Pathology of ischaemic heart disease and hypertension Flashcards
How many men die of heart die of heart disease?
Around 30%
Laminar flow
Away to avoid clotting
Cells go down centre of artery
-endothelial cells are like Teflon coat so cells don’t tend to stick to them
-if endothelial cells flap up, reveals collagen cells and platelets love collagen and stick to it and release signals for other platelets to stick to them and aggregation occurs
Fibrinogen –> fibrin –> clot
Thrombosis triangle - Virchow’s triad
Change in vessel wall
Change in blood flow
Change in blood constituents
Causes of ischaemic heart disease
Myocardial hypertrophy
Small vessel disease
Atherosclerosis
-these overlap
Thrombosis causes
Heart attacks
AND?
Ischaemia
a restriction in blood supply to tissues, causing a shortage of oxygen that is needed for cellular metabolism (to keep tissue alive)
Atherosclerosis
-porridge + stiffening
A disease in which plaque (atheroma?) builds up inside your arteries
Risk factors for athersclerosis
Social deprivation Men more than women Cigarette smoking Hypertension Diabetes (if poorly controlled) Hyperlipidaemia
Cigarette smoking as a risk factor
Rubbish diffuses into blood and causes endothelial cell damage
Left ventricular hypertrophy
Too much heart muscle
Will have same amount of blood going into it so less flow through it
Can be huge
What is deposited in plaque
Continuous little areas of damage to the endothelial cells and thrombosis forms on top
High BP causes shearing of endothelial cells - could have effect
Plaque made up of fat, cholesterol, calcium, and other substances found in the blood
-over time, plaque hardens and narrows your arteries
Bleeding within plaque
Not very stable
New BVs grow into them but not very stable
Bleeding within it causes expansion / growth
Atherosclerosis causes
Chest pains on exercise
MI
-but very slow process over many years
What can cause left ventricular hypertrophy
Stenosis of aortic valve
Small vessel changes
At arteriolar level
Inappropriate vasoconstriction
–< production of nitric oxide
– > destruction of nitric oxide
What does ischaemic heart disease look like?
Regional transmural myocardial infarction
Subendocardial myocardial infarction
Chronic ischaemia
Regional transmural myocardial
infarction
Acute occluding event in one of the three
main coronary arteries
Lack of collateral circulation from the other
vessels
Patch of dead heart muscle in one area of the heart the whole thickness of the wall because 1 artery is blocked off
Subendocardial myocardial
infarction
Severe coronary artery atherosclerosis in
all three main coronary arteries
Some sudden reduction in blood flow e.g.
hypotension during an operative procedure
Just beneath endocardium
Or around left ventricle but not all the way through
Chronic ischaemia
‘Fixed’ atherosclerotic lesions Angina Myocardial fibrosis Hibernating myocardium Stunned myocardium
Complications of myocardial infarction
Sudden death Arrhythmias Cardiac failure Mitral incompetence Pericarditis Cardiac rupture Mural thrombosis Ventricular aneurysm Pulmonary emboli
Sudden death
Arrhythmias such as ventricular fibrillation
-not really pumping any blood round
Rational for acute coronary care services
Cardiac failure
Arrhythmias
-complete heart blocks
Loss of myocardium and so reduced pump
function
Mitral incompetence
Rupture or necrosis of papillary muscles
Pan systolic murmur
Cardiac rupture
Weakening of wall due to muscle necrosis and acute inflammation 3-7 days after infarction Rupture into pericardial sac Rupture of interventricular septum
Mural thrombosis
Thrombosis on the abnormal endothelial
surface following infarction
7-14 days after infarction
Embolisation to any arterial site
Ventricular aneurysm
Stretching of newly-formed collagenous scar tissue 4 weeks or more after infraction May be associated with cardiac failure May contain thrombus
Clinical importance of hypertension
Commonest cause of heart failure in most
countries
Major risk factor for atherosclerosis
Major risk factor for cerebral haemorrhage
Hypertension
High blood pressure
One year survival failure of heart failure
Around 60%
Measuring blood p
We measure a smoothed out version of what happens in the heart on the arm
Goes down in the night
What is high blood pressure (TABLE)
A high systolic (130 and over) or diastolic (80 and over) can count as high blood pressure
Classification of high blood presure
Primary
– no definitely identified cause
Secondary
– identifiable cause
Primary hypertension
Adrenalin Sodium control Renin angiotensin aldosterone -these overlap -poorly understood
Secondary hypertension
Renal – renin dependent – salt and water overload Endocrine – Cushing’s, Conn’s, phaeochromocytoma Coarctation of aorta Drug therapy – corticosteroids, NSAIDs
Clinicopathological classification
Benign – long asymptomatic period – increased frequency of complications later Malignant – markedly raised diastolic pressure – symptomatic – rapidly fatal if untreated
Effects of hypertension
- accelerated atherosclerosis
- sclerosis of smaller vessels
- microaneurysms and haemorrhages
- heart failure
- kidney failure
- cerebral haemorrhages = ‘strokes’