Ischemic Heart Disease Histology Flashcards
hypoxia
reduced oxygen supply to a tissue with normal perfusion
ex. cyanotic congenital heart disease, severe anemia, carbon monoxide poisoning
clinical syndromes that can result from ixchemia
angina pectoris
myocardial infarction
chronic ischemic heart disease
sudden cardiac death
risk factors of HD
Heredity
Age
Sex
Lipidemia
Increased weight
Pressure
Inactivity
Diabetes
Smoking
“HAS LIPIDS”
reperfusion injury
reversible or irreversible injury caused by repurfusion
this includes myocardial stuning, srrythmias, microvascular injury, and irreversible cell damage
factors reducing coronary blood flow
decreased aortic diastolic pressure
increased intraventricular pressure and myocardial contraction
coronary artery stenosis
aortic valve stenosis and regurgitation
increased right atrial pressure
etiologies of coronary artery stenosis
fixed coronary stenosis
acute plaque change (rupture, hemorrhage)
coronary artery thrombosis
vasoconstriction
What is the most sensitive region to ischemia?
subendocardium
wave front moves outward from there
most common sites for thrombosis
LAD, right coronary, and left circumflex artery, in approximately a 3:2:1 ratio
complications of an MI
sudden cardiac death
congestive heart failure
aneurysm with mural thrombus formation
cardiac arrythmia
free wall rupture with resulting cardiac tamponade
Dresler’s syndrome (fibrinous pericarditis)
papillary muscle dysfunction with resultant valvular dysfunction usually of the mitral valve
1-4 hours of MI
usually no major changes
could be presence of wavy fibers due to inactive fibers being pulled on from the ends by live contracting myocytes
6-12 hours of MI
coagulative necrosis beings to appear
12-24 of MI
infarct becomes infiltrated by neutrophils, and the muscle cells begin to lose their nuclei and cross-striations
4-24 hours of MI
pale
swelling
contraction band necrosis
PMNs
3-5 days of MI
mottled yellow, red
hemorrhage
heavy PMNs
lowest degree of mechanical integrity and most prone to rupture
5-7 days of MI
mottled
macrophages and fibroblasts
lowest degree of mechanical integrity and most prone to rupture
2-4 weeks of MI
mottled
granulation tissue
5-8 weeks of MI
scarring
gradual replacement with fibrotic tissue
risk of rupture is low because the scar is thin but strong
can billow out forming an aneurism
What time do these events happen?
usually no major changes
could be presence of wavy fibers due to inactive fibers being pulled on from the ends by live contracting myocytes
1-4 hours of MI
What time do these events happen?
coagulative necrosis beings to appear
6-12 hours of MI
What time do these events happen?
infarct becomes infiltrated by neutrophils, and the muscle cells begin to lose their nuclei and cross-striations
12-24 of MI
What time do these events happen?
pale
swelling
contraction band necrosis
PMNs
4-24 hours of MI
What time do these events happen?
mottled yellow, red
hemorrhage
heavy PMNs
lowest degree of mechanical integrity and most prone to rupture
3-5 days of MI
What time do these events happen?
mottled
macrophages and fibroblasts
lowest degree of mechanical integrity and most prone to rupture
5-7 days of MI
What time do these events happen?
mottled
granulation tissue
2-4 weeks of MI
What time do these events happen?
scarring
gradual replacement with fibrotic tissue
risk of rupture is low because the scar is thin but strong
can billow out forming an aneurism
5-8 weeks of MI
coagulation necrosis
cells are dead but can still see outlines
nuclei are gone
contraction band necrosis
hyper dense eosinophilic bands
clearing of the cytoplasm - cells become hydropic
contractile proteins no longer present, instead hyper condensed in the band
calcium rushing into the cell through the leaky membranes cause the Z line to condense
calcification of the coronary arteries
calcific atherosclerosis are typically stable
nut much lipid and not prone to rupture
a high number of stable placques indicates the presence of unstable placques
most frequent cause of coronary occlusion
rupturing of mild to moderate stenoses (<80% of baseline)
this is because there are so many more of these stenoses as opposed to the highyl obstructive plaques
cardiac allograft vasculopathy
major cause of death following cardiac transplantation as soon as 1 year following engraftment
many transplants fail to reinervate and angina is not common
clinical presentation includes arrythmias, CHF, or sudden death
affects intramural and epicardial coronary arteries and veins
thought to result form repeated endothelial injury followed by reiapr response
inciting agents of CAV
autoimmune response to allograft
CMV
ischemia reperfusion injury
baseline HLD, HTN
early CAV histology
diffuse fibrous intimal thickening or vasculitis
late CAV histology
focal atherosclerotic plaques, diffuse intimal thickening, or a mixture of both
complications of angioplasty
causes tearing and usually when effective causes dissection
complications of stents
thrombogenic
complications of vein grafts
grafts undergo arterialization
complications of allografts
recipients lose their hearts due to diffuse arteriosclerosis
creatine kinase
found in heart muscle, skeletal muscle, and brain
increased in over 90% after MIs
begins to rise 4-6 hours after MI and peaks at 24 hours
returns to normal in 3-4 days
MB fraction returns to normal in 2 days
lactic dehydrogenase (LD or LDH)
found in heart muscle, skeletal muscle, liver, erythrocytes, kidney, and some neoplasms
increased in over 90% of MIs
begins to rise 24 hours after MI and peaks in 3 days
returns to normal in 8-9 days
myoglobin
found in striated muscle
damage to skeletal or cardiac muscle releases myoglobin into circulation
rises 2 hours after MIs and peaks at 6-8 hours
returns to normal in 20-36 hours
troponin T and I
high sensitivity, preferred markers
very specific for cardiac injury
rises in 4-6 hours
peaks in 12-16 hours
stays elevated for up to 10 days
