It usually starts with a condition called atherosclerosis. In simple terms atherosclerosis is a narrowing of the arteries due to the build up of plaque.
How does this happen? To use the scientific lingo, what is the aetiology of atherosclerosis?
The short answer, as I discovered to my surprise, is that we do not yet know the full story. I shall now summarise what we do know.
To understand the aetiology of atherosclerosis you need to stop thinking of arteries as simple pipes through which blood flows. As this Encyclopaedia Britannica graphic demonstrates, arterial walls have a complex layered structure.
The innermost layer is called the endothelium. It comprises a single layer of epithelial cells. These provide an even, low-friction inner surface which facilitates the smooth flow of blood.
The next two layers, moving outwards, comprise connective tissue and the inner elastic membrane.
The endothelium, the layer of connective tissue and the inner elastic membrane together form the “tunica intima” or just plain “intima.” It is here, inside the intima, that a process leading to the formation of atherosclerotic plaque seems to start.
In broad outline here’s what happens. Recall those invaluable trucks, the LDL particles, that ferry cholesterol and triglycerides to where they’re needed in the body. The LDL particles are constantly darting in and out of the intima. The higher the concentration of LDL particles in the blood, the more likely some are to enter the intima.
Sometimes an LDL particle will get stuck inside the intima. Usually this does not matter. An HDL particle will come along, suck out any cholesterol jammed inside the intima and transport it to the liver for recycling or disposal. If for some reason that doesn’t happen we get an accumulation of cholesterol and triglycerides inside the intima.
The LDL particles and their contents accumulating in the intima undergo chemical changes. Specifically their contents, those cholesterol molecules and triglycerides, are oxidised while their proteins are both oxidised and glycated.
For reasons that are not fully understood cells in the arterial wall interpret these chemical changes as a threat and trigger the body’s immune response. What happens then is complicated but the end result is the emergence of an atherosclerotic plaque. You can think of a plaque as a little boil or pimple protruding into the bloodstream with its roots inside the arterial wall. A fibrous “cap” walls off the contents of the plaque from the bloodstream.
In most cases, so long as the plaque is stable, there are no adverse consequences. Occasionally a plaque may grow so big that it significantly constricts the flow of blood. If this happens in the coronary arteries the result may be angina pectoris.
Sometimes, perhaps due to inflammation, the cap of the plaque disintegrates exposing all the detritus inside the plaque to the bloodstream. When that happens a clot forms. If the clot is small and the artery wide enough it will dissolve before any harm is done. Sometimes, however, the clot will completely block an artery. If that happens in a coronary artery the result is a myocardial infarction.
Recall that your heart is a muscular little pump that needs lots of oxygenated blood and nutrients. Any part of your heart muscle that is deprived of its blood supply due to a blockage in a coronary artery quickly dies. Once dead it is gone forever. Heart muscle does not regenerate.
And that, in a nutshell, is how most heart attacks occur.
