|

Acute Coronary Syndrome

Last updated:

Overview

Acute coronary syndrome (ACS) is a medical emergency characterized by signs and symptoms that occur due to ischaemia in the myocardium. It is an umbrella term for diagnoses including:

  • ST-elevation myocardial infarction (STEMI)
  • Non-ST-elevation myocardial infarction (NSTEMI)
  • Unstable angina

The initial management of ACS is similar up to the point of using investigations to identify the specific diagnosis. 

Presentation

The main presenting complaint is chest pain:

  • Usually retrosternal, crushing, central, heavy, severe, and diffuse
  • Sometimes patients describe pressing or squeezing
  • May radiate to the left arm or jaw
  • Some patients may not have pain at all e.g. diabetics, elderly people, female sex
  • Sometimes they may have atypical pain:
    • They may describe it as:
      • Indigestion
      • Epigastric pain
      • Interscapular pain in the back
      • Neck or jaw pain

Other associated features:

Some patients may go into cardiogenic shock, which has a high mortality rate:

  • Systolic blood pressure <90mmHg despite volume replacement
  • Reduced urine output
  • Cool extremities
  • Altered mental status
  • Pale appearance
  • Tachypnoea and tachycardia
  • Severe dyspnoea

Signs on Examination

Patients usually have very few examination findings. If they develop complications, there may be some significant findings.

Investigations

Overview

All patients with suspected ACS should have the following investigations performed:

  • 12-lead ECG:
    • Additional leads should be recorded if the standard leads are inconclusive or the patient has signs or symptoms of ongoing myocardial ischaemia
  • Cardiac troponins: – if this does not delay treatment of a STEMI
    • This can confirm the diagnosis, but an ECG alone can suffice

Diagnosis

ST-Elevation Myocardial Infarction (STEMI)

STEMI is diagnosed if there are ECG changes. Cardiac troponins can be used to confirm the diagnosis but should not delay treatment:

  • ST-elevation in at least 2 contiguous leads:
    • ≥2.5mm in men <40 years old
    • ≥2mm in men >40 years old
    • ≥1.5mm in women of all ages
  • A new left bundle branch block
  • ST depression in V1-V3 suggests a posterior STEMI

Non-ST-Elevation Myocardial Infarction (NSTEMI)

NSTEMI is diagnosed using an ECG and cardiac troponins:

  • No ST-elevation may be seen
  • ST depression – worse prognosis
  • T wave inversion
  • Troponins are raised

Unstable Angina

The diagnosis of unstable angina is usually made by a cardiologist:

  • ECG may be normal
  • Troponins are not raised

Troponins can rise a few hours after unstable angina’s onset, making it difficult to distinguish unstable angina from an NSTEMI. Elevated troponins point the diagnosis towards NSTEMI.

Management

All patients with ACS

The initial management of all patients with suspected ACS is the same:

  • Loading dose of aspirin 300 mg immediately
  • Oxygen only if saturations are <94%
  • Morphine only if severe pain is present
  • Nitrates may be given if there is ongoing chest pain or hypertension
    • Should be used with caution if the patient is hypotensive.

Following an ECG, the next steps vary depending on the diagnosis.

ST-Elevation Myocardial Infarction (STEMI)

Once a diagnosis of STEMI has been made, patients should immediately be assessed for coronary reperfusion therapy which involves a percutaneous coronary intervention (PCI) or fibrinolysis.

Percutaneous coronary intervention (PCI) is offered if the patient presents within 12 hours of symptom onset and PCI can be delivered within 120 minutes after presentation. It is also considered if the patient is presenting >12 hours and has continuing myocardial ischaemia/cardiogenic shock. Other points include:

  • Radial access is preferred to femoral access
  • Drug-eluting stents are used
  • Pre-PCI antiplatelet treatment:
    • If the patient is not taking an oral anticoagulant: offer prasugrel with aspirin
    • If the patient is taking an oral anticoagulant: offer clopidogrel
  • Drug therapy during PCI:
    • If undergoing PCI with radial access:
      • Unfractionated heparin and bailout glycoprotein IIb/IIIa inhibitor (GPI) (e.g. tirofiban)
        • “Bailout” means it is used as a rescue therapy to manage complications
    • If undergoing PCI with femoral access:
      • Bivalirudin and bailout GPI
  • Other procedures during PCI:
    • Thrombus aspiration should be considered
    • Complete revascularisation should be considered in patients with multivessel coronary artery disease without cardiogenic shock

Fibrinolysis is performed if the patient presents within 12 hours of symptom onset but PCI is not possible within 120 minutes of presentation. Other points include:

  • Patients should be given an antithrombin drug (e.g. low molecular weight heparin, fondaparinux, or bivalirudin) at the same time
  • An ECG should be performed 60-90 minutes after thrombolysis
    • If there is evidence of ongoing myocardial ischaemia (e.g. ST elevation), offer immediate coronary angiography and PCI and do not repeat fibrinolysis

If patients are not treated with reperfusion therapy they are medically managed:

  • If the patient is not taking an oral anticoagulant: offer prasugrel with aspirin
  • If the patient is taking an oral anticoagulant: offer clopidogrel with aspirin or aspirin alone if the bleeding risk is high

Non-ST-Elevation Myocardial Infarction (NSTEMI)/unstable angina

The Global Registry of Acute Coronary Events (GRACE) score is calculated which then guides treatment. This calculates the risk of mortality within the next 6 months:

  • If ≤3% (low risk)– medical management:
    • Give ticagrelor and aspirin
    • If high-bleeding risk: clopidogrel and aspirin or aspirin alone
    • If ischaemia develops or is shown on testing: angiography with PCI
  • If >3% (intermediate/high risk)– PCI within 72 hours if stable, immediately if unstable:
    • See PCI management above
  • Additional drug therapy for NSTEMI/unstable angina:
    • If no high bleeding risk and not immediately having angiography: offer fondaparinux
    • If there is significant renal impairment (creatinine >265 µmol/L): consider unfractionated heparin instead of fondaparinux

All patients after treatment

  • Pre-discharge echocardiogram to assess left ventricular function.
  • Establish secondary prevention after an acute MI:
    • People after an acute MI should be offered an angiotensin-converting enzyme (ACE) inhibitor, aspirin, another antiplatelet for 12 months, a beta-blocker, and a statin.

Absolute contraindications to fibrinolysis

  • History of intracranial haemorrhage at any time
  • History of haemorrhagic stroke at any time
  • Ischaemic stroke in the last 6 months
  • Major surgery/trauma in the last 1 month
  • Gastrointestinal bleeding within the last 1 month
  • Bleeding disorders
  • Aortic dissection
  • Non-compressible punctures within the last 24 hours e.g. liver biopsy/lumbar puncture
  • Central nervous system neoplasm or arteriovenous malformation

Monitoring

  • Patients are usually followed up 1-2 weeks following discharge
  • Patients are given indefinite medications for secondary prevention
  • Patients have follow-up echocardiograms to check left ventricular function

Patient Advice

  • Patients should be followed up 1-2 weeks following discharge
  • Patients should be educated on their medications post-MI
  • Patients should be given instructions on what to do if they experience recurrent symptoms and should go to the emergency department
  • For patients that drive a car or motorcycle, they must:
    • Stop driving for:
      • 1 week if they had successful treatment
      • 4 weeks if treatment was not successful
      • 4 weeks if they were managed medically
    • They do not need to tell the DVLA
  • For patients that drive a bus, coach, or lorry, they must:
    • Tell the DVLA and stop driving for 6 weeks
    • Fill in a VOCH1 form and send it to the DVLA
    • Be assessed by a clinician after 6 weeks to see if they can drive again

Complications

Cardiac arrest

This may be due to:

Patients are managed as per the Advanced Life Support protocol.

Chronic heart failure

Ventricular damage and remodelling may impair function leading to chronic heart failure.

Cardiogenic shock

If significant damage to the heart occurs, it may fail as a pump leading to cardiogenic shock characterised by hypotension and tachycardia. This may occur due to: 

  • Papillary muscle rupture
  • Ventricular septal rupture
  • Left ventricular free wall rupture and subsequent pericardial tamponade
  • Right ventricular infarction

Acute pericarditis

Usually occurs within 48 hours of a myocardial infarction. Patients have pleuritic chest pain that’s relieved when leaning forward/sitting up and worsened lying down

Dressler’s syndrome

Usually occurs 2-6 weeks after an MI. Patients have fever, pleuritic chest pain, raised ESR, and pericardial effusions. It is managed with aspirin or NSAIDs

Left ventricular aneurysm

Ischaemia can weaken the ventricular walls leading to an aneurysm. Patients have persisting ST elevation and left ventricular failure. Thrombi can form within the aneurysm so patients are anticoagulated to reduce the risk of stroke.

Left ventricular free wall rupture and acute pericardial tamponade

Necrosis may thin the ventricular walls leading to rupture and allowing blood to leak out into the pericardium. This leads to a cardiac tamponade which requires urgent pericardiocentesis and thoracotomy.

Ventricular septal defect

Interventricular septal ruptures can lead to a ventricular septal defect. This can lead to acute heart failure and patients have a pansystolic murmur. It is managed with urgent surgery.

Acute mitral regurgitation

Rupture of the papillary muscles can lead to acute mitral regurgitation and acute pulmonary oedema and hypotension. This is more common in inferior and anterolateral MIs and is treated with emergency surgery.

Prognosis

  • People with NSTEMIs have a high incidence of recurrent myocardial ischaemia and a worse prognosis than those with unstable angina
  • Factors associated with a poorer prognosis are:
    • Advancing age
    • Presence and severity of ischaemia-related ECG changes
    • Size of troponin rise
    • Complications arising
    • Arrhythmias
    • Renal impairment
    • Diabetes mellitus
    • Anaemia
    • Cerebrovascular disease
    • Peripheral arterial disease

Author