QuestionSBA
QuestionChoice
This patient has multiple risk factors for MI, including diabetes, hypertension and obesity. Diaphoresis (sweating) and nausea are both important symptoms to recognise as potential indicators of cardiac pathology. They can also present with shortness of breath as the primary symptom. In addition, older male patients are the most likely demographic to experience MI without chest pain
33253
a
Myocardial infarction (MI)
QuestionChoice
DKA occurs more often in type 1 diabetes compared with type 2, however, some patients with type 2 diabetes are ketone producing. It would be unlikely for ketoacidosis to cause collapse without first experiencing notable vomiting, confusion or drowsiness, none of which are mentioned in the stem
33257
e
Diabetic ketoacidosis (DKA)
QuestionChoice
A TIA is characterised by sudden onset neurological deficit that usually lasts for minutes to hours, but resolves within 24 hours. A TIA could be an explanation for a patient presenting following a collapse. However, it is not classically preceded by an extended period of symptoms from other systems, such as nausea and sweating
33255
c
Transient ischaemic attack (TIA)
QuestionChoice
This patient does have a risk factor for pulmonary embolism in his obesity, but his risk profile for a MI is greater. In addition, there are no other identifiable triggers for pulmonary embolism in the history, such as recent long distance travel or immobility
33254
b
Pulmonary embolism
QuestionChoice
It is always important to consider arrhythmia as a potential cause of collapse. However, there is no mention of preceding palpitations, shortness of breath or pre-syncopal episodes. Given the diaphoresis, nausea and risk factors for MI, this would be a more likely explanation
33256
d
Arrhythmia
Concept
Chapter
# Summary

Acute coronary syndrome (ACS) refers to a set of symptoms and signs that occur due to reduced blood flow to the heart at rest. It encompasses 3 distinct diagnoses: unstable angina, non-ST elevation myocardial infarction (NSTEMI), and ST elevation myocardial infarction (STEMI). In the case of infarction, this is a medical emergency requiring urgent treatment. ACS is most commonly caused by the rupture of atherosclerotic plaques in coronary arteries leading to further narrowing, and potentially complete occlusion, of these critical blood vessels. Diagnosis involves clinical evaluation, ECGs, and troponin levels. Treatment strategies differ for STEMI and NSTEMI/unstable angina but include oxygen therapy if hypoxic, antiplatelet medication, glyceryl trinitrates, morphine, and percutaneous coronary intervention (PCI). Post-MI management includes aspirin, dual antiplatelet therapy, beta-blockers, ACE inhibitors, high-dose statins, and cardiac rehabilitation. There are many complications to be aware of post-ACS and these include arrhythmias, heart failure, and cardiac tamponade, and others.

# Definition 

Acute coronary syndrome is a set of symptoms and signs that occur due to decreased blood flow to the heart at rest. It broadly refers to three distinct diagnoses: unstable angina, non-ST elevation myocardial infarction (NSTEMI) and ST elevation myocardial infarction (STEMI). 

# Epidemiology 

In the UK, there are over 80,000 hospital admissions due to ACS every year. Coronary artery disease remains the largest cause of death in the UK. 

# Pathophysiology

Coronary artery disease refers to the narrowing of coronary arteries by atherosclerosis and plaque formation. In stable angina, when the demand for myocardial oxygen increases with exertion, narrowed coronary arteries cannot meet this increased demand leading to myocardial ischaemia and pain. Conversely, in ACS, the symptoms occur at rest. This is because there is sudden plaque rupture and clot formation in the narrowed coronary arteries. If there is partial occlusion of the coronary artery this leads to ischaemia and chest pain at rest (unstable angina). If the coronary artery becomes more occluded or fully occluded this leads to significant hypoperfusion of the myocardium and ultimately leads to infarction (death) of the myocardial tissue (NSTEMI or STEMI). 

# Risk Factors

Coronary artery disease and the development of plaques can be attributed to non-modifiable and modifiable risk factors. Modifiable risk factors must be addressed in the management of IHD. 

* Non-modifiable:
  * Age
  * Male sex
  * Family history
  * Ethnicity (particularly South Asians)
* Modifiable:
  * Smoking
  * Hypertension
  * Hyperlipidaemia
  * Hypercholesterolaemia
  * Obesity
  * Diabetes
  * Stress
  * High fat diets
  * Physical inactivity

# Classification 

Acute coronary syndrome can be split up into three distinct diagnoses: 

1. **Unstable angina**: caused by partial occlusion of a coronary artery. Troponin negative chest pain with normal/abnormal ECG signs. 
2. **Non-ST Elevation Myocardial Infarction**: caused by severe but incomplete occlusion of a coronary artery. Troponin positive chest pain without ST elevation. 
3. **ST-Elevation Myocardial Infarction**: caused by complete occlusion of a coronary artery. Troponin positive chest pain with ST elevation on ECG. 

*Myocardial Ischaemia vs. Myocardial Infarction and the Release of Troponin*

It is important at this stage to distinguish between angina (stable angina is on exertion and unstable angina is at rest) and myocardial infarction. Angina refers to myocardial ischaemia that causes chest pain but does not lead to the death of myocardial tissue and does not lead to a troponin rise. In myocardial infarction, the hypoperfusion of the myocardium is so profound that it leads to the death of myocardial tissue. It is when there is myocardial tissue death that troponin is released into the bloodstream and a troponin rise is found on blood tests.

*Type 2 Myocardial Infarction* 

It is also important to mention that some patient may have myocardial infarctions due to cardiac hypoperfusion for other reasons (e.g. severe sepsis, hypotension, hypovolaemia or coronary artery spasm). These are usually termed type 2 myocardial infarctions and may not require the conventional treatment outlined below. 

# Symptoms and Signs

* Chest pain - the classical presentation can be considered in terms of the SOCRATES mnemonic:
  * Site - Central/left sided
  * Onset - Sudden
  * Character - Crushing ('like someone is sitting on your chest')
  * Radiation - Left arm, neck and jaw
  * Associated symptoms - Nausea, sweating, clamminess, shortness of breath, sometimes vomiting or syncope
  * Timing - Constant
  * Exacerbating/relieving factors - Worsened by exercise/exertion and may be improved by GTN
  * Severity - Often extremely severe
* Atypical presentations may include:
  * Epigastric pain
  * No pain (more common in elderly and **patients with diabetes**):
    * Acute breathlessness
    * Palpitations
    * Acute confusion
    * Diabetic hyperglycaemic crises
    * Syncope

# Differential Diagnoses

It is important to remember that there are non-MI causes of chest pain and these should be considered when making a diagnosis:

* Cardiac
  * Myocarditis
  * Pericarditis
  * Cardiomyopathy
  * Valvular disease
  * Cardiac trauma
* Pulmonary
  * PE
  * Pneumonia
  * Pneumothorax
* Vascular
  * Aortic dissection
* GI
  * Oesophageal spasm
  * Oesophagitis
  * Peptic ulcer
  * Pancreatitis
  * Cholecystitis
* MSK
  * Rib fracture
  * Costochondritis
  * Muscle injury
  * Herpes zoster

# Diagnosis of ACS 

Diagnosis depends on a combination of clinical, ECG and biochemical findings which helps distinguish between the various types of ACS.

* Unstable angina - cardiac chest pain at rest + abnormal/normal ECG + **normal troponin**.
* NSTEMI - cardiac chest pain at rest + abnormal/normal ECG (but not ST-elevation) + **raised troponin**
* STEMI - cardiac chest pain at rest + **persistent ST-elevation/new LBBB** (note that there is no need for a troponin in this case).

## Diagnosis of STEMI

* ST segment elevation **>2mm** in adjacent chest leads
* ST segment elevation **>1mm** in adjacent limb leads
* New left bundle branch block (LBBB) with chest pain or suspicion of MI

## Diagnosis of NSTEMI

Diagnosis of NSTEMI requires two of the following:

* Cardiac chest pain
* Newly abnormal ECG which does not demonstrate ST-elevation e.g. ST depression, T wave inversion or non-specific changes. 
* Raised troponin (with no other reasonable explanation)

# Investigations

## Bedside 

* ECG 
	* Looking for ST-elevation, LBBB or other ST abnormalities
	* This is the most important investigation and should not be delayed for other investigations (e.g. bloods) because this will define immediate management.
	* If an ECG shows STEMI then troponin is essentially irrelevant and the patient requires immediate treatment.

## Bloods 

* Troponin: performed **at least 3 hours** after pain starts. It will also need to be repeated (usually 6 hours after the first level) in order to demonstrate a dynamic troponin rise. 
* Renal function: good renal function is required for coronary angiogram +/- PCI due to the use of contrast. 
* HbA1c and lipid profile: looking for modifiable risk factors for coronary artery disease. 
* FBC and CRP - rule out infectious causes of chest pain
* D-dimer - may be used in _appropriate_ patients to rule out PE. *Be very careful about who you do a D-dimer on!*

## Imaging 

* CXR: should be completed in all those presenting with a chest symptoms. It will help to rule out other causes of chest pain (e.g. pneumothorax) and look for complications of a large MI (e.g. pulmonary oedema in acute heart failure). 

# ECG Interpretation - Cardiac Territories and Affected Vessels

The importance of a 12-lead ECG is that it allows one to view electrical activity of the heart from different "views". In MI (particularly STEMI) this allows you to understand which territory (and therefore which vessel) is being affected.

| Location of ST elevation   | Area of myocardium | Coronary artery      |
| -------------------------- | ------------------ | -------------------- |
| II, III, aVF               | Inferior           | RCA                  |
| V1-2                       | Septal             | Proximal LAD         |
| V3-4                       | Anterior           | LAD                  |
| V5-6                       | Apex               | Distal LAD/ LCx/ RCA |
| I, aVL                     | Lateral            | Lcx                  |
| V7-V9 (ST depression V1-3) | Posterolateral     | RCA/ LCx             |


RCA: right coronary artery, LAD: left anterior descending, LCx: Left circumflex

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NSTEMIs may also show T wave abnormalities (such as ST depression and T wave inversions) in vascular territories as above. However, changes can also often not include all the specific leads of that territory in an NSTEMI.

# Troponin Interpretation

Troponin is a myocardial protein that is released into the bloodstream when cardiac myocytes are damaged. Serum levels typically rise **3 hours** after myocardial infarction begins.

Different hospitals have differing guidelines (and assays) for interpretations of results. In general there are three groups of troponin levels:

* Low - definitely no myocardial cell death. The patient is not having an MI although they may be experiencing unstable angina.
* Mildly raised - This is an equivocal result and may be due to other non-MI related factors (see below). These patients usually need a <u>6-12 hour repeat test</u>.
  * If repeat troponin is raised on the repeat they are having an MI.
  * If repeat troponin is stable or falling then they are unlikely to be having an MI.
* Definitely raised with sequential dynamic troponin rises - MI confirmed (be aware of the possibility of a Type 2 MI)

## Non-ACS causes of a raised troponin

Although troponin is often used diagnose myocardial infarction, there are in fact many causes of a raised troponin:

* Myocardial infarction
* Pericarditis
* Myocarditis
* Arrythmias
* Defibrillation
* Acute heart failure
* Pulmonary embolus
* Type A aortic dissection
* Chronic kidney disease
* Prolonged strenuous exercise
* Sepsis

It is therefore critical to have good clinical grounds to test a troponin in order to avoid unnecessary treatments and investigations.

# Management

Acute management depends on the type of acute coronary syndrome. It is broadly split into the management of STEMI and the management of NSTEMI/unstable angina. 

# Management of STEMI

[lightgallery5]

For emergencies, always follow A-E structure. 

1. Targeted oxygen therapy (aiming for sats >90%)
2. Loading dose of **PO aspirin 300mg**
   - Note that some hospital protocols will also call for a loading dose of a second anti-platelet agent such as clopidogrel (300mg) or ticagrelor (180mg)
   - For those going on to have PCI, NICE guidance suggests adding prasugrel (if not on anti-coagulation) or clopidogrel (if on anti-coagulation)
3. **Sublingual GTN spray** - for symptom relief
4. **IV morphine/diamorphine** - in addition this causes vasodilation reducing preload on the heart
5. Primary percutaneous coronary intervention (PPCI) for those who:
   - Present **within 12 hours of onset of pain** AND
   - Are **<2 hours** since <u>first medical contact</u>

Remember that (particularly in STEMI) _time is heart_ therefore urgent treatment, escalation, and delivery of PPCI is critical to good outcomes.

# Management of NSTEMI/Unstable Angina

[lightgallery6]

For emergencies, always follow A-E structure. 

1. Targeted oxygen therapy (aiming for sats >90%)
2. Loading dose of **PO aspirin 300mg** and fondaparinux
   * Patients should have their 6 month mortality score (often the GRACE score) calculated as early as possible - all those who are anything other than lowest risk should also be given **prasugrel or ticagrelor** unless they have a high risk of bleeding where **PO clopidogrel 300mg** is more appropriate.
3. **Sublingual GTN spray** - for symptom relief
4. **IV morphine/diamorphine** - in addition this causes vasodilation reducing preload on the heart
5. Start antithrombin therapy such as **treatment dose low molecular weight heparin** or **fondaparinux** if they are for an immediate angiogram
6. Patients with <u>high 6 month risk of mortality</u> should be offered an angiogram within 96 hours of symptom onset.

Note that management of unstable angina is similar to that of NSTEMI with aspirin for all patients and fondaparinux and early angiography for those at high risk.

# Post-MI management

[lightgallery7]

* ALL patients post-MI patients should be started on the following 5 drugs:
  1. **Aspirin 75mg OM** + second anti-platelet (**clopidogrel 75mg OD** or **ticagrelor 90mg OD**)
  2. **Beta blocker (normally bisoprolol)**
  3. **ACE-inhibitor (normally ramipril)**
  4. **High dose statin (e.g. Atorvastatin 80mg ON)**
* All patients should have an **ECHO** performed to assess systolic function and any evidence of heart failure should be treated.
* All patients should be referred to **cardiac rehabilitation**.
* Patients who have been treated without angiography should be considered for ischaemia testing to assess for inducible ischaemia. 

# Complications

* Ventricular arrhythmia
* Recurrent ischaemia/infarction/angina
* Acute mitral regurgitation
* Congestive heart failure
* 2nd, 3rd degree heart block
* Cardiogenic shock
* Cardiac tamponade
* Ventricular septal defects
* Left ventricular thrombus/aneurysm
* Left/right ventricular free wall rupture
* Dressler's Syndrome
* Acute pericarditis

## Ventricular Arrhythmias

* Ventricular arrhythmias can occur as a consequence of MI, during cardiac catheterisation, or after reperfusion.
* Most post-MI ventricular arrhythmias are short lived and self-resolve.
* However if sustained VT or VF occurs they should be treated as per the Advanced Life Support protocols.

## Recurrent Ischaemia/Infarction/Angina

* Occasionally inserted stents can thrombose requiring reintervention.
* New infarcts can occur in different vascular territories - this is less likely in the age of PCI where all territory are imaged during the procedure.
* Angina and chest pain can continue for some time after an MI and is more common in NSTEMI patients.

## Congestive Heart Failure

* Heart failure can occur as a consequence of impairment heart muscle function secondary to ischaemia.
* It should be treated as any other acute heart failure.
* Ventricular function may improve over months as the heart muscle recovers.

## Heart Block

* Various levels of heart block are common - particularly following **inferior** infarcts (because the right coronary artery supplies the SAN).
* These may be treated with:
  * Simple observation (as many will revert back to sinus rhythm)
  * Transcutaneous/venous pacing (if symptomatic)
  * Permanent pacing (if failing to resolve)

## Left Ventricular Thrombus/Aneurysm

* Aneurysm can occur following an anterior MI where the myocardium can be susceptible to wall stress leading to an aneurysm.
* It may be silent, cause arrhythmias or embolic events.
* It is definitely diagnosed on ECHO but ECG may show persisting ST elevation.
* Thrombus can form either within an above described aneurysm or around hypokinetic regions of the myocardium.
* Thrombi can embolise causing complications such as stroke, acute limb ischaemia and mesenteric ischaemia.

## Left/Right Ventricular Free Wall Rupture

* Necrosis of the free walls of either ventricle can lead to rupture allowing blood into the pericardial space.
* This leads to a rapid tamponade and normally leads to cardiac arrest/death within seconds.
* Treatment includes pericardiocentesis and surgery but prognosis is extremely poor.

## Acute Mitral Regurgitation

* This can occur because of papillary muscle rupture and carries a poor prognosis. Occurs commonly due to infero-osterior MI. 
* This presents with:
  * Pansystolic murmur heard best at the apex
  * Severe and sudden heart failure
* It is diagnosed on echocardiogram and may require surgical correction.

## Ventricular Septal Defect

* Interventricular septal rupture is a short-term complications of myocardial infarction.
* Rupture caused by an anterior infarct is generally apical and simple.
* Rupture caused by an inferior infarct is generally basal and more complex.
* Without reperfusion, septal rupture typically occurs within the first week after the infarction.
* Features of septal rupture include:
  * Shortness of breath
  * Chest pain
  * Heart failure
  * Hypotension
  * Harsh, loud pan-systolic murmur along the left sternal border.
  * Palpable parasternal thrill.
* Diagnosis is with echocardiogram.
* Patients are managed with emergency cardiac surgery.

## Dressler's syndrome

* Dressler's syndrome or post-infarction pericarditis typically presents with persistent fever and pleuritic chest pain **2-3 weeks** or up to a few months after an MI.
* Note that patients can get pericarditis immediately following MI which is NOT considered Dressler's syndrome.
* Symptoms usually resolve after several days.
* Occasionally it can also present with features of pericardial effusion and has become relatively uncommon since the introduction of PCI.
* Management: **high dose aspirin**

# Prognosis 

Due to the development of PPCI and post-MI care (cardiac rehabilitation) the mortality rates following myocardial infarction continue to decline. Those patients who go on to develop heart failure after myocardial infarction have a significantly worse prognosis than those who do not. 

# NICE Guidelines

[NICE Guidelines for Unstable Angina and NSTEMI](https://www.nice.org.uk/guidance/cg94)

[NICE Guidelines for STEMI](https://www.nice.org.uk/guidance/cg167)

# References

[Patient UK Information on Acute Coronary Syndrome](<https://patient.info/doctor/acute-coronary-syndrome-pro>)
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A posterior STEMI.
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An anterolateral STEMI.
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An anterior STEMI.
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A left bundle branch block.
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An inferior STEMI.
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6651
A 75 year old man presents to the emergency department (ED) after a sudden collapse at home. This was preceded by a four hour history of feeling clammy and nauseous. He has a past medical history of type 2 diabetes and hypertension. He also has a body mass index (BMI) of 38.

Observations show: HR 112 bpm, RR 20 bpm, SpO2 92% on air, BP 88/74 mmHg and temperature of 37.6.

What is the most likely cause of the patient's symptoms?
a