IHD Flashcards
Define ischaemic heart disease
Decreased perfusion or increased demand to the heart
Non-modifiable RFs
Male, post-menopausal female
Age range to be considered SIGNIFICANT FHx?
Males
Co-morbidities as RFs
CKD
HT
DM
Obesity/hyperlipidaemia
Lifestyle factors as RFs
Smoking
Obesity, diet, sedentary lifestyle
Stress
Depression
Top 4 triggers of ischaemic event
ECEM Exercise Cold Air Emotions Meals
Some medical triggers of ischaemic event
Anaemia
Infection
Thyroid
RFs/Causes of atherosclerosis
Hypertension
High LDL
Smoking
DM
Process of atherosclerosis
- Endothelial injury
- LDL monocytes and platelets adhere and enter endothelium
- Macrophages ingest LDL to form foam cells
- Foam cells accumulate and form fatty streaks in intima
- Cytokines/growth factors cause Smooth Muscle migration into intima
- Formation of fibrous cap, which can calcify
Cells that migrate into intima during atherosclerosis
LDL monocytes, platelets, lymphocytes, macrophages, smooth muscle
Percent occlusion that is bad and when collaterals develop
70%
Percent occlusion that is serious and can cause resting myocardial flow impairment
90%
Inferior MI may be caused by occlusion of?
RCA, LCs
Anteroseptal MI may be caused by occlusion of?
LAD
Posterior MI may be caused by occlusion of?
LCx
Anterolateral MI may be caused by occlusion of?
LCA
Pathology immediately after MI?
No significant change
Pale, acute inflammation, necrosis (striations disappear)
Pathology 24-28h after MI
Yellow rubbery centre with hemorrhagic border, obvious necrosis and inflammation, early granulation at periphery
Pathology 3-4 days after MI
Area of infarction progressively replaced by granulation tissue
Pathology 10 days after MI
Paler and thinner fibrous tissue
Pathology 1-3 weeks after MI
Silvery fibrous scar tissue
Pathology 3-8 weeks after MI
Acute Coronary Syndrome (ACS) encompasses which conditions?
Unstable angina
NSTEMI
STEMI
Define NSTEMI
Partial thickness damage, no ST elevation seen on ECG