Ischaemic Heart Disease Flashcards
What is the definition of Ischaemic heart disease?
Definition: An imbalance between myocardial oxygen supply and demand
What are some acute and chronic forms of ischaemic heart disease?
Acute
Unstable angina
Myocardial infarction
Sudden cardiac death
Chronic
Stable angina
Chronic myocardial ischaemia
Give an idea of cardiac anatomy.
The heart is like a modified blood vessel:
- Solid organs generally have a hilum and flow is from hilum to capsule/periphery. - Hollow organs have a fatty external layer containing vessels and the flow is from outside to inside. - Infarcts occur at the end of the blood supply.
Explain some features of the vulnerable subendocardium.
Due to the physiology and anatomy, the subendocardium is the first area targeted, infarcts start from inside can spread outwards.
The endocardium is spared because it has some direct diffusion from the blood in the chambers.
The names of the coronary arteries that we use in clinical practice might be different to what you’ve learned.
Explain some features of the vulnerable subendocardium.
Due to the physiology and anatomy, the subendocardium is the first area targeted, infarcts start from inside can spread outwards.
The endocardium is spared because it has some direct diffusion from the blood in the chambers.
The names of the coronary arteries that we use in clinical practice might be different to what you’ve learned.
What are some strategies you can use to identify the directions of a heart dissection?
- Flattening posteriorly
- Papillary muscles and chordae
- PD at septum
- LAD branches lateral off-septum
- Size differential superior and inferior surfaces
- More pericardial fat anterior than inferior
Explain the vascular supply of the heart?
- Anterior wall and 2/3 septum supplied by LAD
- Lateral wall supplied by LCX
- Posterior wall (Inferior wall) supplied by PD
– Right dominant heart PD is from RCA (majority of people)
– Left dominant heart PD is from LCX
What is an MI? What are some key pathological features?
– An imbalance between the supply and demand of the myocardium resulting in ischaemia and cell death.
– Most commonly caused by an acute plaque event with rupture or haemorrhage of atherosclerotic plaque and formation of an occlusive thrombus within a coronary artery
- Has all the features of what you already know:
– Necrosis
– Acute inflammation
– Granulation tissue
– Fibrosis / Scar
- Occurs in a timely progression and allows us to predict complications
What kind of injury occurs with an MI within 0-30 minutes?
Angina/Reversible Injury: (0 min - 30 min)
– No macroscopic changes
– No microscopic changes
BUT
– Intracellular changes (eg mitochondrial swelling, myofibril relaxation) are present, visible only on electron microscopy
– Functionally there is a rapid loss of contractility
– May see ECG changes
- ST depression and/or T wave inversion
What kind of injury occurs with an MI within 30mins to 12 hours?
Irreversible Injury: (30 min - 12 hours)
– Includes disruption of the cell membrane (sarcolemma)
- Levels of cardiac enzymes start to rise and become detectable in the blood during this time (approx 3-4 hours post infarction) [troponin, creatine kinase]
- These tests are the mainstay of diagnosis of myocardial infarction
What are some complications that can occur with an MI between 30 mins and 4 hrs of the event?
Complications: (30 min - 4 hours)
- The damaged myocytes are unstable →ARRHYTHMIA
- The damaged myocytes cannot contract properly → CARDIAC FAILURE
Irreversible Injury:
Cell Death: (30 min - 12 hours)
Haemorrhage:
Oedema:
What is a STEMI?
STEMI: ST elevation myocardial Infarction: completely occluded artery
NSTEMI: any kind of MI where the ECG do not have ST elevation
What complications occur with an MI between 12 hours and 24 hours of the event?
Necrosis and Early Acute Inflammation
What complications occur with an MI between 1 and 3 days after the event?
Acute Inflammation - troponin peaks and can still be detectable up to 2 weeks post infarct
What occurs at the end of acute inflammation after an MI?
End of Acute Inflammation & Start of Early Grandulation:
- Macrophages ingest dead myocytes
- Fibroblasts and vessels of granulation tissue appear
- Collagen starts being laid down at 5-6 days
What are some serious complications that occur between 1 and 3 days of an MI?
Complications: (1 day - 3 days)
- The damaged myocytes are unstable → ARRHYTHMIA
- The damaged myocytes are being destroyed → CARDIAC FAILURE
- Inflammatory mediators abound → PERICARDITIS
- The damaged wall isn’t moving normally → MURAL THROMBUS
- The wall is necrotic and weakened → RUPTURE
What are three ways the heart can rupture?
- Haemopericardium/cardiac tamponade
- Rupture of papillary muscle
- Rupture of IV septum
What events occur after 1-8 weeks after an MI?
Early And Late Granulation: (1 week - 8 weeks)
- Initially high cellularity, high vascularity with little collagen
- Gradual reduction in cells and vessels with increasing collagen.
- The granulation tissue has collagen and is getting stronger and slowly becoming fixed in position
- At this point it is flexible and may stretch, causing thinning of the wall
What are some complications that occur after an MI? (1 - 8 weeks)
- The damaged myocytes have been cleared, leaving islands of viable myocytes in healing tissue → ARRHYTHMIA
- The damaged myocytes will not be replaced → CARDIAC FAILURE
- The damaged wall isn’t moving normally → MURAL THROMBUS
- With collagen the wall is strong again, but flexible to wall stress and may stretch, thin and bulge out → ANEURYSM (Infarct Expansion)
MURAL THROMBUS
↑
ANEURYSM (Infarct Expansion)
What are the events and possible complications that can occur after 8 weeks post MI?
Fibrosis/Scar: (8+ weeks)
- dense collagen
- fibrosis is blue in a Trichrome stain.
Complications: (8+ weeks)
- The damaged myocytes have been cleared, leaving islands of isolated myocytes in healing tissue → ARRHYTHMIA
- The damaged myocytes will not be replaced. Long term, the remaining left ventricle may undergo remodeling, including hypertrophy and eventually decompensate → CARDIAC FAILURE
- Any aneurysm formed now will not regress. Over time, there may be some increase in aneurysm size. However, with the formation of scar tissue, it is very unlikely to rupture.
→ ANEURYSM MURAL THROMBUS
What are some other causes of MI?
Other Vascular Pathology (Non Atherosclerosis)
- Coronary Artery Dissection
- Thrombosis due to Vasculitis
- Thromboembolism from the heart
Reduced Flow / Oxygenation
- Hypotension (Shock)
- Rapid Tachycardia
- Hypoxaemia
What is the difference between stable and unstable angina?
Both stable and unstable angina represent transient ischaemia, symptomatic with chest pain.
Stable Angina
Presents as reproducible cardiac chest pain that occurs on exertion and goes away with rest
• Due to atherosclerotic narrowing of a vessel
• Endothelial dysfunction
• Symptoms generally start at 70% stenosis
Unstable Angina
Presents as cardiac chest pain that may occur at rest or minimal exertion
• Acute plaque event
• Coronary artery thrombosis
• Resolves
• No irreversible damage
• Clinically: cardiac type chest pain, can occur at rest or with exertion.
What is Chronic Myocardial Ischaemia?
With chronic atherosclerotic narrowing of vessels:
- Small areas of subendothelial ischaemia
- Patchy myocyte necrosis and replacement by fibrosis
- Similar to the sort of fibrosis you might see in myocardial hypertrophy
- Carries similar risk of cardiac failure and arrhythmia
Define and give features of sudden cardiac death?
- Defined:
– unexpected death
– due to cardiac causes
– in a short time period (
