Laboratory Tests and Ancillaries
Electrocardiogram (ECG)
Obtain and interpret
an ECG as soon as possible, preferably within 10 minutes of emergency
department (ED) arrival, since even at the early stage, ECG is rarely normal; compare with previous ECGs if available. If the ECG shows ST-segment elevations or new or presumed new
LBBB, then the patient should be immediately evaluated for primary percutaneous coronary intervention or if
this cannot be performed in a timely manner by experienced operators, for fibrinolytic
therapy. If the resting ECG is without ST elevation (eg ST-segment depressions
or deep T-wave inversions without Q waves) or is non-interpretable (eg new
RBBB, paced rhythm), consider NSTE-ACS (eg NSTEMI or unstable angina).
Myocardial Infarction w ST-Segment Elevation_Diagnostics 1ECG changes of AMI are evolutionary. Hyperacute changes of a tall peaked T wave or ST-segment elevation followed by development of a Q wave. In resource-limited settings, development of pathological Q waves can confirm the diagnosis of MI only if the patient’s clinical history and previous ECG or cardiac biomarker results are available. Then, there is a return of ST-segment to isoelectric and T-wave inversion.
ST segment elevation in two contiguous leads in a patient with ischemic symptoms is the cardinal feature of STEMI. It is a new or presumed new ST-segment elevation at the J point in ≥2 contiguous leads that should be considered at ≥0.2 mV for men ≥40 years, ≥0.25 mV for men <40 years, or ≥0.15 mV for women regardless of age in leads V2-V3, and/or ≥0.1 mV in other contiguous leads, without LV hypertrophy or LBBB. ST-segment depression and T-wave changes are new horizontal or downsloping ST-segment depression ≥0.05 mV in ≥2 contiguous leads or T-wave inversion ≥0.1 mV in two contiguous leads with prominent R wave or R/S ratio >1.
Diagnosis of STEMI can also be made in patients with alternative ECG changes that are suggestive of acute coronary occlusion or in those who present late, where the ST-segment changes have evolved; alternative ECG features indicating possible acute coronary occlusion include the following:
- Reciprocal ST-segment depression
- ST-segment depression V1-V4 with posterior ST-segment elevation V7-V9
- De Winter’s T waves: Tall, prominent, symmetrical T waves with upsloping ST-segment depression in the precordial leads
- New LBBB
- LBBB with concordant or excessively discordant ST-segment change (Sgarbossa’s criteria)
- Refractory ventricular arrhythmia
A completely normal ECG
does not exclude the possibility of ACS. The ECG may be vague
in the early hours and may not show ST-segment elevation or new Q waves. A repeat
or serial ECG every 10 to 15 minutes should be taken to compare with previous
records and detect evolving infarction or transient changes.
Additional chest leads (V7-V9) and right ventricular leads may be helpful. Posterior leads (V7-V9)
should be obtained in patients with suspected left circumflex occlusion,
particularly in the setting of isolated ST-segment depression ≥0.5 mm in leads
V1-V3, to assess for ST-segment elevation in the posterior leads, which could
indicate a posterior STEMI.
Confirmatory Tests
for the Diagnosis of MI
Elevated biochemical markers of myocardial necrosis, including a
rise and/or fall of cTn values with at least one value above the sex-specific
99th percentile URL in combination with other clinical criteria, rule in MI.
Acute myocardial injury is defined as a rise and/or fall in cTn I or T values,
with at least one value above the sex-specific 99th percentile URL, without
evidence of ischemia, while chronic myocardial injury has ≥2 persistently
elevated cTn I or T values due to an underlying cardiac condition or a
non-cardiac condition associated with cardiac remodelling. These can confirm
the diagnosis of MI in the absence of ECG changes. 2D echocardiography and perfusion
scintigraphy, if available, can be used to look for (presumed) new regional wall
motion abnormalities or loss of viable myocardium consistent with an ischemic
cause. Intracoronary thrombus may be identified by angiography or autopsy.
Biochemical
Indicators for Detecting Myocardial Necrosis
cTn (T or I), measured using a high-sensitivity assay, is the
preferred and most sensitive and specific biomarker for myocardial injury,
necrosis, and infarction. High-sensitivity cTn (hs-cTn) assays can detect
significantly lower levels of cTns and have a higher negative predictive value
for AMI than conventional assays, allowing earlier diagnosis of ACS. In
patients with STEMI, cTn is not recommended for diagnostic evaluation, as
clinical history and ECG are generally sufficient, with cardiac biomarkers
serving to support the diagnosis. Blood samples should be taken on first
assessment and repeated in 1 to 3 hours for high-sensitivity troponin and 3 to
6 hours later for conventional troponin assays if the initial result was
non-diagnostic and the clinical suspicion of MI and/or the pretest probability
of MI is high. In the acute phase of STEMI, routine blood sampling for serum markers
is indicated as soon as possible, but it should not delay initiation of
reperfusion therapy. If a single cTn measurement is used, sampling should be
performed at least 3 hours after symptom onset for hs-cTn and at least 6 hours
after symptom onset for conventional cTn.
Indications for serial cTn measurements include the following:
- Early presentation: When the patient presents soon after symptom onset as cTn elevation may not yet be detectable even with high-sensitivity assays
- Recurrent or persistent ischemic symptoms: Prior to excluding MI
- Elevated cTn without confirmed MI: To differentiate acute from chronic myocardial injury
Myocardial Infarction w ST-Segment Elevation_Diagnostics 2If both high-sensitivity and conventional cTn assays are not available at the time of first assessment, CK-MB measured by mass assay is the preferred alternative. It may be measured in patients presenting within 6 hours of symptom onset as an early biomarker of MI. The values for CK-MB should rise and fall. If the values remain elevated without change, this is typically not due to MI. In STEMI with clear ECG changes, a single CK-MB or cTn measurement obtained >8 hours after symptom onset may be sufficient to support the diagnosis. A diagnosis of reinfarction is supported by a value increase of ≥20% between two samples of troponins or CK-MB collected 3 to 6 hours apart.
Other Diagnostic Tests
The following laboratory investigations should be performed, as clinically indicated, in patients with suspected STEMI: Complete blood count, renal profile, blood glucose, and lipid profile.
Imaging
Imaging is used to confirm MI,
identify its underlying mechanism, differentiate true ischemic MI from
non-ischemic myocardial injury, assess myocardial viability and function, and
detect alternative diagnoses or complications. Without any delay to therapy, obtain a chest
X-ray and in doubtful presentations, perform transthoracic and/or
transesophageal echocardiography, coronary computed
tomography angiography (CCTA), magnetic resonance imaging (MRI), and
radionucleotide techniques, as appropriate, to differentiate STEMI from aortic
dissection, pulmonary embolism, pulmonary edema, pneumothorax or pneumonia.
Perform echocardiography to allow risk stratification of
patients with chest pain upon emergency department (ED) arrival and in those whose
diagnosis is unclear and ECG is not diagnostic, especially in patients with
LBBB or pacing and suspicion of posterior STEMI with anterior ST-segment
depressions. In the presence of normal or uninterpretable ECG
and ongoing chest pains suggestive of myocardial ischemia, echocardiogram may
be helpful to look for new/presumed new wall motion abnormalities. A transthoracic echocardiography may provide evidence of focal
wall motion abnormalities and facilitate triage in patients with ECG findings
that are difficult to interpret.
Invasive Imaging Modalities
Invasive coronary angiography is the gold-standard
assessment of coronary anatomy. It identifies obstructive disease, acute
coronary pathology and indications for revascularization, while intravascular
imaging (intravascular ultrasound [IUS]/optical coherence tomography [OCT]) confirms
atherothrombosis and the type of plaque morphology (rupture, erosion,
intraplaque cavity, mural thrombus) and/or identifies an alternative acute
coronary pathology. Lastly, invasive functional testing, like provocation
testing, identifies coronary spasm. Other tests such as fractional flow reserve
(FFR) or resting indices (eg resting full-cycle ratio [RFR] or instantaneous
wave-free ratio [iFR]) may be helpful detecting functionally significant
stenosis that could cause myocardial ischemia in the context of supply-demand
mismatch.
Non-invasive Imaging Modalities
Echocardiography is a rapid bedside tool for
assessment of regional wall motion abnormalities, infarct extent, ventricular
thrombus, pseudoaneurysm, pericardial effusion/hematoma, and valvular
dysfunction. It also excludes mechanical complications and alternative
diagnoses. CMR imaging is preferred for tissue characterization, while confirming
infarction, assessing edema, microvascular obstruction, intramyocardial
hemorrhage, infarct extent, and complications. CMR also differentiates MI from
myocarditis or Takotsubo syndrome. CCTA is used in the assessment of coronary
atherosclerosis, plaque composition, selected spontaneous coronary artery
dissection, obstructive CAD, and graft patency. It is useful in selected
low-risk patients or when invasive angiography is not indicated. Lastly, nuclear
imaging (positron emission tomography-CT [PET-CT]/single photon emission CT
[SPECT]) assesses myocardial blood flow and viability but has limited spatial
resolution and limited clinical use in AMI.
Myocardial Infarction w ST-Segment Elevation_Diagnostics 3