Ischaemic Heart Disease

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Ischaemic heart disease is the most common type of cardiac disease and the leading cause of death in the Western world, accounting for about 30% of all male deaths and 23% of all female deaths.

The main cause of ischaemic heart disease, also called coronary heart disease, is atheroma of coronary arteries. The risk factors predisposing to development of ischaemic heart disease are similar to those predisposing to development of atheroma.

Because of its greater bulk and work requirement, the myocardium of the left ventricle has the higher oxygen demand and is more prone to ischaemia.

Stable angina is caused by low flow in atherosclerotic coronary arteries
Angina is episodic chest pain that takes place when there is a demand for increased myocardial work, usually through exercise, in the presence of impaired perfusion by blood.
Pathological studies of patients with angina show that they have at least one stenosis over 50% of the lumen in a main coronary artery (high-grade stenosis).

The high-grade stenosis limits flow, but this may be modifiable by drugs, depending on the nature of the plaque. Atheromatous plaques in coronary arteries may be one of two types.
Over a long period, repeated episodes of impaired flow may lead to development of fine fibrosis in the myocardium, with death of individual cardiac muscle fibres.
Anastomotic vessels frequently develop to compensate for areas of vascular stenosis.

Unstable angina is caused by fissuring of atherosclerotic plaques.
Fissuring of plaques may cause a syndrome of sudden-onset angina that increases in frequency and severity, termed crescendo angina or unstable angina.
As there is a plaque fissure and thrombosis has been initiated, there is a risk of subsequent total thrombotic occlusion of the vessel. A proportion of patients with unstable angina will progress to myocardial infarction or may die from secondary development of a ventricular arrhythmia Plaques in coronary arteries.
Eccentric plaques, often rich in lipid, affect only one segment of the wall of a coronary artery. Improvement of flow at the site of such plaques may be achieved by vasodilator drugs, which can cause relaxation of the normal (unaffected) part of Concentric plaques, usually mostly collagenous, affect the whole of the arterial wall and, as the whole wall is abnormal, drug therapy cannot improve flow over
a narrowed segment.

Acute ischaemic heart disease is largely caused by complications to atheromatous plaques
Thrombus formation, stimulated by the presence of an atheromatous plaque, is the main cause of episodes of acute ischaemic heart disease. Thrombosis at this location is caused by two main processes:
• 25% of cases are due to superficial ulceration of endothelium over a plaque.
• 75% of cases are due to plaque fissuring, resulting in a deep cleft in a lipid-rich plaque that either precipitates thrombus development in the lumen or causes bleeding into the body of the plaque, with resultant ballooning into the lumen.

Importantly, such complications may be in low-grade stenoses, areas that will not have caused previous angina on exertion. The initial manifestation of coronary artery atherosclerosis may therefore be sudden cardiac death, with no history of previous chest pain on exertion.

Acute myocardial infarction may be regional or subendocardial
There are two main patterns of myocardial infarction, each having a somewhat different pathogenesis.
Regional myocardial infarction (90% of cases) involves one segment of the ventricular wall. The cause of this pattern of infarction is nearly always thrombus formation on a complicated atheromatous plaque.
If there is complete persisting occlusion of the arterial branch supplying that area, the infarct is full thickness.
If there is lysis of the thrombus or a collateral supply to the myocardium, the infarct will be limited to the subendocardial zone (regional subendocardial infarction).

Circumferential subendocardial infarction (10% of cases) involves the subendocardial zone of the ventricle and is caused by a general hypoperfusion of the main coronary arteries.
This is usually due to an episode of modest hypotension.
critically reducing flow in arteries already affected by high-grade atherosclerotic stenoses.
The region at the end of the arterial perfusion zone, the subendocardial zone, fails to be perfused and undergoes necrosis.

The three main patterns of myocardial infarction are regional full-thickness, regional subendocardial, and circumferential subendocardial.
The full thickness of the lateral wall of the left ventricle is infarcted.
The subendocardial zone around the whole circumference of the left ventricle is infarcted and dark in colour.
The site of regional myocardial infarction depends on which vessel is involved.
The extent and distribution of the area of myocardial infarction depends upon
which coronary artery branch is occluded. The vast majority of infarcts affect the left ventricle and the septal region. Infarction of the right ventricle can occur but is very rare by comparison.

Site of myocardial infarction and vessel

Myocardial infarction induces acute inflammation, followed by organization and scarring
The end result of myocardial infarction is replacement of the necrotic area by collagenous scar.
The entire process, from fibre necrosis to scar formation, takes 6-8 weeks, the macroscopic and histological appearances of the infarct changing with time.
Between 0-12 hours an infarct is not macroscopically visible; however the ischaemic muscle can be detected by showing loss of oxidative enzymes by nitro blue-tetrazolium (NBT) when the infarcted area appears uncoloured.

Between 12 and 24 hours the infarcted area is macroscopically pale with blotchy discoloration. Histologically infarcted muscle is brightly eosinophilic with intercellular oedema.

Between 24 and 72 hours the infarcted area excites an acute inflammatory response.
Macroscopically the dead area appears soft and pale with a slight yellow colour.
Histologically neutrophils infiltrate between dead cardiac muscle fibres.
Organization of the infarcted area occurs between 3 and 10 days.
Macroscopically a hyperaemic border develops around the yellow dead muscle.
Histologically there is replacement of the area by vascular granulation tissue.
With time, progressive collagen deposition occurs and over a period of weeks to months the infarct is replaced by collagenous scar.

Myocardial infarcts go through a series of changes with time.
Many complications of myocardial infarction occur in the first two weeks
If the patient survives the immediate impact of acute myocardial infarction, or is successfully resuscitated from cardiac arrest or acute pulmonary oedema, the next hurdle is the short-term complications. These include:
• Further episodes of cardiac dysrhythmia,particularly ventricular fibrillation. Bradyarrhythmias
are particularly seen with posterior (inferior)infarcts, as the AV node is often involved.
• Development of left ventricular failure is most common with very large areas of infarction, which
cause cardiac dilatation as the necrotic wall softens in organization.
•Rupture of the ventricula wall at any time,usually 2- 10 days after the infarct, particularly during
early organization and softening, Blood bursts through the wall, instantly filling the pericardial cavity (haemopericardium). The sudden rise in intrapericardial cavity pressure prevents cardiac filling (cardiac tamponade), leading to rapid death. Rarely, intracardiac rupture may occur through the septum, causing a left-to-right shunt and development of severe left ventricular failure if large.
• Papillary muscle dysfunction or infarction leads to mitral valve incompetence, as one valve leaflet is no longer able to close during systole.
• Mural thrombus formation on the inflamed endocardium over the area of infarction.
Fragments can break off and embolize to various organs (particularly the brain, spleen, kidney, gut
and lower limbs, producing infarction.

• Acute pericarditis may occur due to inflammation over the infarct surface.
Because blood flow is slower, patients may be confined to bed, and there is a phase of hypercoagulability of blood, increasing the risk of leg-vein thrombosis.
The area of infarction has ruptured and a track of blood runs from the ventricular chamber to the epicardial surface. In this instance death was rapid after development of haemopericardium.
•A plaque of mural thrombus lies over an area of infarction at the apex of the left ventricle.
The area of infarction has ruptured and a track of blood runs from the ventricular chamber to the epicardial surface. In this instance deathwas rapid after development of haemopericardium.
The area of infarction has ruptured and a track of blood runs from the ventricular chamber to the epicardial surface. In this instance death was rapid after development of haemopericardium.

A plaque of mural thrombus lies over an area of infarction at the apex of the left ventricle.
Long-term complications of myocardial infarction.
If patients survive the immediate and short-term effects of myocardial infarction, long-term complications may arise, among which is chronic intractable left-heart failure due to inadequate left ventricular
pumping action. This is particularly common when the infarct has been extensive and full-thickness.

There may be ventricular aneurysm formation due to gradual distension of that part of the left ventricular wall where the muscle has been replaced by rigid but inelastic fibrous scar.
Ventricular aneurysms frequently become filled with laminated thrombus, but embolic complications are uncommon.
This occurs in around 10% of long-term survivors.
Recurrent myocardial infarction is a risk because of the underlying coronary artery insufficiency.
A patient who has had a myocardial infarct is always prone to develop a further episode.

Dressler's syndrome is a form of immune-mediated pericarditis associated with a high ESR.
It develops in a very small number of cases after infarction (2-10 months after the acute event).
After an infarct, stretching of collagenous scar causes aneurysmal bulging of the ventricular wall.
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Revised: 02-11-2014.