Myocardial Infarction

§ Immediately after an acute coronary occlusion, blood flow ceases in the coronary vessels beyond the occlusion. The area of myocardium that has either zero blood flow or so little blood flow that it cannot sustain muscle function is infarcted.

§ The overall process is called a myocardial infarction

§ When myocardial ischaemia is severe or prolonged (> 1/2 hour), the cardiac tissue that is deprived of oxygen & glucose will die & undergo necrotic changes. Such necrosis induced by ischaemia is called an infarction (or infarct).

§ The death of myocardial cells caused by coronary artery occlusion is referred to as a myocardial infarction (MI) .

§ Infarcted myocardium is dead heart muscle resulting, usually, from an occluded coronary artery.

§ Infarct: localised area of necrosis in a tissue, vessel or organ resulting from tissue anoxia caused by an interruption in the blood supply to the area

§ Almost all myocardial infarctions result from atherosclerosis of coronary arteries

Mechanism of vascular occlusion leading to infarction

1) Spastic constriction

• usually early stages of CHD
• local spasm of a coronary artery secondary:
1. Nervous reflex: exposure to wind or cold
2. Local irritation of smooth muscle adjacent to atherosclerotic plaque eg: nicotine or caffeine; spontaneous

• could potentially lead to MI if already have a compromised blood supply to a region of myocardium with increased work load.

2) Occlusion

• usually later stages of CHD
• characteristically progressive & irreversible
• when plaque breaks through intima

—> contact with blood

—> initiate thrombus —> occlude vessel —> MI

—> portion of clot breaks away —> distal vessel embolisation —> MI

3) Myocardial infarction caused by myocardial ischaemia but WITHOUT coronary thrombosis

• a large percentage of deaths post MI are not associated with coronary thrombosis however do have atherosclerotic narrowing of major coronaries
• -Increased stress on heart (exercise, emotional, anything that increases load on heart or decreases blood supply)

—> decreased O2 supply/ O2 demand ratio of myocardium

—> non contracting myocardium (in this region)

—> increased work load on rest of heart

—> increased O2 demand in rest of heart

—> myocardium with marginal blood supply becomes noncontracting

—> oedema in ischaemic myocardium

—> release of local vasoconstrictors

—> further diminution of local blood supply

—> myocardial infarction

Sequelae of myocardial infarction

1. When the area of ischaemia is large, within about one hour in an area of total cessation of coronary blood supply, some of the muscle fibres in the very centre of the area die rapidly (zone of infarction)

2. Immediately around the dead area is a nonfunctional area (zone of injury) because of failure of contraction & often impulse conduction

3. Extending circumferentially around the zone of injury is an area that is weakly contracting because of mild ischaemia (zone of ischaemia) -Note that this zone of ischaemia is barely adequately supplied by small coronary collaterals provided the patient is kept at rest — any extra work load on the heart may divert blood to normal musculature thereby rendering this region nonfunctional

Replacement of dead muscle by scar tissue

1. Shortly after occlusion:

- the muscle fibres die in the very centre of the ischaemic area

2. During the following days:

- this area of dead fibres grows because many of the marginal fibres finally succumb to the prolonged ischaemia

- area of nonfunctional muscle becomes smaller due to enlargement of collateral blood vessels

3. During few days to 3 weeks

- most of nonfunctional area becomes either functional or dead

- dead muscular tissue is replaced by fibrous tissue

- note that most severe complications after a MI occur within 2 weeks of the event (eg: VSD, free wall rupture, papillary muscle rupture)

4. Several month to year

- size of fibrous zone becomes progressively smaller due to property of fibrous tissue to undergo progressive contraction & dissolution

—> functional musculature able to contract more efficiently without having to stretch dead area of heart

- compensation of rest of heart for missing musculature by hypertrophy

- Over several years with repeated regions of infarctions see development of ischaemic cardiomyopathy

Window of opportunity for the restoration of blood flow to obviate infarction

§ Myocardial ischaemia may result in myocardial necrosis if not rapidly treated

§ Myocardial ischaemia may be associated with regional wall abnormalities and papillary muscle dysfunction resulting in mitral regurgitation & pulmonary oedema

§ The goal of the operation is to provide myocardial revascularisation as rapidly as possible — the sooner the patient is placed on CPB, the fewer myocytes will die

§ Time spent on taking down IMA may not be prudent

§ Saphenous vein grafting is performed swiftly; the most critical lesions performed first with cardioplegia given down the grafts as soon as they are completed

§ Other adjunctive measures include:

• extra attempts to cool the heart

§ Retrograde coronary perfusion

§ Warm induction

§ period of controlled perfusion post completion of grafting

§ IABP; to reduce myocardial work

§ Myocardial revascularisation for acute infarcts greater than a few hours old is of reduced benefit?

• degree of cellular death is determined by: degree of ischaemia x degree of metabolism

• Post MI must maintain an optimal balance between myocardial blood supply and demand so as to salvage as much as the ischaemic zone around the infarct as possible

• By delivering O2 to ischaemic myocardium, reperfusion has the potential to relieve ischaemia thereby limiting infarct size

• Clinical & experimental evidence show improved mortality & morbidity the earlier the reperfusion post MI

• Surgical reperfusion [CABG] of ischaemic myocardium is only successful in limiting infarct size if performed within 4 — 6 hours post MI [preferably first 2 hours]

• CABG is contraindicated in patients with uncomplicated transmural infarcts > 6 hours post MI as is associated with increase risk of haemorrhage into area of infarct

Value of rest post MI

- increased myocardial metabolism [eg exercise, stress]

—> increased myocardial demands for O2 and nutrients

—> vessels of normal vasculature become dilated

—> most blood flows into normal myocardium at expense of blood flow to ischaemic regions [“coronary steal” syndrome]

—> exacerbate ischaemia

- Therefore the greater the degree of rest post MI for first few weeks the less cellular death