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cardiovascular system
atherosclerosis
diagnoses

definition and etiology

definition:
Intimal thickening of one or many arteries due to localized accumulation of fatty material (atheromas).

etiology:
There are several types of arteriosclerosis, the global term for formation of atheromas in the arteries. Atherosclerosis is the most important kind of arteriosclerosis. Atherosclerosis sequelae are the major cause of mortality from illness in the U.S. (at least 33%). The disease seems to favor blood vessels of high importance (cardiac, kidney, cerebral), and the peripheral arteries (causing much morbidity). The mechanism of atheromatous development is still theoretical, but suggests that injury to the lining of the blood vessel from turbulence, hypertension, hypoxia, hyperglycemia or free radicals causes smooth muscle cells to proliferate at the lesion site to initiate regrowth of tissues. LDL attaches to the smooth muscle cells to stimulate them to multiply. But the uptake of cholesterol (a major component of LDL) into the intima leads to the formation of an atheroma that is later hardened by calcium deposits.

Other implicated factors include the following:

Homocysteine is believed to contribute directly to the early stages of atherosclerosis by damaging the intima, the cells that line blood vessels. Elevated serum homocysteine levels are found in 20 - 40% of the population. Patients with even slightly elevated homocysteine have more than three times the risk of suffering a heart attack compared to those showing normal homocysteine levels. (Stampfer, MJ, et al. JAMA 1992;268:977-981. Many cardiovascular patients have mild elevations. (Franken, DG, et al. Amer J Clin Nutr 1993; 57:47-53). Studies have revealed that homocysteine levels strongly correlated with blood and dietary folic acid and dietary intake of Vitamin B-6. (Selhub, J, et al. JAMA 1993;270:2693-8.) Likewise, similar, though weaker, inverse correlations were found for blood levels of Vitamins B-12 and B-6 and homocysteine. The lowest homocysteine levels corresponded with dietary intakes of folic acid and Vitamin B-6 well above the RDA.

Hydrogenated oils (including partially hydrogenated oils) are significantly atherosclerotic. Ironically, hydrogenated oils such as margarine were for man years believed to be healthier because they were cholesterol-free. However, the rise of myocardial infarctions and heart disease in general can be traced back to the 1920s and 1930s, when hydrogenated oils were first being introduced and used in foods. Hydrogenated oils are unsaturated oils which are heated, pressurized and then chemically altered with nickel (or a similar metal), changing the biochemical formation from the natural "cis" formation (liquid state at room temperature) into the synthetic "trans" formation (solid state at room temperature). It is now suggested that the synthetic and foreign quality of the trans oil creates damage to body tissues causing atherosclerotic formation and cancer. Furthermore, polyunsaturates allow significant formation of free radical compounds, thought to cause endothelial damage and predispose to formation of atheromas. Epidemiological research shows that people were eating high cholesterol diets for hundreds or thousands of years (meat, cream, butter, eggs, lard), and yet the epidemic of heart disease began only earlier this century, after the introduction of hydrogenated oils. Of course, this is one among many other contemporary factors related to heart disease, including pollution, sedentary lifestyle, refined sugar and flour products, and poor meat quality due to chemicals, hormones, antibiotics and other additives. Almost all the long-lived, healthy communities where degenerative disease and heart disease were unknown included significant meat or dairy in their diets (Schmid). It seems that the argument that cholesterol alone is the villain in heart disease falters at the evidence of those communities. It now seems that use of monounsaturated oils such as olive an canola, and moderate use of short-chain fatty acids (butter) may be the best way of maintaining "healthy" fat intake.

Risk factors for atherosclerosis include: high blood pressure, cigarette smoking, diabetes mellitus (hyperglycemia), obesity, family history, increased serum lipids, diet high in fats (unsaturated, hydrogenated and hydrogenated oils), sedentary lifestyle, aging, men in general, and women after menopause.

signs and symptoms

The development of atherosclerosis is insidious and occult until a complication develops.

complications:
sequelae include: thrombosis, stenosis, aneurysm, myocardial infarction, angina, TIA or CVA, intermittent claudication
essential hypertension may suggest but is not diagnostic of atheromas

lab findings (these are suggestive, not definitive):
elevated plasma homocysteine levels
amino acid analysis shows high levels of homocysteine
cholesterol >200 mg/dl (180 mg/dl is normal)
chronic hyperglycemia
elevated triglycerides and LDLs, decreased HDLs
increased lipoprotein B and decreased lipoprotein A
cholesterol/HDL ratio > 4.5
(+) cardiac angiography for occluded coronary arteries (definitive)

course and prognosis

The best treatment is prevention. Weight loss, dietary counseling and nutritional supplementation, exercise programs, cessation of smoking, control of blood pressure and blood sugar are ways to control or prevent the development of atheromas. Epidemiological evidence strongly supports the claim that atherosclerosis is a "disease of affluence" which is relatively absent in cultures with different dietary and lifestyle patterns. Recent research demonstrates that appropriate dietary and lifestyle treatment may substantially reduce intimal plaques, confirming the empirical evidence gathered by naturopathic physicians and others that symptoms resulting from the presence of atheromas may be ameliorated or reversed entirely in patients undergoing treatment. However, while there is now considerable evidence supporting those treatments, there is controversy over the extent to which sufferers will comply with such actively participant regimes.

differential diagnosis

Symptoms and signs of atherosclerosis vary according to the area affected, and must be differentiated from other conditions which may present locally.


footnotes

Franken, DG, et al. Treatment of mild homocysteinemia in vascular disease patients. Amer J Clin Nutr 1993; 57:47-53.

Stampfer, MJ, et al. A Prospective study of plasma homocyst(e)ine and risk of myocardial infarction in US physicians. JAMA 1992;268:977-981.

Selhub, J, et al. Vitamin status and intakes as primary determinants of homocysteinemia in an elderly population. JAMA 1993;270:2693-8.