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This week, I thought I’d talk about a disease that many Americans will face in their lifetime: cardiovascular disease (CVD). CVD killed an estimated 900,000 Americans last year, so it’s something we have to be familiar with. CVD could be a forever-long post, and all the science and medical mumbo-jumbo would probably cause the average person (aka. my wife) to keel over. So I thought I’d break it up and start with the disease atherosclerosis because it’s pretty much what starts CVD.

Now to understand the pathogenic process of the disease, I think it’s important to establish the “normal” artery. Blood vessels have three layers in them: the tunica intima, the tunica media, and the tunica adventitia (tunica externa). Normally, arteries regulate the diameter of their lumen by the contraction or relaxation of the smooth muscles in the vessels. This is one of the factors controlling blood pressure.

Image Credit: www.arteryplaque.com

In atherosclerosis, the endothelial cells of the intima are injured. This can be caused by factors like hyperlipidemia, hypertension, toxins, and/or inflammation. With this injury, the body responds by forming a clot via platelets. It’s typically a common thing in the body to form clots in arteries, but excessive injury leads to excessive clot formation, but not before the injury. Then, lipids (fats) start to pass through the intima and collect in the media layer. A type of white blood cell, macrophages, enter the media layer and ingest the fats, thus becoming foam cells. This begins to cover this now swollen layer of foam cells and starts to obstruct the artery, thus starting a vicious cycle of more turbulence in the artery, causing more injury, causing more clotting, and forming what’s called a thrombus.

Eventually, that thrombus will break off from all the pressure built up behind it and continue down the artery until the artery starts to get smaller (leading to the capillaries) and blocks the rest of the circulation. This leads to lack of blood and oxygen getting to tissues and forces the heart to work harder, but it can only do that for long before it fails.

The best form of treatment for this is the prevention of it happening: lowering the rates of Type 2 diabetes, smoking, and over consumption of alcohol. The drug treatments include combinations of statins, niacin (aka. vitamin B3), and intestinal cholesterol absorption-inhibiting supplements (like ezetimibe). Vitamin B3 in pharmacological doses (generally 1,000 to 3,000 mg/day) tends to improve HDL (good cholesterol) levels, and change the composition of LDL that can lower the subset of LDL linked with atherosclerosis. Always consult your doctor if you have a family history of CVD or if you have any concerns about these conditions. They should get you on a good lifestyle change, which is ultimately what you need, but it could be paired with statin drugs or combination therapy in severe cases.

Image Credit: dr gil frias

Above is a pretty decent model of atherosclerotic plaque in an artery. Not a pretty picture.

Before I wrap this up, I just want to stress that your circulatory system is linked directly with a lot of systems in your body that you need in order to live: lungs, brain, kidneys, etc. I’ll go into the links of CVD with those organs as well, but I’ll let you recover from this post first.

So this was the basics of atherosclerosis. Moral of the story is that you should avoid excess plaque build up in your arteries. Remember, what you eat goes through your blood before you get the Buddha belly, so eat and stay healthy.

Image Credit: kathy789

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Tags: atherosclerosis, cardiovascular