Acute coronary syndrome (ACS) refers to three states of myocardial ischaemia: unstable angina (UA), non-ST elevation myocardial infarction (NSTEMI) and ST elevation myocardial infarction (STEMI).
ACS is a medical emergency requiring urgent admission. Around 100,000 people are admitted with ACS in the UK each year. Atherosclerosis represents the most significant aetiological factor.
ACS is classified into one of three conditions according to clinical features, ECG findings and cardiac enzymes:
ACS is typically triggered by rupture of an atheromatous plaque in the coronary arterial wall. For completeness, a number of less common causes are also mentioned below.
Modifiable risk factors
Non-modifiable risk factors
Other causes of emboli
Other causes of coronary occlusion
Changes in oxygen demand and / or delivery
Atherosclerosis is an inflammatory process which predisposes individuals to ACS. It is a complex cellular process involving lipids, macrophages and smooth muscle.
The first step is endothelial injury. This causes a local inflammatory response. If the injury recurs or healing is incomplete, inflammation may continue leading to the accumulation of low-density lipoproteins (LDL). These become oxidised by local waste products creating reactive oxygen species (ROS).
In response to these irritants, endothelial cells attract monocytes (macrophages). These engulf (phagocytose) the LDLs swelling to become foam cells and ‘fatty streaks’.
Continued inflammation triggers smooth muscle cell migration. This forms a fibrous cap, which together with the fatty streaks, develops into an atheroma.
The top of the atheroma forms a hard plaque. This may rupture through its endothelial lining exposing a collagen-rich cap. Platelets aggregate on this exposed collagen forming a thrombus that may occlude or severely narrow the vessel. Alternatively, the thrombus may break lose, embolising to infarct a distant vessel.
The signs and symptoms of ACS are those of myocardial ischaemia and an elevated autonomic (sympathetic) response. However, some patients may have a ‘silent MI’. This is typically seen in elderly and diabetic patients.
ACS necessitates a quick and accurate diagnostic process combining history, examination, ECG results and laboratory findings (e.g. cardiac enzymes).
ECG: ST elevation in leads II, III & AVF - indicative of an acute inferior MI.
Image courtesy of Wikimedia commons.
Cardiac enzymes are biomarkers of myocardial ischaemia. They include:
Troponins (T or I) have become the gold standard test. They begin to rise hours after the event. It may be measured 6-12 hours post-event, typically 8 hours. It also has prognostic input, the degree to which the troponin is raised is related to risk of death.
NOTE: new 'sensitive' troponin tests allow for diagnostic measurements just 3 hours post-event.
Troponins may be raised (though typically to a lesser degree) in a number of other settings such as heart failure, chronic kidney disease and pulmonary embolisms.
Immediate managment of all suspected ACS can be remembered using the mnemonic MONA - morphine, oxygen, nitrates, aspirin.
NICE guidelines recommend IV morphine (administered with an anti-emetic) in sufficient dosage to relieve chest pain, in addition to loading-dose aspirin (300mg) and sublingual (under the tongue) GTN, a potent vasodilator. Oxygen appears to be of limited benefit in patients with preserved oxygen saturations (94% or greater), and may indeed be harmful.
Patients with STEMI require emergency reperfusion to restore coronary flow and minimise myocardial injury. PCI is the preferred strategy.
Primary percutaneous coronary intervention (PCI) should ideally be undertaken within 120 minutes. If this is unavailable, fibrinolytic agents such as alteplase or reteplase may be given IV. Provided coronary stenting is performed in the next 6-24 hours, this is an effective alternative.
Patients should be initiated on aspirin and a second anti-platelet drug prior to PCI. Typically, clopidogrel is used, however, preference is now being given to prasugrel and ticagrelor. Dual anti-platelet therapy (e.g. lifelong aspirin and 12 months of clopidogrel / prasugrel / ticagrelor) should be continued post-PCI.
Anticoagulation with heparin (LMWH or UFH) or bivalirudin should be offered prior to PCI.
If angiography is likely within 24 hours unfractionated heparin should be offered. If angiography is not likely within 24 hours (and the patient does not have a high bleeding risk) fondaparinux should be offered.
Management of NSTEMI and UA is guided by the estimated six-month mortality risk calculated using the GRACE score.
GRACE (Global Registry of Acute Coronary Events) is a scoring system which estimates six-month mortality risk in patients with NSTEMI / UA. It is calculated by clinicians by entering simple clinical risk factors into a web-based model.
Long-term management requires both medical therapy and patient education. Advise patients on modifiable risk factors: smoking cessation, dietary changes and mild exercise.
Beta-blockers and ACE-i should be given in the absence of contra-indications, continue aspirin and clopidogrel (when indicated). Statin therapy is often initiated.
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