1,564 patient receiving unfractionated heparin in the ESSENCE trial, and 1,607 receiving enoxaparin in the ESSENCE trial. They included UA/NSTEMI patients with chest pain at rest who presented within 24 hours of symptoms who had ST-segment deviation on their presenting EKG, history of coronary artery disease, and a measured cardiac enzyme that was elevated. Patients were excluded if revascularization was within 24 hours or if the patient had a contraindication to anticoagulation. The primary endpoints were composite all-cause mortality, myocardial infarction, or urgent revascularization up to 14 days.

    By the end of the 14 days, 16.7% of the derivation group died, had a myocardial infarction, or needed urgent revascularization. An increase of the TIMI 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 its derivation.

    Scirica et al (2002) externally validated the TIMI Score in 1,137 UA/NSTEMI patients from 9 sites in the TIMI III Registry. They included UA/NSTEMI patients with ischemic chest pain lasting more than five minutes, presenting 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 endpoints were death, myocardial infarction, 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 Score. However, they modified the TIMI Score definitions to some degree: they substituted a patient’s history of MI or revascularization history for “known coronary artery stenosis >50%” and assigned 1 point for aspirin use in the past 24 hours, not 7 days as in the original trial by Antman et al. Still, this population was in a registry for patients with known UA/NSTEMI. Thus, this validation is less useful for undifferentiated chest pain patients seen in the acute care setting of the emergency department.

    Pollack et al (2006) externally validated the TIMI Score in a prospective observational cohort study of 3,929 adult chest pain patients in the ED. They included adult chest pain patients older than 24 years old evaluated with EKG. Adults under 24 years old were included if the chest pain was preceded by cocaine use within the week prior. Patients were excluded if they had a STEMI. Whereas the original derivation study looked at adverse outcomes within 14 days and Scirica et al validated the risk score looking up to 6 weeks and even 1 year, Pollack et al followed-up patients up to 30 days from presentation for adverse outcomes of death, myocardial infarction, or revascularization. As in prior studies, the higher the TIMI Score, the higher the likelihood of adverse outcome within the measured time period, in this study 30 days. 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 zero was assumed and assigned to the category of cardiac enzymes.

    Chase et al (2006) externally validated the TIMI Score in a prospective observational study of 1,458 patient visits in the ED. They included non-traumatic chest pain patients older than 30 years old who had an EKG done 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, this study assigned a score of zero to cardiac enzymes if they were not drawn. Chase et al also followed patients 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 Score of zero, 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; this study had patients with mostly low TIMI scores and also included STEMI patients into the study population.


    Dr. Elliott M. Antman

    About the Creator

    Elliott M. Antman, MD, is a professor and associate dean for Clinical/Translational Research at Harvard Medical School. He is also a senior physician in the Cardiovascular Division of the Brigham and Women's Hospital in Massachusetts and President of the American Heart Association (2014-2015). As a senior investigator in the TIMI Study Group, Dr. Antman has published on the use of serum cardiac markers for diagnosis and prognosis of patients with unstable angina and acute myocardial infarction, cyclooxygenase and cardiovascular risk, and antithrombotic therapy for acute coronary syndromes.

    To view Dr. Elliott M. Antman's publications, visit PubMed

    About the Creator
    Dr. Elliott M. Antman
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