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
- Look particularly for some of the following abnormalities: ST elevation; peaked T waves (early); T wave inversion (later); pathological Q waves
- 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
- Guidelines (NICE and SIGN) recommend Clopidogrel 300mg should also be given to patients
- 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
- 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)
- This usually involves stenting the affected artery.
- Should ideally present within 12 hours of symptom onset and receive PCI as soon as possible (<120 minutes)
- 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
- Patients should be given unfractionated heparin.
- 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