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

• 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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