DIAGNOSIS

ACS is a clinical syndrome that includes MI and unstable angina. An MI can present as either a STEMI or NSTEMI. A STEMI typically occurs as a result of plaque rupture and subsequent thrombosis of a coronary artery that leads to infarction and subsequent ECG changes. An NSTEMI does not have the ECG changes seen in STEMI but can also occur secondary to plaque rupture (Type 1 NSTEMI) or to inadequate blood flow to meet the metabolic demands of the myocardium in conditions like sepsis, pulmonary embolism, or coronary vasospasm (Type 2 NSTEMI). In either case, both STEMI and NSTEMI will result in an elevated troponin. Unstable angina is characterized by new onset chest pain, pain lasting greater than 20 minutes or pain at rest or with minimal exertion. While unstable angina can occur with ECG changes not diagnostic of STEMI, it does not have elevated troponins.10 It is essential to differentiate between STEMI and NSTEMI since those with STEMI require emergent coronary intervention.9 NSTEMI is more common than STEMI, representing 60-70% of myocardial infarctions.14 NSTEMI with coronary occlusion is present in 25% of cases.15

ACS pain is classically described as exertional, pressure-like chest pain with radiation to the jaw, neck, one or both arms/shoulders, or back. Associated symptoms include nausea/vomiting, shortness of breath, and diaphoresis.10 Atypical symptoms (dyspnea alone, fatigue, weakness, epigastric pain, palpitations, syncope, nausea alone, and cardiac arrest) are more common in the elderly, women, and diabetics. Atypical symptoms are presented symptoms in one-third of confirmed myocardial infarctions.16

Troponin is a protein released from myocardial tissue and is indicative of cardiac cell death. Serum troponin levels begin to rise measurably as early as 2 to 3 hours after onset and can remain elevated for up to 7 days.10 When available, cardiac troponin assays (cardiac specific I or T) should be used in the diagnosis of MI. A troponin value above the 99th percentile upper reference limit (determined by the assay type) is considered positive. Troponin values may continue to rise, or they may decline depending on the timing of the clinical event, and both situations should raise concern for ACS.10,17 Due to the time elapsed between cardiac cell death and laboratory detectable rise in troponin levels, the troponin level may be checked serially, usually every 3 to 6 hours.18

The following are clinical findings in combination with a rise and/or fall in troponin values that constitute the diagnosis of acute MI:19

- Symptoms of ischemia (See above paragraph.)
- New ischemic ECG changes
- Development of pathological Q waves
- Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
- Identification of an intra-coronary thrombus on angiography or autopsy

Other clinical conditions may present with elevated troponin. Some of these conditions may manifest symptoms similar to ACS (myocarditis, pulmonary embolism, and aortic dissection), while other conditions may present without features of ACS (such as rhabdomyolysis, sepsis and renal failure) and their management is distinct from that of ACS.19 It is therefore important to consider the clinical manifestations and additional studies (ECG, echocardiography) in addition to troponin in the diagnosis of ACS. Keep in mind that in forward deployed locations, laboratory testing for troponin may not be available, and a high index of suspicion must be maintained in the presence of appropriate symptoms.

DIAGNOSIS OF ACS BY ECG CHARACTERISTICS

The 12-lead ECG of STEMI follows an anatomical distribution based on the infarcted artery. ST-elevation in one region should manifest with reciprocal ST-depression in the opposite anatomic region. ST-elevation must be present in two contiguous leads to be diagnostic. Figure 1 shows proper ECG lead placement for a typical 12-lead ECG.

In conjunction with symptoms consistent with myocardial ischemia, the following are the ECG criteria diagnostics of STEMI:19

- New ST-elevations ≥ 0.1 mV in 2 or more contiguous leads except V2-V3
- New ST-elevations in V2-V3 with the below criteria:
- ≥ 0.25 mV in men aged < 40 years
- ≥ 0.2 mV in men aged ≥ 40 years
- ≥ 0.15 mV in women

Figures 2 - 4 demonstrate typical patterns of anterior, inferior, and lateral wall STEMI, respectively.

Outside of the standard ECG findings which are diagnostic of a STEMI previously mentioned, there is currently only one universally recognized “STEMI equivalent,” which is a left bundle branch block (LBBB) meeting the Sgarbossa’s criteria.19

There are other highly concerning ECG patterns that include the de Winter pattern, the left main pattern, hyperacute T waves, Wellen’s syndrome and posterior MI. These patterns are not considered a STEMI equivalent but emergent/urgent revascularization with PCI that should be considered.24 ECG interpretation may be complex and urgent teleconsultation with a cardiologist should be considered. ECG changes that should also raise concern for ischemia include ST depressions ≥ 0.5 mm (in ≥ 2 contiguous leads) or T-wave inversion.

1. LBBB with Sgarbossa’s criteria – Sgarbossa’s criteria was developed to identify an acute MI in the setting of a LBBB since this pattern can cause ST- and T-wave changes that make it difficult to identify an MI. The ECG is considered consistent with MI if any of the following three criteria are met and combine to equal ≥ 3 points:25

- ≥ 1 lead with ≥ 1 mm of concordant ST-elevation with the QRS complex (5 points)
- ≥ 1 lead of V1-V3 with ≥ 1 mm of concordant ST-depression with the QRS complex (3 points)
- ST- elevation of ≥ 5 mm that is discordant with the QRS complex (2 points)

2. Modified Sgarbossa criteria (listed below) may outperform the original proposed criteria.26 Any of the changes listed below are diagnostic of MI in the modified criteria.

- ≥ 1 lead with ≥ 1 mm of concordant ST elevation with QRS
- ≥ 1 lead of V1-V3 with ≥ 1 mm of concordant ST depression with QRS
- ≥ 1 lead anywhere with ≥ 1 mm ST-elevation and proportionally excessive discordant ST-elevation, as defined by ≥ 25% of the depth of the preceding S-wave (an ST:S ratio of ≤ -0.25)

ECG Patterns Highly Concerning for Myocardial Infarction

1. De Winter pattern – ST-depressions at the J point in V1-V6 and tall, peaked, symmetric T-waves are consistent with a de Winter pattern and associated with proximal left anterior descending artery (LAD) occlusion.

2. Left main pattern - Multi-lead ST-depression with coexistent ST-elevation in lead aVR has been described in patients with left main artery or proximal LAD occlusion. This is referred to as a left main pattern.

3. Hyperacute T waves – broad, asymmetrically peaked T-waves can be seen in early STEMI.

4. Wellen’s syndrome – Biphasic T-waves (Type A) or deep, symmetric T-wave inversions (Type B) in leads V2-V3 are strongly associated with proximal LAD occlusion. This is referred to as Wellen’s syndrome.

Another indication of acute cardiac ischemia on the ECG is flat or down-sloping ST-depression ≥ 0.5 mm in 2 contiguous leads (Figure 11). If the ST-depressions are seen in leads V1-V3 then the next step should be to obtain a 12-lead ECG with posterior leads. This is accomplished by removing leads V4-V6 from the patient and placing them at the inferior margin of the left scapula, as shown in Figure 12. If these leads (now called V7-V9) show ST-elevation this will be consistent with a posterior STEMI (Figure 13).

Similarly, if the initial ECG shows evidence of an inferior STEMI (ST-elevation in lead II, lead III, and aVF with reciprocal changes), then consider placing leads V1-V6 on the patient as a complete mirror reflection (as shown in Figure 14). If these leads (now called V1R-V6R) show ST-elevation this will be consistent with right ventricular infarction.

If the initial ECG is non-diagnostic (i.e. only one lead meeting ST-elevation criteria but the second contiguous lead ST-elevation is less than 0.1 mV) but the suspicion for ACS is present, then serial ECGs (every 15 minutes for the first hour) should be performed to ensure STEMI is not missed.17,19

In contrast to STEMI, UA/NSTEMI can present with a myriad of ECG findings. These may include normal ECGs, nonspecific T-wave inversions, ST-depression or transient ST-elevation.