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Cardiac and arterial aging 68

They say we are only as old as our arteries, and, with few exceptions, this is true!

The most tragic aspect of cardiovascular diseases, and heart attacks in particular, is their brutality! One minute everything seems fine, the next we are overcome with pain, we panic, even worse, we die suddenly, without warning. Our arterial networks take years to age and can remain silent for a long time, without exhibiting any clinical symptoms. There are occasional warning signs of course, pain which flares up during physical exertion… But we often blame it on the physical effort itself.

Although the term ‘cardiovascular’ is often used, it is important to understand that the vascular system is the first to deteriorate, shutting off blood flow and depriving the body of oxygen, and leading to kidney, heart or brain damage.

The more we age, the more our arteries harden: this is what we call arteriosclerosis. But this hardening is often accompanied by cholesterol plaques which cling to the walls of the blood vessels. When this happens, as is most often the case, it is called atherosclerosis or atheromatous disease. Vascular walls are made up of several layers of cells. The first to be damaged is the one in direct contact with the blood stream, which is made of endothelial cells. These cells weaken with time and progressively lose the ability to synthesize collagen and elastin, two substances which are essential to arteries’ flexibility. They become more and more rigid and less and less able to react to the heart’s constant requests for them to expand or shrink depending on our body’s oxygen needs. As damage accumulates, every layer of the arterial wall becomes inflamed, leading to scarring which will serve as an anchor point for cholesterol. It will continually deposit itself until it completely plugs the artery’s lumen; circulation is then partially or completely stopped and oxygen and nutrition is no longer transported downstream. If this plumbing issue takes place in the renal arteries, it leads to kidney failure; in the coronary arteries (those which irrigate the heart), it leads to heart attacks, the severity of which will depend on the degree of obstruction; in the carotid arteries, it leads to strokes (Cerebrovascular Accidents or CVAs), resulting in the paralysis of the limbs on the side of the body opposite the damage, with or without aphasia (speech impairment). Our organism has however designed a cholesterol cleanup system, which we can measure via HDL (High Density Lipoprotein) blood levels, but it unfortunately also has a system which promotes cholesterol accumulation, measured in LDL (Low Density Lipoprotein) blood levels.

Hypertension is another consequence of arterial wall rigidity, and is assessed via two components. Systolic pressure, which reflects pressure variations during peak cardiac contraction; this value isn’t constant as it is influenced by stress, anxiety, whether we are standing or sitting, physical activity and many other factors. Diastolic pressure reflects how our heart behaves when it refills with blood; it is more stable and a better indicator of our arteries’ condition. Arterial pressure is measured with a sphygmomanometer or blood pressure monitor, the normal range being between 120 mm and 140 mm of mercury for systolic pressure and between 70 and 90 mm of mercury for diastolic pressure (these values vary from country to country).


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