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Original Contribution
August 16, 2000

The TIMI Risk Score for Unstable Angina/Non–ST Elevation MI: A Method for Prognostication and Therapeutic Decision Making

Author Affiliations

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).

JAMA. 2000;284(7):835-842. doi:10.1001/jama.284.7.835
Abstract

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 = .02).

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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