Coronary heart disease/athersclerosis Flashcards by rachael a

modifiable risk factors of coronary heart disease

smoking
lipids
blood pressure
diabetes
obesity
sendentary lifestyle

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non modifiable risk factors of coronary heart disease

age
sex
genetic background

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what combination of risk factors has the greatest impact on coronary heart disease

hypertension
smoking
high cholesterol

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where is athersclerosis most likely to develop

at branches of vessels

e.g carotid, coronary and iliac arteries

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why is atherosclerosis more likely to develop at artery branches

turbulent flow causing inflammation

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where does athersclerosis happen within a blood vessel

between endothelium and internal elastic layer (intima)

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what do coronary arteries do at lesion prone locations

adaptive thickening of the smooth muscle - intima widens and is larger

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what is a type II lesion

macrophage foam cells infiltrate intima

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what is a type III lesion/preatheroma

small pools of extracellular lipid form around the macrophage foam cells

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what is a type IV lesion/atheroma

a core of extracellular lipid forms (small pools have joined up) around macrophage foam cells

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what is a type V lesion/fibroatheroma

fibrous thickening around core of extracellular lipid and macrophage foam cells, hardening of vessel constriction

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what is a type VI or complicated lesion?

a rupture/surface defect caused by a haematoma and fissure within intima causes a thrombus to form on outer layer of intima/lumen

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when is the best time to intervene with atherosclerosis

intermediate or advanced lesions

for primary prevention of rupture/stenosis - lifestyle changes and risk factor management

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what interventions are needed for complicated lesions?

stenosis/plaque rupture treatment
catheter based interventions
revascularisation surgery
treatment of heart failure

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what cells are involved in athersclerosis

vascular endothelium
macrophages
vascular smooth muscle cells
T lymphocytes
platelets

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how are vascular endothelial cells involved in athersclerosis

barrier function against athersclerosis

leukocyte recruitment

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how are macrophages involved in athersclerosis

foam cell formation
major source of free radicals and metalloproteinases
cytokine and growth factor release

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how are vascular smooth muscle cells involved in athersclerosis

migration and proliferation
collagen synthesis
remodelling, fibrous cap formation

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how are t lymphocytes involved in athersclerosis

macrophage activation

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how are platelets involved in athersclerosis

thrombus generation

cytokine/growth factor release

what are the two main classes of macrophages

inflammatory macrophages - kill germs

resident macrophages - homeostasis e.g osteoclasts, alveolar macrophages, spleen macrophages

what is low density lipoprotein

bad cholesterol synthesised in liver

carries cholesterol from liver to body tissues

what is high density lipoprotein

good cholesterol

reverse cholesterol transport

what are oxidised/modified LDLs

impact of free radicals on LDL

highly inflammatory and toxic forms of LDL in vessel walls

structure of low density lipoprotein

``` docking molecules for fat delivery lipid monolayer (micelle) cargo fat ```

how do LDLs cause athersclerosis

lwak through endothelial barrier binds to proteoglycans in sub-endothelial layer oxidated by free radicals, phagocytosed by macrophages CREATES FOAM CELLS and stimulates chronic inflammation

what is familial hypercholesterolaemia

autosomal genetic disease elevated cholesterol failure to clear LDL from blood early athersclerosis - MI before 20

what are statins

HMG-CoA reductase inhibitors

how do macrophages impact atherosclerosis inflammation

generate free radicals to oxidise lipoproteins phagocytose lipoproteins and become foam cells express cytokines that recruit monocytes express chemoattractants and growth factors for VSMC generate proteinases to degrade tissue

what free radicals do macrophages produce

NADPH oxidase | myeloperoxidase

what cytokines do macrophages express to recruit monocytes

IL-1 upregulates VCAM-1 | vicious cycle of self-perpetuating inflammation

what chemoattractants do macrophages express

protein growth factors for vascular smooth muscle cells, stimulate them to proliferate and deposit ECM platelet derived growth factor (PDGF) - VSMC chemotaxis, survival and cell division transforming growth factor beta (TGFb) - increased collagen synthesis and matrix deposition

what are metalloproteinases

degrade collagen by zinc based mechanism

what is the fate of macrophages involved in athersclerosis

protective systems overwhelmed die by apoptosis release toxic lipids and tissue factors into lipid necrotic core builds up until plaque ruptures and these are spilled out into the blood encouraging a clot

what is nuclear factor kappa B

transcription factor activated by scavenger receptors, cytokines etc switch on inflammatory genes for metalloproteinases, nitric oxide synthase, IL-1

what macrophage scavenger receptors bind to oxidised LDL

scavenger receptor A and B (CD204, CD36)

first line management of a STEMI

antiplatelet and anti-ischaemic/coagulant treatment then PCI/CABG

long term management of STEMI

``` antiplatelet therapy statin beta blocker ACEi cardiac rehabilitation + lifestyle changes ```

pathophysiology of STEMI

nearly always coronary plaque rupture resulting in thrombosis formation, occluding a coronary artery

pathophysiology of NSTEMI

incomplete thrombus formation, doesnt stop blood and oxygen completely but restrictio is great enough that oxygen is used up quickly. in distal arteries and arterioles, tissue death occurs due to oxygen starvation affected area is small to not cause ST elevation but causes depression and Troponin elevation

pathophysiology of unstable angina

plaque becomes unstable, fibrous cap disrupts and forms thrombus but enough for lumen to meet demand during rest

clinical difference between unstable angina and NSTEMI

NSTEMI shows raised Troponin levels

typical angina components

precipitated by physical exertion retrosternal pain in chest relieved by rest or glyceryl trinitrate (GTN)

what do blood troponin levels indicate

elevated in heart damage, remain elevated for 2wk normal levels = less likelihood of muscle damage, more likely angina rise/fall in series of troponin results indicates heart attack

treatment of unstable angina and NSTEMI first steps

risk assessment for future coronary events

low risk NSTEMI and unstable angina patient management

conservative treatment aspirin, clopidogrel, heparin, nitrates, b blockers stress test

low risk patients NSTEMI and unstable angina stress test results mean

negative - discharge | positive - coronary angiography (PCI, CABG etc)

high risk NSTEMI and unstable angina patients management

invasive management | coronary angiography - PCI, CABG

assessment of patient who is at high risk of future coronary events

positive troponin, ST changes, patient generally unstable