Ischaemic Heart Disease Flashcards
What is the definition of ischaemic heart disease?
pathophysiological syndromes due to inadequate blood supply to the myocardium
What are the 2 reasons why there may be inadequate blood supply to the myocardium in IHD?
- reduced coronary blood flow due to atheroma +/- thrombus
2. myocardial hypertrophy due to systemic hypertension
What are the 5 factors involved in preventing IHD?
- stop smoking
- lose/manage weight
- lower blood pressure
- encourage exercise
- calculate risk and prescribe relevant treatment
What is the main risk score calculation used in IHD?
The Framingham risk score calculation
It estimates a patient’s 10 year risk of having a heart attack
What are 2 other commonly used risk calculators?
- SCORE
2. QRISK3
What is involved in the pathogenesis of IHD?
- acute and/or chronic ischaemia
- loss of autoregulation of coronary blood flow with >75% vessel occlusion
- low diastolic flow leading to subendocardial hypoperfusion
- myocyte dysfunction/death from ischaemia
When is recovery possible from IHD?
If there is rapid reperfusion within 15-20 minutes
At what point does IHD become symptomatic?
When there is >75% vessel occlusion
This is critical stenosis and gives angina-like symptoms
What are the 4 IHD syndromes?
- angina pectoris
- acute coronary syndrome
- sudden cardiac death
- chronic ischaemic heart disease
What typically causes acute ischaemia?
- atheroma + acute thrombosis/haemorrhange
Lipid rich plaques are most at risk
What does acute ischaemia in the heart lead to?
regional transmural myocardial infarction
this is different to a subendocardial MI
If someone has an MI and dies within 24 hours, what morphology would be present?
Morphology would be normal
e.g. in a sudden cardiac death
What would the MI morphology look like after 1-2 days?
it would be pale and oedematous
there would be neutrophils and myocyte necrosis
What would the MI morphology look like after 3-4 days?
it would be yellow with a haemorrhagic edge
there would be macrophages and myocyte necrosis
What would the MI morphology look like after 1-3 weeks?
it would be red-grey to grey-white
it becomes pale and thin
granulation tissue forms, followed by fibrosis
What would the MI morphology look like after 3-6 weeks?
there would be a dense fibrous scar
What is a ‘STEMI’?
ST-elevation myocardial infarction
What causes a STEMI?
blockage of one of the major coronary arteries
this is the most serious type of heart attack caused by COMPLETE OCCLUSION of a coronary artery
What is an example of an NSTEMI?
subendocardial MI
What is an NSTEMI?
non-ST-elevation myocardial infarction
an acute ischaemic event causing myocyte necrosis
What is the perfusion of the subendocardial myocardium like under normal conditions?
it is relatively poorly perfused under normal conditions
What can lead to the subendocardial myocardium infarcting without any acute coronary occlusion?
- stable atheromatous occlusion of the coronary circulation
- an acute hypotensive episode
this can lead to subendocardial MI
What is the most common blood marker of cardiac myocyte damage?
Troponins T and I
Under what circumstances may troponins T and I be raised?
- post-MI
- pulmonary embolism
- heart failure
- myocarditis
When are troponins T and I detectable?
When do they peak?
detectable after 2-3 hours
peaks after 12 hours
still detectable for up to 7 days
When is creatine kinase MB detectable as a sign of cardiac myocyte damage?
detectable after 2-3 hours
peaks at 10-24 hours
detectable for up to 3 days
What are 3 other cardiac enzymes that can show damage to the cardiac myocytes?
- myoglobin
- lactate dehydrogenase isoenzyme 1
- aspartate transaminase
What is the problem with using myoglobin as a marker of cardiac injury?
When does it peak?
It peaks after 2 hours
It is also released from damaged skeletal muscle
When is lactate dehydrogenase isoenzyme 1 detectable?
When does it peak?
Peaks after 3 days
Detectable for up to 14 days
Why is aspartate transaminase less useful as a marker of myocardial damage?
it is also present in the liver
What % of MI patients experience sudden cardiac death?
20%
They have 1-2 hour mortality
What is the prognosis of MI patients who do not experience sudden cardiac death?
10-15% = early hospital mortality
7-10% - further 1 year mortality
3-4% mortality per year in subsequent years
What % of MI patients experience complications?
80-90%
What are the 4 main complications of MI?
- arrhythmias, ventricular fibrillation & sudden death
- left ventricular failure and shock
- pericarditis
- cardiac mural thrombus and emboli
What are the 4 less common complications of MI?
- DVT and pulmonary embolus
- myocardial rupture
- ventricular aneurysm
- autoimmune pericarditis +/- pleurisy for 2 weeks-months post MI
What tends to be involved in myocardial rupture?
tamponade, ventricular septal perforation and damage to papillary muscle
What are the 3 stages involved in MI diagnosis?
- taking a history and finding the symptoms
- examination - pulse, breathing
- investigations - ECG, cardiac enzymes
What is the MONA of MI treatment?
M - morphine
O - oxygen
N - nitrates
A - aspirin
What reperfusion technique is used to treat MI?
PCI - percutaneous coronary intervention
this is better than thrombolysis
What are the further measures for treating MI?
managing the complications of MI and secondary prevention
What drugs are given in the secondary prevention of MI?
- ACEi, anti-platelets and anti-coagulants
- anti-arrhythmics and beta-blockers
- statins
What causes chronic ischaemic heart disease?
decompensated myocardium or coronary artery atheroma produces relative myocardial ischaemia
It may be a result of previous MIs or congestive heart failure
What does the heart look like in congestive heart failure?
it is enlarged, hypertrophied and dilated
What is the risk of chronic ischaemic heart disease?
risk of sudden cardiac death or MI
What causes familial hypercholesterolaemia?
mutations in genes involved in cholesterol metabolism
What are the most common mutations in familial hypercholesterolaemia?
- low density lipoprotein receptor gene
2. apolipoprotein B
What is the most common symptom of someone who is heterozygous for familial hypercholesterolaemia?
development of xanthomas and early progressive atherosclerosis
xanthomas develop in the tendons, periocular and corneal arcus
What is the treatment for heterozygous familial hypercholesterolaemia?
early primary treatment with statins
How does treatment for homozygous hypercholesterolaemia differ to heterozygous?
treatment is more complex and less effective
