Figure 1. Acute Coronary Syndromes

Figure 1 Notes

The top half of the figure illustrates the progression of plaque formation and onset and complications of NSTE-ACS, with management at each stage. The numbered section of an artery depicts the process of atherogenesis from 1) normal artery to 2) extracellular lipid in the subintima to 3) fibrofatty stage to 4) procoagulant expression and weakening of the fibrous cap. ACS develops with 5) disruption of the fibrous cap, which is the stimulus for thrombogenesis. 6) Thrombus resorption may be followed by collagen accumulation and smooth muscle cell growth. Thrombus formation and possible coronary vasospasm reduce blood flow in the affected coronary artery and cause ischemic chest pain.

The bottom half of the figure illustrates the clinical, pathological, electrocardiographic, and biomarker correlates in ACS and the general approach to management. Flow reduction may be related to a completely occlusive thrombus (bottom half, right side) or subtotally occlusive thrombus (bottom half, left side). Most patients with ST elevation (thick white arrow in bottom panel) develop QwMI, and a few (thin white arrow) develop NQMI. Those without ST elevation have either UA or NSTEMI (thick red arrows), a distinction based on cardiac biomarkers. Most patients presenting with NSTEMI develop NQMI; a few may develop QwMI. The spectrum of clinical presentations including UA, NSTEMI, and STEMI is referred to as ACS. This NSTE-ACS CPG includes sections on initial management before NSTE-ACS, at the onset of NSTE-ACS, and during the hospital phase. Secondary prevention and plans for long-term management begin early during the hospital phase. Patients with noncardiac etiologies make up the largest group presenting to the ED with chest pain (dashed arrow).

Figure 2. GRACE Risk Model Nomogram

1. Find Points for Each Predictive Factor: Killip Class Points SBP (mmHg) Points Heart Rate (beats/min) Points Age (years) Points Creatinine Level (mg/dL) Points I 0 ≤ 80 58 ≤ 50 0 ≤ 30 0 0 – 0.39 1 II 20 80 – 99 53 50 – 69 3 30 – 39 8 0.40 – 0.79 4 III 39 100 – 119 43 70 – 89 9 40 – 49 25 0.80 – 1.19 7 IV 59 120 - 139 34 90 – 109 15 50 – 59 41 1.20 – 1.59 10     140 – 159 24 110 – 149 24 60 – 69 58 1.60 – 1.99 13     160 – 199 10 150 – 199 38 70 – 79 75 2.00 – 3.99 21     ≥ 200 0 ≥ 200 46 80 - 89 91 > 4.0 28             ≥ 90 100

Other Risk Factors	Points
Cardiac Arrest at Admission	39
ST-Segment Deviation	28
Elevated Cardiac Enzyme Levels	14

2. Sum Points for All Predictive Factors: Killip Class SBP Heart Rate Age Creatinine Level Cardiac Arrest at Admission ST-Segment Deviation Elevated Cardiac Enzyme Levels = Total Points

3. Look Up Risk Corresponding to Total Points:
Total Points	≤60	70	80	90	100	110	120	130	140	150	160	170	180	190	200	210	220	230	240	≥250
Probability of In- Hospital Death, %	≤0.2	0.3	0.4	0.6	0.8	1.1	1.6	2.1	2.9	3.9	5.4	7.3	9.8	13	18	23	29	36	44	≥52

Table 1. TIMI Risk Score^a for NSTE-ACS

TIMI Risk Score/ All-Cause Mortality, New or Recurrent MI, or Severe Recurrent Ischemia Requiring Urgent Revascularization Through 14 Days After Randomization, %

0-1

4.7

2

8.3

3

13.2

4

19.9

5

26.2

6-7

40.9

^a The TIMI risk score is determined by the sum of the presence of 7 variables at admission; 1 point is given for each of the following variables: ≥65 years of age; ≥3 risk factors for CAD; prior coronary stenosis ≥50%; ST deviation on ECG; ≥2 anginal events in prior 24 h; use of ASA in prior 7 d; and elevated cardiac biomarkers.
Modified with permission from Antman EM et al. JAMA. 2000;284:835-842.

Table 2. Clinical Assessment and Initial Evaluation

Recommendation	COR	LOE
Patients with suspected ACS should be risk stratified based on the likelihood of ACS and adverse outcome(s) to decide on the need for hospitalization and assist in the selection of treatment options.	I	B

Table 3. ED or Outpatient Facility Presentation

Recommendations	COR	LOE
Patients with suspected ACS and high-risk features such as continuing chest pain, severe dyspnea, syncope/presyncope, or palpitations should be referred immediately to the ED and transported by emergency medical services when available.	I	C
Patients with less severe symptoms may be considered for referral to the ED, a chest pain unit, or a facility capable of performing adequate evaluation depending on clinical circumstances.	IIb	C

Table 4. Prognosis—Early Risk Stratification

Recommendations	COR	LOE
In patients with chest pain or other symptoms suggestive of ACS, a 12-lead ECG should be performed and evaluated for ischemic changes within 10 min of the patient’s arrival at an emergency facility.	I	C
If the initial ECG is not diagnostic but the patient remains symptomatic and there is a high clinical suspicion for ACS, serial ECGs (e.g., 15- to 30-minute intervals during the first hour) should be performed to detect ischemic changes.	I	C
Serial cardiac troponin I or T levels (when a contemporary assay is used) should be obtained at presentation and 3-6 h after symptom onseta in all patients who present with symptoms consistent with ACS to identify a rising and/or falling pattern of values.	I	A
Additional troponin levels should be obtained beyond 6 h after symptom onseta in patients with normal troponin levels on serial examination when changes on ECG and/or clinical presentation confer an intermediate or high index of suspicion for ACS.	I	A
Risk scores should be used to assess prognosis in patients with NSTE-ACS.	I	A
Risk-stratification models can be useful in management.	IIa	B
It is reasonable to obtain supplemental electrocardiographic leads V7-V9 in patients whose initial ECG is nondiagnostic and who are at intermediate/high risk of ACS.	IIa	B
Continuous monitoring with 12-lead ECG may be a reasonable alternative in patients whose initial ECG is nondiagnostic and who are at intermediate/high risk of ACS.	IIb	B
Measurement of B-type natriuretic peptide or N-terminal pro–B-type natriuretic peptide may be considered to assess risk in patients with suspected ACS.	IIb	B
a If the time of symptom onset is ambiguous, the time of presentation should be considered the time of onset for assessing troponin values (COR I, LOE A).

Table 5. Cardiac Biomarkers and the Universal Definition of MI

Recommendations	COR	LOE
Diagnosis
Cardiac-specific troponin (troponin I or T when a contemporary assay is used) levels should be measured at presentation and 3-6 h after symptom onset in all patients who present with symptoms consistent with ACS to identify a rising and/or falling pattern.	I	A
Additional troponin levels should be obtained beyond 6 h after symptom onset in patients with normal troponins on serial examination when electrocardiographic changes and/or clinical presentation confer an intermediate or high index of suspicion for ACS.	I	A
If the time of symptom onset is ambiguous, the time of presentation should be considered the time of onset for assessing troponin values.	I	A
With contemporary troponin assays, creatine kinase myocardial isoenzyme (CK-MB) and myoglobin are NOT useful for diagnosis of ACS.	III: No Benefit	A
Prognosis
The presence and magnitude of troponin elevations are useful for short- and long-term prognosis.	I	B
It may be reasonable to remeasure troponin once on day 3 or day 4 in patients with an MI as an index of infarct size and dynamics of necrosis.	IIb	B
Use of selected newer biomarkers, especially B-type natriuretic peptide, may be reasonable to provide additional prognostic information.	IIb	B