Atherosclerosis and Ischaemic Heart Disease Flashcards
effects of atherosclerosis
elastic arteries - aorta, carotid, iliac arteries
large and medium muscular arteries - coronary and popliteal
which layer of the blood vessel does this affect
there is an intimal lesion - forms an atheromatous plaque underneath
distribution of atherosclerotic plaques
decreasing order of frequency
- abdominal aorta
- coronary arteries
- popliteal arteries
- descending thoracic aorta
- internal carotid arteries
- circle of willis
when can atheromatous plaques develop
develop throughout life with a fatty streak beginning in childhood
becomes symptomatic in middle age or later
consequences of athersclerosis
MI/ chronic IHD/ suddne death stroke/ CVA AAA gangrene of legs - critical limb ischaemia gut ischaemia
what can happen to the vessel as a result of a plaque formation
narrowing as increase in plaque size - there can be an overlying thrombus which can dislodge and form a clot in a smaller vessel - lead to ischeamia of that beyond the vessel
haemorrhages
dilation of the vessel - aneurysm - rupture, mural thrombi
features of an atheromatous plaque
fibrous cap
cells - smooth muscle and inflammatory - foamy macrophages common feature
lipids
connective tissue and extracellular matrix
healing response - platelets can be found with the inflammatory cells
types of plaque
stable and unstable
stable - thick fibrous cap
unstable plaque - no thick cap - at risk of rupture/fissure, emboli +/- thrombosis
increased risk of a haemorrhage into the plaque
risk factors for atherosclerosis
non modifiable - increasing age - male - family history - genetic abnormalities modifiable - hyperlipidaemia -hypertension - smoking - diabetes
pathogenesis of atherosclerosis
- response to injury hypothesis
chronic inflammatory response of arterial wall initiated by chronic endothelial injury
what is ischaemic heart disease
characterised by - myocardial ischaemia = imbalance between the supply and demand of the heart fro oxygenated blood
90% due to atherosclerosis of coronaries
remaining 10% due to congenital defects, anaemia, lng disease
can be aggrevated by :
- hypertrophy
- hypotension
- hypoxaemia
- increased heart rate
what increases the risk of developing ischaemia heart disease ( athersclerotic things)
- no of vessels involved
- distribution of the vessels
the degree of narrowing of the vessels
how can you decrease the risk and effects of ischaemic heart disease
1) prevention: modification of the risk factors - smoking, hypercholesterolaemia, sedentry life style
2) therapeutic advances: new medications, CCU, angioplasty, stents, CABGs, improved control of arrythmias
4 syndromes associated with athersclerosis
- MI
- angina
- chronic IHD
- sudden cardiac death
what is the difference between angina and an MI
is cell death - no necrosis in angina
in MI - necrosis - myocyte necrosis, elevated enzymes - creatinine kinase, elevated cardiac specific proteins - troponins
what are the enzymes that rise in MI and how long for
creatinine kinase - rise within 4-8 hours and elevated for 3 days
what are the cardiac specific proteins that rise in MI and how long for
troponins - rise in 4-8 hours and last for 7-10 days
when does the stenosis of a vessel become critical
when it reaches less than 75% of the cross sectional area so compensatory vasodialtion is not enough to meet the demands
vessels that are involved
= proximal left anterior descending
- proximal left circumflex
- entire length of the RCA
where does the left anterior descending supply
septum; anterior, lateral and apical wall of the left ventricle; most of the left and right bundle branches; and the anterior papillary muscle of the bicuspid valve (left ventricle)
where does the left circumflex supply
most of the left atrium the posterior and lateral free wall of the left ventricle and part of the anterior papillary muscle
where does the right coronary artery supply
right atrium and right ventricle inf/post wall LV posterior IV septum AV node SA node
what are the most dangerous lesions
where there is 50-75% stenosis with a lipid rich core and a minimal fibrous cap - alone this is not enough to produce symtpmatic angina, but there is risk of acute plaque change -
also no development of colaterals and potentially a lack of preconditioning
types of MI
transmural and subendocardial
- transmural is full thickness of the wall
usually associated with acute thrombosis/occlusion of the vessel
occasionally related to vasospasm or emboli
- subendocardial
inner 1/3 -1/2 of myocardium
may extend beyond the perfusion territory of a single artery
subendothelila zone is the least well perfused so most as risk when there is reduced coronary flow
usually critical stenosis but no acute plaque change
How long after can you histologically see there has been an MI
4hours
How long after can you see microscopically there has been an MI
12 hours
What allows it to be seen earlier
Some dyes
What can salvage the heart
Early reperfusion, thrombolysis
What does earlier reperfusion do
Salvages sublethally injured myocytes and minimises infarct size, haemorrhage into the area
What risk with reperfusion
Reperfusion injury
Induces a new element of injury due to free radicals
Why might not the myocytes function for a few days
Stunned myocardium
So may not function
What may be protective to the myocardium
Repetitive short lived ischamia may be protective
Preconditioning mechanisms
Collateral development
Complications of MI
Contractile dysfunction - heart failure- cardiogenic shock
Arrhythmia
Myocardial rupture
- of the free wall - tamponade
- IVS left to right shunt
- papillary muscle - acute severe mitral regurgitation
Pericarditis early or several weeks (Dressler syndrome=autoimmune)
Mural thrombosis - at risk of embolising
Ventricular aneurysm
Papillary muscle dysfunction - MR
Progressive late heart failure
Normal heart role and weight
Pump
250-300g female
300-350g males
What is increased size weight called
Cardiomegaly
Hypertrophy
Increased chamber size is
Dilated
Role of cardiac myocytes
Cell of contraction
What are the specialised myocytes for conduction
SAN
AVN
bundle of His
Heart failure is also called
CCF
congestive cardiac failure
It is failure of the pump
What are the adaptive mechanisms to prevent/ postpone failure
- dilation - inc preload - frank starling mechanisms
- hypertrophy - inc size of cardiac myocytes
- activation of neural humoral mechanisms
- NA released from adrenergic cardiac nerves
- activation of RAA system
- release atrial natriuretic peptide
What causes heart failure
Usually due to systolic function - heart can’t contract enough
Occasionally due to diastolic function - chamber walls stiff and unable to stretch to allow filling with blood
Left heart failure what happens
LV can’t pump to the body
Leading to organ ischaemia - impaired renal function
Pulmonary oedema due to back pressure
What happens in right heart failure
RV can’t pump to the lungs
Leading to a back pressure in the body causing peripheral oedema
Congestion in the organs
As cites/ pleural effusion
What is usually heart failure
Left
Right usually occurs secondary
Pure right heart failure income - cor pulmonale
What is the response of the heart to increased demands
Inc pressure - left sided - systemic hypertension
Pulmonary hypertension - right sided cor pulmonale
What does hypertension lead to
Hypertrophy
Adaptive response to pressure overload
What can hypertrophy lead to
Myocardial dysfunction
Cardiac dilation
Congestive heart failure
Sudden death
Diagnostic criteria for systemic hypertensive heart disease
Left ventricular hypertrophy (concentric)
History/pathological evidence of hypertension
Even prolonged mild hypertension can lead to hypertrophy
Presentation of systemic hypertensive heart disease
Asymptomatic
ECG/echo - show increased size
Atrial fibrillation - left atrial enlargement
CCF
What is the gross morphology of systemic hypertensive heart disease
Circumferential LV hypertrophy No dilation of LV Inc heart weight Thick wall Thick wall = stiff --> impaired diastolic filling --> left atrial enlargement
Histology of systemic hypertensive heart disease
Inc myocytes size
Increased nuclear size
Interstitial fibrosis
What is cor pulmonale
Pulmonary hypertensive heart disease
Secondary to pulmonary hypertension
Is caused by a lung abnormality/lung vasculature abnormalities
Need to EXCLuDe pulmonary hypertension secondary to congenital heart disease
Diseases of the left side of the heart
Acute cor pulmonale
Sudden increase in pulmonary blood pressure
E.g. Massive PE
–> marked dilation of the right ventricle
No hypertrophy
Chronic cor pulmonale
Prolonged pressure overload
Right ventricular hypertrophy
