Use of aspirin, age >= 65 years & presence of Congestive Heart Failure (CHF) were stronger predictors of Modified Gensini score. Multiple linear regressions, Student's t-test and Pearson's coefficient 'r' were also used. Correlation with Modified Gensini score and percentage stenosis in culprit artery was done.ĭata were summarized in the form of Mean, Standard Deviation and Proportions. All patients underwent coronary angiography. One hundred and sixty patients with acute unstable angina were evaluated for presence of 9 clinical predictors and their 3 risk scores were calculated. This was a hospital based single centre, cross-sectional, observational, descriptive study conducted at a tertiary care teaching institute. To know the correlation of clinical risk scores with angiographic extent of coronary artery disease. JAMA.The correlation of clinical risk predictors and clinical risk scores: Thrombolysis in Myocardial Infarction (TIMI), Platelet Glycoprotein IIb-IIIa in Unstable Angina, Receptor Suppression Using Integrilin Therapy (PURSUIT) and Global Registry of Acute Coronary Events (GRACE) scores in Unstable Angina with angiographic extent of Coronary Artery Disease (CAD) is not known. 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. 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 =. The pattern of increasing event rates with increasing TIMI risk score was confirmed in all 3 validation groups (P<.001). 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. 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. 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. ![]() 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. 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. The 3 validation cohorts were the unfractionated heparin group from ESSENCE and both enoxaparin groups. A total of 1957 patients with UA/NSTEMI were assigned to receive unfractionated heparin (test cohort) and 1953 to receive enoxaparin in TIMI 11B 15 were assigned respectively in ESSENCE. Two phase 3, international, randomized, double-blind trials (the Thrombolysis in Myocardial Infarction 11B trial and the Efficacy and Safety of Subcutaneous Enoxaparin in Unstable Angina and Non-Q-Wave MI trial ). 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. 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.
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