Lecture DetailsEdit

Karlheinz Peter; Week 11 MED1022; Physiology

Lecture ContentEdit

There are three branches of the coronary artery, left circumflex artery, left descending artery, right main artery. Venous blood from the right ventricle, anterior cardiac veins, right atrium. Left ventricle, coronary sinus, atrium. Atherogenesis is erosion of the endothelial layer. Leukocytes and platelets adhere to the endothelium. Atheroschlerosis is expression of endothelial molecules on the endothelium. Monocytes and macrophages are involved, T lymphocytes cause clonal expansion, CRP (C-reactive protein which is expressed in inflammation), amyloid, fibrinogens, infections (Chlamydia pneumonia), plaque stability (inflammatory protease activity), hot plaques.

Vascular cell adhesion molecule is expressed a lot, leukocytes recognise and adhere, invade tissue and cause inflammation. Atherogenesis is leukocyte adhesion and transmigration, fatty streak of platelet adhesion, formation of foam cells. There is then the proliferation and necrosis stage, macrophages accumulate, necrotic cells form and a fibrous cap is formed. Progression of stable atheroschlerosis causes angina which requires intervention such as stenting. Rupture prone plaques can cause MI. Rupture is due to thinning of fibrous cap, haemorrhage from plaque microvessels. Acute MI is caused by coronary thrombosis (emboli from platelet aggregates), identification is done by CRP/soluble adhesion molecules, imaging is ultrasound, IVUS, CT, MRI, possibly angiography. There can be atheroschlerosis without luminal loss.

Calcification is the easiest method of telling if a plaque is stable or unstable, very common in stable plaques as is extent of stenosis (>75/<50). Ischaemia leads to ST depression. Infarction leads to ST elevation and T inversion. Troponin and creatine kinase are blood markers.


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