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ACS include:
1. STEMI
2. NSTEMI
3. Unstable angina (UA)
* The difference between UA & NSTEMI is that in the latter, there is occluding thrombus, which leads to myocardial
necrosis and a rise in serum troponins or creatine kinase-MB (CK-MB).
Pathophysiology
Mechanism which is common to ACS 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. The presence of rich lipid pool within the plaque and a thin, fibrous cap is associated with an
increased risk of rupture. Platelet release of serotonin and thromboxane A2 result in myocardial ischaemia due to
reduction of coronary blood flow.
Symptoms Signs
1. Acute central chest pain >20 mins, may radiate to 1. Pallor, Sweatiness, anxiety, distress
arm or jaw 2. Pulse > or <
2. Ass. with nausea, dyspnea, sweatiness & 3. Hyper or hypotension
palpitation. 4. 4th heart sound (atrial gallop)
3. May present without chest pain in elderly & 5. May present with signs of heart failure (JVP,
diabetics (such Pt may present with syncope, 3rd heart sound, basal crepitation)
pulm. oedema, epigastric pain & vomiting)
Investigation
1. Electrocardiogram (ECG) 2. Biochemical Markers
NSTEMI
ST depression and T-wave inversion
ECG should be repeated when patient is in pain
STEMI
New & persistent ST elevation or left bundle
branch block pattern
ECG changes confined to the leads that face the
infarction
Transient ST elevation is seen with coronary
spasm or Prinzmetals angina