Coronary heart disease (CHD) is the leading cause of death in the UK, responsible for more than 73,000 deaths each year. It is estimated that 2.3 million people are living with CHD in the UK – over 1.4 million men and 850,000 women. The incidence of CHD increases with age and it is more common in people with type 1 or type 2 diabetes, high blood pressure or high cholesterol and in those who smoke (British Heart Foundation 2015).
CHD is characterised by narrowing (stenosis) of the coronary arteries caused by the development of an atherosclerotic plaque, which consists of fat, cholesterol and other blood-borne substances. Atherosclerotic plaques may be stable, often causing no symptoms, or unstable where the material inside the plaque may be exposed to the circulation. This can lead to blood clots forming in the arteries, reducing blood flow and consequently oxygen supply to the heart.
Acute coronary syndrome refers to a group of acute conditions caused by the sudden reduction in the oxygen supply to the heart muscle. This can trigger a myocardial infarction (MI), which may result in long‑term heart muscle dysfunction and death. There are 3 main types of acute coronary syndrome:
ST-elevation myocardial infarction (STEMI) in which the vessel is completely occluded, which can cause extensive damage to a large area of the heart
non-ST-elevation myocardial infarction (NSTEMI) in which the blood vessel is partially occluded, resulting in damage to a smaller area of the heart
unstable angina, in which the blood flow is restricted but there is no permanent damage to the heart.
Percutaneous coronary intervention (PCI) is a procedure used to widen the coronary artery. NSTEMI and STEMI account for 65% and 35% of respective cases of acute coronary syndromes where PCIs are performed (British Cardiovascular Intervention Society 2013). Myocardial infarction is associated with the formation of blood clots (unstable angina tends not to be, so is outside the scope of this briefing). In NSTEMI, and after opening the artery in STEMI, dislodged blood clots can lead to downstream microvascular impairment and the no-reflow phenomenon, where blood flow to the ischaemic tissue may still be impeded even after the blockage is removed. This is caused by platelet-fibrin aggregates in the distal arterial bed, which stimulate an inflammatory cascade that can perpetuate myocardial oedema, vessel spasm and endothelial dysfunction.