Acute Coronary Syndrome (ACS)

Chest pain is one of the commonest presenting complaints encountered and the diagnosis of an ‘acute coronary syndrome’ is frequently suspected. ACS encompasses a variety of diagnoses and we will examine each one in detail.

They can be divided into:

  • Unstable Angina
  • Non-ST elevation myocardial infarction
  • ST elevation myocardial infarction

What is a myocardial infarction?

Let’s first look at what we define as a ‘Myocardial infarction’.  The ESC handily created a lengthy document entitled ‘Third Universal Definition of Myocardial Infarction‘.


Here’s how they define a myocardial infarction

Detection of a rise and/or fall in cardiac biomarker values (preferably troponin) with at least one value above the 99th percentile (upper reference limit) with at least one of the following:

  • Symptoms of ischaemia – Clinical presentation and the history you take are vital to guide your interpretation of the tests you are about to do!
  • New or presumed new significant ST segment or T wave changes or new left bundle branch block (LBBB)



A ‘new left bundle branch block’ does not mean ‘a left bundle branch block that has just been found because the patient has never had an ECG before‘. Nor does it mean ‘a left bundle branch block that is present now but was not present on an ECG in 2006’.

A NEW LBBB due to ischaemia is generally the result of an occluded proximal LAD or left main stem – it requires a large amount of myocardium and conductive tissue to be affected to cause this ECG appearance and these patients are SICK.



Development of Q waves on the ECG

The Q wave is a reflection of septal depolarisation. This is usually hidden behind the much more forceful and electrically active ventricular wall depolarisation – if the ventricular wall is dead, a ‘window’ is created that allows the septal depolarisation to show up on the surface ECG.


Imaging evidence of new regional wall abnormality

There is a phenomenon called the ischaemic cascade which is worth a brief explanation. The sequence of changes and signs of ischaemia on various tests is as follows…

Ischaemic cascade flowchart

Hint: The important point here is that the troponin level is ONLY A NUMBER. It is not a magic diagnostic test and is only relevant when applied in the context of other clinical findings / history points / investigations. Just to emphasise this, here is a (not exhaustive) list of the causes of a raised troponin (1)

Causes of raised Troponin
Causes of raised Troponin

Clinical examples

Patient 1

  • Typical cardiac chest pain for 1 hour and still ongoing
  • On examination, cold, clammy and sweaty
  • ECG below
  • Troponin awaited
  • What’s the diagnosis?


Patient 1 ECG
Patient 1 ECG

Patient 2

  • Thirty minutes of typical cardiac chest pain earlier today
  • Normally have well controlled angina but it has been getting progressively worse
  • On examination –  pale conjunctivae, tachycardic with a tender epigastrium
  • Rectal examination reveals malaena. Hb 56 (normal range 115 – 135)
  • ECG below
  • High sensitive Troponin – 450 (normal range < 40)
  • Diagnosis?
Patient 2 ECG
Patient 2 ECG


Patient 3

  • One hour of chest pain worse on lying flat and better whilst sitting forward
  • Spent the night sat up in bed
  • Preceding viral illness for 3 – 4 days
  • ECG below
  • High sensitive Troponin – 2000 (normal range < 40)
  • Diagnosis?
Patient 3 ECG
Patient 3 ECG


Running each patient through the diagnostic criteria

Patient 1

  • Typical symptoms
  • ECG demonstrating clear anterior ST elevation
  • A bedside echo would demonstrate a large anterior wall motion abnormality (and is useful if there is some debate regarding whether the infarct is new or old – although not in this case with such clear ECG abnormalities)
  • The troponin came back at 3,000 rising to > 50,000 at 12 hours
  • Diagnosis – Myocardial infarction (STEMI)
  • Treatment – anti-platelets and immediate angiography


Patient 2

  • Typical symptoms with history of background stable angina
  • ECG looks ischaemic with ST depression globally
  • Troponin raised
  • Diagnosis – Myocardial Infarction (NSTEMI)
  • However, there is clear evidence of gastrointestinal bleeding and profound anaemia. What is the underlying mechanism of ischaemia?

Classification by pathophysiology

By our definitions, both patients have had a ‘myocardial infarction’. However, there is clearly different pathophysiology at work. The ESC has again come to the rescue with a helpful classification system.


Type 1 MI – Spontaneous myocardial infarction (ACS)

Patient 1 has suffered a type 1 MI. This is your ‘typical’ myocardial infarction. Atherosclerosis (as shown in the diagram below from the Encyclopedia Britannica) originates from damage the endothelium and a buildup of cholesterol. The inflammatory reaction to this by macrophages then causes the plaque of foam cells, lipids, cellular debris and (eventually) calcium to build up with a fibrous cap on top. When this cap cracks, the exposed debris triggers your body’s natural healing mechanisms and thrombus forms – in the confines of a coronary artery (between 2 and 5mm in diameter), this causes partial or total occlusion of the artery (hence the name acute coronary syndrome!)


Type 1 MI
Type 1 MI




The specific treatment for a type I MI

Stop platelet aggregation and thrombus formation:

  • Dual antiplatelet drugs (aspirin and one of clopidogrel / ticagrelor / prasugrel)
  • Heparinoids
    • Low molecular weight heparin (1mg / kg bd)
    • Fondaparinux – lower bleeding risk (only inhibits about 50% of platelets but this is enough to get a similar effect as LMWH) (2.5mg SC od)


Stabilise the cap of the ruptured plaque:

  • Atorvastatin 80mg od has been shown to reduce death and major cardiovascular events after ACS (PROVE-IT TIMI 22 trial (2))


Other agents are less specific to type I MI’s but play key roles:

  • Reduce myocardial workload by slowing the pulse
    • Beta blockade (or equivalent)
  • Prevent myocardial remodelling / control blood pressure
    • ACE inhibitor (or equivalent)


The next phase is to assess the coronary arteries via invasive angiography if felt appropriate and treat any culprit lesions by angioplasty or bypass grafting. We’ll cover this in more detail later.


Type 2 MI – Myocardial infarction secondary to an ischaemic imbalance

A type 2 myocardial infarction is a common event in hospitals where patients with stable coronary artery disease +/- previous coronary intervention (PCI or CABG) are unwell and put additional stress on their heart that would not normally be present.


If there is sufficient imbalance between…

  • Supply of blood (with or without stable coronary artery disease), for example:
    • Anaemia / hypovolaemia
    • Coronary vasospasm


  • Demand for blood, for example:
    • Sepsis / hypovolaemic shock
    • Tachyarrhythmia


…the myocardium can become ischaemic WITHOUT a plaque rupture event as seen in a type 1 MI event.


This is exactly what happened to patient 2, who probably has some stable coronary artery disease judging by his history of stable angina. On this occasion they have become profoundly anaemic, leading to a SUPPLY-DEMAND MISMATCH, causing ischaemic chest pain and ECG changes. A picture demonstrating the different scenarios is seen below¹

Type 2 MI
Types of MI



  • If anaemic, transfuse
  • If septic, treat the sepsis
  • If hypovolaemic, correct the volume status
  • If tachycardic, correct the cause of the tachycardia (+ /- rate control if the tachycardia IS the primary problem)


As there is no thrombus formation, there is NO ROLE for anti-platelets in these patients (and in the case of patient 2, giving aspirin, clopidogrel and heparin could have potentially fatal consequences!!)


Other types of MI

Type 3 MI – Diagnosed post-mortem. Clearly suboptimal.


Type 4a MI – Related to percutaneous coronary intervention (i.e. caused by an angioplasty procedure blocking a side branch or damaging the main coronary artery causing ischaemia)


Type 4b MI – Related to stent thrombosis – if patients stop anti-platelets early post angioplasty or continue to smoke, stents can occlude (usually results in a STEMI if complete sudden thrombosis or NSTEMI if gradual restenosis over time)


Type 5 MI – Related to a bypass graft (CABG) operation

What about patient 3?

The third patient illustrates the importance of the clinical history. The investigations alone could be interpreted as:

  • Troponin raised
  • ECG showing ST elevation
  • Therefore, “it must be a myocardial infarction”……Call cardiology registrar.


However, the clinical history is the key:

  • This patient has symptoms typical of PERICARDITIS (postural changes in pain and preceding viral illness) – NOT typical symptoms of ischaemia.
  • The ECG demonstrates saddle shaped ST segment elevation and PR segment depression (see lead 2) – which again confirms the suspicion that this is PERICARDITIS.
  • If the inflammation of the pericardium affects the myocardium, a troponin release can occur – this is then called MYOPERICARDITIS.


Again, the treatment here is not strong anti-platelets and angiography (indeed there is a small risk of haemorrhage from the inflamed pericardium leading to tamponade. Not great.).


Non-steroidal anti-inflammatories, colchicine and support of any LV dysfunction are the key.

Classification by clinical presentation

So now we have defined the pathophysiology at work, we can look at more clinical definitions. The ESC guidelines are again very clear on their definitions (see below).

Classification of MI by clinical presentation
Classification of MI by clinical presentation4


A STEMI is an EMERGENCY. The ST elevation is a sign of complete occlusion of an epicardial coronary artery by thrombus causing immediate myocardial death and relates to the territory affected:

  • Anterior – V1 – V4
  • Inferior – II,III,aVF
  • High lateral – I,aVL
  • Low lateral – V5,V6
  • Posterior – Dominant R wave in V1 – 3 with ST depression in V1 – 3 (the mirror image of an anterior MI)


The recommended treatment USED to be thrombolysis to try and break down the clot in the artery:

  • However, this has significant bleeding risks attached to it and often failed to open the artery up requiring the patient to undergo ‘rescue angioplasty’ – with higher bleeding risks associated due to the pre-medication


The current gold standard is immediate angioplasty or ‘primary PCI‘ to allow the vessel to be opened as quickly as possible (‘time is muscle‘):

  • Studies have shown that it is beneficial to delay treatment up to 90 minutes to allow transfer to a primary PCI centre rather than resorting to thrombolysis.
  • There is benefit in primary PCI up to 12 hours from the onset of pain. After that point, the OAT trial (4) suggests that there is limited benefit in opening up the occluded artery as the damage is already done.



Immediate assessment is key – these patients are at high risk of ventricular arrhythmias and myocardial damage can be minimised by rapidly opening the artery.


Clinical assessment:

  • Confirm the diagnosis (symptoms + ECG changes)
  • Brief screen for significant co-morbidities:
    • Advanced dementia /  Acute bleeding / Advanced malignancy


  • Stabilise:
    • Morphine
    • Oxygen only if low SATS
    • Nitrates
    • Aspirin (and second rapid-acting antiplatelet – Ticagrelor or Prasugrel)


  • Contact your local friendly interventional cardiology centre and we will do the rest
    • Time-to-reperfusion is critical!


The actual STEMI procedure will be covered in a different article.



Non-ST elevation myocardial infarctions are often seen as a more ‘routine’ heart attack. However, they actually have WORSE long term outcomes than STEMIs (although a lower risk of death in the short term). They tend to be associated with partial coronary occlusion.




  • Clinical assessment, troponin measurement and ECG analysis
  • Risk factors of coronary artery disease
  • Try and decide Type I vs Type II MI



  • Morphine / Oxygen if needed / Nitrates
  • Aspirin and second antiplatelet (Clopidogrel or Ticagrelor)
  • Beta blockade (or alternative rate limiting agent if contraindicated – aim HR of 50 – 60)
  • ACE inhibitor (unless contraindicated – aim for SBP of 120 or less)
  • Atorvastatin 80mg od
  • Initiate medical treatment once diagnosis confirmed (with serial troponin measurement)


Risk stratification

Once someone is diagnosed with a type I NSTEMI and commenced on appropriate medical therapy, there are various risk scores that can be calculated to assess the value of invasive angiography.


GRACE score (

  • Used to predict in-hospital and post-discharge to 6 month mortality


CRUSADE score (

  • Used to predict bleeding risk following ACS
    • Other bleeding scores are available


Other factors that should be taken into account before proceeding to angiography:

  • Renal function (there is a risk of contrast nephropathy and this can leave predialysis patients permanently dependent on dialysis)


  • Bleeding risk (as above)


  • Can the patient lie flat?
    • Whilst angiography can be done sat up on patients in intractable heart failure, it is not fun for the operator, cath lab team or patient and in a non-urgent setting should be delayed until the patient is able to tolerate lying flat!


  • Other significant co-morbidities
    • Patients with poor quality of life and/or short life expectancy (age / dementia / malignancy etc) may not gain any prognostic benefit from the procedure and should be managed medically.


If the patient is deemed suitable for coronary angiography, there is an ‘ideal’ window of 48 – 96 hours to perform this, allowing medical therapy to be initiated first. If you work in a hospital that does not do angioplasty on ACS patients, this means the patients will be waiting prior to being transferred. Patients who should be ‘fast-tracked’ include:

  • Ongoing ischaemic pain despite optimal medical therapy
  • Ventricular arrhythmias due to ongoing ischaemia
  • Haemodynamic instability (i.e cardiogenic shock)

So where does ‘Unstable Angina’ fit into all this?!

Stable (or ‘exertional’) angina is defined as:

  • Typical cardiac pain
  • Brought on by exertional and relieved by rest
  • Lasting less than 20 minutes


Unstable angina has several features with distinguish it from its stable cousin:

  • ‘Crescendo’ angina is typical angina occurring on rapidly decreasing levels of exertion often leading to…
    • Anginal pain at rest lasting more than 20 minutes
    • New onset angina fitting one of these two criteria


Troponin measurement will be normal as there has not been any ischaemic damage (YET!) and the ECG may be normal for similar reasons, although there are some signs not to miss (see below). This means the diagnosis is often ALL on your clinical assessment!

Wellen’s syndrome is a specific pattern of ECG changes indicating a critical proximal LAD lesion – it is defined by its deep arrowhead T wave inversion in the anterior chest leads. Even if the story is not particularly exciting, this is HIGH RISK ECG and should prompt inpatient treatment and investigation.

Wellen's syndrome
Wellen’s syndrome


ACS is a cluster of different diagnoses with a common pathophysiology (partial or complete coronary occlusion due to plaque rupture and subsequent thrombus formation). It causes significant mortality and should be aggressively treated.

A good clinical history is essential to allow accurate interpretation of the investigations that will follow. Make sure you clarify the nature, duration and pattern of the pain and identify underlying risk factors for coronary disease.


  1. Third Universal Definition of Myocardial Infarction. European Heart Journal (2012) 33, 2551 – 2567.
  2. Type 1 MI – staff. “Blausen gallery 2014”. Wikiversity Journal of Medicine. DOI:10.15347/wjm/2014.010. ISSN 20018762. (Own work) [CC BY 3.0 (], via Wikimedia Commons
  3. Cannon et al. Intensive versus Moderate Lipid Lowering with Statins after Acute Coronary Syndromes. N Eng J Med 2004; 350: 1495 – 1504
  4. Rotti et al. 2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. Published online in European Heart Journal Aug 2015.
  5. Yousef ZR, Redwood SR, Bucknall CA, Sulke AN, Marber MS. Late intervention after anterior myocardial infarction: effects on left ventricular size, function, quality of life, and exercise tolerance: results of the Open Artery Trial (TOAT Study). J Am Coll Cardiol 2002;40:869-876


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