The Conversation – 21st July 2017
Heart disease is among the leading causes of death globally and imposes a significant burden on the health-care system. We know some of the causes of heart disease: smoking, unhealthy diet, obesity, high blood pressure, diabetes and genes.
But there are also a lot of people who die from heart disease who don’t have any of these risk factors. Studies are trying to find out why, and it appears the immune system and inflammation in the body could be to blame.
The most common type of heart disease is coronary artery disease, which affects the blood vessels of the heart. Coronary artery disease is mainly caused by blockages that affect blood flow to the heart muscle, which interrupts the supply of oxygen and other important nutrients.
The most common cause of this blockage is the build-up of fatty molecules called lipids (which largely consist of cholesterol) leading to plaque forming inside the vessels, and swelling (inflammation) within the walls of the blood vessels. This process is called atherosclerosis.
These plaques don’t usually cause any symptoms for the first few decades, until there is significant narrowing of the vessel or there is disruption of the plaque surface (a piece of the plaque breaks off, causing a blood clot) which leads to a heart attack.
Recent evidence suggests cholesterol crystals in the plaque that builds up in atherosclerosis trigger the release of molecules from the immune system. These molecules cause inflammation and promote blood vessel injury and plaque instability, leading to heart attacks, strokes and death.
Immune cells have receptors that serve as sentry guards. They sense various potentially harmful molecules (such as foreign proteins, cell debris or damaged DNA), then send out molecules (like soldiers) to remove these “threats”. The strength of this response can be heightened as a result of a person’s genes – as is the case in some autoimmune diseases. READ MORE AT: https://theconversation.com/how-our-immune-system-causes-heart-disease-78532?utm_source=twitter&utm_medium=twitterbutton