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Antman EM, Cohen M, Bernink PJLM, et al. The TIMI Risk Score for Unstable Angina/Non–ST Elevation MI: A Method for Prognostication and Therapeutic Decision Making. JAMA. 2000;284(7):835–842. doi:10.1001/jama.284.7.835
Author Affiliations: Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Boston, Mass (Drs Antman and Braunwald and Ms McCabe); Division of Cardiology, Hahnemann University Hospital, Philadelphia, Pa (Dr Cohen); Department of Cardiology, Martini Hospital, Groningen, the Netherlands (Dr Bernink); Evangelisches Krankenhaus, Witten, Germany (Dr Horacek); Washington County Hospital, Hagerstown, Md (Dr Papuchis); Fundacion Favaloro, Buenos Aires, Argentina (Dr Mautner); Pontificia Universidad Catolica de Chile, Santiago (Dr Corbalan); and Rhône-Poulenc Rorer, Collegeville, Pa (Mr Radley).
Context Patients with unstable angina/non–ST-segment elevation myocardial
infarction (MI) (UA/NSTEMI) present with a wide spectrum of risk for death
and cardiac ischemic events.
Objective To develop a simple risk score that has broad applicability, is easily
calculated at patient presentation, does not require a computer, and identifies
patients with different responses to treatments for UA/NSTEMI.
Design, Setting, and Patients Two phase 3, international, randomized, double-blind trials (the Thrombolysis
in Myocardial Infarction [TIMI] 11B trial [August 1996–March 1998] and
the Efficacy and Safety of Subcutaneous Enoxaparin in Unstable Angina and
Non-Q-Wave MI trial [ESSENCE; October 1994–May 1996]). A total of 1957
patients with UA/NSTEMI were assigned to receive unfractionated heparin (test
cohort) and 1953 to receive enoxaparin in TIMI 11B; 1564 and 1607 were assigned
respectively in ESSENCE. The 3 validation cohorts were the unfractionated
heparin group from ESSENCE and both enoxaparin groups.
Main Outcome Measures The TIMI risk score was derived in the test cohort by selection of independent
prognostic variables using multivariate logistic regression, assignment of
value of 1 when a factor was present and 0 when it was absent, and summing
the number of factors present to categorize patients into risk strata. Relative
differences in response to therapeutic interventions were determined by comparing
the slopes of the rates of events with increasing score in treatment groups
and by testing for an interaction between risk score and treatment. Outcomes
were TIMI risk score for developing at least 1 component of the primary end
point (all-cause mortality, new or recurrent MI, or severe recurrent ischemia
requiring urgent revascularization) through 14 days after randomization.
Results The 7 TIMI risk score predictor variables were age 65 years or older,
at least 3 risk factors for coronary artery disease, prior coronary stenosis
of 50% or more, ST-segment deviation on electrocardiogram at presentation,
at least 2 anginal events in prior 24 hours, use of aspirin in prior 7 days,
and elevated serum cardiac markers. Event rates increased significantly as
the TIMI risk score increased in the test cohort in TIMI 11B: 4.7% for a score
of 0/1; 8.3% for 2; 13.2% for 3; 19.9% for 4; 26.2% for 5; and 40.9% for 6/7
(P<.001 by χ2 for trend). The pattern
of increasing event rates with increasing TIMI risk score was confirmed in
all 3 validation groups (P<.001). The slope of
the increase in event rates with increasing numbers of risk factors was significantly
lower in the enoxaparin groups in both TIMI 11B (P
= .01) and ESSENCE (P = .03) and there was a significant
interaction between TIMI risk score and treatment (P
Conclusions In patients with UA/NSTEMI, the TIMI risk score is a simple prognostication
scheme that categorizes a patient's risk of death and ischemic events and
provides a basis for therapeutic decision making.
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