Histopathology - CVD Flashcards
(35 cards)
Most important independent RF for atherosclerosis/ CVD
FHx
What is the role of the factor released after platelets adhere to the injured endothelium?
Intimal smooth muscle proliferation
ECM deposition
Fatty streak - mature atheroma + growth
PDGF, FGF, TGF-alpha implicated
Early atheroma arises in ___ epithelium
intact
What does endothelial damage cause
Increase in permeability
Altered gene expression
Adhesion
Where do atheromatous plaques form?
In areas where there is flow disturbance
What do we mean by acute plaque change?
Rupture - exposes prothrombogenic plaque contents
Erosion - exposes prothrombogenic subendothelial basement membrane
Haemorrhage - into plaque (increases size)
Majority of plaques which show acute change only show mild to moderate luminal stenosis prior to acute change not enough narrowing to cause ischaemia – therefore, there are numerous asymptomatic potential victims
Characteristics of vulnerable plaques
- Thin fibrous cap
- Lots of foam cells and extracellular lipid
- Clusters of inflammatory cells
- Few smooth-muscle cells
What causes sudden death in people with vulnerable palques?
Emotional stress
- Adrenaline increases BP and causes vasoconstriction
- Increases physical stress on plaque
• Circadian periodicity to sudden death (6am-noon)
What is IHD
Group of conditions arising from myocardial ischaemia
% of stenosis required for
stable
unstable
angina
stable - 75%
unstable - > 90%
In which coronary arteries are plaques mainly found?
First few cm of LCA, LCX
Entire length of RCA
What happens during ACS?
Stable plaque undergoes acute plaque change and a thrombus forms which increases occlusion
(due to rupture, erosion, haemorrhage)
Most common death in postmenopausal women
IHD
Coronary arteries affected during MI
LAD > RCA > LCx
During an MI when is there
loss of nuclei
necrotic cell death
infiltration by neutrophils and then macrophages
new blood vessel formation + collagen synthesis + granulation tissue + myofibroblasts
loss of nuclei
6-24h
necrotic cell death
6-24h
infiltration by neutrophils and then macrophages
1-4 DAYS
new blood vessel formation + collagen synthesis + granulation tissue + myofibroblasts
1-2 WEEKS
Gross change in the heart after an MI
1-18h 24h 3-4D 1-3W 3-6W
1-18h
No change
24h
Pale, edema
inflammation, edema
3-4D
Haemorrhage
necrosis
1-3W
thin yellow
granulation tissue
3-6W
tough white
fibrosis
Temporal sequence in the appearance of cells infiltrating a MI
neutrophils –> macrophages –> angioblasts –> fibroblasts + collagen
What is a reperfusion injury
reversible cardiac failure post MI lasting a few days
arrhythmias
due to oxidative stress, Ca overload, inflammation
What is hibernating myocardium?
Chronic sublethal ischaemia –> lower metabolism in myocytes
reversed with revascularisation
Myocardial rupture post MI which places are the most common
free wall > septum > papillary muscle
What is a mural thrombus and why is it dangerous?
Infarct expansion – necrotic muscle stretches -> mural thrombus
can form a clot that can fly out in the heart –> clots/emboli from ventricular aneurysm can also block other capillaries/arteries in the body (e.g. bowel ischaemia, stroke, embolic damage to other organs)
rupture can lead to hemopericardium
MI complications
o Complications (DARTH VADER) D Death A Arrhythmia R Rupture (papillary muscle) T Tamponade H Heart Failure
V Valvular disease A Aneurysm of ventricle D Dressler’s syndrome (pericarditis; 2nd or 3rd day) E Embolism (i.e. bowel ischaemia) R Recurrence
Chronic IHD w HF causes
previous MI or previous ischaemic myocardial damage e.g. severe obstructive coronary artery disease
Define sudden cardiac death
o “Unexpected death from cardiac causes in individuals without symptomatic heart disease or early (1 hour) after onset of symptoms”
Usually due to lethal arrhythmia (from ischaemia-induced electrical instability)
Usually on background of IHD (90%)
Acute myocardial ischaemia is usual trigger
Usually causes electrical instability at sites distant from conduction system (near scars from old MIs)
50% have plaque rupture
10% non atherosclerotic cause e.g. long QT
