Acute coronary syndrome

Notes

Definition & classification

Acute coronary syndrome (ACS) refers to three states of myocardial ischaemia: unstable angina (UA), non-ST elevation myocardial infarction (NSTEMI) and ST elevation myocardial infarction (STEMI).

ACS is a medical emergency requiring urgent admission. Around 100,000 people are admitted with ACS in the UK each year. Atherosclerosis represents the most significant aetiological factor.

ACS is classified into one of three conditions according to clinical features, ECG findings and cardiac enzymes:

  1. STEMI: ST-segment elevation, new-onset left bundle branch block and raised troponins.
  2. NSTEMI: Non-specific signs of ischaemia or normal ECG, raised troponins.
  3. UA: Characteristic clinical features, non-specific signs of ischaemia or normal ECG, normal troponins.

Aetiology

ACS is typically triggered by rupture of an atheromatous plaque in the coronary arterial wall. For completeness, a number of less common causes are also mentioned below.

Coronary atherosclerosis

Modifiable risk factors

  • ​High cholesterol
  • Hypertension
  • Smoking
  • Diabetes
  • Obesity

Non-modifiable risk factors

  • Age
  • Family history
  • Male sex
  • Premature menopause

Other

Other causes of emboli

  • Valvular disease

Other causes of coronary occlusion

  • Vasculitis (e.g. Kawasaki disease)
  • Coronary vasospasm (e.g. cocaine)

Changes in oxygen demand and / or delivery

  • Anaemia
  • Hyperthyroidism

Pathophysiology

Atherosclerosis is an inflammatory process which predisposes individuals to ACS. It is a complex cellular process involving lipids, macrophages and smooth muscle. 

Step 1 - endothelial dysfunction

The first step is endothelial injury. This causes a local inflammatory response. If the injury recurs or healing is incomplete, inflammation may continue leading to the accumulation of low-density lipoproteins (LDL). These become oxidised by local waste products creating reactive oxygen species (ROS).

Step 2 - plaque formation

In response to these irritants, endothelial cells attract monocytes (macrophages). These engulf (phagocytose) the LDLs swelling to become foam cells and ‘fatty streaks’.

Step 3 - plaque rupture

Continued inflammation triggers smooth muscle cell migration. This forms a fibrous cap, which together with the fatty streaks, develops into an atheroma

The top of the atheroma forms a hard plaque. This may rupture through its endothelial lining exposing a collagen-rich cap. Platelets aggregate on this exposed collagen forming a thrombus that may occlude or severely narrow the vessel. Alternatively, the thrombus may break lose, embolising to infarct a distant vessel.

Clinical features

The signs and symptoms of ACS are those of myocardial ischaemia and an elevated autonomic (sympathetic) response. However, some patients may have a ‘silent MI’. This is typically seen in elderly and diabetic patients.

Symptoms

  • Chest pain > 15 minutes
  • Shortness of breath
  • Sweating
  • Nausea and vomiting

Signs

  • Pale 
  • Clammy
  • Tachycardic
  • Cardiac failure (e.g. pulmonary oedema, hypotension)

Investigations & diagnosis

ACS necessitates a quick and accurate diagnostic process combining history, examination, ECG results and laboratory findings (e.g. cardiac enzymes).

Diagnosis of ACS

12-lead ECG

  • STEMI: ST-segment elevation is seen. Changes, however, evolve over time:
    • Minutes to hours: hyperacute T-waves
    • 0-12 hours: ST-elevation
    • 1-12 hours: Q-wave development
    • Days: T-wave inversion
    • Weeks: T-wave normalisation and persistent Q-waves
  • NSTEMI & UA: may have signs of myocardial ischaemia, T-wave inversion or ST-segment depression or no signs.

ECG: ST elevation in leads II, III & AVF - indicative of an acute inferior MI.

Image courtesy of Wikimedia commons.

Cardiac enzymes

Cardiac enzymes are biomarkers of myocardial ischaemia. They include:

  • Troponins (T or I) - gold standard
  • Creatine kinase (CK, specifically CK-MB)
  • Myoglobin

Troponins (T or I) have become the gold standard test. They begin to rise hours after the event. It may be measured 6-12 hours post-event, typically 8 hours. It also has prognostic input, the degree to which the troponin is raised is related to risk of death.

NOTE: new 'sensitive' troponin tests allow for diagnostic measurements just 3 hours post-event.

Troponins may be raised (though typically to a lesser degree) in a number of other settings such as heart failure, chronic kidney disease and pulmonary embolisms.

Cardiac markers

Bedside

  • ECG
  • Blood pressure
  • Blood glucose (BM)

Bloods

  • FBC
  • U&Es
  • LFTs
  • TFT
  • CRP
  • Cholesterol

Imaging

  • Chest XR - may demonstrate signs of heart failure
  • Echocardiogram - may demonstrate reduced ejection fraction and / or valvular pathology

Special

  • Coronary angiogram - see management below

Immediate management

Immediate managment of all suspected ACS can be remembered using the mnemonic MONA - morphine, oxygen, nitrates, aspirin.

NICE guidelines recommend IV morphine (administered with an anti-emetic) in sufficient dosage to relieve chest pain, in addition to loading-dose aspirin (300mg) and sublingual (under the tongue) GTN, a potent vasodilator. Oxygen appears to be of limited benefit in patients with preserved oxygen saturations (94% or greater), and may indeed be harmful.

Hospital management

STEMI

Patients with STEMI require emergency reperfusion to restore coronary flow and minimise myocardial injury. PCI is the preferred strategy.

Primary percutaneous coronary intervention (PCI) should ideally be undertaken within 120 minutes. If this is unavailable, fibrinolytic agents such as alteplase or reteplase may be given IV. Provided coronary stenting is performed in the next 6-24 hours, this is an effective alternative.

Patients should be initiated on aspirin and a second anti-platelet drug prior to PCI. Typically, clopidogrel is used, however, preference is now being given to prasugrel and ticagrelorDual anti-platelet therapy (e.g. lifelong aspirin and 12 months of clopidogrel / prasugrel / ticagrelor) should be continued post-PCI.

Anticoagulation with heparin (LMWH or UFH) or bivalirudin should be offered prior to PCI.

Management of STEMI

NSTEMI / UA

If angiography is likely within 24 hours unfractionated heparin should be offered. If angiography is not likely within 24 hours (and the patient does not have a high bleeding risk) fondaparinux should be offered. 

Management of NSTEMI and UA is guided by the estimated six-month mortality risk calculated using the GRACE score.

  • Intermediate - high risk (> 3%): angiography within 72 hours with a view to cardiac stenting / CABG. Dual anti-platelet therapy (e.g. life-long aspirin and clopidogrel for 12 months). Consider a glycoprotein IIb/IIIa inhibitor (IV eptifibatide or tirofiban) if chest pain continues.
  • Low risk (1.5-3%): Dual antiplatelet therapy (e.g. life-long aspirin and clopidogrel for 12 months).
  • Lowest risk (<1.5%): Life-long aspirin only.

Management of NSTEMI / UA

GRACE scoring

GRACE (Global Registry of Acute Coronary Events) is a scoring system which estimates six-month mortality risk in patients with NSTEMI / UA. It is calculated by clinicians by entering simple clinical risk factors into a web-based model.

GRACE Scoring - ACS Risk Score

  • Age
  • Heart rate
  • Systolic BP
  • Renal function
  • CHF
  • ST-segment deviation
  • Cardiac arrest
  • Elevated biomarkers

Reproduced from: www.gracescore.org

Long-term management

Long-term management requires both medical therapy and patient education. Advise patients on modifiable risk factors: smoking cessation, dietary changes and mild exercise.

Beta-blockers and ACE-i should be given in the absence of contra-indications, continue aspirin and clopidogrel (when indicated). Statin therapy is often initiated.

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