Acute Coronary Syndrome

Pathophysiology

Acute Coronary Syndrome is usually the result of a thrombus from an atherosclerotic plaque blocking a coronary artery. When a thrombus forms in a fast flowing artery it is made up mostly of platelets. This is why anti-platelet medications such as aspirin, clopidogrel and ticagrelor are the mainstay of treatment.

 

The Coronary Arteries

The Left Coronary Artery becomes the Circumflex and Left Anterior Descending (LAD).

Right Coronary Artery (RCA) curves around the right side and under the heart and supplies the:

  • Right atrium
  • Right ventricle
  • Inferior aspect of left ventricle
  • Posterior septal area

Circumflex Artery curves around the top, left and back of the heart and supplies the:

  • Left atrium
  • Posterior aspect of left ventricle

Left Anterior Descending (LAD) travels down the middle of the heart and supplies the:

  • Anterior aspect of left ventricle
  • Anterior aspect of septum

 

Three types of Acute Coronary Syndrome

  • Unstable Angina
  • ST Elevation Myocardial Infarction (STEMI)
  • Non-ST Elevation Myocardial Infarction (NSTEMI)

 

Making a Diagnosis

When a patient presents with possible ACS symptoms (i.e. chest pain) perform an ECG:

If there is ST elevation or new left bundle branch block the diagnosis is STEMI.

If there is no ST elevation then perform troponin blood tests:

  • If there are raised troponin levels and/or other ECG changes (ST depression or T wave inversion or pathological Q waves) the diagnosis is NSTEMI
  • If troponin levels are normal and the ECG does not show pathological changes the diagnosis is either unstable angina or another cause such as musculoskeletal chest pain

 

Symptoms

Central, constricting chest pain associated with:

  • Nausea and vomiting
  • Sweating and clamminess
  • Feeling of impending doom
  • Shortness of breath
  • Palpitations
  • Pain radiating to jaw or arms

Symptoms should continue at rest for more than 20 minutes. If they settle with rest consider angina. Diabetic patients may not experience typical chest pain during an acute coronary syndrome. This is often referred to as a “silent MI”.

 

ECG Changes in Acute Coronary Syndrome

STEMI:

  • ST segment elevation in leads consistent with an area of ischaemia
  • New Left Bundle Branch Block also diagnoses a “STEMI”

NSTEMI:

  • ST segment depression in a region
  • Deep T Wave Inversion
  • Pathological Q Waves (suggesting a deep infarct – a late sign)

 

Artery

Heart Area

ECG Leads

Left Coronary Artery

Anterolateral

I, aVL, V3-6

LAD

Anterior

V1-4

Circumflex

Lateral

I, aVL, V5-6

Right Coronary Artery

Inferior

II, III, aVF

 

Troponins

Troponins are proteins found in cardiac muscle. The specific type of troponin, the normal range and diagnostic criteria vary based on different laboratories (so check your policy). Diagnosis of ACS typically requires serial troponins (e.g. at baseline and 6 or 12 hours after onset of symptoms). A rise in troponin is consistent with myocardial ischaemia as the proteins are released from the ischaemic muscle. They are non-specific, meaning that a raised troponin does not automatically mean ACS.

There are alternative causes of raised troponins:

  • Chronic renal failure
  • Sepsis
  • Myocarditis
  • Aortic dissection
  • Pulmonary embolism

 

Other Investigations

Perform all the investigations you would normally arrange for stable angina:

  • Physical Examination (heart sounds, signs of heart failure, BMI)
  • ECG
  • FBC (check for anaemia)
  • U&Es (prior to ACEi and other meds)
  • LFTs (prior to statins)
  • Lipid profile
  • Thyroid function tests (check for hypo / hyper thyroid)
  • HbA1C and fasting glucose (for diabetes)

Plus:

  • Chest xray to investigate for other causes of chest pain and pulmonary oedema
  • Echocardiogram after the event to assess the functional damage
  • CT coronary angiogram to assess for coronary artery disease

 

Acute STEMI Treatment (always check local protocol)

Patients with STEMI presenting within 12 hours of onset should be discussed urgently with local cardiac centre for either:

  • Primary PCI (if available within 2 hours of presentation)
  • Thrombolysis (if PCI not available within 2 hours)

The local cardiac centre will advise about further management (such as further loading with aspirin and ticagrelor).

Percutaneous Coronary Intervention (PCI) involves putting a catheter into the patient’s brachial or femoral artery, feeding that up to the coronary arteries under xray guidance and injecting contrast to identify the area of blockage. This can then be treated using balloons to widen the gap or devices to remove or aspirate the blockage. Usually a stent is put in to keep the artery open.

Thrombolysis involves injecting a fibrinolytic medication (they break down fibrin) that rapidly dissolves clots. There is a significant risk of bleeding which can make it dangerous. Some examples of thrombolytic agents are streptokinase, alteplase and tenecteplase.

 

Acute NSTEMI treatment: BATMAN

B – Beta blockers unless contraindicated

A – Aspirin 300mg stat dose

T – Ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative)

M – Morphine titrated to control pain

– Anticoagulant: Low Molecular Weight Heparin (LMWH) at treatment dose (e.g. enoxaparin 1mg/kg twice daily for 2-8 days)

N – Nitrates (e.g. GTN) to relieve coronary artery spasm

Give oxygen only if their oxygen saturations are dropping (i.e. <95%).

 

GRACE Score to assess for PCI in NSTEMI:

This scoring system gives a 6-month risk of death or repeat MI after having an NSTEMI:

  • <5% Low Risk
  • 5-10% Medium Risk
  • >10% High Risk

If they are medium or high risk they are considered for early PCI (within 4 days of admission) to treat underlying coronary artery disease.

 

Complications of MI (Heart Failure DREAD)

DDeath

RRupture of the heart septum or papillary muscles

E Edema” (Heart Failure)

AArrhythmia and Aneurysm

D Dressler’s Syndrome

 

Dressler’s Syndrome

This is also called post-myocardial infarction syndrome. It usually occurs around 2-3 weeks after an MI. It is caused by a localised immune response and causes pericarditis (inflammation of the pericardium around the heart). It is less common as the management of ACS becomes more advanced.

It presents with pleuritic chest pain, low grade fever and a pericardial rub on auscultation. It can cause a pericardial effusion and rarely a pericardial tamponade (where the fluid constricts the heart and prevents function).

A diagnosis can be made with an ECG (global ST elevation and T wave inversion), echocardiogram (pericardial effusion) and raised inflammatory markers (CRP and ESR).

Management is with NSAIDs (aspirin / ibuprofen) and in more severe cases steroids (prednisolone). They may need pericardiocentesis to remove fluid from around the heart.

 

Secondary Prevention Medical Management (6 As)

  • Aspirin 75mg once daily
  • Another antiplatelet: e.g. clopidogrel or ticagrelor for up to 12 months
  • Atorvastatin 80mg once daily
  • ACE inhibitors (e.g. ramipril titrated as tolerated to 10mg once daily)
  • Atenolol (or other beta blocker titrated as high as tolerated)
  • Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily)

Dual antiplatelet duration will vary following PCI procedures depending on the type of stent that was inserted. This is due to a higher risk of thrombus formation in different stents.

 

Secondary Prevention Lifestyle:

  • Stop smoking
  • Reduce alcohol consumption
  • Mediterranean diet
  • Cardiac rehabilitation (a specific exercise regime for patients post MI)
  • Optimise treatment of other medical conditions (e.g. diabetes and hypertension)

 

Types of MI

This is slightly unnecessary knowledge for everyday practice but worth being aware of. It is worth avoiding as it could confuse people unless they are a medical registrar or cardiologist.

  • Type 1: Traditional MI due to an acute coronary event
  • Type 2: Ischaemia secondary to increased demand or reduced supply of oxygen (e.g. secondary to severe anaemia, tachycardia or hypotension)
  • Type 3: Sudden cardiac death or cardiac arrest suggestive of an ischaemic event
  • Type 4: MI associated with PCI / coronary stunting / CABG

 

Last updated October 2018
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