Myocardial infarction

• Discuss the aetiology and pathogenesis of the changes in the coronary arteries.
• Describe the areas of the heart affected by blockage of each of the main coronary artery branches.
• Describe the macroscopic and microscopic changes that occur in the coronary arteries in ischaemic heart disease.
• Describe the gross and microscopic changes in a myocardial infarct.
• Describe the complications of a myocardial infarct.

• The pathophysiology of a myocardial infarction is very important.
• If you haven’t already revised the CALs on atheroma and thrombosis it would be useful to look at these first.

Ischaemic heart disease is defined as an insufficient blood supply to the heart to meet its metabolic demands.

It can be divided into 2 categories – deficiency supply and excessive demand.

Deficient supply –

• Coronary artery disease (commonest)
• Reduced coronary artery perfusion
• Shock
• Severe aortic valve stenosis

Excessive demand

• Pressure overload: e.g. hypertension, valve disease
• Volume overload: e.g. valve disease

Atheroma is a key pathophysiological process which affects the coronary arteries and predisposes to myocardial infarction.

An atheroma would need to be quite significant in order to obstruct >70% of the lumen, often it is complicated atheroma which will lead to a sudden decrease in blood flow.

The plaque will disrupt laminar flow in the coronary artery and predispose to a superimposed thrombus on top which can lead to further myocardial ischaemia.

If a fissure develops in the plaque it can haemorrhage into the lumen and lead to myocardial infarction.

Sometimes myocardial ischaemia can happen even if there is no evident atheroma. This occurs when the artery spasms leading to a reduction in blood flow.

• An embolism is a very uncommon cause of obstruction of the coronary arteries. This is largely due to the anatomy of the coronary arteries and how they articulate with the aortic valve.

• The ostia are located just above the valve, at right angles to the wall of the aorta and are partly covered by the cusp of the valve
• A thrombus would need to turn at right angles and if it were a few millimetres long it would not be able to turn down the coronary arteries

• It is more likely that a thrombus passes through the aorta rather remaining around the valves during diastole
• Most thrombi in coronary arteries are adherent to the wall and superimposed on an atheromatous plaque, suggesting they are formed in situ.

To summarise then – the most common aetiological factor for myocardial infarction is complicated atheroma which has resulted in haemorrhage into the lumen or a superimposed thrombus, resulting in decreased blood flow through the coronary artery.

• It is very important to ascertain what areas of the heart are supplied by each of the main coronary artery branches.
• They are generally organised into 3 broad categories, which can be mapped to the leads of an ECG.

• Chronic pyelonephritis results in systemic hypertension leading to ventricular hypertrophy.
• The hypertrophied (enlarged) left ventricle is at increased risk of ischaemic damage and hypertension also predisposes to atherosclerosis and thrombotic occlusion.
• This leads to myocardial infarction, which can lead to rupture of the left ventricle due to softening of the myocardium.

• An infarct develops with necrosis in an area of myocardium.
• An acute inflammatory reaction occurs with neutrophil infiltration.
• A subsequent chronic inflammatory reaction occurs with healing.
• Granulation tissue appears and collaged in laid down.
• This results in a scar forming which can contract over time.
• The adjacent heart muscle may undergo compensatory hypertrophy to take over the work done by the lost heart muscle.

The picture below shows scar formation in the yellow circle on the posterior aspect of the left ventricle.

Scar tissue leads to a decrease in the amount of functioning cardiac muscle, it is also weaker than the surrounding myocardium and is at risk of stretching and bulging outwards forming an aneurysm.

• This image is taken at the interface of infarcted myocardium and normal myocardium
• The normal cells are located in the upper right corner of the image
  • Note the nucleus (a) and myofibrils (long pink filaments running lengthwise along the cells)

• The necrotic cells are in the middle-bottom half of the picture.
  • Note absent nucleus (c), loss of myofibrils (d), increased eosinophilia (pinkness! – necrotic fibres take up the pink (eosin) stain more readily than normal fibres)

• The body then mounts an acute inflammatory reaction to the necrotic tissue via the innate immune system

• After the acute inflammatory reaction, a chronic inflammatory reaction occurs and the body responds with repair & healing process to organise the area of necrotic tissue
• This type of necrosis is called coagulative necrosis

• In this picture, the necrotic cardiomyocytes still retain their architecture but on close inspection are anucleate.
• The collagen is identified by an anucleate pale pink/purple sheet, with individual stands visible.

• It’s worth knowing that the morphological appearance of an infarct changes macroscopically and microscopically with its age
• The table below breaks down morphological change into macroscopic & microscopic changes over time
• Interestingly – if someone were to die immediately (i.e. drop dead) of a coronary artery thrombus the myocardium would appear normal, as there wouldn’t be enough time for the changes to develop

• As the cardiomyocytes break down post-MI they release enzymes into the blood
• These enzymes can be detected in the blood and used as biomarkers for diagnostic testing of myocardial ischaemia

Symptoms –

• chest pain – severe central crushing chest pain radiating to the left arm & jaw
• nausea
• dyspnoea

Complications of an MI can be roughly divided into early (occurring in the first 2 weeks post-MI) and late (occurring 2-6 weeks post-MI)

• Arrhythmias are very common early complications of an MI.
• If the conduction system is affected then it can lead to a bradyarrhythmia e.g. bradycardia, heart block.

• Other arrhythmias are very common after an MI, that is why it is important that a patient is kept in a monitored bed in hospital

• Most infarcts affect the muscle of the left ventricle, as such a patient is at a much greater risk of developing left ventricular failure due to pump failure.
• This will lead to a backlog of blood in the lungs which will manifest as pulmonary oedema.
  • This can present with breathlessness, frothy sputum and develop into congestive cardiac failure or respiratory failure if it is very severe.
• An arrhythmia can also lead to cardiac failure, particularly if a patient develops an unstable tachycardia.

• Inflammation & irritation of the pericardial sac can lead to chest pain & fever.
• It is identifiable on an ECG and is treated with non-steroidal anti-inflammatory drugs e.g ibuprofen

• The infarcted area of tissue is often weaker than the surrounding cardiac muscle after an MI.
• Depending on the area of infarction different areas of the heart muscle can rupture.
  • Ventricular rupture – can occur after an anterior MI where there is a weakening of the left ventricular wall – this can lead to a cardiac tamponade.
  • Septal rupture – can occur after an anterior or posterior MI and will lead to a left-right shunt.
  • Papillary muscle rupture – can occur after an inferior MI and lead to mitral regurgitation & heart failure.

• This usually occurs 4-6 weeks after an MI after the infarcted tissue has developed into a scar.
• This scar tissue can dilate forming an aneurysm.
• This can lead to left ventricular failure, arrhythmias and systemic embolus formation.

• If the MI involves the endocardium it can result in a mural thrombus forming on the endocardial surface.
• This can dislodge and lead to a systemic embolus.

• Dressler’s syndrome usually occurs 2-6 weeks after an MI.
• It is due to antibodies which mount an inflammatory response to the myocyte sarcolemma.
• It presents with pericarditis and pleural effusion.

Myocardial infarction is an extremely important condition and is responsible for a large proportion of morbidity and mortality in Scotland. It’s important that you understand:

1. The aetiology & pathophysiology of myocardial ischaemia
2. The morphological changes over time
3. The clinical presentation of an MI
4. The regions of the heart supplied by the coronary arteries
5. The complications of an MI