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A User鈥檚 Guide to Understanding Your Cardiologist

If you have ever met with a Cardiologist, no doubt you have heard the terms "arterio" and/or "athero" referred to more than once. So - what do these mean?

When talking about heart disease, you often hear several different terms being bandied about and very often no one actually explains what they mean. So here is a quick cheat sheet to help you understand.

What exactly is the difference between arteriosclerosis and atherosclerosis?

The short answer is nothing. Arteriosclerosis means hardening of the arteries. Sclerosis (蟽魏位萎蚁蝇蟽喂蟼) coming from the Greek word to harden and arterio (伪蟻蟿蔚蟻委伪) obviously meaning artery. Atherosclerosis does have a slightly different meaning. It refers to a hardening of the arteries due to the build-up of plaque. Athero- derives from the ancient Greek word for gruel or porridge, and early anatomists thought that the clogged arteries of patients looked as if they were filled with coagulated porridge. They are in fact clogged with plaque lining the wall of the arties that is a combination of lipids, immune cells, and connective issue that calcified over time.

So arteriosclerosis is a more general term that refers to hardening of the arteries due to any cause, whereas atherosclerosis refers to clogging of the arteries due to plaque build-up. However, for most people plaque build-up is the main reason why arteries harden over time, and the two terms are often used interchangeably.

Is measuring arterial stiffness something I should be doing?

As we age, a few things start to happen. The arteries in our body, both large and small, lose some of their elasticity. Every time the heart beats and pushes blood out into the circulation, the arteries stretch a little to accommodate the pulse of blood and then slowly recoil to keep pushing the blood forward after the heart has relaxed. This is why your blood pressure has two numbers: both a systolic (high) and diastolic (low). As we age and arteries stiffen, they are less accommodating to these jets of blood from the heart and the two blood pressure numbers tend to spread. The higher number gets higher and the lower number gets lower. The difference between these numbers is what we call the pulse pressure. There are ways to get around this, and that involves measuring the mean blood pressure which is one-third of the systolic pressure + two-thirds of the diastolic pressure. Some, but not all machines, give you this number automatically.

So, you can get a quick assessment of your arterial stiffness by looking at your pulse pressure but more formal ways obviously exist. Now your pulse pressure can widen for other reasons like a leaky aortic valve so it is an imperfect marker of arterial stiffness. These involve measuring the pulse wave velocities of blood flow in your arteries and seeing how quickly they strike the walls of the arteries and then reflect backwards. It is fascinating science and often done for research purposes, but not really used in the clinical setting. There are a few reasons for this, but mainly it鈥檚 not entirely clear that measuring arterial stiffness would change the treatment we give patients. We generally advise patients to exercise regularly, stop smoking, eat right, and lower their blood pressure, blood sugar, and cholesterol. We would continue to do that regardless of what arterial stiffness says.

What exactly is endothelial dysfunction and why is everybody talking about it?

The walls of your arteries are made up of three layers: the intima (inner layer), the media (middle layer) and the adventitia (outer layer). The outer layer is connective tissue, which is not relevant to our discussion today. The media is mainly smooth muscle cells that can contract to narrow and widen arteries to regular blood flow. The intima, the inner layer, is what contains the endothelium; the cells that line the interior surface of the artery.

When the endothelial cells do not work properly, hence endothelial dysfunction, there are a number of implications for cardiovascular disease. Although the biology is very complicated, the main mechanism seems to be the disruption of how these cells release nitric oxide, which is necessary for how blood vessels dilate, narrow and regulate blood clotting. Of course, endothelial dysfunction is involved in causing heart attacks, stroke and cardiovascular disease in general.

So what causes endothelial dysfunction? Smoking, diabetes, high blood pressure, and high cholesterol are all involved here so, much like with arterial stiffness, measuring endothelial dysfunction doesn鈥檛 really change what we need to do to treat cardiovascular disease. This essentially involves reducing the cardiac risk factors. So while endothelial dysfunction may be the mechanism by which these risk factors affect the heart, treating these underlying risk factors is still the important thing to do.

While it鈥檚 tempting to get caught up in new terminology, it鈥檚 important to remember the fundamentals. These are often the most important things for improving your long-term well-being. So while it鈥檚 interesting to understand exactly how smoking affects your heart, by promoting inflammation which is associated with endothelial dysfunction which in turn is associated with arterial stiffness, the only thing that really matters is if you stop.

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