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Your heart is an engine and its job is to pump fresh blood to all the organs of your body so that they may remain healthy and function properly. It pumps the blood out through the artery system, which is a branching network of "pipes" which go to every living part of your body. This artery system includes the coronary arteries which bring fresh blood to the heart muscle itself so that it may work as a pump. The harder that your heart needs to work, the more fresh blood it will need.


These arteries provide a route for your heart to distribute crucial "fuel" (important nutrients like oxygen, glucose, etc) to all your body's organs so that they may function properly. The veins then bring the waste material away from the organs ( like carbon dioxide, lactic acid, etc) so that it may be disposed of at the kidneys, lungs or liver. 


Atherosclerosis refers to the concept of arterial “hardening” which may occur in any/or all of the arteries throughout your body. When the arterial hardening becomes significant, and the arteries start to clog up, then that body part will struggle to work properly due to it not being able to get enough fuel to function , and it may even fail. As you will read below, atherosclerosis may occur slowly and cause a progressively worsening blockage or it may occur rapidly (plaque rupture) and cause a sudden blockage.


Your Coronary arteries provide a route for fresh blood and its fuel to be self-distributed within the heart muscle itself. 

Without fresh fuel, your heart would have problems functioning properly, because it is an engine and can't "work for free". 


ANGINA :  When these coronary arteries get partly blocked up with atherosclerosis, a patient may experience chest symptoms during periods of exertion. The idea here, is that when this patient isn't doing very much activity, his heart may be able to function sufficiently despite its blockages, because the heart may not need very much fuel to pump. But, if the patient needs his heart to pump harder (as when playing sports or rushing about), his ability for his heart to get the fuel that it needs may be hampered by these “blocked up” arteries. The worse the blockages get, the more noticeable your symptoms may get with lesser and lesser amounts of activity.


HEART ATTACK :  The above view of atherosclerosis (as a progressive narrowing of arterial tubes) makes sense when we are faced with a patient who is experiencing activity induced angina. But, it doesn’t account for the fact that most heart attacks occur in patients who don't have  significant blockages or even high cholesterol levels. There are many patients who aren’t even recognized as having heart disease until they present with an unexpected heart attack, or even worse, with sudden death. That is why this initial concept of atherosclerosis as a “hardening of the arteries” was an oversimplified view.

Risk Factors are:

  • smoking

  • diabetes or metabolic syndrome

  • hypertension

  • inactivity, obesity

  • sleep apnea

  • stress

  • male gender

  • androgen deficiency

  • estrogen deficiency

  • older age 

  • genetically prone

  • bad cholesterol

  • poor Diet  (“saturated” or “trans” fats)


These may all contribute to a patient’s level of vascular inflammation.

We now think of atherosclerosis as a dynamic and ever changing inflammatory disease in which there appears to be a wide variety of vascular risk factors that may directly cause damage to the vessel walls through the process of:

  • An inflammatory response

  • An immunological response

  • Oxidiative stress

  • Thombosis (blood clotting)


Atherosclerosis  all begins as a stiffening of the inner lining of vessel walls (endothelial dysfunction) which affects the elasticity of the vessels and may be associated with small fatty deposits located within the walls that are called fatty streaks.This may lead to thickening of the inner lining of the blood vessel (intima). This all appears to start at a young age (as early as age 18).  

But, if it is left untreated, the fatty streak may expand into a swollen fatty plaque and with time, this plaque may either :


  1. Continue to expand and slowly block up the artery. With time it may become scarred and/or calcified and will be less and less prone to reverse as it "ages". This type of patient will complain of activity related Angina. 

  2. Become “vulnerable” and burst open or rupture thereby  provoking an intense inflammatory reaction within the vessel wall and its lumen that may threaten to block up the antire artery with a gruel like mixture of fat cells, blood cells and clotting factors. This is how an "unexpected heart attack" may occur.

  3. A comination of both types of plaque may occur in the same patient

How can we detect it before it's too Late?

Most patients at different stages in their lives may have a mixture of scarred, calcified, and vulnerable plaque and usually if the plaque is present in one part of the body, then the odds are high that it is present “all over the place”.  So, you can see why it is a good idea to avoid those risk factors that may cause atherosclerosis to develop in the first place, especially since it is widely believed that the early stages of plaque formation are entirely reversible.


It is a good idea for doctors to identify patients with vascular disease at an early stage, and especially before advanced disease has developed. We have many available tools at our disposal.

Coronary angiogram

This involves the injection of an iodine based dye into the opening of the coronary artery, which allows the cardiologist to view the artery (under Xray guidance) and see the number, location and severity of the blockages. It is the gold standard test and is absolutely necessary prior to heart surgery or angioplasty. It's limitations are that it has some risks (which your cardiologist will discuss with you) and it may not detect vascular disease at its most early stages of developement such as seen with endothelial dysfunction, intima thickening or fatty streaks and early noncalcified plaques.


Stress echo or Stress Nuclear

This involves the use of ultrasound imaging or nuclear imaging while a patient is running on a treadmill, which allows the cardiologist to see if part of the heart is struggling when you are needing it to pump harder. It is not perfect, but, is less invasive than an angiogram and has lower risks. When it is coupled with intelligent decision making, it can be very useful in determining whether or not a person has "significant" coronary artery disease. However, its weakness is that it is imperfect, and incapable of detecting minor (early) blockages.


CT Coronary Angiogram

This is a CT scan taken of your coronary arteries during an injection of iodine contrast dye into a vein in your arm. The advantage is that it is safer than an actual angiogram, due to the fact that the injection is into the arm vein rather than directly into the coronary artery. But, the disadvantage is that it is not as accurate. Some Cardiologists will use this test to help them sort out whether or not a patient has coronary artery disease, when the stress echo or stress nuclear in that patient was not definitive. 


Calcium Score (Agatston)

This is best thought of as a "low dose" CT scan. There is no iodine injection. It simply measures the presence and quantity of calcium in the coronary arteries. Its advantage is that a normal test is very meaningful, especially in older patients. Older patients with vascular disease would be expected to have calcified atherosclerosis, and so, a normal study is a very favorable finding. On the other hand, younger patients with vascular disease would be expected to have fatty (noncalcified) plaque. So, the art of using this test, is in knowing in which patient you can trust it.


Carotid intimal Media Thickness (CIMT)

When atherosclerosis begins to appear in the arterial wall, it doesn't necessarily cause a blockage. In fact, it may often accumulate to a significant degree even without affecting the blood flow at all. This is frequently seen in women with heart disease and they tend to experience symptoms relate to arterial spasm rather than to "blockage". Tests that are usually used in heart patients, like stress echo or stress nuclear, may appear  "normal" in a patient like this despite them having significant vascular abnormalities. The CIMT measure looks at the thickness of the inner lining (intima-media layer) of your artery and is measured at the level of the carotid artery. 


  • When your body's arteries are in the early stages of atherosclerosis, this section will begin the thicken with fat, inflammatory cells, etc. Remember, that when you have begun to develop atherosclerosis, it is very likely that it is occuring throughout your entire body. The carotid artery is an easily accessible artery to do this measurement on,  and provides an excellent opportunity to measure this. CIMT is an extremely useful test, and can help your doctor spot the earliest stage of your atherosclerosis, even before you have developed even minor blockages (let alone calcified lesions). An abnormally thickened carotid intima-media layer is abnormal, and is a warning to you and your doctor that you need to make some very serious lifestyle changes, and possibly even consider cardioprotective medication. But, like all tests, it is important to have it measured by an individual and/or lab  who is very experienced in this technique.

Inflammatory and Genetic markers of Atherosclerosis

It is a good idea for doctors to learn how to identify those patients who are at risk for having a plaque burst before it actually happens. 

This concept of inflammation as the cause of atherosclerosis has led to the discovery of certain inflammatory biomarker blood tests which can be used to predict patients who may be at an increased risk of cardiovascular events (see inflammatory markers of heart diseasegenetic markers of heart disease).


The trick is to figure out which of these markers have the most value as a novel risk predictor and in whom should we be measure them.

hsCRP is one of the best studies inflammatory biomarkers. Its value is recognized and discussed in several association guidelines (most recently CCS 2013). But, there are also many other markers that are being discovered and reviewed, and with time, some of these will be likely used in screening for patients who are at increased risk of vascular events.

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