Atherosclerosis (hardening of the arteries) is the most common form of arteriosclerosis, a class of diseases in which the walls of a person's artery become thicker and less elastic through deposits along the arteries that often contain calcium.
Atherosclerosis is the leading cause of illness and death in the United States and most other Western countries. It causes about one million deaths per year in the United States alone, double the number of deaths from cancer.
The disease develops slowly. It shows few symptoms until the arteries have narrowed severely or have actually become obstructed.
Fatty material (atheromas or plaque) accumulates under the inner lining of arterial walls, resulting in narrowing and eventual impairment of blood flow. It can affect medium and large arteries in the brain, heart, kidneys, other vital organs, and arms and legs.
Risk factors include male gender, menopause in women, hypertension, elevated levels of low-density lipoprotein (LDL), decreased levels of high-density lipoprotein (HDL), quitting smoking, diabetes, obesity, having a personal or family history of heart disease, sedentary lifestyle, increasing age, high fat or sucrose intake, hyperhomocysteinemia, elevated fibrinogen, CRP and Lp(a) levels, deficiency of Coenzyme Q10 and L-carnitine, air pollution, stress, sleep deficiency, social isolation, high degrees of negative attitudes (such as hostility and cynical distrust), excessive experience of negative emotions (such as depression, anger, and anxiety), and high ratio of free radical markers to antioxidants.
Pain and cramps at the site of the narrowed artery, such as chest pain or leg cramps when walking; a hardened feel, like small, hard pipes, of arteries in forearms or carotid arteries in the neck. Clinical signs and symptoms include aneurysm, thrombosis, embolus, and stenosis; lowered or absent pulses; vascular (blood vessel) bruit (whooshing or blowing sound heard over the artery with a stethoscope); (in more severe cases) muscle atrophy, ulceration, or gangrene.
The doctor will listen for a bruit during a stethoscope examination of the patient's neck, abdomen, or groin area. The sound may indicate turbulence in the blood flow caused by a narrowing of the arteries. He/she will check blood pressure, and estimate blood flow by feeling for pulsations in the wrists, legs, and feet; a decrease in pulsations may indicate partly obstructed blood flow. An ankle-arm index (systolic blood pressure at the ankle divided by the brachial systolic blood pressure in the arm) of less that .9 is a highly accurate quantitative indicator of significant arteriosclerosis.
Laboratory tests that indicate atherosclerosis (or complications thereof)
The doctor will check the blood-sugar level for diabetes and additional tests indicating cardiovascular risk including total cholesterol, LDL, HDL, triglycerides, CRP, Lp(a), fibrinogen, and homocysteine.
Conventional X-rays of the chest and blood vessels provide limited diagnostic information. Ultrasound or computed tomography (CT scan) can help to locate the presence and measure the extent of decreased blood flow. Arteriography of the appropriate organ or limb can locate the site of damage more precisely.
Other Diagnostic Procedures
To some extent, the body will protect itself by forming new blood vessels (collateral circulation) around the affected area. Follow your health care provider's recommendations for treatment and control of hypertension, diabetes, and other diseases.
Nutritional supplements can be very effective and counseling strategies and behavioral techniques help patients to manage stress, move toward more positive attitudes, and establish broader, supportive social relationships. There is increasing evidence that elevated levels of homocysteine may be important in the genesis of atherosclerosis and cardio-vascular disease, and that nutrition can be helpful at modifying those levels.
The final outcome varies, but atherosclerosis is usually progressive and frequently leads to complications that include:
The authors of one study state, "This... study suggests that high hostility levels may contribute to early subclinical atherosclerotic coronary artery disease." According to background information in the study, hostility is a personality and character trait with attitudinal (cynicism and mistrust of others), emotional (anger) and behavioral (overt and repressed aggression) components. [Journal of the American Medical Association. 2000; 283: pp.2546-51]
Numerous studies have confirmed premature, accelerated atherosclerosis in SLE patients. Although the exact cause is not known at this point, atherosclerotic heart disease is a common cause of morbidity and death amongst lupus patients.
Peripheral artery disease is a likely sign of more widespread accumulation of fatty deposits in your arteries: Atherosclerosis of the peripheral arteries is by far the most common cause of peripheral vascular disease.
Tobacco smoke contains more than 4,000 chemicals, more than 50 of which have been identified as carcinogens. These chemicals are extremely damaging to the cardiovascular system. Specifically, these chemicals are carried in the bloodstream on LDL cholesterol, where they either damage the lining of the arteries directly or they damage the LDL molecule which then damages the arteries. High cholesterol levels compound the risks.
Low estrogen levels raise LDL-C (bad) cholesterol, while lowering HDL (good) cholesterol, both of which contribute to atherosclerosis. Supplemental estrogen reduces this risk, at least partially by increasing the HDL particle size which confers some protection against heart disease.
Researchers at Columbia University Medical School found that serum testosterone levels were about 90ng/dl lower in patients who had suffered myocardial infarctions (MI) than in those who had not. These results suggest that low testosterone levels predispose men to MI and are lower in men with severe coronary artery atherosclerotic disease than in controls.
LDL is the cholesterol type most commonly thought of as a strong risk factor for atherosclerosis and heart disease. Oxidized LDL and the fraction called Lp-a produce a greater risk. Since HDL cholesterol reduces the risk, low HDL levels are not desirable.
Multiple studies indicate that 15-30% percent of patients with premature occlusive vascular disease have moderately elevated total plasma homocysteine concentrations. [ JAMA 1992; 268: pp.877-81]
Circulation, the journal of the American Heart Association, reports on a study that has correlated the degree of carotid arterial atherosclerosis with exaggerated response to mental stress in men under the age of 55. Patients whose blood pressure responses to stressful situations were the strongest were found to have significantly more advanced atherosclerosis in the carotid arteries than those whose blood pressure responses were less salient.
Although researchers are careful not to say that stress causes atherosclerosis, the evidence clearly points to cardiovascular reactivity to stress as an atherosclerotic risk factor of the same magnitude as smoking, hypertension, insulin resistance, and elevated cholesterol levels. The hypothesis is that, "Frequent and prolonged periods of elevated blood pressure during mental stress may promote mechanical injury to the endothelial lining or cause release of hormones that can promote the build up of plaque." [Circulation Vol. 96, No. 11: pp. 3842-3848]
Moscow scientists stated in October, 2000 that they have shown atherosclerotic plaques in blood vessels are formed because of adrenaline, a hormone that releases during stress.
Depression is emerging as a risk factor for heart disease. A study of 688 women showed that depression and anger are associated with hardening of the arteries in women, in part through physical and behavioral risk factors such as bad cholesterol levels, obesity and smoking. [Psychosomatic Medicine, March/April 2001]
Experimental studies have demonstrated a correlation between magnesium deficiency and atherosclerosis, but without any clear evidence to determine the mechanisms involved. Magnesium deficiency may affect the atherosclerosis process through several different mechanisms.
While there has been much emphasis on low fat diets, there are some intriguing studies that show that a low fat diet may actually increase LDLs and that it may be more important to alter the fats in the diet, decreasing saturated fats and trans fatty acids, and replacing them with poly- and mono-unsaturated fats. Hydrogenated oils are at least, if not more, atherogenic than saturated fats.
High-potency antioxidant supplements can reduce atherosclerosis in humans. A study involving 11,178 elderly people over a 9 year period showed that the use of the antioxidant vitamin E reduced the risk of death from all causes by 34%. This effect was strongest for coronary artery disease, where vitamin E reduced death from heart attack by 63%. [American Journal of Clinical Nutrition, Aug. 1996]
The vegetarian diet promotes stabilization or possible reversal of the atherogenic process.
Hawthorn is particularly recommended. Proanthocyanadins stabilize collagen to prevent cholesterol deposits on arterial walls, prevent free radical damage, reduce peripheral vascular resistance, angina, cholesterol, and increase coronary and myocardial perfusion; hawthorn has a historic use in congestive heart failure; dosage 3 to 5gm as either dried herb, solid extract, or liquid extract.
Ginkgo (250mg tid) is also recommended. Concentrated extracts may be required to achieve the recommended doses. In addition, a tincture (30 to 60 drops tid) or tea (1 cup tid) of one to four of the suggested herbs, taken before meals, may be helpful.
A mechanism by which atherosclerotic plaque accumulates on the walls of arteries is the oxidation of LDL cholesterol. Garlic has been shown in repeated studies to protect against LDL cholesterol oxidation and oxidation in the linings of the arteries themselves. Garlic, ginger and onions all have a beneficial effect on platelet aggregation which reduces the tendency to form clots too easily, thus preventing the blockage of narrowed arteries.
A low-fat, low-cholesterol diet is recommended, as is an increase fiber (especially water-soluble fibers), fruits, vegetables, and vegetarian sources of protein.
Dosage: 150 to 250mg qid away from meals. Inhibits platelet aggregation and breaks down plaque.
Regular aerobic exercise lowers fibrinogen levels – a risk factor for atherosclerosis of equal or greater predictive value than cholesterol. Additionally, exercise improves the production of nitric oxide within the blood vessel wall, which should limit the progression of atherosclerosis. Exercise improves the fitness of the heart as well as circulation.
Even damage from a history of heavy smoking can be reversed by quitting. The longer the period of time that passes after quitting, the greater the return toward normal vascular health.
Considered to be from 200 to 500 times more potent an antioxidant than vitamin E, selenium and vitamin E are synergistic as antioxidants and inhibit or prevent the damage to tissues by free radicals which have been cited as causal factors in heart disease, atherosclerosis, arthritis and aging. Dosage: 200mcg per day.
Chromium is often deficient in those with atherosclerosis; supplementation may result in plaque regression. Chromium is used to help reduce atherosclerosis, especially in those who show low chromium levels. Cultures with higher tissue levels of chromium also appear to have lower incidences of atherosclerosis and heart disease. Dosage: 200mcg/day.
Mind/body techniques, such as yoga, meditation, relaxation, and biofeedback show promise in increasing cardiovascular health.
Recycles vitamins E and C when they've been used. Dosage: 50mg bid.
Dosage: 1,000mg tid.
Dosage: 400 IU per day.
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