Investigations
1st investigations to order
ECG
Test
Perform a 12-lead ECG within 10 minutes of first medical contact in any patient who presents with chest pain and/or other signs of possible STEMI.[1][2]
If the patient presents in the community, obtain a pre-hospital ECG and send it digitally to the receiving hospital as quickly as possible.[2][82]
If the ECG is equivocal despite a high clinical suspicion of acute MI, perform serial ECGs in the appropriate hospital setting and compare these with historical ECGs, if available.[1][2][82]
In the appropriate clinical context (chest pain or other symptoms of ischaemia), make a clinical working diagnosis of STEMI if there is new (or increased) and persistent ST-segment elevation in two or more contiguous leads.[2][71]
Make the diagnosis when these criteria are met in the absence of left ventricular hypertrophy, left bundle branch block (LBBB), or a paced rhythm on the ECG.
Severe cases of left ventricular hypertrophy can appear identical to LBBB.
A paced rhythm can appear identical to LBBB.
Note that the presence of left ventricular hypertrophy, LBBB, or a paced rhythm does not preclude a diagnosis of STEMI if the patient presents with typical symptoms of myocardial ischaemia.
See Less common ECG presentations below for more on diagnosis of STEMI in the presence of LBBB.
Consult a cardiology specialist immediately if the ECG changes are equivocal.
An urgent transthoracic echocardiogram to look for regional wall motion abnormalities is indicated.[120]
Measure ST-segment elevation from the J point.[1][2]
As soon as a clinical diagnosis of STEMI is made based on ECG changes together with symptoms or signs of ischaemia, start treatment and make an immediate assessment of eligibility for coronary reperfusion therapy (irrespective of age, ethnicity, sex, or level of consciousness).[2][71][75]
Alert the interventional cardiology team straight away.
Do not wait for cardiac biomarker results or other laboratory or imaging investigations. Assessment and diagnosis of STEMI is a time-critical process.
For a library of ECGs with learning points, see Diagnosis recommendations.
Less common ECG presentations
Posterior STEMI[1][2]
Consider this when there is ST-segment depression in leads V1-V3 along with characteristic signs and symptoms of myocardial ischaemia.
Confirm with posterior lead ECG: ST-segment elevation ≥0.5 mm in V7-V9.
Right ventricular infarction[1][83]
Can complicate an inferior STEMI.
Check right precordial leads (V3R and V4R).
Look for ST elevation ≥1 mm in aVR and V1.
Confirmation will have an impact on choice of therapeutic intervention.
Left main coronary obstruction[2][84]
Consider complete left main coronary artery obstruction if the following are both present, especially if the patient has haemodynamic compromise:
ST depression ≥1 mm in ≥6 surface leads (i.e., inferolateral ST depression)
ST elevation in aVR or lead V1.
STEMI in the presence of LBBB[86][122]
ECG diagnosis of STEMI is trickier in the presence of LBBB.[2]
Bundle branch block (BBB) precludes accurate assessment, but it may be possible to make the diagnosis if marked ST-segment abnormalities are present.[2]
The presence of concordant ST-segment elevation (i.e., in leads with positive QRS deflections) is one of the best indicators of total coronary occlusion and ongoing MI in the context of a patient with concomitant LBBB.[85]
Manage any patient with BBB and clinical suspicion of ongoing myocardial ischaemia as per the standard STEMI protocol. This applies to both left and right regardless of whether or not the BBB was previously known.[2]
Presumed new LBBB alone does not indicate the presence of a STEMI.[87][88]
If in doubt, seek immediate input from the cardiology team.
More info: Sgarbossa criteria for diagnosis of MI in the presence of LBBB
Consider using the Sgarbossa criteria to improve the diagnostic accuracy for STEMI in patients who have LBBB at presentation.
ST elevation of ≥1 mm, concordant with the QRS complex: 5 points.
ST depression ≥1 mm in leads V1, V2, or V3: 3 points.
This has a sensitivity of 19% and a specificity of 81% to diagnose acute MI.[123]
ST elevation ≥5 mm, discordant with the QRS complex: 2 points.
This has a sensitivity of 10% and a specificity of 99% to diagnose acute MI.[123]
An aggregated score of 3+ is 90% specific for MI but only 36% sensitive.
Components of the Sgarbossa criteria have high specificity but low sensitivity so are useful to confirm acute MI but less useful to rule it out.[124]
The low sensitivity means you must maintain a high index of suspicion if the presentation is consistent with MI regardless of the criteria score.
'Weighted' Sgarbossa criteria rely on the points system; however, only two of the criteria carry a score ≥3 to make the diagnosis of acute MI.[125]
'Unweighted' Sgarbossa criteria are applied without the points system – this is more sensitive but less specific.[125]
The criteria were originally based on the outcome of acute MI as measured by creatine kinase-MB rather than angiographic evidence of acute coronary occlusion – further reducing sensitivity because the criteria encompass both STEMI and non-ST-elevation MI (NSTEMI).[125]
[Figure caption and citation for the preceding image starts]: Sgarbossa criteria for MI in the presence of LBBBCreated by the BMJ Knowledge Centre [Citation ends].
The modified Sgarbossa criteria have better sensitivity but worse specificity for STEMI.[125][126]
The original rule for >5 mm discordance is replaced with a proportionately excessive discordance: ST-elevation/S-wave amplitude ≤-0.25.
The modified criteria were found to be more sensitive versus the ‘weighted’ (80% vs. 49%; P <0.001) and ‘unweighted’ (80% vs. 56%; P <0.001) Sgarbossa criteria.[125]
[Figure caption and citation for the preceding image starts]: ST/S ratio under the modified Sgarbossa criteriaCreated by the BMJ Knowledge Centre [Citation ends].
Previous silent/unrecognised STEMI
Be aware of the possibility that abnormal ECG features might be due to a previous silent/unrecognised STEMI.[1]
Residual ST elevation on the ECG from an old STEMI may be detected either incidentally in an asymptomatic patient who is having an ECG for another reason, or occasionally in a patient with symptoms of ischaemia who is experiencing an NSTEMI against the background of a previous history of STEMI.
In such cases, there may be ST-segment elevation on the current ECG that was already present on old ECGs (e.g., in the case of left ventricular aneurysm formation). It is important to distinguish this from new ST elevation as management will differ.
The historical STEMI may have been 'silent' and gone unrecognised at the time. The resulting old ECG features will usually be fixed.
It is helpful to take a thorough history, together with diligent ECG interpretation and comparison with old ECGs (plus medical records) if available.
Seek specialist input from the cardiology team.
The following criteria for previous (or silent/unrecognised) MI can be helpful. There may be:[1]
Pathological Q waves with or without symptoms, in the absence of non-ischaemic causes[1]
Loss of viable myocardium in a pattern consistent with a coronary artery territory (regional wall abnormality) seen on cardiac imaging:
Echocardiography
Myocardial perfusion scintigraphy (MPS)
Positron emission tomography (PET)
Cardiac magnetic resonance imaging
Pathological findings of a healed or healing MI on cardiac imaging.
Practical tip
A Q wave is defined as any negative deflection preceding an R wave in the QRS complex.
A Q wave represents the normal left-to-right depolarisation across the interventricular septum.
Small Q waves tend to be normal in most leads (e.g., left-sided leads such as I, aVL, V5, and V6).
More pronounced Q waves (>2 mm deep) may be seen in lead III or aVR as a normal variant.
Q waves are not usually seen in the right-sided leads (V1-V3).
Pathological Q waves can be a sign of previous MI. The precise definition of pathological Q waves has been debated. The 2018 Fourth Universal Definition of MI defines them as follows:[1]
Any Q wave in leads V2-V3 >20 milliseconds (0.02 seconds) or any QS complex in leads V2 and V3
Q wave ≥30 milliseconds (0.03 seconds) and ≥1 mm deep or QS complex in leads I, II, aVL, aVF, or V4-V6 in any two leads of a contiguous lead grouping (I, aVL; V1-V6; II, III, aVF)
R wave >40 milliseconds (0.04 seconds) in V1-V2 and R/S >1 with a concordant positive T wave in the absence of a conduction defect.
Result
a STEMI is diagnosed in the appropriate clinical context (a patient with chest pain or other symptoms consistent with myocardial ischaemia) when there is new (or increased) and persistent ST-segment elevation in at least two contiguous ECG leads of ≥1 mm in all leads other than leads V2-V3 where the following cut-off points apply:[1]
≥2.5 mm in men <40 years old
≥2 mm in men >40 years old
≥1.5 mm in women regardless of age
coronary angiography
Test
After making a clinical diagnosis of STEMI, offer coronary angiography, with follow-on primary percutaneous coronary intervention (PCI) if indicated, as the preferred coronary reperfusion strategy, if:[75]
The patient presents within 12 hours of onset of symptoms, and
Primary PCI can be delivered within 120 minutes of the ECG-based diagnosis. When primary PCI is not an immediate option and cannot be provided within 120 minutes of ECG diagnosis, fibrinolysis should be initiated expeditiously as part of a pharmaco-invasive strategy, provided the patient has presented within 12 hours of symptom onset.[75]
Seek immediate specialist advice from cardiology to discuss management options for any STEMI patient who presents >12 hours after symptom onset. Coronary angiography ± primary PCI should be considered if there is evidence of continuing myocardial ischaemia, haemodynamic instability or cardiogenic shock, or life-threatening arrhythmias.[2]
If a patient with acute STEMI has had fibrinolysis, offer angiography:[75]
Immediately if an ECG 60-90 minutes after fibrinolysis shows residual ST-segment elevation (rescue PCI)
After seeking specialist cardiology advice if the patient has recurrent myocardial ischaemia after fibrinolysis
During the same hospital admission if the patient is stable after successful fibrinolysis (routine PCI strategy).
Radial arterial access is preferred to femoral access in all patients undergoing coronary angiography.[75]
Result
acute occlusion or critical stenosis
cardiac troponin
Test
Request a baseline high-sensitivity cardiac troponin (cTn) along with your set of routine blood work whenever a patient presents with a possible acute MI.
A pathological rise in troponin level followed by a later fall provides definitive confirmation of an acute MI in a patient who has clinical/ECG evidence of ongoing myocardial ischaemia (although STEMI can usually be diagnosed by ECG alone).[1][89]
However, do not delay coronary reperfusion to wait for troponin results.
Start treatment and immediately assess eligibility for coronary reperfusion therapy as soon as a clinical diagnosis of STEMI is made based on ECG signs in a patient with chest pain or other symptoms consistent with myocardial ischaemia.[1][82]
Troponin I and T are the preferred biomarkers for definitive confirmation of an MI, with high-sensitivity assays preferred to standard ones.[1][82]
Cardiac troponins are biological markers of cardiac muscle death (cardiomyocyte necrosis) that are released into the circulation when damage to cardiac muscle has occurred.[1][89]
Creatine kinase-MB fraction is less sensitive and less specific and is now rarely used or measured.[1]
Troponin level deviations and normal cut-offs are assay-specific so check local protocols.
Note there is significant variability in:[1]
The time to peak value – levels usually begin to rise around 2-3 hours after onset of myocardial ischaemia but this varies according to the underlying mechanism
The time when a normal value may become greater than the 99th percentile of the upper range limit[127]
The time window to observe a fluctuating pattern of values.
Because assays are not standardised, values from one assay cannot be compared with those from a different assay.[1]
Always interpret troponin values in the context of:[1][82]
Current and previous ECGs
Signs and symptoms reported by the patient (in particular, the time since symptom onset)
The possibility of an alternative cause for an elevated troponin. This may be cardiac (e.g., myocarditis, aortic dissection, severe heart failure) or non-cardiac (e.g., pulmonary embolism, impaired renal function, underlying sepsis)[82]
The demonstration of a rising and/or falling pattern is important to distinguish acute myocardial injury from a chronically elevated cTn[1]
Historical troponin levels recorded for the individual patient (e.g., measured during previous admissions)
Some patients may have a higher baseline compared with the general population.[82]
[Figure caption and citation for the preceding image starts]: Cardiac troponin kinetics after acute myocardial injury including acute MICreated by the BMJ Knowledge Centre [Citation ends].
glucose
Test
Look for uncontrolled hyperglycaemia in all patients (not just those with diabetes).[2]
Hyperglycaemia is common in the setting of acute MI, with or without a history of diabetes.
Also check for hypoglycaemia in critically ill patients.
Do not delay coronary reperfusion treatment to wait for blood results.[2]
Result
normal or elevated plasma glucose
full blood count
Test
Look for anaemia, which may influence the duration of dual antiplatelet therapy prescribed.
Raised inflammatory markers may be a direct result of the acute-phase response to acute MI or may point to a concomitant infection.
Do not delay coronary reperfusion treatment to wait for blood results.[2]
Result
normal range but can be elevated or reduced
electrolytes, urea, creatinine, and estimated glomerular filtration rate (eGFR)
Test
Potassium, calcium, and magnesium homeostasis is crucially important to prevent both bradyarrhythmias and tachyarrhythmias during the peri-infarct interval.
Baseline renal function at the time of hospital admission will provide a benchmark to allow for subsequent up-titration of medications and allow for the identification of contrast-induced nephropathy after primary angioplasty (if the patient is eligible for coronary reperfusion therapy).
Note patients on potentially nephrotoxic drugs on admission, especially if they are eligible for primary angioplasty.
Reduce the risk of contrast-induced nephropathy if an invasive strategy is planned in a patient with chronic kidney disease.[2]
Also note that chronic kidney disease is a cardiac risk factor.
Result
normal range but can be elevated or reduced
C-reactive protein (CRP)
Test
May be raised as a direct result of the acute-phase response to acute MI but may also point to a concomitant infection.
Not useful in the acute period of STEMI management but an elevated level may inform assessment of the patient’s continued risk for recurrent cardiovascular events.[128]
In a secondary analysis of the VISTA-16 trial, elevated levels of high-sensitivity CRP during the index admission and the subsequent 16 weeks after an acute coronary syndrome were associated with a higher risk of the combined end point of cardiovascular death, myocardial infarction, non-fatal stroke, unstable angina, and all-cause death.[128]
Result
normal range or elevated
serum lipids
Test
Not useful in the acute period of STEMI management but will inform assessment of the patient’s risk factor profile for recurrent cardiovascular events, and aid in setting targets for lipid-lowering therapy.
Cholesterol levels may be lowered by high catecholamine levels mediated by an acute MI in its early phases.
Serum lipids should, therefore, be repeated in 30-60 days.
Irrespective of serum lipid levels, high-intensity statins are mandated after STEMI.
Result
normal range or elevated
Investigations to consider
arterial blood gas
Test
Patients may be hypoxaemic and require supplemental oxygen.
Check arterial blood gases only when there is severe dyspnoea, hypoxia, and/or clinical evidence of pulmonary oedema or cardiogenic shock, and in survivors of cardiac arrest.
Patients may require airway stabilisation and oxygen supplementation before proceeding to primary percutaneous coronary intervention.
This should not be performed routinely and must not delay coronary reperfusion therapy if there is no current or impending objective respiratory compromise.
Taking an arterial blood gas may cause trauma to the radial artery, which is typically the access point for coronary angiography.
Result
oxygen is indicated when:[2]
arterial oxygen saturation (SaO2) <90% or
PaO2 <7.9 kPa (<60 mmHg)
chest x-ray
Test
Use a chest x-ray to exclude alternative causes and to aid indirect assessment of cardiac function.[82]
Widened mediastinum may indicate acute aortic dissection.
Pulmonary oedema suggests impaired left ventricular systolic function.
A large globular cardiac contour or significantly increased cardiothoracic ratio may suggest pericardial effusion.
Imaging tests must not delay coronary reperfusion therapy.
Result
possible findings:
pulmonary oedema
widened mediastinum
cardiomegaly
permanent pacemaker
biventricular pacemaker
sternal wires
clear lung fields
normal cardiac contour
point-of-care transthoracic echocardiogram
Test
Use a point-of-care transthoracic echocardiogram to:[1][2]
Look for regional wall motion abnormalities of the left ventricle in patients with an atypical presentation or equivocal ECG[120][131]
Assess the patient’s eligibility for coronary reperfusion therapy in the event of a delayed presentation
In practice, however, the patient's clinical status and the presence of pathological Q waves in the ECG are usually enough to assess their eligibility for coronary reperfusion therapy if presentation is delayed
Look for mechanical complications of acute MI:[131]
Left ventricular function
Right ventricular function
Ventricular septal rupture
Left ventricular free wall rupture
Acute mitral regurgitation
Pericardial effusion
Cardiac tamponade.
An echocardiogram can also be used to:
Exclude STEMI in patients who present with global saddle-shaped ST-segment elevation (as seen with acute pericarditis)[131]
Confirm the diagnosis of takotsubo cardiomyopathy (usually after normal coronary arteries are found on a STEMI angiogram)[1][131]
Suggest alternative aetiologies associated with chest pain (e.g., acute aortic disease, pulmonary embolism).[2][131]
Imaging tests must not delay coronary reperfusion therapy.
A pre-discharge echocardiogram is indicated for all patients post-acute MI to assess left ventricular function after coronary reperfusion therapy.[71][75]
Result
left ventricular regional wall motion abnormalities
valvular defects
right ventricular function
pericardial effusion
left ventricular mural thrombus
Emerging tests
cardiac myosin-binding protein C (cMyC)
Test
CMyC may perform better than cardiac troponin T or I in patients who present early after symptom onset.[132]
CMyC is a cardiac-restricted protein that is released more rapidly than cardiac troponin after acute MI.
CMyC is also more abundant than cardiac troponins.
It may become the gold standard test for the early diagnosis of acute MI, though it is not currently used in clinical practice.
Result
elevated
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