After infiltrating the artery wall, LDLs are oxidized, or converted to harmful forms that are toxic to endothelial and smooth muscle cells, thus further damaging the artery lining.
The risk factors for cardiovascular disease have been categorized by the american heart association (AHA) as follows: Major risk factors that cannot be changed (increasing age,
male gender, and heredity) Major risk factors that can be changed (elevated blood cholesterol levels, high blood pressure, cigarette smoking, and physical inactivity Other contributing factors (obesity, diabetes, and stress). Major Risk Factors That Cannot Be Changed Age Approximately 55% of all heart attacks occur in people who are 65 years of age or older. This age group accounts for more than 80% of the fatal heart attacks. Male Gender Until recently, the incidence of coronary heart disease among women has been largely unexplored. Men have been the primary subjects in the coronary heart disease and risk factor studies because of the high incidence of both among men. However, coronary heart disease is also the leading cause of death and disability among women, accounting for almost 250,000 deaths annually. Women have less heart disease than men, particularly before menopause. The reasons for the difference include the following: The female hormone estrogen protects the coronary arteries from atherosclerosis Women have higher circulating levels of high density lipoprotein (HDL) cholesterol, which also protects the arteries. After menopause, though, the heart attack rate among women increases significantly until the mid-60s, when women's risk is equal to that of men the same age. An alarming trend in recent years is the increased incidence of heart attacks in premenopausal women who have been smoking cigarettes long enough for it to affect their health, especially when combined with oral contraceptive use. Heredity According to the AHA, "A tendency toward heart disease or atherosclerosis appears to be hereditary, so children of parents with cardiovascular disease are more likely to develop it themselves." A history of first degree male relatives (father, grandfather, and brothers) who died of coronary heart disease before the age of 55 or first degree female relatives (mother, grandmother, and sisters) who died of coronary heart disease before the age of 65 indicates a strong familial tendency. If the family history is positive, the modifiable risk factors must be controlled. Major Risk Factors That Can Be Changed Cholesterol Cholesterol is a steroid that is an essential structural component of neural tissue; it is used in the construction of cell walls and for the manufacture of hormones and bile (for the digestion and absorption of fats). A certain amount of cholesterol is required for good health, but high levels in the blood are associated with heart attacks and strokes. The AHA suggests that Americans reduce cholesterol consumption to less than 300 milligrams per day (300 mg/day), that fat intake be reduced to a maximum of 30% of the total calories consumed, and that saturated fat be reduced to no more than 10% of the total calories. Many authorities are convinced that limiting total fat and saturated fat is more important than being overly restrictive of cholesterol. Americans have made substantial progress in reducing cholesterol consumption. The average cholesterol consumed by men and women respectively in 1960 was 704 mg/day and 493 mg/day. By 1994, How LDL cholesterol contributes to coronary artery disease is not completely understood, but the "lipid oxidation theory" appears to have the support of the scientific community. According to this theory, LDLs do not latch on to the artery linings, depositing the cholesterol that eventually forms plaque. Instead, high circulating levels of LDL in the blood stimulate the cells beneath the artery lining to transport the LDLs into the artery wall. This process is facilitated when artery linings are damaged by any one or a combination of the following: cigarette smoking, high blood pressure, diabetes mellitus, viruses, and other toxic substances. After infiltrating the artery wall, LDLs are oxidized, or converted to harmful forms that are toxic to endothelial and smooth muscle cells, thus further damaging the artery lining. This process triggers the body's immune system, which responds by sending white blood cells, called monocytes, that also penetrate into the inner layer of the artery. The monocytes turn into macrophages, which engulf oxidized LDLs in an effort to protect the artery from further damage. The macrophages become bloated from gobbling up LDLs, and in this condition they eventually develop into foam cells. Foam cells in turn stimulate the smooth muscle cells in the affected arteries to grow in size and number. This adds to the thickness of the artery walls. Concurrently, blood platelets congregate at the sites of disease, further adding to the thickening process. The culmination of these events results in the development of fatty streaks in the arteries. This is an initial sign of coronary artery disease. Some of these streaks develop into atherosclerotic plaques, which are the lesions that define diseased coronary arteries. In some instances the cells lining the artery flake off or retract, exposing the foam cells lying beneath. Once again, the body attempts to repair the damage, but the restoration process causes the wounded artery to scar down as a fibrous plaque. This represents a later-stage lesion in the development of atherosclerotic plaque. Lesions grow over time by accumulating fibrous tissue, cholesterol, and other debris from the blood stream. Concomitantly, the channel narrows severely, diminishing blood flow to the myocardium. At this point the lesion has progressed to a mature plaque. Finally, further damage to the artery wall may cause either a blood clot to develop or bleeding to occur into the core of the plaque, or the artery may go into spasm. Any of these events can abruptly interrupt or block the flow of blood to a portion of the heart muscle, resulting in a heart attack. Heart attacks are rare when LDL values in the blood are below 100 mg/dl. A national panel of experts has developed guidelines for safe and unsafe levels of LDL. A high circulating level of LDL cholesterol is positively related to cardiovascular disease. Weight loss, a diet low in saturated fat and total fat, exercise, and medication (if needed) will lower LDL levels in the blood. HDLs are involved in reverse transport; that is, they accept cholesterol from the blood and tissues and transfer it to VLDLs and LDLs for transport to the liver, where it can be degraded, disposed of, or recycled. HDLs protect the arteries from atherosclerosis by clearing cholesterol from the blood. Cardiovascular health depends greatly on low levels of total cholesterol and LDLs and a high level of HDLs. Cigarette smoking, diabetes, elevated triglyceride levels, and anabolic steroids lower HDL, whereas physical exercise, weight loss, and moderate alcohol consumption raise it. Moderate alcohol consumption (two drinks or less per day) increases HDL cholesterol levels. An alcoholic drink is defined as a 5 ounce glass of wine, or a 12 ounce beer, or 11/2 ounces of 80 proof spirits. However, alcohol is a depressant that is responsible for nearly 50,000 traffic deaths annually and contributes to one third of all drownings and boating deaths. Alcohol impairs judgment and removes inhibitions so that people under its influence behave in ways they ordinarily would not while sober. Alcohol consumption is not an acceptable way to raise HDL cholesterol. The higher the HDL, the greater the protection from cardiovascular disease. The average value for men is 45 mg/dl, and for women it is 55 mg/dl. This biological difference in HDL levels between genders partly explains the lower incidence of heart disease in premenopausal women as compared with men. After menopause, HDL levels in women begin to decrease, as does their protection provided by this subfraction of cholesterol. The ratio between total cholesterol (TC) and HDL (TC/HDL) should also be considered when the risk is interpreted. This ratio is determined by dividing TC by HDL. Another blood fat, the serum triglycerides, is involved in the development and progression of atherosclerosis. Average serum triglycerides, depending on age and gender, range from 50 mg/dl to 200 mg/dl. Elevated triglycerides may not directly cause atherosclerosis, but they often accompany and add to the severity of other blood fat abnormalities. For example, high triglycerides tend to be accompanied by low HDLs, high LDLs, and high total cholesterol. This profile is predictive of the development of atherosclerosis and coronary heart disease. A number of studies have shown that sedentary hypertriglyceridemic people can reduce serum triglycerides by as much as 45% when they participate regularly in moderately intense exercise. Physically fit people metabolize serum triglycerides more effectively than sedentary people and are able to clear them from the blood more rapidly after a high-fat meal.
