Atherosclerosis and Heart Disease

Atherosclerosis is a disease process that significantly contributes to the development of coronary heart disease. Not to be confused with Arteriosclerosis which is a hardening and loss of elasticity in the artery wall, this process is characterized by inflammation, fatty deposits along with the formation and accumulation of plaque on the inside wall (intima) of the artery.

Most people are aware these days that certain lifestyle choices such as poor diet, stress and inactivity play a significant role in the onset and development of coronary artery disease...but exactly how does this process work? How do arteries such as your coronary arteries become narrowed and 'clogged'?

Click here to read about how Blood Clots form in your arteries

How do Coronary Arteries Narrow?

The Atherosclerosis process begins with minute damage to the endothelial cells lining the inside of the vessel wall (tunica intima). this damage can occur as a result of exposure to...

• Environmental Toxins; cigarette smoke and oxidative stress-causing synthetic chemicals
  
• Poor food choices containing too few protective compounds and excessive 'bad fats'
  
• Inflammation caused by unbalanced dietary choices
  
• Viruses and bacteria
  
• Physical trauma to the endothelial cells such as can occur during coronary angioplasty and stent implantation
  
• Artery cellular damage caused by radiation therapy to the chest area
  
• Hypertension; causing hardening and fibrosis of artery walls
•  Negative emotional stress causing free radical formation and blood pressure abnormalities

Coronary Angiography is a routine test to look for the presence of narrowed and blocked areas in your coronary arteries

As you will be aware from having a scrape or cut on your hand, any damage to your skin cells is followed by an inflammatory response which initiates the process of healing and renewal. The renewal process usually lays down replacement tissue that is not identical to the tissue you had before your injury...this new tissue is called scar tissue. In the same way as your skin reacts to an injury...leaving a scar behind as a reminder of your accident, the delicate endothelial layer of your coronary arteries (and other arteries) also react similarly to any assault or injury.

The 'Problem' with the Healing Response

As soon as an injury occurs to the endothelium of your coronary arteries, white blood cells...Monocytes (which later become Macrophages)...travel to the damaged area acting as scavengers at the injury site to pick up dead and dying cells, bacteria or debris which have resulted from the injury.

The presence of the monocytes coincides with the onset of the inflammation process, (a natural process...but you don't want this to occur in your coronary arteries) which in turn encourages more monocytes to show up on duty.

Normally, the monocytes...turned macrophages...would migrate away from the injury site after scavenging...but abnormally high blood levels of a certain type of cholesterol called LDL cholesterol, often referred to as 'bad cholesterol' can encourage the macrophages to clump together.

Cholesterol Cholesterol is a very important natural substance that is meant to be present in your body in normal amounts...even so called 'bad cholesterol'. Bad Cholesterol is not bad as such. LDL Cholesterol has very important functions to fulfill in the body, namely to help build your hormones and build and repair damaged cellular membranes, however the presence of higher than normal levels and the process of oxidation of the LDL molecules is thought to impact normal body processes and contribute to the Atherosclerosis process. In an individual with a normal healthy cholesterol ratio, HDL cholesterol...often referred to as 'good cholesterol' is in plentiful supply in the blood stream. HDL cholesterol provides the mechanism by which excess LDL cholesterol is cleared away. This is why in your cholesterol results a high HDL and a low LDL is thought to be favorable.

LDL cholesterol to the 'Rescue'

When you suffer coronary artery inflammation and injury, LDL molecules 'enquire' of the damaged area via the process of cellular communication how much cholesterol is needed to repair the cellular damage in the artery wall. Once this is established, the LDL molecules transport the cholesterol to the site of injury to help with the repair process.

Excessive amounts of LDL Cholesterol and Triglycerides (which are also transported by LDL molecules) can oxidise...or turn 'rancid' when you have insufficient blood levels of antioxidants present to neutralize the oxidation process. This oxidation can damage the neighbouring cellular structure of the artery and also attract monocytes (white blood cells) to the injured area.

The Monocytes 'stick-to' the injured area of the artery wall and then begin to migrate through the first layer of the artery (endothelium) becoming Macrophages in the process.

Defective cellular communication and high blood levels of LDL cholesterol can lead to an over-supply of LDL cholesterol to the injury site, causing the macrophages to become overwhelmed as they try to ingest the oxidised cholesterol. This forces them to clump together and become Foam Cells. Effectively the macrophages have over-eaten, losing their scavenging ability in the process.

Fatty Streaks

Smooth muscle cells from the middle layer of the artery (tunica media) join the 'clumped' macrophages and also become foam cells due to the presence of the oxidised LDL cholesterol. This accumulation of foam cells causes Fatty Streaks to form in the wall of the artery.

Atherosclerotic Plaques

The smooth muscle cells also lay down collagen and elastin fibres which begins to thicken the inside wall of the artery (tunica intima) and produce fibrous lesions. These lesions contain dead and dying foam cells which are given the name Atherosclerotic Plaques.

As this process continues, the fibrous lesions can grow into the artery lumen...the 'free space' where the blood normally flows and start to affect normal blood transport. Atherosclerosis can start to become symptomatic as the blood supply is reduced to the down-stream tissue.

If the passage of blood continues to be hindered at the injury site, death to the blood vessel cells can occur as they become starved of vital nutrients and oxygen. The affected vessel becomes more and more rigid over time as healthy endothelial cells that line the artery wall begin to die and are replaced by a fibrotic and hardened cell structure.

Vicious Cycle

As the blood vessel becomes more and more rigid...its normal elasticity lost, the pressure required to push blood through that vessel increases which in-turn causes yet more damage to the vessel wall...more damage means renewed sites of injury, inflammation, monocyte/macrophage migration and LDL cholesterol showing up to help repair the damage...and so the Atherosclerosis cycle continues.

Click here to go from Atherosclerosis to Causes of Coronary Heart Disease

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