Cardiovascular disease processes

Cardiovascular disease processes

Dale Pinnock
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Published by
Quadrille Publishing
978 184949 542 4

Heart disease isn’t something you just get struck down with. It is the result of a lot of small changes coming together over time. Many of the things that you have heard of as being risk factors for heart disease – such as high blood pressure, or smoking – essentially set the stage for a series of events to occur which can lead to the condition ultimately known as heart disease.

There are several pathological (disease causing) events that take place. There isn’t always a specific order for these occurring and, very often, one gives rise to another in a vicious cycle. Here are the main events, the key pathological processes and certainly the ones that have been at the centre of most studies. Understanding them properly will help you get a better grasp on how nutrition and lifestyle can be one of the most powerful parts of your armoury against cardiovascular disease.

Endothelial dysfunction

The endothelium, as we have seen earlier in this book, is the skin that lines the inside of our blood vessels. This thin skin is absolutely vital in maintaining the function of the rest of the blood vessel and, when it goes wrong in some way, the consequences can be devastating to cardiovascular health.

And one of the fundamental areas where the endothelium can start to malfunction is when it has a reduced production or utilisation or release of nitric oxide. This is a chemical that is naturally made by – and released by – the endothelial cells, and which controls several aspects of vascular biology. It reduces blood clotting, reduces the movement of white blood cells into the vessel walls (see plaque formation), and also reduces the oxidation of LDL cholesterol. The major and most widely understood role for nitric oxide, however, is vasodilation, which means the widening of blood vessels (remember from when we explored blood pressure). This is the relaxation of the muscular walls of the blood vessels. It is normally stimulated mostly by sheer stress placed on the vessel walls by blood flowing through. Nitric oxide is produced and released by endothelial cells in response to immediate localised changes that signal a need for a change in blood pressure or vessel function.

Problems arise when nitric oxide release or utilisation is impaired. The first and most obvious consequence is the reduced capacity for the vessels to widen under stress. Lets use the analogy of a hose pipe to give some clarity to this. Imagine you have two hose pipes. One is made of flexible, responsive rubber, the other of stiff, inflexible plastic. When water runs through them at a normal and steady pace, they both perform perfectly well. But, what happens if you should turn on the taps at full pelt? The rubber hose, when faced with the sudden rise in pressure, will simply stretch and expand and ‘go with the flow’. The plastic one has no give, so begins to crack and split under the pressure.

Well, this gives you an idea of how things go awry when our blood vessels are less responsive to changes in pressure. Suddenly we are at more risk of damage to the endothelium from the increased pressure against the vessel walls, and any areas of repaired damage and plaques are more susceptible to further damage and rupture. The initial stages of endothelial damage, whether induced by physical stress or other events, involve and lead to…


We are now at the point, with research going in the direction that it is, where we can say with certainty that, despite whatever else is going on in the body, cardiovascular disease is essentially an inflammatory condition. Inflammation that causes damage to the vital endothelium and then fuels further pathophysiological changes in the body.

Inflammation is a normal, natural and vital thing. It aids our immune system in dealing with pathogens, infection or damaged tissue. In cardiovascular disease, it seems there is a two-way street, or a vicious cycle. Inflammation can cause endothelial dysfunction; endothelial dysfunction can cause inflammation.

One of the main and most widely established causes of inflammation within the endothelium is the oxidation of LDL cholesterol. LDL cholesterol can become damaged by circulating free radicals (reactive oxygen molecules that cause damage) and be readily oxidised (damaged and chemically altered). When this happens, the oxidised cholesterol can cause damage to the endothelium. Oxidation makes LDL far more able to penetrate the endothelium and cause some of the damage outlined over the page (plaque formation). Other factors that can trigger inflammation are smoking, high insulin levels – caused by eating too many fast-release carbohydrates for too long – and stress.

But, probably, the biggest factor of all for most of us in the Western world is the wrong types of fats in our diet. I am going to go into much more detail in the next chapter on nutrition and heart disease and heart health, but in the Western world we are eating too much of a type of fat that may be killing us slowly. Now, before you think this may be that old-school message about saturated fat that you have heard a million times for decades and that has now been proven to be wrong, think again. Listen up: saturated fat is not the villain that you might have thought.

In fact, the wrongdoer was the thing we moved over to when we all began abandoning butter for ‘heart-healthy’ margarines! We are consuming too much of something called omega 6. Omega 6 is a polyunsaturated fatty acid that, when metabolised by the body in more than minuscule amounts, actually exacerbates inflammation.

When inflammation arises within the endothelium, the next series of events that can occur are…

Plaque formation

Plaques are the things that form in the blood vessels walls during what is called atherosclerosis. This is what people are referring to when they use the rather crude terminology of ‘furring up’, or ‘clogging’, of the arteries. They are the result of a series of events and knowing some of the stages will allow you to understand those elements of diet and lifestyle that may offer help in the prevention and management of the condition.

The first stage of this process stems from damage to the endothelium, that thin inner skin that lines the blood vessel. This can be susceptible to damage, given the right circumstances. When this damage occurs, circulating materials in the bloodstream – such as cholesterol and fats – can get trapped in the area of damage. Cholesterol that has become trapped in this area suddenly becomes more susceptible to oxidation and damage, due to the array of chemical responses taking place as all this circulatory junk accumulates. When the cholesterol oxidises, it triggers an inflammatory response. This then alerts circulating white blood cells, which move to the site of vascular injury. White blood cells, being what they are, wade in and try to help clean up the mess because, after all, this consistent oxidation of cholesterol can cause untold damage if not managed. So, in order to contain this, the white blood cells begin to swallow up oxidised cholesterol.

When white blood cells do this, they begin to change and transform and become what is known as foam cells. When they have changed in this way, their normal ability to move and circulate disappears and they stay put at the site of injury. This is the first stage of what is termed a fatty streak, or fatty build-up within the blood vessel wall.

As this matures, smooth muscle cells from the muscular walls of the vessel also begin to move into the mass of foam cells and aid in supplying a matrix of fibres that can make this fatty streak more stable. It becomes a collection of fatty material, topped with a fibrous cap that is essentially holding everything in place.

This plaque can sometimes be very stable and lay unaffected in the blood vessel for a whole lifetime. At other times, plaques can be very unstable, meaning that the slightest increase in blood pressure, or increased force on the vessel wall from blood flow, can cause the plaque to rupture, which gives rise to a thrombus. Also, chronic inflammation that has built up over a long time can give rise to the release of enzymes that can break down the fibrous cap, again leading to rupture. When this happens, the next stage is…

Thrombus formation

When atherosclerotic plaques rupture, a blood clot quickly forms around the site of rupture. This can be likened to the formation of a scab when you cut your finger. When damage occurs, the affected area sends out chemicals that activate platelets in the blood. Platelets are known as cell fragments. They are cells without a nucleus and contain much less complicated machinery than most cells in our bodies.

When the platelets are activated, they become sensitive to the effects of different clotting factors. These varying clotting factors come into play, binding platelets together using a fibrous mesh called fibrin. This ends up almost like a layer of netting that holds everything in place.

This clot can grow quite large, sometimes large enough to completely block the blood vessel it is inside. When this happens, the tissue it supplies becomes oxygen starved. Depending on how long this state lasts, the tissue may lose some of its function, or die completely. This is what is known as infarction.

In a heart attack, this occurs in a vessel that supplies blood to the heart muscle. In a stroke, this happens in a vessel that supplies blood to the brain.

Sometimes, the clot forms in a relatively wide blood vessel and is in no way big enough to cause occlusion (blockage) of the vessel. But, with changes in blood pressure and the force exerted on to the blood vessel wall from blood flow, clots (thrombus) can be dislodged. They can then move through the circulatory system.

As the blood vessels get closer to key tissues, they get smaller and smaller and their networks more intricate. As a thrombus moves through this seemingly endless network, sooner or later it will end up reaching a vessel that is just too small to accommodate it, where it will then cause a blockage.

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