Time to get Smart with your Heart

It really is time to get smart with your heart. Cardio Vascular Disease is a big deal. It kills annually 18 million people a year, almost the entire population of Australia. A year! It is the biggest killer worldwide, accounting for 31% of all deaths; most of which are preventable.

But what causes Cardio Vascular Disease? Atherosclerosis is the major contributor responsible for the cases of cardiovascular disease in the world, for developing and developed countries alike.

The exact cause of atherosclerosis is unknown but there are several known risk factors which are listed in the table below.

Risk Factors for Cardio Vascular Disease.

Irreversible Male
Increasing age
Genetic/ Family traits
Body Build – Apple higher risk to Pear shapes
Potentially reversible
High cholesterol – Total cholesterol and LDL cholesterol
Physically inactive
High blood pressure
Unhealthy diet
Stressful situations
Coronary prone behaviour patterns : Type A


Atherosclerosis is a disease in which plaque builds up in arteries. This occurs through  repeated exposure to circulating factors in the blood such as LDL cholesterol and saturated fat.

What is atherosclerosis?

Well it looks like this.

This is similar to brushing our teeth. When we eat unhealthy foods we get a furry fuzzy feeling on our teeth which is the buildup of plaque. In the morning and at night we brush our teeth and this is the cleaning mechanism to remove the plaque.

But within the body, with many many years of exposure to such things as unhealthy eating habits, high blood pressure, smoking, extra weight and the like, the body cannot continue to ‘clean’ at such high intensity and so plaque begins to build up in the arteries.

Atherosclerosis develops in 4 key stages:

Stage 1 – Initial Lesion

To begin, the arteries transport oxygen enriched blood to the heart which is then transported around the body to fuel all movements necessary for life. The arteries have a smooth inner lining, making it easy for red blood cells to pass through undisturbed when performing this essential role.

But over time and many years, with poor diet and poor habits, little lesions occur in the smooth lining of the artery. Once it’s damaged, LDL cholesterol particles, also traveling in the blood can get into this lesion and bury into the wall of the artery.

Hang on.. LDL cholesterol? LDL stands for Low Density Lipoprotein. Cholesterol is a type of fat. But water and fat don’t mix. To solve this problem and to allow the transport of fat through the bloodstream, cholesterol (and other fats) are packaged into particles called lipoproteins, of which LDL-cholesterol is only one type.

Stage Two – Under Attack: Release the Macrophages

Once the LDL cholesterol enters into the cell wall, the body sees this as an attack and tries to defend this by activating macrophages to consume the LDL cholesterol. Macrophages are a type of white blood cell which engulfs and digests foreign particles and thereby protects the body.

These macrophages, large and full of LDL cholesterol, are then termed foam cells which are imbedded in the artery wall. These foam cells over time accumulate and can be seen in scans as yellow fatty streaks in the artery walls.

Sadly, this can be seen in children as young as 10 years old…

Stage Three – Build a Wall

As the fatty streaks continue to grow in size with time, the body tries to protect the artery and smooth cells surround the fatty deposits, creating a fibrous capsule that will thicken with time. At this stage the growth is called a plaque.

Over time the plaque may continue to expand, eventually intruding upon the inner opening of the artery. At this stage the artery cannot stretch enough to preserve the blood flow to the rest of the body, leading to a buildup of pressure.


Stage Four – Eruption

The pressure of blood flow through such a tight gap causes damage to the fibrous capsule covering the plaque, resulting in a rupture. This rupture exposes the cholesterol and tissue underneath. The body reacts as it would to a cut on the finger and forms a blood clot which can then completely block the artery.

The symptoms will correspond to with where this occurs in the body. In the chest area, blockage of the arteries can result in chest pain, known as angina and eventually a heart attack. In the brain, starvation from oxygen can result in strokes or TIA. Cramping is experienced in the legs, a condition known as intermittent claudication.

In other cases, atherosclerosis can cause the integrity of the artery wall to weaken and bulge under the pressure of blood flow. This is called an aneurysm and if the condition of the artery worsens, it can rupture and the resulting hemorrhage could be fatal.


All of us will experience heart disease at some point in our lives, whether ourselves or the people we most care about. My mum experienced a heart attack in her 50’s. Starting off as irregular chest pains during work, overtime the arteries could not cope and she passed out.

Luckily, she was rushed to hospital in time and is alive today. Since then she has quit smoking, opted for a vegan lifestyle during weekdays and walks to keep active. I am thankful for these changes, but sadly, many people don’t make them until it’s too late.

Do you have any stories you wish to share of heart disease, the good and the bad? Please feel free to do so in the comments below.

Over the coming week I will be posting about how a vegan diet helps to prevent cardio vascular disease. We’ll also explore the difference between ‘good’ and ‘bad’ cholesterol.




Heart Foundation – https://www.heartfoundation.org.au/your-heart/know-your-risks/risk-factors

Word Health Organisation – http://www.who.int/cardiovascular_diseases/en/

Australian Bureau of Statistics – http://www.abs.gov.au/ausstats/[email protected]/Lookup/by%20Subject/4364.0.55.001~2014-15~Main%20Features~Heart,%20stroke%20and%20vascular%20disease~13

National Heart, Lung and Blood Institution – https://www.nhlbi.nih.gov/health/health-topics/topics/atherosclerosis


Barth, J. D., & Arntzenius, A. C. (1991). Progression and regression of atherosclerosis, what roles for LDL-cholesterol and HDL-cholesterol: a perspective. European heart journal, 12(8), 952-957.

Badimon, L., & Vilahur, G. (2012). LDL‐cholesterol versus HDL‐cholesterol in the atherosclerotic plaque: inflammatory resolution versus thrombotic chaos. Annals of the New York Academy of Sciences, 1254(1), 18-32.


Essentials of Human Nutrition (4th ed.) by Jim Mann and Stewart Truswell

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