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CLINICAL STATEMENTS AND GUIDELINES

Circulation. 2025;151:e771–e862. DOI: 10.1161/CIR.0000000000001309 April 1, 2025 e785

percentile upper reference limit and believed caused by myocardial ischemia.21 With the development of hs-cTn assays enabling detection of circulating cTn at lower concentrations, CDPs using serial testing of hs-cTn at presentation (0 hours) and 1 to 2 hours later provide high negative predictive value, as well as accelerated recognition of myocardial injury.9,1012 Clinicians should be familiar with both the evidence-based CDPs and the analytical characteristics of the cTn assay (ie, limit of quantification, 99th percentile upper reference limit, and criteria for significant change) used in their practice.24,26 Men and women may have different cutoff values with hs-cTn assays. With hs-cTn assays, changes in hs-cTn concentration within the normal reference range but below the 99th percentile upper reference limit can signal cardiac ischemia and may warrant further evaluation. CDPs incorporating hscTn assays with repeat sampling at 1 or 2 hours from ED arrival with calculation of the change or “delta” hs-cTn can identify patients at very low risk (eg, negative predictive value >99.5%) based on assay-specific diagnostic thresholds.8,11,27–30 However, when using conventional cTn assays, the sampling timeframe is extended to 3 to 6 hours from ED arrival.31 cTn may be within normal range early after symptom onset especially when a high-sensitivity assay is not used. When using a CDP that incorporates a single hs-cTn value, the troponin should be obtained at least 3 hours after the onset of symptoms.32

3.1.3 Risk Stratification Tools for Patients With STEMI and NSTE-ACS

Synopsis Substantial variability in short-term mortality and MACE risk exists among patients with ACS. Individual risk assessment can inform discussions with patients and decisions regarding therapeutic interventions. Several risk scores have been developed and validated to help assess a patient’s short- and long-term risk in established ACS using commonly available clinical and laboratory variables. Although several risk scores exist,1–3 the GRACE (Global Registry of Acute Coronary Events) and TIMI (Thrombolysis in Myocardial Infarction) Risk Scores for NSTE-ACS and STEMI (Table 5) are well validated and may be useful for helping to guide some therapeutic decisions (Section 6.1., “Rationale and Timing for a Routine Invasive or Selective Invasive Approach”).4–7 These scores are not to be used as diagnostic tools, because they stratify patient risk in the setting of suspected or confirmed ACS. Risk assessment using the GRACE Risk Score has been found to be superior to subjective physician assessment for the prediction of death or MI in patients with STEMI or intermediate-risk NSTE-ACS.8 However, there is insufficient evidence that routine use of risk scores in patients hospitalized for STEMI/ NSTE-ACS translates into reduced risk of cardiovascular events.9,10

Evidence of HF, such as pulmonary congestion detected by physical examination, chest x-ray, or lung ultrasound, is an important risk marker and integral part of the Killip classification (and thereby the GRACE Risk Score and TIMI Risk Score for STEMI) in patients with ACS.11–15 Similarly, elevated cardiac biomarkers provide prognostic information and also are key elements of the GRACE and TIMI Risk Scores. Higher cTn levels in patients with ACS are associated with an increased risk of death and MACE16,17 and similarly may be useful for helping to guide some treatment decisions.4,18 Several other serum or plasma biomarkers may provide additional prognostic information. In particular, natriuretic peptides (including B-type natriuretic peptide and N-terminal pro-

Table 5.  Selected Risk Stratification Tools for Patients With ACS

GRACE Risk Score (2.0)6,7 TIMI Risk Score for Unstable Angina/NSTEMI*4 TIMI Risk Score for STEMI5

Target population ACS Unstable angina or NSTEMI STEMI Target outcome(s) In-hospital, 6-mo, 1-y, 3-y, death or death/MI 14-d all-cause death, MI, or urgent revascularization 30-d all-cause death Variables used In-hospital risk score

Age Killip class Systolic blood pressure Heart rate ST-segment deviation Cardiac arrest on admission Serum creatinine Elevated cardiac biomarkers Age ≥65 y

≥3 risk factors for CAD Known coronary stenosis (≥50%) ST-segment deviation ≥0.5 mm ≥2 anginal events in prior 24 h Aspirin use in prior 7 d Elevated cardiac biomarkers (CK-MB or troponin) Age (65-74 y/≥75 y) (2-3 points)

Killip class II-IV (2 points)* Systolic blood pressure (<100 mm Hg, 3 points) Heart rate >100 bpm (2 points) Anterior ST-segment elevation or LBBB (1 point) Diabetes/hypertension/angina (1 point) Weight (<67 kg, 1 point) Time to treatment >4 h (1 point)

*Score 1 point for each characteristic that is present. ACS indicates acute coronary syndromes; bpm, beats per minute; CAD, coronary artery disease; CK-MB, creatine kinase-myocardial band; GRACE, Global Registry of Acute Coronary Events; LBBB, left bundle branch block; MI, myocardial infarction; NSTEMI, non–ST-segment elevation myocardial infarction; STEMI, ST-segment elevation myocardial infarction; and TIMI, Thrombolysis in Myocardial Infarction.

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