Although testing can be valuable in detecting existing blockages in your coronary arteries before sudden death, angina pectoris, or a heart attack occurs, ideally you should try to prevent blockages from forming in the first place. This why it is important for you to understand how Atherosclerosis develops, and what factors accelerate it. Even if you already have coronary heart disease and have had coronary artery bypass surgery, you will want to decrease the chance that the blockages will return.
Coronary heart disease results from the gradual development of Atherosclerosis in the coronary arteries. The term Atherosclerosis comes from the greek atheroma, meaning porridge, and skleros, meaning hard. At birth our coronary arteries are completely open, no blockages are present, and blood flow is unimpaired. Between the ages of 10 and 20, small deposits of lipid, called "fatty streaks," beginning to appear in the lining of the coronary arteries. Over time, some fatty streaks change gradually into larger deposits, called "fibrous Plaques." As the fibrous plaque forms, it protrudes into the opening of the coronary artery.
These early stages of Atherosclerosis progress slowly through the teen age years and through the twenties and thirties, but by age 45 or 50 many people in our society have more advanced Atherosclerosis that may lead to coronary heart disease. If you have risk factors or have inherited a genetic problem in processing fat in your body, you are much more likely to have Atherosclerosis. The same factors may accelerate the early deposits of fatty streaks in the coronary arteries of your children.
Atherosclerosis has afflicted many populations throughout the history of mankind. For example, it has been found in Egyptian mummies, but not all mammals are not susceptible to this disease. rats and dogs are quite resistant, at least partly because most of their blood cholesterol is in high density lipoproteins (HDL), the "good" cholesterol. In contrast, humans carry most of their blood cholesterol in low density lipoproteins (LDL), which promote atherosclerosis. When animals consume diets rich in cholesterol or saturated fat, those that are intolerable, such as some nonhuman primates and rabbits, develop Atherosclerosis; those that are resistant, such as dogs and rats, do not.
The relationship between cholesterol in the diet and Atherosclerosis was first observed in rabbits in 1908 by a Russian pathologist name Ignatowsky. Later studies of nonhuman primates demonstrated the direct relationship between cholesterol and saturated fat in the diet, cholesterol level in the blood, and the development of Atherosclerosis.
Can The Process of Atherosclerosis Be Reversed?
The answer is yes. Studies have shown that when the level of cholesterol in the blood of nonhuman primates is lowered by diet or drugs, the deposits of Atherosclerosis in their coronary arteries become smaller. A study has also shown this to be true in humans.
In the 1960s, medical researchers established that not all countries had the same amount of Atherosclerosis in their populations. The international Coronary Heart Disease and Atherosclerosis project studied people in 14 different countries. Arteries from 22,509 people who died between the ages of 10 and 69 years were examined under the microscope. In his book Geographic Pathology Of Coronary Heart Disease and Atherosclerosis DR. Henry McGill ranked twelve of the four populations according to fat intake, blood cholesterol level, and Coronary Heart Disease and Atherosclerosis. He found a direct and highly significant relationship between these factors; locations with greatest amount of Coronary Heart Disease and Atherosclerosis, such as the United States and Norway, had significantly higher average blood cholesterol levels and a significantly greater fat consumption.