18. Pathogenesis of coronary insufficiency. Risk factors

Last updated on May 24, 2019 at 17:47

Summary

The oxygen delivery to the myocardium can only be increased by increasing the coronary blood flow. If the coronary blood flow can’t be increased to meet the oxygen demand of the myocardium coronary insufficiency and ischaemia develops.

Coronary circulation

The myocardial metabolism is highly aerobic, meaning that the coronaries must supply a lot of oxygen to the heart muscle. The coronary circulation is 80 mL/100g/min, which is higher than the cerebral blood flow at 60 mL/100g/min. The oxygen extraction from the coronary blood to the myocardium is close to the max, from 10 to 14%. The O2 consumption is 8-15 mL/100g/min.

The subendocardial myocardium of the left ventricle are the unluckiest. During systole the arteries in the subendocardial myocardium are compressed, and therefore perfusion of this area is decreased. The majority of the perfusion of the subendocardial myocardium therefore occurs during diastole. Because of this is the diastolic time important for the coronary circulation. This puts an upper limit on how high the heart rate can become before the subendocardial myocardium is underperfused.

The coronary blood flow is autoregulated, so that the coronary blood flow stays constant despite large fluctuations in the mean arterial pressure. Coronary blood flow is autoregulated between 60 and 150 mmHg MAP.

β1 adrenergic activity decreases coronary blood flow, while the following factors increase it:

  • Hypoxia
  • Adenosine
  • K+
  • Lactate
  • NO
  • Prostacyclin
Coronary insufficiency

When the myocardium must work harder must the coronary circulation also increase. In healthy hearts the myocardial perfusion demand and coronary supply are equal, so that the myocardium always receives the perfusion it needs. When the myocardium has a higher oxygen demand than the coronary circulation can provide we have a coronary insufficiency, and so the myocardium becomes ischaemic.

The myocardial oxygen demand increases when heart rate and/or contractility increases.

Coronary insufficiency has many consequences. Having your myocardium underperfused can be very painful, causing the characteristic chest pain called angina, as we will see later. Ischaemia decreases the contractility of the ventricles. It also causes ECG changes which can be used to diagnose it.

If the insufficiency is severe the ischaemia can cause necrosis, eventually causing acute myocardial infarction.

Factors affecting oxygen demand

Three major points affect the oxygen demand of the myocardium: the heart rate, the contractility and the tension in the ventricular wall. Let’s go through all of them.

The increase in oxygen demand with an increased heart rate is simple to explain. Each beat requires energy. When the heart rate increases will the heart beat more often, increasing the energy and therefore oxygen demand.

Contractility is the measure of force of contraction. When the force of contraction increases will the myocardial cells do more work, meaning that they require more oxygen.

The role of ventricular wall tension in oxygen demand can be hard to understand. When the wall has higher tension, it’s like the wall and the myocytes in the wall are stretched. Myocytes have a harder time contracting when they’re stretched compared to when they’re not. This can be seen by how a bicep curl with a dumbbell is hardest in the beginning when the elbow is fully extended (and the biceps is stretched), and gradually becomes easier as the biceps contracts. This means that the myocardium has a higher oxygen demand when the tension increases.

Then, what increases the tension in the ventricular wall? To understand that we must look at the Law of Laplace. This law states that the tension is directly proportional to the pressure inside the ventricle and to the radius of the ventricle but indirectly proportional to the thickness of the wall. The law can be formulated like this:

From this law we can derive that an increase in either intraventricular pressure or radius will increase the wall tension and therefore the oxygen demand. Increased ventricular wall thickness however decreases the tension, reducing the oxygen demand.

Three important pathophysiological conclusions can be drawn from this:

  • An increase in ventricular wall thickness is beneficial to decrease the myocardial oxygen demand
  • Any increase in the diameter of the lumen will increase the wall tension and therefore the oxygen demand
  • Any increase in end-diastolic pressure will increase tension

Several pathologies cause increased oxygen demand by increasing either the heart rate, contractility or wall tension. Here are some:

  • Increased afterload
    • Systemic hypertension
  • Exercise
  • Assuming upright position
Factors affecting oxygen supply

As noted in the beginning of this topic is the myocardial oxygen extraction from the blood close to maximum, even at rest. This means that the oxygen supply can’t be increased by increasing the oxygen extraction, as it is already at its highest level. Oxygen supply can only be increased by increasing the blood flow.

The coronary circulation depends on the difference between the aortic diastolic pressure and the pressure inside the coronary sinus. This difference is called the perfusion pressure. When the perfusion pressure increases will the oxygen supply increase as well.

Factors affecting the coronary reserve

The coronary reserve is the maximum increase in coronary blood flow that can be achieved. It’s essentially how large of an increase in coronary blood flow that can be provided when needed. A large coronary reserve is a good thing, as the coronaries have a large capacity to supply the myocardium with blood even when the myocardial oxygen demand increases.

Coronary reserve is the maximum amount of blood flow that can be achieved minus the blood flow in rest.

Many factors can decrease the coronary reserve. Many of them do it by decreasing the lumen of the coronaries. Atherosclerotic plaques in the coronaries are the most common cause. When the plaques occlude more than 70% of the lumen will angina develop.

The smooth muscle in the coronary wall can also spasm, decreasing coronary perfusion. This is characteristic in Prinzmetal’s angina.

If the blood contains low amounts of oxygen, like in anaemia the coronary reserve will be decreased.

Risk factors

The definite biggest risk factor for coronary insufficiency is atherosclerosis. The pathomechanism and risk factors of atherosclerosis are detailed in the pathology 1 topic.


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17. Tissue hypoxia, ischemia, reperfusion and tissue metabolism

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19. Pathomechanism and consequences of acute myocardial infarction

2 thoughts on “18. Pathogenesis of coronary insufficiency. Risk factors”

  1. I told my examiner that the coronary arteries are compressed during systole, and he said that it is not correct. It is due to the high systolic intraventricular pressure and the ventricular contraction (the blood won’t go from a lower to a higher pressure.) In my opinion, I think the vessels get compressed aswell.

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