Coronary artery disease is the most common type of cardiovascular
disease and is the leading cause of mortality in the UK and worldwide1.
It usually occurs when there is rupture of an atherosclerotic plaque leading to
occlusion or narrowing of the coronary vessels that supply the muscles of the
heart2. This leads to symptoms such as chest pain and tightness
that can radiate to the arms, neck, jaw back or stomach, sweating,
light-headedness, dyspnoea and nausea or vomiting3. In the 1960s
the mortality rate for myocardial infarction was estimated around 70% but today
at least 70% of patients tend to survive which reflects great improvement in
the management and prevention1,4.
The general aim of treatment is reperfusion of the heart
musculature through unblocking the coronary arteries, reducing ischaemia and to
modify future risk factors; however, acute management is dependent on the type
of myocardial infarction: ST-elevation MI (STEMI) or Non-ST-elevation MI (NSTEMI)5,6.
Both types of myocardial infarctions are given an immediate loading dose of
300mg aspirin and 300mg clopidogrel to reduce the size of the clot and further
clotting with a known decrease mortality of at least 50%5,6,9. In acute
STEMIs, patients undergo prompt revascularisation with primary percutaneous
coronary intervention (pPCI) if within 90 minutes of initial presentation,
thrombolysis if >90 minutes and within 12 hours of symptom onset or a
coronary artery bypass graft (CABG) dependent upon haemodynamic instability as these
revascularisation therapies can prevent or decrease damage to the myocardium7,9.
In acute NSTEMIs, the initial treatment involves symptom control through pain
relief, treating any life-threatening instability and observation in contrast
to immediate revascularisation8,9.
The current NICE guidelines regarding pharmacological
management for both types of post-myocardial infarction consists of dual
antiplatelet therapy of aspirin 75mg given indefinitely in combination with
P2Y12 inhibitor such as clopidogrel 75mg for up to 12 months in addition to
other therapies such as an ACE inhibitor, beta-blocker and statin9.
There is already a well documented benefit of dual antiplatelet
therapy in acute coronary syndromes compared to aspirin alone established by
CURE11, COMMIT/CCS-212 and CLARITY-TIMI 2813
trials which showed an approximate 20% reduction in 1-year incidence of
cardiovascular events but a subsequent increase in bleeding risk10.
However, few studies have used P2Y12 inhibitors alone and there are theories as
to why aspirin may diminish the vascular benefits of P2Y12 inhibitors.
clopidogrel monotherapy produces at least the
same benefit if not more than aspirin alone therefore there is a possibility
that the supposed benefit from dual antiplatelet therapy comes from clopidogrel
alone. There is a lack of data in this area when it comes to the treatment of
MI with the possibility that the addition of aspirin to clopidogrel may give
little or no reduction in infarctive events at the cost of an increased risk of