11/14/24, 10\:43 AM ST-Elevation Myocardial Infarction (STEMI)

ST-Elevation Myocardial Infarction (STEMI)

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ST-elevation myocardial infarction (STEMI)\: characterised by transmural myocardial ischaemia causing myocardial
injury/necrosis; diagnosed by acute anginal chest pain and ST elevation on an ECG.
Aetiology\: caused by complete occlusion of one or more coronary arteries, usually due to a thrombus.
Risk factors\: Non-modi
(smoking, longstanding hypertension, hyperlipidaemia, obesity, sedentary lifestyle).
History\: Typical features include central/left-sided chest pain lasting >15 minutes, described as pressure, heaviness,
squeezing, and aching; radiation to the left arm, shoulders, neck, or jaw; associated symptoms like sweating, nausea,
vomiting, dyspnoea, fatigue, and palpitations.
Clinical examination\: Comprehensive cardiovascular examination is necessary;
include hypotension/hypertension, low-grade fever, pale/cool/clammy skin, signs of acute heart failure, systolic murmur,
or pericardial rub.
Di
pulmonary embolism, pneumonia, pneumothorax, oesophageal spasm, oesophageal rupture, GORD, acute gastritis,
cholecystitis, acute pancreatitis, costochondritis.
Investigations\: Primary investigation is a 12-lead ECG to identify ST elevation in at least two contiguous leads; other tests
(e.g., troponin, full blood count, urea & electrolytes, liver function tests, lipid pro
help guide management and identify complications.
Imaging\: Chest X-ray to identify other causes of chest pain and pulmonary oedema.
Immediate management\: Use the ABCDE approach, continuous monitoring, and provide analgesia, aspirin loading dose
(300mg), and oxygen if SpO2 \<94%. Use the MONA mnemonic\: Morphine, Oxygen, Nitrates, Aspirin.
Reperfusion therapy\: Urgent discussion for primary percutaneous coronary intervention (PCI) if available within 120
minutes of presentation, or thrombolysis if PCI is not possible within 120 minutes.
Secondary prevention\: Long-term management includes ACE inhibitor/ARB, dual antiplatelet therapy, beta-blocker, statin,
and cardiac rehabilitation.
Complications\: Includes tachyarrhythmias, bradyarrhythmias, re-infarction, ventricular rupture, acute mitral regurgitation,
left ventricular aneurysm, stent thrombosis, bleeding following thrombolysis, pericarditis (Dressler's syndrome), depression.
Prognostic factors\: Worse prognosis associated with greater severity of myocardial necrosis, anterior myocardial infarction,
delayed reperfusion, comorbidities, and older age.
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A comprehensive topic overview

Introduction

An acute ST-elevation myocardial infarction (STEMI) is a clinical event characterised by transmural myocardial
ischaemia resulting in myocardial injury or necrosis. It is one of three types of acute coronary syndrome. The other forms
include unstable angina and non-ST-elevation myocardial infarction (NSTEMI).
The diagnosis of STEMI requires the presence of acute anginal chest pain and ST elevation on an electrocardiogram.
Elevated biomarkers such as troponin do not contribute to diagnosing a STEMI.
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Aetiology

A STEMI is caused predominantly by complete occlusion of one or more coronary arteries that supply the heart, usually
due to a thrombus. A thrombus is mostly made up of aggregated platelets and thrombin.
The disruption of blood
thickness, resulting in a transmural infarction.

Risk factors

Risk factors for STEMI include any cardiac risk factors which increase the risk of coronary artery atherosclerosis.
Non-modi
Male sex
Older age
Previous history of ACS/ischaemic heart disease
Family history of ACS/ischaemia heart disease
Renal insu
Diabetes
Modi
Smoking
Longstanding hypertension
Hyperlipidaemia
Obesity & sedentary lifestyle

Clinical features

History

Initial assessment of anyone with acute chest pain involves a thorough history. For more information, see the Geeky Medics
guide to chest pain history taking.
Typical features of cardiac chest pain include\:
Site\: central or left-sided chest pain (usually lasting > 15 minutes)
Onset\:
“crescendo pain” with increasing severity over several minutes
Character\: described as substernal pressure, heaviness, squeezing, and aching
Radiation\: left arm, shoulders, neck, or jaw
Severity\: variable, can range from 1 to 10 out of 10
Associated symptoms may include sweating, nausea, vomiting, dyspnoea, fatigue and/or palpitations.

Clinical examination

All patients with suspected ACS require a comprehensive cardiovascular examination. However, examination
be non-speci
Examination
septal rupture\:
Hypotension or hypertension may occur depending on the extent of the myocardial infarction
Low-grade fever
Pale, cool and/or clammy skin
Signs of acute heart failure\: tachycardia, gallop rhythm, third and fourth heart sounds, bibasal crackles, peripheral
oedema, elevated jugular venous pressure and/or tender hepatomegaly
Systolic murmur due to acute mitral regurgitation or ventricular septal rupture and/or pericardial rub
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Di

Chest pain has a wide range of potential causes. Di
include\:
Cardiovascular\: other forms of ACS (unstable angina or NSTEMI), acute pericarditis, myocarditis, aortic stenosis, aortic
dissection
Respiratory\: pulmonary embolism, pneumonia, pneumothorax
Gastrointestinal\: oesophageal spasm, oesophageal rupture, GORD, acute gastritis, cholecystitis, acute pancreatitis
Musculoskeletal\: costochondritis

Investigations

The most important investigation in the context of ACS is a 12-lead ECG. The diagnosis of STEMI requires the presence of
acute anginal chest pain and ST elevation on an ECG.
Other investigations (including troponin) do not contribute to diagnosing a STEMI. However, these investigations may
identify complications (e.g. signs of heart failure on a chest X-ray) or help guide management.

Bedside investigations

When ACS is suspected, a 12-lead ECG should be acquired and interpreted within 10 minutes or as soon as possible.
In the proper clinical context, a STEMI is diagnosed when there is a new and persistent ST-segment elevation in at least
two contiguous leads of ≥1mm in all leads except V2-V3 with the following cut-o
≥2.5 mm in men \<40
≥2 mm in men >40
≥ 1.5 mm in women regardless of age
1mm = 1 small square (in a standard ECG strip)
ST elevation
It’s important to consider patients with left bundle branch block (LBBB) can mimic acute ischemia and should be further
evaluated using Sgarbossa’s criteria.
Contiguous ECG leads lie next to each other anatomically and indicate speci
of individual coronary anatomy, these patterns are generalisations and not hard and fast rules.
Left anterior descending (LAD) occlusion produces ST elevation in the precordial leads (V1-3)
Right coronary artery (RCA) occlusions produce ST changes in the inferior leads (II-III-AVF)
Left circum
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Figure 1. An anterior STEMI with ST elevation in the precordial leads
Figure 2. An inferior STEMI with ST-elevation in leads II, III and aVF
See the Geeky Medics guides to ECG interpretation for more information.

Laboratory investigations

Relevant laboratory investigations include\:
Troponin
Full blood count\: check for anaemia
Urea & electrolytes\: renal function may a
cardiovascular disease
Liver function tests
Lipid pro
Thyroid function tests\: check for hypo/hyperthyroidism
HbA1C and glucose\: hyperglycaemia is common in ACS and associated with worse outcomes
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Troponin
Troponin is released from ischaemic muscle. Cardiac troponins T and I are highly sensitive and speci
myocardial damage. Serum levels increase within 3-12 hours from the onset of chest pain, peak at 24-48 hours, and
can remain high for up to 14 days in the presence of normal creatine clearance.
Other cardiac enzymes (e.g. CK-MB) increase within 3-12 hours of the onset of chest pain. However, these are not
routinely measured since sensitivity and speci
ACS is not the only cause of a raised troponin, and troponin levels must be interpreted in the clinical context. Other
causes of raised troponins include\:
Tachy/bradyarrhythmias
Aortic dissection
Heart failure
Myocarditis
Chronic kidney disease
Sepsis

Imaging

Relevant imaging investigations include\:
Chest X-ray\: to identify other causes of chest pain and pulmonary oedema

Management

STEMI is an emergency situation, and an initial ABCDE approach should be taken.
All patients should be placed on continuous monitoring (including ECG, pulse, blood pressure, and oxygen saturation) to
identify life-threatening arrhythmias (e.g. ventricular
Arranging rapid reperfusion therapy is essential to reduce further ischaemic cardiac injury and avoid complications.

Immediate management

Immediate management of STEMI includes\:
Analgesia
Loading dose (300mg) of aspirin
Oxygen if SpO2 \<94%
MONA
MONA is a mnemonic for the initial management of a STEMI.
Morphine
Oxygen (saturations under 94%)
Nitrates
Aspirin (300mg loading dose)

Reperfusion therapy

The NICE guidelines advise that patients with a STEMI presenting within 12 hours of the onset of symptoms should be
discussed urgently for either\:
Primary percutaneous coronary intervention (if available \<120 minutes of presentation)
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Thrombolysis (if PCI is not possible within 120 minutes)
The current gold standard treatment option is primary percutaneous intervention (PCI) to allow the vessel to be opened
as quickly as possible, as ‘time is muscle’
.
Primary percutaneous coronary intervention
Percutaneous coronary intervention (PCI) involves catheterising the patient’s radial or femoral artery and feeding up a
guide wire to the coronary arteries under X-ray guidance.
Contrast is injected to identify the occlusion, which can be opened with a balloon. A stent is placed to maintain artery
patency. Aspiration of the thrombus can be performed in selected cases.
Figure 3. A patient with STEMI being
treated with PCI, showing partial
occlusion of the left circum
artery. The guide wire has traversed the
occlusion and its tip is visible at the
bottom of the image.
Thrombolysis
Thrombolysis involves injecting a
agents include streptokinase, alteplase and tenecteplase.
However, this has signi
angioplasty’ with higher bleeding risks.

Secondary prevention

All patients diagnosed with acute coronary syndrome require long-term management and prevention strategies.
The following medications are recommended to reduce the risk of future events (secondary prevention) and improve
myocardial function\:
ACE inhibitor or ARB\: continued inde
Dual antiplatelet therapy (aspirin plus a second agent)\: for up to 12 months
Beta-blocker for at least 12 months\: continued inde
Statin\: continued inde
Cardiac rehabilitation should be o
Advice on lifestyle, driving,
Tailored physical activity
Stress management
Health and lifestyle education

Complications

Complications of a STEMI include\:
Tachyarrhythmias\: sinus tachycardia, atrial , atrial
(mono/polymorphic ectopic)
Bradyarrhythmias\: sinus bradycardia, atrioventricular blocks, atrial
Re-infarction or infarct extension\: most common in the initial few days
Ventricular free-wall/septal rupture
Acute mitral regurgitation
Left ventricular aneurysm
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Stent thrombosis following PCI
Bleeding (e.g. intracranial, gastrointestinal) following thrombolysis
Pericarditis (Dressler's syndrome)
Depression

Prognostic factors

The following features are associated with a worse prognosis\:
Greater severity of myocardial necrosis (based on serum troponin, ECG changes and degree of LV dysfunction on
echocardiography)
Site of the infarction\: anterior myocardial infarction generally has a less favourable prognosis than inferior myocardial
infarction
Delayed reperfusion with short-term and long-term treatment
Comorbidities (e.g. hypertension, chronic kidney disease, anaemia and diabetes mellitus)
Older age

References

NICE. Acute coronary syndromes. 2020. Available from\: [LINK]
BMJ Best Practice. Overview of Acute Coronary Syndrome. 2022. Available from\: [LINK]
de Luna, A. B., Fiol-Sala, M., & Antman, E. M. (2008). T h e 1 2 l e a d E C G i n S T e l e v a t i o n m y o c a r d i a l i n f a r c t i o n \: a p r a c t i c a l
a p p r o a c h f o r c l i n i c i a n s . John Wiley & Sons.
Watson, T. J., Ong, P. J., & Tcheng, J. E. (2018). Primary angioplasty\: a practical guide.
Albarran, J., & Tagney, J. (Eds.). (2008). C h e s t P a i n \: A d v a n c e d A s s e s s m e n t a n d M a n a g e m e n t S k i l l s . John Wiley & Sons.

Image references

Figure 1. Various authors. S T e l e v a t i o n m y o c a r d i a l i n f a r c t i o n E C G ( c r o p p e d ) . License\: [CC BY]
Figure 2. Glenlarson. E C G 0 0 1 . License\: [CC BY-SA]
Figure 3. Todt T, Maret E, Alfredsson J, Janzon M, Engvall J, Swahn E. C o r o n a r y a n g i o g r a p h y o f a S T E M I p a t i e n t , s h o w i n g
p a r t i a l o c c l u s i o n o f l e f t c i r c u m CC BY]

Reviewer

Dr Abubakr Khalil
Consultant Cardiologist
Altnagelvin Hospital, Londonderry

Acute Coronary Syndrome (ACS)
Acute Heart Failure
Atrial Fibrillation (AF)
Atrioventricular Block
Brugada Syndrome

Test yourself

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