Acute coronary syndrome is a constellation of symptoms and clinical findings which results from impaired cardiac perfusion at rest
Aetiology
Usually the result of a thrombus from an atherosclerotic plaque blocking a coronary artery
Pathophysiology
The mechanism that is common to all acute coronary syndromes is rupture or erosion of the fibrous cap of a coronary artery plaque
This leads to platelet aggregation and adhesion, localized thrombosis, vasoconstriction and distal thrombus embolization
Thrombus formation and the vasoconstriction produced by platelet release of serotonin and thromboxane A2 result in myocardial ischaemia due to reduction of coronary blood flow
Myocardial infarction is caused by underperfusion of the myocardium leading to death of myocardial tissue
It is distinguished from angina by this death of tissue
Subtypes of ACS
Unstable angina: subtotal occlusion, supply led ischaemia without infarction, high (50%) risk of MI in subsequent 30 days
NSTEMI: subtotal occlusion
STEMI: complete occlusion
Types of MI
Type 1: Traditional MI due to an acute coronary event
Type 2: Ischaemia secondary to increased demand or reduced supply of oxygen (e.g. secondary to severe anaemia, tachycardia or hypotension)
Type 3: Sudden cardiac death or cardiac arrest suggestive of an ischaemic event
Type 4: MI associated with PCI/coronary stunting/CABG
Clinical features
Symptoms
Chest pain (SOCRATES)
Site - central/left sided
Onset - often sudden
Character - crushing ('like someone is sitting on your chest')
Radiation - left arm, neck and jaw
Associated symptoms - nausea, sweating, clamminess, shortness of breath, sometimes vomiting or syncope
Timing - constant, 30 mins or longer
Exacerbating/relieving factors - worsened by exercise/exertion and may be improved by GTN (but not completely relived or else angina)