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Acute coronary syndromes
Acute coronary syndromes

Acute coronary syndromes

Acute coronary syndromes (ACS) are 3 conditions that acutely affect the heart and have a similar presentation of crushing chest pain.

We will discuss all 3 of these conditions in a lot more detail in their relevant CCCs, however, to name them we have:

  1. ST elevation myocardial infarction (STEMI)
  2. Non-ST elevation myocardial infarction (NSTEMI)
  3. Unstable angina

Pathophysiology

ACS usually results from a thrombus due to an atherosclerotic plaque that ruptures to occlude a coronary artery.

Atherosclerotic plaques rupture/erode to form a thrombosis. Arteries are platelet-rich, therefore the thrombus is a platelet rich thrombus (white thrombus), as opposed to RBC rich thrombi in veins (red thrombi). The thrombus then occludes the coronary artery → ischaemia/infarction of the myocardium → myocardial death. Depending on the extent of damage as well as the ECG presentation, it is classified as a STEMI, NSTEMI, unstable angina.

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Let’s recap our anatomy of the coronary arteries briefly:

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We have 2 main coronary arteries which come off of our aortic sinus:

  1. Left coronary artery - comes off the left aortic sinus to give off 2 main branches:
    1. Left anterior descending (LAD)/anterior interventricular artery - found in the anterior interventricular sulcus. It supplies the right ventricle, left ventricle and anterior 2/3rds of the interventricular septum.
    2. Left circumflex (LCx) - travels in the coronary sulcus towards the base of the heart. It supplies the left atrium and left ventricle. It also gives off the left marginal branch.
      1. Left marginal artery - travels along the obtuse margin of the heart and supplies the left ventricle.
  1. Right coronary artery - comes off the right aortic sinus also travelling in the coronary sulcus towards the diaphragmatic surface (base of the heart). It itself has 4 main branches:
    1. Atrial branch - found in between the right auricle and ascending aorta. It gives rise to the SA nodal branch.
      1. SA nodal branch - supplies SA node.
    2. Right marginal artery - travels from the acute margin to the apex, supplying the right ventricle.
    3. Atrioventricular branch - a small branch for the AV node.
    4. Posterior interventricular artery/posterior descending artery (PDA) - it is found in the posterior interventricular sulcus, travelling to the base of the heart also. It supplies the posterior 1/3rd of the interventricular septum.

😷 Presentation

  • ⭐️ Chest pain - this is the classical, most notable symptom. It is typically on the left side of the chest and may radiate to the left arm, jaw, or back. It is described as a crushing chest pain as if there was a heavy pressure sitting on the chest. However, this presentation differs sometimes. Pain is also reported in the neck and shoulder blades.
  • Palpitations
  • Dizziness
  • Dyspnoea
  • Nausea and vomiting
  • Sweating (diaphoresis)

On examination, we may notice changes to the pulse, blood pressure, temperature and SpO2. However, these are often normal.

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🔍 Investigations

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ECG

🥇 ECG is the first-line investigation. It is needed to distinguish between a STEMI, and NSTEMI/UA:

ECG changes
Coronary artery affected
Anterior
V1-v4
LAD
Inferior
II, III, aVF
Right coronary
Lateral
I, V5-V6, aVL
Left circumflex
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Interpretation of ECGs with the clinical and previous histories taken into account.

  • ST-segment elevation - ST-segment elevation > 1 mm in 2 contiguous limb leads OR > 2 mm in 2 contiguous chest leads indicates STEMI.
  • New-onset left bundle branch block (LBBB) - for STEMI.

💡 STEMI in leads II, III and aVF, and inferior ST depression in leads V1-V3 is highly indicative of a posterior infarct.

Inferior STEMI
Inferior STEMI
Anterior STEMI
Anterior STEMI
Lateral STEMI
Lateral STEMI
⚛️
Troponin

Troponin <14ng/L more than 6 hours after symptoms rules out an MI.

Troponin is a regulatory protein that is found in the cardiac muscle. The troponin complex is made up of 3 regulatory proteins: TnI, TnT, and TnC. It is important for muscle contraction and the actin-myosin sliding filament theory. TnC is non-specific to skeletal muscle, however TnI and TnT are specific to cardiac muscle.

Troponin is attached to tropomyosin, and blocks the myosin binding site from being exposed. However, during a muscle contraction, it undergoes a change of shape and exposes the myosin binding site to allow for contraction of the muscle as myosin slides over the actin filaments.

Troponin is excreted by the kidneys.

Why is this relevant?

Troponin is a biochemical marker that can be used to detect myocardial infarction as it is released in high levels into the blood as we get myocardial death. Troponin levels rise 4-6 hours after symptom onset and peak at 18-24 hours. They then decline over the next 10 days after the MI.

A rise in troponin levels followed by a later fall provides definitive confirmation of an acute MI in a patient who has clinical or ECG evidence of ongoing myocardial ischaemia.

What else can elevate troponins?

  1. PE
  2. Chronic renal failure
  3. Sepsis
  4. Myocarditis
  5. Aortic dissection
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  • Creatine kinase MB (CK-MB) - creatine kinase is found in both skeletal and cardiac muscle, but creatine kinase MB is found in higher concentrations in cardiac muscle and therefore is more specific to cardiac damage (CK-MM is more specific to skeletal muscle). It remains elevated for 3-4 days after MI but is useful in detecting re-infarction 4-10 days after the initial MI.

🧰 Management

When we have identified ACS we need to primarily focus on 3 aspects with management:

  1. Pain relief
  2. Preventing deterioration
  3. Revascularisation

NICE divides ACS into 2 groups for management:

  1. STEMI
  2. NSTEMI

Let’s look at the common management of all ACS patients then we will look at the management of these 2 groups specifically:

🎨
MONA:
  1. Morphine - given IV. It is given with an anti-emetic agent (such as ondansetron) to prevent the patient vomiting the oral loading dose of dual anti-platelet therapy. IV GTN can be given if the patient has ongoing chest pain.
  2. Oxygen - if SpO2 <94% on air.
  3. Nitrates - given sublingually as GTN spray. It can be given as an IV infusion if the patient has ongoing pain despite the morphine, or if they have refractory hypertension. Caution should be taken in hypotensive patients.
  4. Aspirin - a loading dose of 300mg is given.
  • We then need to do an ECG to determine the subtype of ACS that the patient has
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STEMI management:

If the patient does not meet the criteria for reperfusion therapies, dual antiplatelet therapy with aspirin and ticagrelor is recommended. If the bleeding risk is high then consider clopidogrel

If the patient meets the criteria for STEMI (to be discussed in the MI CCC) then we need to assess their eligibility for percutaneous coronary intervention or fibrinolysis, both are which are types of coronary reperfusion therapies.

  1. Percutaneous coronary intervention

    2. This entails coronary angioplasty along with stenting. It is performed through catheterisation via the radial artery (although femoral access may be used).

    Stenting is done using drug-eluding stents. They are covered in drugs such as sirolimus or paclitaxel as these inhibit cell proliferation and restenosis.

    PCI is offered if the patient is presenting within <12 hours of symptom onset and the PCI can be delivered within 2 hours of the time when fibrinolysis could have been given.

    It is considered if the patient presents after 12 hours with signs of ongoing coronary ischaemia.

  • Prior to PCI:
    1. Angiography
    2. Dual anti-platelet therapy

      3. → Aspirin

      → Prasugrel (P2Y12 inhibitor) if they are not taking an oral anticoagulant already or clopidogrel if they are already taking an oral anticoagulant.

  • During PCI:
    1. IV anticoagulants (alongside dual-platelet therpay)

      2. If they are undergoing PCI with radial access → unfractionated heparin (UFH) with bailout glycoprotein IIb/IIIa inhibitor (tirofiban and eptifibatide) which are used in case of any complications that may arise during PCI.

      If they are undergoing PCI with femoral access → bivalirudin (a direct thrombin inhibitor) along with bailout GPI.

  1. Fibrinolysis

      2. Fibrinolytic agents such as streptokinase, alteplase, urokinase. These promote plasminogen conversion into plasmin. As we know, plasmin is a fibrinolytic enzyme which breaks down fibrin into fibrin degradation products.

      It needs to be offered within 12 hours of symptom onset if PCI cannot be delivered within these 120 minutes (for example if they need to be transferred to a larger hospital from a district hospital). However, if the ECG taken 90 minutes after does not show resolution, then PCI will be considered again.

    1. During fibrinolysis:

      2. We need to give an antithrombin agent such as enoxaparin, fondaparinux, or UFH.

    2. After fibrinolysis:

      3. Give dual antiplatelet therapy if not treated with PCI. We give clopidogrel if the bleeding risk is high but the P2Y12 inhibitor of choice depends on the bleeding risk ultimately.

      An ECG should be done 60-90 minutes after fibrinolysis: if the ECG still shows STEMI → offer immediate coronary angiography and consider PCI.

  2. Treat the hyperglycaemia if present. This is a common finding in patients after having an acute MI. NICE recommends a dose-adjusted insulin infusion with regular monitoring of blood glucose levels to glucose below 11.0 mmol/l.
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Absolute contraindications to fibrinolysis:
  • History of spontaneous intracerebral haemorrhage
  • Ischaemic stroke within last 6 months
  • CNS damage, neoplasm or AV malformation
  • Major trauma, surgery, head injury within last 1 month
  • GI bleeding within last 1 month
  • Bleeding disorder
  • Aortic dissection
  • Non-compressible punctures within last 24 hours - such as liver biopsy or lumbar puncture.
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Relative contraindications to fibrinolysis:
  • Chronic oral anticoagulant usage
  • Pregnancy or <1 week postnatally
  • Refractory hypertension (systolic BP >180mmHg and/or diastolic BP >110mmHg).
  • TIA within last 6 months
  • Advanced liver disease
  • Infective endocarditis
  • Active peptic ulcer
  • Prolonged or traumatic CPR
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NSTEMI/unstable angina management:

Once diagnosis of NSTEMI or UA is made:

  1. Aspirin - 300mg loading dose and continue on 75mg OD lifelong.
  2. Antithrombin therapy
    1. Fondaparinux - unless patient has high risk of bleeding or is going for immediate coronary angiography.
    2. Enoxaparin - if the patient has renal impairment (creatinine >265umol/L).
  3. GRACE risk assessment - to formally assess risk of future CVS event.

GRACE risk assessment:

The Global Registry of Acute Coronary Events (GRACE) is the most widely used tool for risk assessment. It predicts 6-month mortality using:

  1. Age
  2. Heart rate and BP
  3. Cardiac function (Killip classification) and renal function (serum creatinine)
  4. Cardiac arrest on presentation
  5. ECG findings
  6. Troponin levels

It can be calculated online with a predicted risk outcome:

Predicted 6-month mortality
Risk of future CVS events
<1.5%
Lowest
1.5% - 3%
Low
3% - 6%
Intermediate
6% - 9%
High
9%
Highest

Low risk patients (<3%):

  • Conservative management without coronary angiography - this involves dual antiplatelet therapy.

Intermediate - highest risk patients (>3%):

  • If clinically unstable:
    • Immediate coronary angiogrpahy + revascularisation with PCI or CABG
    • Dual antiplatelet therapy
    • Anticoagulant (heparin)
  • If clinically stable:
    • Coronary angiography ± revascularisation within 72 hours
    • Dual antiplatelet therapy
    • Anticoagulant (heparin)
    • ACEI or ARB
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How do we define clinical instability?
  1. Ongoing or recurrent pain refractory to treatment
  2. Haemodynamic instability
  3. Dynamic ECG changes
  4. Left ventricular failure
  5. Life-threatening arrhythmia
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Secondary prevention:

All 3 types of ACS need lifelong drug treatment to reduce the risk of another CVS event. This includes:

  1. Dual antiplatelet therapy - continue 75mg aspirin lifelong and stop the P2Y12 inhibitor after 1 year.
  2. Start/continue B-blocker (bisoprolol) or a non-dihydropyridine CCB (verapamil or diltiazem)
  3. Start/continue ACEI (enalapril) or ARB if the ACEI is not tolerated.
  4. Start statin (atorvostatin)
  5. Cardiac rehab - with exercise, health education, stress management and psychological + social support.