Chest Pain and Breathlessness Flashcards
(34 cards)
Name the three clinical syndromes of ischaemic heart disease
- Angina (stable and unstable)
- Myocardial infarction
- Sudden cardiac death
What can cause ischaemic heart disease
- Atheroma of coronary arteries (95% cause)
- coronary artery vasculitis (inflammation of the vessel)
- coronary artery vasospasm
- anaemia
What is the primetime for males to have there first heart attack
55
- Women have ischaemic heart disease later in life
What are the risk factors for ischaemic heart disease
- sex (male)
- age
- family history
- hyperlipidaemia
- hypertension
- diabetes mellitus
- smoking
- obesity
- stress
- lack of exercise
Name differences between stable and unstable angina
unstable
- comes on at rest
- unpredictable
- unstable plaque of atheroma that is changing and growing and complicating
stable
- coronary artery disease causing the atheroma is stable
- plaque is not changing a lot
- lasts about 5-15 minutes, with exercise and emotional stress, reduces when relaxing or taking nitrates
What is the main cause of IHD
- Atheroma of coronary arteries (95% cause)
What are the theories as to how atheroma has formed
- Encrustation (Rokitansky) - platelet thrombi over injured endothelium
- Imbibition (Virchow) - low grade inflammation leads to increase plasma filtration
- Reaction to injury (Ross and Glomset) - endo injury with increase permeability and macro/smooth muscle accumulation
Describe Rokitansky theory as to how atheroma has formed
- platelets stick to the inside of the platent wall and this is due to the endothelium being injured
Describe Virchow theory as to how an atheroma has formed
- cells - low grade inflammation leads to increased plasma filtration
Describe Ross and Glomset theory as to how an atheroma has formed
- idea that there is a reaction to a vessel wall due to endothelium injury, this increases permeability and macro/smooth muscle accumulation
What part of the artery is the atheroma in
Tunica intima
Describe the pathogenesis of atherosclerosis
- At some stage there is a problem
- contents get stuck to the vascular wall
- platelets get stuck and form a thrombi
- endothelium cells either damaged directly or due to the turbulence get dislodged and expose the underlying connective tissue
- this triggers thrombosis due to the damage of the endothelium
- this triggers inflammation
- the plaques becomes more pronounced
- the smooth muscle cells migrate to the intima and become foam cells
- macrophages also take up the fat and become foam cells
- the plaque becomes bigger
- collagen is laid down
- get a plaque that is more fibrous and cellular
- the blood is still trying to get through the lumen
- get necrosis in the centre eventually
- then there is an attempt at healing and vaso vasorum grow into the intima and supply it with blood in an attempt to heal the necrosis
- dyanmic situation has occurred in the coronary artery, the plaque has ulcerated and liberated the necrotic centre and stimulated local thrombosis causing occlusion
- or the atheroma plaque has caused critical thrombi dynamic changes that cause the occlusions of the vessel
What are the complications of an atheroma
- ulceration
- fissuring
- haemorrhage
- thrombosis
- aneurysm - dilatation of a vessel (seen in an abdominal aorta due to atheroma)
What are the two main types of acute myocardial infarction
- Transmural (most cause ST elevation(STEMI))
- Subendocardial (most do not cause ST elevation (NSTEMI))
Describe a transmural actue MI
- involves the whole thickness of the ventricular wall - starts from the endocardium right through the myocardium to the epicardium
What is the most likely cause of a transmural acute MI
- underlying lesions is an atheromatous plaque in a coronary artery that has undergone fissuring and occlusive thrombosis
Describe a subendocardial infarction
- confined to the inner third or half of the myocardium - this gets in oxygen last
What is a subendocardial infarction due to
- results from generalised under-perfusion of the myocardium
- caused by generalised atheroma of all of the coronary circulation
or - e.g. anaemia on top of something else
- Lung disease
If there is an occlusion of
- Main left coronary artery
- Left anterior descending
- Left circumflex
- Right coronary artery
What part of the heart does it affect?
- Main left coronary artery = massive anterolateral MI
- Left anterior descending = anteroseptal MI
- Left circumflex = lateral MI
- Right coronary artery = Posterior (inferior) MI
Describe the macroscopic appearance of the MI
- 0-12 hours
- 12-24 hours
- 24-72 hours
- 3-10 days
- weeks - months
- 0-12 hours = no changes
- 12-24 hours = pale with blotchy discolouration
- 24-72 hours = soft, pale and yellow
- 3-10 days = soft, yellow-brown with hyperaemic border
- weeks - months = white fibrous scar
Describe the histology appearance of the MI
- 0-12 hours
- 12-24 hours
- 24-72 hours
- 3-10 days
- weeks - months
- 0-12 hours = No changes
- 12-24 hours = bright eosinophilia of muscle fibres reflecting onset of coagulation necrosis; intracellular oedema
- 24-72 hours = coagulative necrosis with loss of nuclei and striations, beginning of acute inflammatory response with heavy interstitial neutrophil infiltrate
- 3-10 days = replacement of infarcted area by granulation tissue
- weeks - months = collagenous scar tissue
How does a pathologist diagnose cardiac death due to MI after death
Cut along the coronary artery and find the infract
What are the short term complications of MI
left ventricular failure
cardiac dysrhythmias
rupture of ventricular wall - blood will just go left to right
papillary muscle infarction - can cause mitral regurgitation
mural thrombus - if it embolisms it can convert to stroke
fibrinous pericarditis
deep vein thrombosis
What are the long term complications of MI
intractable left ventricular failure
ventricular aneurysm - thin wall where the scar is
Dressler’s syndrome
recurrent myocardial infarction
