Key PointsACS has evolved as a useful operational term that refers to a spectrum of conditions compatible with acute myocardial ischemia and/or infarction which are usually due to an abrupt reduction in coronary blood flow (Figure 1).
- A key branch point is ST elevation or new left bundle-branch block on the ECG, which are considerations for immediate coronary angiography to determine if there is an indication for reperfusion therapy to open a likely completely occluded coronary artery.
- The imbalance may also be caused by other conditions, including excessive myocardial oxygen demand in the setting of a stable flow-limiting lesion; acute coronary insufficiency due to other causes (e.g., vasospastic [Prinzmetal] angina, coronary embolism, coronary arteritis); noncoronary causes of myocardial oxygen supply-demand mismatch (e.g., hypotension, severe anemia, hypertension, tachycardia, hypertrophic cardiomyopathy, severe aortic stenosis); nonischemic myocardial injury (e.g., myocarditis, cardiac contusion, cardiotoxic drugs); and multifactorial causes that are not mutually exclusive (e.g., stress [Takotsubo] cardiomyopathy, pulmonary embolism, severe HF, sepsis).
- If cardiac biomarkers are elevated and the clinical context is appropriate, the patient is considered to have NSTEMI. Otherwise, the patient is deemed to have UA.
- ST depression, transient ST elevation, and/or prominent T-wave inversions may be present but are not required for a diagnosis of NSTEMI.
- Abnormalities on the ECG and elevated troponins in isolation are insufficient to make the diagnosis of ACS but must be interpreted in the appropriate clinical context.
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:
|Other Risk Factors||Points|
|Cardiac Arrest at Admission||39|
|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:
|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|
For example, a patient has Killip class II, SBP of 100 mm Hg, heart rate of 100 beats/min, is 65 years of age, has serum creatinine level of 1.0 mg/dL, did not have a cardiac arrest at admission but did have ST-segment deviation and elevated enzyme levels. His score would be: 20 53 15 58 7 0 28 14 = 196. This person would have about a 16% risk of having an in-hospital death.
Similarly, a patient with Killip class I, SBP of 80 mm Hg, heart rate of 60 beats/min, is 55 years of age, has serum creatinine level of 0.4, and no risk factors would have the following score: 0 58 3 41 1 = 103, which gives approximately a 0 .9% risk of having an in-hospital death.
To convert serum creatinine level to micromoles per liter, multiply by 88.4.
Modified with permission from Granger CB, Goldberg RJ, Dabbous O, et al. Predictors of hospital mortality in the Global Registry of Acute Coronary Events. Arch Intern Med. 2003;163:2345-2353.
Table 1. TIMI Risk Scorea 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, %
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
|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
|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
|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
|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|
|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|
|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|