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acute coronary syndrome

Written by Luke Zhu

Last Reviewed: June 2019

Review Due: June 2020

 

DEFINITION

‘a spectrum of disorders characterised by myocardial ischaemia, encompassing unstable angina, non-ST elevation myocardial infarction (NSTEMI) and ST-elevation myocardial infarction (STEMI)’

Unstable Angina

'narrowing of the coronary arteries, leading to reduced cardiac perfusion resulting in short episodes of cardiac chest pain at rest with no associated rise in troponin'

Non-ST Elevation Myocardial Infarction

'sub-total narrowing of the coronary arteries, leading to reduced cardiac perfusion resulting in cardiac chest pain with an associated rise in troponin without evidence of ST elevation on ECG'

ST Elevation Myocardial Infarction

'complete occlusion of the coronary artery, leading to loss of blood supply to the cardiac tissue resulting in cardiac chest pain, a rise in troponin and evidence of ST elevation on ECG'

AETIOLOGY

Atherosclerotic plaque rupture

Thrombosis

Coronary vasospasm

risk factors

Dyslipidaemia

Hypertension

Smoking

Diabetes

Obesity

Lack of physical exercise

Older age

Family history of (early) heart disease

Recreational drug use (commonly cocaine)

 

SIGNS AND SYMPTOMS

Anterior, central, crushing chest pain (may or may not radiate down left arm or jaw)

Sweating

Nausea and vomiting

Shortness of breath

Palpitations

Anxiety (“sense of impending doom”)

 

PATHOPHYSIOLOGY

The underlying issue in ACS is reduced oxygenated blood supply to the cardiac muscle. This can be caused by gradual stenosis of the coronary vessels, or by an acute plaque rupture leading to thrombus embolisation that occludes the vessel.

Loss of blood supply will lead to ischaemia in the region of tissue supplied by the affected vessel. If left untreated, irreversible tissue necrosis will occur.

 

Investigations

Electrocardiogram

The main feature to be diagnosed on an ECG is ST elevation, however it is also useful in identifying the vessel(s) affected. See below for more information.

Cardiac Biomarkers

Most centres use a high-sensitivity troponin assay, typically measured at admission and 6-12 hours after onset of pain

CXR

Should be considered in all patients presenting with acute chest pain, to exclude other diagnoses such as pneumonia or pneumothorax

Coronary Angiography

All patients presenting with a STEMI should receive therapeutic coronary angiography (see below) as soon as possible.

For patients with unstable angina/NSTEMI, the GRACE score can be used to calculate 6-month mortality and guide the need for coronary angiography. Medium (5-10%) and high (>10%) risk patients should receive early in-patient angiography.

what is troponin?

electrocardiography

An ECG is a tracing of the electrical activity of the heart, typically obtained by placing 10 electrodes on the chest wall and limbs. A 12-lead ECG is vital in the assessment of patients with acute coronary syndrome, as it helps guide their management and can help determine the site of their disease.

ST Segment Elevation

To be diagnosed with ST Elevation MI, an ECG must show:

  • presence of  ≥1 mm ST elevation in at least two adjacent limb leads

  • ≥2 mm ST elevation in at least two contiguous precordial leads

  • new-onset bundle branch block

Reciprocal ST changes, i.e. ST Depression in the opposite leads to those showing ST Elevation, can help confirm the diagnosis of myocardial infarction.

Location of Infarct

The region of infarcted myocardium, and therefore the affected coronary vessel, can be determined by analysing which leads show ischaemic changes. 

Progression of ECG Changes

An ECG of a patient with an acute MI will change over time, as the myocardium infarcts and tissue death (and eventually healing) occur. The first signs (of a STEMI) will typically be ST Elevation and T-Wave Inversion. This is followed by development of a pathological Q-Wave. While the ST-Segment, QRS Complex and T-Waves will gradually normalise, the Q-Wave will remain.

 

Troponin is a protein integral to muscle contraction, found in skeletal and cardiac muscle.

It is released into the blood following muscle cell death.

Troponin I and T are sensitive markers of myocardial damage.

They are delayed markers of myocardial damage and start increasing 4-9 hours after an acute MI, with peak levels at 12-24 hours,. They may remain elevated for up to 2 weeks.

TREATMENT

risk factor modification

Smoking cessation

Identify and treat hypertension, diabetes and dyslipidaemia

Diet modification

Encourage exercise

unstable angina

Consider oxygen, IV opiates and anti-emetic

Glyceryl Trinitrate (Sublingual or IV)

If pain continues, transfer to a coronary care unit for further management and consideration of revascularisation

non-st elevation mI

Consider oxygen, IV opiates and anti-emetic

PRN Glyceryl Trinitrate

PO Aspirin 300mg (to be continued at 7mg OD)

PO Ticagrelor* 180mg (to be continued at 90mg BD)

SC Fondaparinux 2.5mg (to be continued until discharge depending on creatinine clearance)

If pain continues, transfer to a coronary care unit for further management and consideration of revascularisation

*Other anti-platelets, such as clopidogrel, may also be used. Consult local guidelines for information specific to your hospital.

NB: The above guidance is adapted from the NHS Greater Glasgow and Clyde ACS protocol. Other guidelines may also recommend other medications, such as Beta-Blockers and ACE Inhibitors

ALWAYS CONSULT LOCAL GUIDELINES OR THE BNF FOR UP-TO-DATE DOSING INFORMATION AND GUIDANCE ON policies at your hospital

st elevation mI

Consider oxygen, IV opiates and anti-emetic

PRN Glyceryl Trinitrate

PO Aspirin

PO Ticagrelor (if for PPCI) or Clopidogrel (if for thrombolysis)

IV Heparin

Contact local specialty cardiac centre to arrange for an emergency transfer for primary percutaneous coronary intervention (PPCI)

NB: The above guidance is adapted from the NHS Greater Glasgow and Clyde ACS protocol. Other guidelines may also recommend other medications, such as Beta-Blockers and ACE Inhibitors

revascularisation

Primary Percutaneous Coronary Intervention

  • PPCI (also known as coronary angioplasty) is an invasive, non-surgical procedure in which a catheter is inserted through a peripheral artery (usually the radial or femoral arteries) to gain access to the coronary circulation.

  • A dye is administered to allow the coronary vessels to be visualised with x-ray imaging.

  • Stenosis or occlusion of the vessels can be treated with balloon dilatation and/or the insertion of a stent (a permanent metal scaffolding that helps maintain vessel patency).

  • PPCI is the preferred management option for acute STEMI.

Thrombolysis

  • Thrombolysis involves administration of fibrinolytic drugs (such as recombinant tissue plasminogen activator; tenecteplase) to breakdown clots and restore vascular supply.

  • There are many contraindications to thrombolysis, including recent head injury/surgery, stroke in the past 6 months, history of aortic dissection or recent GI bleed.

  • NICE and SIGN guidelines recommend thrombolysis if PPCI cannot be delivered within 120 minutes.

  • Thrombolysis is only successful in 60-70% of cases, which is why PPCI is the preferred option for patients with acute STEMI.

Coronary Artery Bypass Graft (CABG)

  • CABG is a surgical procedure that aims to restore/improve vascular supply to the myocardium by grafting new vessels to the coronary circulation.

  • Donor vessels are typically obtained from the leg or chest wall.

  • CABG procedures are not typically performed for treatment of acute MI, rather as an elective procedure in patients with ongoing ischaemic heart disease.

secondary prevention

Prior to discharge, patients with a new diagnosis of ischaemic heart disease should be prescribed:

  • Aspirin (plus a second anti-platelet, depending on local guidelines)

  • Beta-Blocker (typically atenolol or bisoprolol)

  • Statin

  • ACE Inhibitor (typically ramipril or lisinopril)

  • Glyceryl Trinitrate Spray

Patients should also be advised on:

  • Smoking cessation

  • Dietary modification

  • Exercise

 
 

EPIDEMIOLOGY

Coronary heart disease is the leading cause of death worldwide. In the UK, 1 in 6 men and 1 in 10 women die from ischaemic heart disease (IHD).

As a whole, risk factors for IHD have been decreasing in developed countries, and increasing in developing ones, likely due to changing lifestyles, diets, urbanisation and increasing life expectancy.

Risk factors are mostly environmental - for example a person of Japanese ethnicity moving to the US may acquire similar IHD risk profiles to someone born in the US.

STEMIs tend to occur at a younger age in men, at an average of 65.1 years old for their first MI. This is in contrast to 72 years for women. The incidence for women increases after menopause

REFERENCES