Acute coronary syndromes Flashcards
definitions
includes unstable angina and evolving MI, which share an underlying pathology - plaque rupture, thrombosis and inflammation
may rarely be due to emboli or coronary spasm in normal coronary vessels, or vasculitis
usually divided into STEMI or new onset LBBB (acute MI), or NSTEMI
the degree of irreversible myocyte death varies
significant necrosis can occur without ST elevation
risk factors
non-modifiable:
age, male gender, FHx of IHD (MI in 1st degree relative <55yo)
modifiable:
smoking, HTN, DM, hyperlipidaemia, obesity, sedentary lifestyle, cocaine use
diagnosis
increase followed by decrease of cardiac biomarkers and either: Sx of ischaemia, ECG changes of new ischaemia, development of pathological Q waves, or loss of myocardium on imaging
Sx
acute central chest pain lasting >20mins
often ass/w. nausea, sweatiness, dyspnoea and palpitations
may be silent
tests
ECG:
classically hyperacute (tall) T waves, ST elevation or new LBBB develop within hours of transmural infarct
T wave inversion and pathological Q waves develop over hours/days
cardiac biomarkers
troponin:
most sensitive and specific markers of cardiac necrosis
serum levels increase in 3-12h after onset of chest pain, peaking after 24-48h, and returning to baseline after 5-14 days
if normal 6h after onset of pain, and ECG normal, very minimal chance of missing MI
creatinine kinase:
CK-MM: found in skeletal muscle, raised after a falls, seizures, prolonged exercise, myosistis
CK-BB: predominantly in the brain
CK-MB: mainly in the heart. levels rise 3-12h after onset of chest pain, peak after 24h, baseline 48-72h. levels peak earlier if reperfusion occurs
myoglobin levels rise 1-4h after chest pain. highly sensitive but not specific
management
STEMI: primary angioplasty of thrombolysis B-blocker ACE-i clopidogrel
NSTEMI:
B-blocker
antithrombotics
assess risk with GRACE score
