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Aging Changes In The Heart And Blood Vessels

The "aging process" causes specific cardiovascular changes. This leads to reduced physical and mental ability. Aging is also a risk factor for cardiovascular disease. Scientists a have learned great deal about the interaction of aging with cardiovascular disease related changes and have identified risk factors for both heart and vascular aging, and heart disease.

 

The "aging process" causes specific cardiovascular changes. This leads to reduced physical and mental ability. Aging is also a risk factor for cardiovascular disease.

 

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The Atherosclerotic Process

With advancing age, as the above changes are occurring within the blood vessel wall, other "intruders" enter into the battle. These "intruders" are constituents of the atherosclerotic process, which has some aspects in common with the aging process. However, unlike the aging process within blood vessels per se, atherosclerosis includes cholesterol accumulation and recruitment of other blood cells to join the battle; these are called inflammatory cells.


Atherosclerosis is so common in older persons (at least one out of two persons over sixty five years of age has atherosclerosis) that some experts had previously thought it was part of the "normal aging process". An alternate view is that atherosclerosis is a disease process that takes advantage of the previously discussed changes that occur within the artery with aging. The vascular aging process and the atherosclerotic process become intertwined as we age, and they influence each other. The more severe your vascular aging process, the easier it is for atherosclerosis to take hold; the more severe your atherosclerosis, the bigger its impact on vascular aging. Thus, it appears that the atherosclerosis process and the aging process combine forces to enable the disease called atherosclerosis to be more visible and more severe in older persons.


Atherosclerosis begins with changes in endothelial cell function that cause white blood cells moving through the blood to stick to the endothelial cells instead of flowing by normally. The barrier normally formed between endothelial cells and the blood becomes weakened and both blood cells and substances circulating in the blood pass through the endothelial cell barrier to join the battleground in the vessel's sub-endothelial space of the intimal compartment. Lipid or fat cell-like substances such as cholesterol in the blood then accumulate there. The lipids become "oxidized" and this enables them to signal the endothelial cells, which then alert others that the battle has begun.

 

Smooth muscle cells that react to endothelial cells and to the fatty infiltration then join in. The smooth muscle cells march from their normal residence in the vascular media and invade the basement membrane by secreting enzymes, which attack the protein in the membrane. Depending on an individual's risk factors (life variables such as a poor diet, lack of exercise, smoking, high blood pressure and the aging process itself) fat accumulation continues and the atherosclerotic process accelerates. White blood cells called macrophages then enlist in the battle and invade the area to digest the fat. Vascular smooth muscle cells that are resident in the intima and that have already changed their nature also scavenge the fat. These fat-laden white blood cells and vascular smooth muscle cells become known as "foam cells". Vascular smooth muscle cells also try to curtail the injury by producing collagen, which forms a cap over the injury site. This fibrous cap is a weapon against disaster, just like scar formation in a wound. Then calcium accumulates and forms a material resembling bone. This complex array of foam cells, calcification, and lipid accumulation it is called an "atherosclerotic plaque". This plaque grows and becomes similar to an armed bomb. As the war progresses the fibrous cap weakens and ruptures due to the action of enzymes called proteases. The plaque cap can explode or rupture, thus exposing the plaque contents to the blood.

 

The "detonation" gives the signal for the "special forces". These are blood cells called platelets. The platelets accumulate, resulting in a blockade, or blood clot on the inner surface of your blood vessel wall. This clot called a "thrombus" can become surprisingly large and occlude the vessel. By this mechanism of rupturing, even small plaques can interfere with blood flow.


Alternatively, atherosclerotic plaques can enlarge to such a degree as to completely block blood flow. When blood flow within an artery is severely compromised by either a larger plaque or a thrombus or both, the cells of  organs that depend upon blood flow from that artery becomes damaged or die. This is similar to an enemy cutting off your food supply. Coronary atherosclerosis cuts off the heart's blood supply by occluding the heart's arteries and thus stopping the oxygen supply to the heart, causing a heart "attack" or myocardial infarction. A stroke results when the atherosclerosis processes cut off the oxygen supply to the brain.

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