Acute Coronary Syndromes

An acute coronary syndrome (ACS) describes a spectrum of clinical manifestations that result from a common pathophysiological process- reduced blood flow to the heart.  It can be classified by degree of infarction (see below) or by evidence from electrophysiology (i.e. ST-elevation vs Non-ST-elevation vs unstable angina).

Background and Epidemiology

  • In the UK about 114000 patients with ACS are admitted a year
  • Coronary heart disease is the most common cause of death in the UK (1 in 5 men and 1 in 7 women)

Risk factors/Aetiology

  • Age; male
  • Social deprivation
  • Smoking (increases mortality due to CHD by 60% and increases risk of CHD by 25%)
  • Poor diet, little exercise and obesity
  • Excess alcohol
  • Hypertension (each 20mmHg rise in systolic, or 10mmHg rise in diastolic, BP doubles risk of death from CHD)
  • Hypercholesterolaemia
  • Diabetes (2-5 fold increased risk of CHD)
  • Family history
  • Ethinicity (more common in those from Indian, Pakistani, Bangladeshi backgrounds)

Pathophysiology

  • Practically all ACSs are caused by corornary arterial thromboses (cf coronary artery disease/angina which is caused only by the precursor to thrombosis- atherosclerosis)
    • See also coronary artery disease for the pathogenesis of atherosclerotic plaques
  • Thrombosis occurs in a number of situations
    • Rupture of the fibrous cap of the plaque (most common)
    • Superficial erosion of the fibrous cap (seen particularly in diabetic/female individuals)
    • Erosion of a calcium nodule deposit (on the fibrous cap)
    • Intraplaque haemorrhage (usually causes a more subacute picture)
  • This is due to the
    • contact of collagen (of the plaques extracellular matrix) with the blood which can trigger platelet activation.
    • factors produced by plaque macrophages can also trigger the coagulation cascade
  • This results in the conversion of fibrinogen to fibrin and cross-linking of platelets (by von Willebrand factor), creating a dense network of platelets trapped in fibrin.  This is known as a ‘white’ arterial thrombus (cf cardiac thrombi- red).
  • This thrombus can either occlude vessels directly at the site of formation or break off and block narrower vessels down stream, causing ischaemia with or without additional infarction.

Presentation

  • Chest pain is the predominant symptom
    • Acute onset; heavy/crushing/squeezing/aching
    • May radiate to the jaw, the left shoulder or down the left arm
    • brought on at rest; worsened by exertion
    • Not relieved by GTN, rest.  Persistent (>20 minutes)
    • May be associated with autonomic features e.g. sweating, nausea/vomiting; shortness of breath; palpitations; fatigue
  • The patient may appear pale, cool, clammy
  • Blood pressure may be low or high

Investigations

  • Troponin
    • Troponins (specifically type T (used in Tayside) and I) are cardiac enzymes only released into the serum if cardiac necrosis has occurred (highly specific and sensitive for cardiac damage- although not always due to CAD)
    • Serum levels increase within 3-12 hours of onset of chest pain (may not be present initially)
      • Two serial measurements: one on admission and one 6-12 hours later, should be taken
      • Reference range in Tayside is <0.045mg/ml (micrograms/l)
        • >0.045 suggests infarction and thus the ACS can be classed either as a STEMI or NSTEMI (see below)
        • <0.045 classifies the ACS as unstable angina (there may still be changes seen on ECG)
  • ECG
    • Classifying ACS by ECG
    • STEMI (ST-elevation myocardial infarction)
      • Look particularly for some of the following abnormalities: ST elevation; peaked T waves (early); T wave inversion (later); pathological Q waves
        • Note that reciprocal leads may show ST-depression

ECG-Anatomy-LITFL

ecg-zones

  • Other tests include FBC (look for any anaemia); U&Es (in particular, deranged potassium may cause arhythmias causing chest pain; also renal function should be determined prior to starting an ACE inhibitor.
  • CXR may be useful to measure heart size for signs of chronic heart failure.
  • Echocardiogram may be used later to identify functional problems post ischaemia/infarction.

Management

Immediate (see also management of the acutely unwell patient)

  • Aspirin 300mg should be given to all patients with a suspected ACS
    • Guidelines (NICE and SIGN) recommend Clopidogrel 300mg should also be given to patients
      • with any signs of ischaemic change on ECG
      • with elevated cardiac enzymes
      • (also who have a predicted 6-month mortality/risk of MI of >1.5%- this can be done using scoring systems e.g. GRACE)
    • MONA
      • Morphine for pain (+anti-emetic)
      • Oxygen
      • Nitrate
      • Aspirin 300mg
  • For Unstable Angina and NSTEMI
    • Consider also unfractionated heparin (adjusted dose) or, if the patient will not be being sent for PCI (see below) within 24 hours, use fondaparinux
    • Based on bleeding risk/risk of ischaemia: consider adding a GPI (e.g. eptifibatide or tirofiban) OR consider bivalirudin as an alternative to Heparin+GPI if the patient is not on fondaparinux+GPI and angiography will be within 24 hours of admission
      • NB Bivalirudin is not currently used in Tayside and Glycoprotein inhibitors should really only be prescribed by a specialist consultant
    • For those at intermediate risk or greater, offer coronary angiogram (with PCI if indicated) within 96 hours of admission
  • For STEMI
    • Patients should be given unfractionated heparin.
      • If PCI cannot be given, fondaparinux should be used instead
      • Patients undergoing PCI are recommended to be treated with GPI drug (see above)
    • Offer Percutaneous Coronary Intervention to all those eligible
      • Should ideally present within 12 hours of symptom onset and receive PCI as soon as possible (<120 minutes)
        • If this is not possible consider fibrinolytic drugs- usually IV Tenecteplase (30-50mg)- given as early as possible (ideally within 6 hours of symptom onset)
          • If patients fail to reperfuse, a rescue PCI procedure can be considered
      • This usually involves stenting the affected artery.
    • NB There may be indications that favour CABG over PCI
      • Longer, calcified vessels involving major bifurcations are affected by CAD
      • Diabetes mellitus (relative)
      • LV dysfunction or strongly positive exercise test
      • Extensive blockage e.g. of the proximal left anterior descending artery
  • Other pharmacological management
    • In patients without bradycardia, hypotenion or underlying cardiac failure, IV and oral beta blockade should be considered
  • Pain relief can be managed with strong opiates e.g. morphine.
  • Anti-nausea drugs may also be required

Long-term treatments/Secondary Prevention

  • Patients should remain on 75-150mg of Aspirin per day
  • Clopidogrel should be continued at 75mg for 3 months in patients with a NSTEMI (not treated with PCI) diagnosis and for at least 1 month (up to 12) in patients with a STEMI (treated with PCI)
    • Consider continuation for up to a year
  • All patients with unstable angina, NSTEMI or STEMI should be offered beta-blocker treatment, ACE inhibitor treatment and statin treatment
    • Offer patients, who are intolerant of an ACEI, an ARB instead.
    • Calcium channel blockers are not recommended first line
  • Omega 3 rich foods e.g. oily fish is recommended

In short:

  • ACE inhibitor
  • Aspirin/Clopidogrel
  • Beta-blocker
  • Statin

Offer an aldosterone antagonist e.g. spironolactone or eplerenone if the patient has symptoms of heart failure (after ACEI treatment)

Comlications of acute MI

  • Cardiac arrest
    • Usually secondary to VF; also VT
    • Most common cause of death
  • Cardiogenic shock
    • If a large part of the ventricular wall is damaged, the ejection fraction may be compromised to the paint that the patient goes into shock
    • Difficult to treat- may require inotropic support
  • Chronic heart failure
  • Heart block
  • Pericarditis (acutely); Dressler’s syndrome (autoimmune pericarditis- pericardial effusion) can occur 2-6 weeks after MI, treated with NSAIDs
  • Left ventricular aneurysm
    • Persistent ST elevation and LVD
    • Risk of stroke- anticoagulate
  • Left ventricular free wall rupture
    • Occurs around 1-2 weeks after
    • Sudden heart failure or collapse with cardiac tamponade (urgent pericardiocentesis)
  • Ventricular septal defect
    • Occurs in 1-2% in the first week post MI
    • Acute heart failure; pansystolic murmur
    • Urgent correction (surgery)
  • Acute mitral regurgitation (ischaemia/ruptured papillary muscle)
    • Early-mid-systolic murmur
    • Often requires emergency repair if associated with acute heart failure
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