Coronary Heart Disease
Description
Coronary heart disease or ischemic heart disease is a result of atherosclerosis of the arteries supplying blood and oxygen to the heart. Over 33% of all deaths in the United States are the result of coronary heart disease. Heart attacks or myocardial infarctions alone account for over 20% of all deaths and are the result of an interruption of blood and oxygen supply to the heart muscle. Several factors can be responsible for this, including blockage of the artery by an atherosclerotic plaque or thrombi, or spasm.
Conventional medical treatment of coronary heart disease is the use of nitrates, coronary artery bypass surgery, and angioplasty, a new technique where a small balloon is inserted into the artery and inflated to flatten nonmineralized fatty deposits. At present, the best approach is a proper prevention plan utilizing diet, exercise and lifestyle modification.
Causes
Primary factors
The primary cause of coronary artery disease is atherosclerosis of the coronary arteries. The atherosclerotic plaque reduces the blood flow through the arteries which may lead to myocardial ischemia.
Predisposing factors
Smoking
High blood pressure
Increased serum lipids (cholesterol and/or triglycerides)
Obesity
Diabetes mellitus
Oral contraceptive use
Genetic predisposition
Aging
Stress
Signs & Symptoms
| Ear lobe crease | Angina Pectoris |
| Nausea | Fainting |
| Cool extremities | Difficulty breathing |
As atherosclerosis is a quiet disease, significant symptoms only appear when the process has advanced to a stage where blood flow to the heart has been greatly reduced. A simple physical finding - a crease in the ear lobe - may offer some warning atherosclerotic processes are occurring.
The ear lobe is richly vascularized, and a decrease in blood flow over a period of time is believed to result in collapse of the vascular bed. This leads to a diagonal ear lobe crease, which has been recognized as a sign of cardiovascular disease since 1973. Since then, over 30 studies have been reported in the medical literature, with the largest to date involving 1,000 unselected patients. The crease is seen more commonly with advancing age, until the age of 80, when the incidence drops dramatically. However, the association with coronary heart disease is age-independent. The ear lobe crease appears to be a better predictor of heart disease than any other known risk factor, including age, smoking, sedentary lifestyle, hyperlipidemia and others. While the presence of an ear lobe crease does not prove coronary artery disease, it strongly suggests it, and examination of the ear lobe should be a useful screening procedure. The correlation does not work with Orientals, native Americans and children with Beckwith's syndrome.
Angina pectoris indicates coronary artery disease. It is characterized by a squeezing, crushing, or burning tightness or pain in the chest which radiates to the left shoulder blade, left arm, or jaw.
Unexpected death may occur without any prior symptoms.
Nutritional Supplements
Structure & Function:
Cardiovascular Support &
Circulatory Support
---------------------------------
General Supplements
---------------------------------
| Adult | ||
| Beta carotene* | ||
| Bromelain | 750 mg | |
| Carnitine | 1,500 mg | |
| Chromium | 200 - 300 mcg | |
| Copper | 2 - 3 mg | |
| CoQ10* | ||
| DHEA* | ||
| EPO* | ||
| Fiber* | ||
| Fish oils | 4 - 10 g | |
| Garlic* | ||
| Ginkgo biloba* | ||
| Green barley* | ||
| Kelp* | ||
| Lecithin* | ||
| Magnesium | 400 - 800 mg | |
| Proanthocyanidins* | ||
| Quercetin* | ||
| Rutin* | ||
| Selenium | 100 - 300 mcg | |
| Superoxide dismutase* | ||
| Vitamin B-6 | 25 mg | |
| Vitamin C | 1,000 - 3,000 mg | |
| Vitamin E | 200 - 600 IU | |
| Wheat germ* | ||
| Policosanol* | ||
| Luteolin* |
* Please refer to the respective topic for specific nutrient amounts.
Notes:
Certainly, in the industrialized world, virtually every adult suffers some degree of atherosclerosis. The array of nutrients used to reverse this trend is extensive. Unfortunately, a majority of the American population still consumes saturated fats, remains sedentary and cannot compensate for these factors simply with nutritional supplements, at any dosage.
Another large group is composed of fibers, some of which are singled out: guar gum and oat bran. Fibers are believed to help cleanse the system, in which process it may also be helpful to boost the beneficial flora with L. acidophilus.
Other plants seem to be useful even without their fibers, in the form of juice, including: chlorella, chlorophyll and green barley. Also, garlic, ginkgo biloba and kelp , which are usually in capsule form, for convenience.
The other listed nutrients are discussed individually:-
Calcium
The daily administration of 800 mg elemental calcium has resulted in a 25% decrease in serum cholesterol in hypercholesterolemic men over a period of one year.
Carnitine
Carnitine has been shown to be therapeutically effective in the treatment of ischemic heart disease. Since long chain fatty acids are the preferred metabolic substrate in well-oxygenated myocardial tissue, normal cardiac function is probably dependent on appropriate myocardial concentrations of carnitine. This is due to carnitine's role as a component of several enzymatic systems which are involved in the transport of fatty acids during energy production.
The normal myocardium stores more carnitine than it needs, but during decreased oxygen supply, carnitine levels quickly decrease.
Supplementation with carnitine normalizes myocardial carnitine levels and allows the ischemic heart muscle to utilize its limited oxygen supply more efficiently. Carnitine also increases HDL levels, while decreasing triglyceride and cholesterol levels.
Chromium
Chromium chloride supplementation (200 mcg per day) results in a decrease in serum triglycerides and total cholesterol, while increasing HDL levels and improving glucose tolerance.
These results have also been duplicated with chromium-rich brewer's yeast, but not chromium-poor torula yeast. The chromium content of the U.S. diet is generally quite low.
Fish oils (EPA)
Clinical studies have shown that the daily ingestion of 10-20 grams of commercially produced EPA results in reduced total cholesterol, increased HDL, reduced platelet aggregation, and increased bleeding time. These effects of EPA are due to its alteration of prostaglandin ratios and competition with arachidonic acid for binding enzyme sites. Increased consumption of EPA results in decreased production of PG2 series prostaglandins and increased levels of PG3 series. This is significant, due to the differing activities of the products of these series: prostacyclin (PGI3) has a greater anti-aggregating effect than PGI2, and thromboxane A3 is a less potent platelet-aggregating factor than thromboxane A2.
Lecithin
Lecithin provides phosphatidylcholine and the essential fatty acid linoleic acid. Lecithin has been used over 4 decades to lower blood levels of cholesterol and triglycerides in individuals with elevated levels. Reports in the medical literature are conflicting on the efficacy of lecithin. The dose that appears most effective is very large, i.e., 25 grams per day. However, most individuals tolerate this dose very well. As most commercially available lecithins are only 20% phophatidylcholine, administration of a more concentrated source of phosphatidylcholine could be at a lower dose.
Magnesium
There is an inverse correlation between total body magnesium and atherosclerosis. Furthermore, it has been observed individuals dying suddenly of ischemic heart disease have significantly lower levels of myocardial magnesium and potassium than matched controls. Such a deficiency may be due to inadequate magnesium intake or excessive vitamin D intake, which intensifies magnesium deficiency. A magnesium deficiency has been shown to produce spasms of the coronary arteries and is thought to be a cause of nonocclusive sudden death ischemic heart disease. Intravenous magnesium is becoming a widely accepted procedure to halt heart attacks. Magnesium supplementation also increases HDL levels, decreases platelet aggregation and prolongs clotting time. Magnesium is also very effective in relieving many cardiac arrhythmias.
Niacin:
Niacin has long been used as a cholesterol lowering agent. However, the dose required (2 to 9 grams) is quite high and usually produces significant side effects including flushing, gastrointestinal distress, gastric ulcer, glucose intolerance and damage to the liver. For these reasons, niacin's use as a cholesterol/triglyceride lowering compound should be reserved for individuals under the care of a physician.
Selenium
Low selenium levels are associated with an increased risk of ischemic heart disease. This observation is based on a study of 11,000 case-controlled pairs from Finland. Restricted selenium intake reduces the levels of glutathione peroxidase, a free radical scavenging enzyme. Deficiency of glutathione peroxidase may lead to increased lipid peroxide-induced vascular endothelial damage. These effects would be aggravated by a vitamin E deficiency as well. Selenium also influences prostaglandin metabolism and decreases platelet aggregation.
Vitamin B-6
One of the theories of atherosclerosis is based on the idea that a vitamin B6 deficiency results in high levels of homocysteine which then damages the arterial wall. Vitamin B6 is indicated in a prevention program due to its role in normal collagen synthesis and platelet inhibiting action.
Vitamin C
Strong clinical and experimental evidence suggests a chronic latent vitamin C deficiency leads to hypercholesterolemia and the accumulation of cholesterol in certain tissues. Vitamin C helps prevent atherosclerosis by directly promoting the catabolism of triglycerides, and through its regulation of arterial wall integrity via its essential role in collagen formation.
Vitamin E
A tocopherol deficiency results in significantly higher levels of lipid peroxides; significantly reduced release of prostacyclin; and lower levels of superoxide dismutase (SOD), glutathione peroxidase and catalase, resulting in increased free radical damage, particularly of the vascular endothelium. Supplemental vitamin E has been shown to prevent atherosclerosis through its inhibition of the platelet-releasing reaction, which produces a marked rise in lipid peroxides; its actions as a free radical scavenger; inhibition of platelet aggregation; and its elevation of HDL levels.
Zinc and Copper
A high zinc-to-copper ratio appears to be a causative factor in atherosclerosis. Zinc and copper compete for binding sites for absorption. High dose zinc administration (160 mg per day) has been shown to lower serum HDL levels in men (but not in women). Lower levels of supplemental zinc (50 mg/day), however, appear to have no ill effects on cholesterol and HDL levels.
High dose zinc supplementation may induce a relative copper deficiency. A deficiency of copper produces results in elevated cholesterol levels. Copper is important both in lipid metabolism and in production of normal connective tissue.
As copper levels are commonly marginal in U.S. diet, supplementation may be appropriate keeping in mind that a balanced zinc-to-copper ratio is necessary for optimal health.
Note: All amounts are in addition to those supplements having a Recommended Dietary Allowance (RDA). Due to individual needs, one must always be aware of a possible undetermined effect when taking nutritional supplements. If any disturbances from the use of a particular supplement should occur, stop its use immediately and seek the care of a qualified health care professional.
Dietary Considerations
Magnesium salts are strongly indicated in this disorder, both in terms of a causal deficiency and a therapeutic supplement.
see Atherosclerosis
Homeopathic Remedy
Congestive Heart Failure (dropsy)
| 1.* Convallaria majalis | 3X to 15C |
| 2.* Digitalis purpurea | 30X |
| 3.* Cainca Racemosa tinct. | 3C |
Coronary Disease
1.* Angina (chest pain) - Glonoinum tinct.- 30C
2.* Irregular Beat - Digitalis purpurea- 6X - 30C
3. Mitral Disease (stenosis) - Crataegus Hawthorn tinct. 6X to 30C
4. Stop/Start - Digitalis purpurea- 30X
5.* Hear tonic - Crataegus Hawthorn tinct.- 6X
6.* Palpitations/Murmurs - Cactus grandiflorus 3C - 30C
7.* Heart Remedy, general - Convallaria majalis 3X - 100X increase heart action
8. Fatty Degeneration - Arsenicum Album 30C
Treatment Schedule
Doses cited are to be administered on a 3X daily schedule, unless otherwise indicated. Dose usually continued for 2 weeks. Liquid preparations usually use 8-10 drops per dose. Solid preps are usually 3 pellets per dose. Children use 1/2 dose.
Legend
X = 1 to 10 dilution - weak (triturition)
C = 1 to 100 dilution - weak (potency)
M = 1 to 1 million dilution (very strong)
X or C underlined means it is most useful potency
Asterisk (*) = Primary remedy. Means most necessary remedy. There may be more than one remedy - if so, use all of them.
References
Boericke, D.E., 1988. Homeopathic Materia Medica.
Coulter, C.R., 1986. Portraits of Homeopathic Medicines.
Kent, J.T., 1989. Repertory of the Homeopathic Materia Medica.
Koehler, G., 1989. Handbook of Homeopathy.
Shingale, J.N., 1992. Bedside Prescriber.
Smith, Trevor, 1989. Homeopathic Medicine.
Ullman, Dana, 1991. The One Minute (or so) Healer.
Herbal Approaches
----------
Herbs
-----------
Ginkgo biloba
Hawthorn berry
Note: The misdirected use of an herb can produce severely adverse effects, especially in combination with prescription drugs. This Herbal information is for educational purposes and is not intended as a replacement for medical advice.
Discussion:
Heart disease, like angina pectoris, may benefit from the use of the following herbs at suggested dosages:
| Ginkgo biloba | 40 mg t.i.d. |
| Hawthorn berry extract | 100 mg t.i.d. |
Several herbs with cardiactive ingredients have been listed by Newall:
| Herb | Effect |
| Broom | Alkaloids, depressant effect |
| Calamus | Antiarrhythmic |
| Cereus | Tyramine, cardiotonic |
| Cola | Caffeine |
| Coltsfoot | Calcium channel blocker |
| Devil's Claw | Activity, in vivo |
| Fenugreek | Activity, in vitro |
| Figwort | Activity, in vitro |
| Fumitory | Alkaloids, |
| Ginger | Activity, in vivo |
| Ginseng, Panax | Activity, in vivo |
| Goldenseal | Berberine, cardioactive alkaloid |
| Hawthorn | Tyramine, activity, in vivo |
| Horehound, White | Activity, in vivo |
| Lime Flower | Activity with excessive ingestion |
| Mate | Caffeine |
| Mistletoe | Viscotoxin, negative inotropic effect |
| Motherwort | Activity, in vitro |
| Parsley | Apiole poisoning in high doses |
| Pleurisy Root | Cardenolides, activity, in vivo |
| Prickly Ash | Interaction with Na, K, ATPase |
| Quassia | Activity, in vitro |
| Shepherd's Purse | Activity, in vitro |
| Squill | Cardiac glycosides |
| Wild Carrot | Depressant activity, in vivo |
Reference:
Newall CA, Anderson LA, Phillipson JD. Herbal Medicines: A Guide for Health-care Professionals. London: The Pharmaceutical Press, 1996:21,45,63,282.
Aromatherapy - Essential Oils
Cardiac Fatigue:
| Aniseed Essence, | (Borneo) Camphor Essence, |
| Garlic Essence. |
Palpitations ( due to nervousness):
| Aniseed Essence, | Caraway Essence, |
| Orange Essence, | Peppermint Essence, |
| Rosemary Essence. |
Tachycardia:
| Garlic Essence, | Ylang-Ylang Essence. |
Related Health Conditions
Arteriosclerosis
Atherosclerosis
Heart disorders
References
General:
Barker DJ: Fetal nutrition and cardiovascular disease in later life. Br Med Bull, 1997 Jan, 53:1, 96-108.
Barker ME et al., Do type As eat differently? A comparison of men and women. Appetite, 1996 Jun, 26:3, 277-85.
Bidlack WR: Interrelationships of food, nutrition, diet and health: the National Association of State Universities and Land Grant Colleges White Paper. J Am Coll Nutr, 1996 Oct, 15:5, 422-33.
Brett KM & Madans JH: Long-term survival after coronary heart disease. Comparisons between men and women in a national sample [see comments]. Ann Epidemiol, 1995 Jan, 5:1, 25-32.
De Lorgeril M et al., Effect of a Mediterranean type of diet on the rate of cardiovascular complications in patients with coronary artery disease. Insights into the cardioprotective effect of certain nutriments [see comments]. J Am Coll Cardiol, 1996 Nov 1, 28:5, 1103-8.
Dreher ML et al., The traditional and emerging role of nuts in healthful diets. Nutr Rev, 1996 Aug, 54:8, 241-5.
Eddy, L. et al: A Protective Role For Ascorbate in Induced Ischemic Arrest Associated with Cardiopulmonary Bypass. J of Appd Cardiology, 1990;5:409-414.
Elliott H Community nutrition education for people with coronary heart disease--who attends? Aust J Public Health, 1995 Apr, 19:2, 205-10.
Elliot, WJ: Ear lobe crease and coronary artery disease. Am J Med 75: 1024-32, 1983.
Eric B. et al: Prospective Study of Alcohol Consumption and Risk of Coronary Disease in Men. The Lancet, August 24, 1991;338:464-468.
Frost G: The effect of low-glycemic carbohydrate on insulin and glucose response in vivo and in vitro in patients with coronary heart disease. Metabolism, 1996 Jun, 45:6, 669-72.
Gale CR et al., Vitamin C and risk of death from stroke and coronary heart disease in cohort of elderly people [see comments]. BMJ, 1995 Jun 17, 310:6994, 1563-6.
Gartside PS & Glueck CJ: The important role of modifiable dietary and behavioral characteristics in the causation and prevention of coronary heart disease hospitalization and mortality: the prospective NHANES I follow-up study. J Am Coll Nutr, 1995 Feb, 14:1, 71-9.
Grundy SM: Cholesterol and coronary heart disease. The 21st century. Arch Intern Med, 1997 Jun 9, 157:11, 1177-84.
Harris TB et al., Cohort study of effect of being overweight and change in weight on risk of coronary heart disease in old age. BMJ, 1997 Jun 21, 314:7097, 1791-4.
Jackson, R. et al: Alcohol Consumption and The Risk of Coronary Heart Disease. British Medical Journal, July 27, 1991;303:211-215.
Klevay, L.M. Ischemic Heart Disease: Nutrition or pharmacotherapy? J. Trace Element. Electrolytes Health Dis. 1993, 7: 63-69. (Review)
Kok, F.J. et al: Do Antioxidants and Polyunsaturated Fatty Acids Have a Combined Association With Coronary Atherosclerosis? Arteriosclerosis, 1991;31:85-90.
Kl”r HU et al., Nutrition and cardiovascular disease. Eur J Med Res, 1997 Jun 16, 2:6, 243-57.
Lamon-Fava S et al., Impact of body mass index on coronary heart disease risk factors in men and women. The Framingham Offspring Study. Arterioscler Thromb Vasc Biol, 1996 Dec, 16:12, 1509-15.
Manson, J.E. et al: A Prospective Study of Antioxidant Vitamins and Incidence of Coronary Heart Disease in Women. Journal of The American College of Nutrition, October 1992;11(5):633/Abstract 119.
Martyn CN et al., Mothers' pelvic size, fetal growth, and death from stroke and coronary heart disease in men in the UK [see comments]. Lancet, 1996 Nov 9, 348:9037, 1264-8.
McCully, Kilmer S., Micronutrients in Health and In Disease Prevention, Bendrich, Adrianne, Butterworth, C. E., Jr. (eds), Marcel Dekker, Inc., New York, Basel, Hong Kong, 1991, pp. 69-93.
McCully, Kilmer S., Chemical pathology of homocysteine I. Atherogenesis, Annals of Clinical and Laboratory Science, Vol. 23, No. 6, 1993, pp. 477-493.
Mickle, D. A.G. et al: Effect of Orally Administered Alpha-Tocopherol Acetate on Human Myocardial Alpha-Tocopherol Levels. Cardiovascular Drugs and Therapy, 1991;5:309-312.
Mirotznik J et al., The health belief model and adherence with a community center-based, supervised coronary heart disease exercise program. J Community Health, 1995 Jun, 20:3, 233-47.
Morrison HI et al., Serum folate and risk of fatal coronary heart disease [see comments]. JAMA, 1996 Jun 26, 275:24, 1893-6.
Mustad V et al., Seasonal variation in parameters related to coronary heart disease risk in young men. Atherosclerosis, 1996 Sep 27, 126:1, 117-29.
O'Connor, G. T. et al: A Regional Prospective Study of In-Hospital Mortality Associated With Coronary Artery Bypass Grafting (individual physician and hospital variation). JAMA, August 14, 1991;266(6):803-809.
Oliver, M.F.: Linoleic Acid, Antioxidants and Coronary Heart DiseaseBiochemical Society Transactions. 1990;18:1049-1051.
Olsewski, A et al., Reduction of plasma lipid and homocysteine levels by pyridoxine, folate, cobalamin, choline, riboflavin, and troxerutin in atherosclerosis, Atherosclerosis, 75, 1989, 1-6.
Oshaug A et al., Use of anthropometric measurements in assessing risk for coronary heart disease: a useful tool in worksite health screening? Int Arch Occup Environ Health, 1995, 67:6, 359-66.
Oster G & Thompson D: Estimated effects of reducing dietary saturated fat intake on the incidence and costs of coronary heart disease in the United States. J Am Diet Assoc, 1996 Feb, 96:2, 127-31.
Pacala-JT et al: Management of older adults with hypercholesterolaemia. Drugs-Aging. 1994 May; 4(5): 366-78.
Page M & Ward SL: The role of diet in coronary heart disease. Prof Nurse, 1995 Aug, 10:11, 691-2, 694, 696.
Peiss B et al., Physicians and nurses can be effective educators in coronary risk reduction. Gen Intern Med, 1995 Feb, 10:2, 77-81.
Petersdorf, R. Harrison's Principles of Internal Medicine. 10th Ed., McGraw-Hill, New York, NY. 1983.
Pietinen P et al., Changes in diet in Finland from 1972 to 1992: impact on coronary heart disease risk. Prev Med, 1996 May-Jun, 25:3, 243-50.
Pizzorno, Joseph E. & Murray, Michael T. A Textbook of Natural Medicine. JBC Publications, Seattle, WA. 1985.
Powell AJ et al., Health risk appraisal and serum cholesterol nutrition education: an outcome study. Mil Med, 1996 Feb, 161:2, 70-4.
Prielpp, R. C. et al: Magnesium Inhibits the Hypertensive But Not the Cardiotonic Action of Low-Dosed Epinephrine. Anesthesiology, 1991;74:973-979.
Rehm JT et al., Alcohol consumption and coronary heart disease morbidity and mortality. Am J Epidemiol, 1997 Sep 15, 146:6, 495-501.
Riemersma, R.A. et al: Anti-Oxidants and Pro-Oxidants in Coronary Heart Disease. The Lancet, March 16, 1991;337:677.
Rimm EB et al., Vitamin E consumption and the risk of coronary heart disease in men. New Eng. J.Med. 328:1450-6, 1993.
Rimm EB et al., Vegetable, fruit, and cereal fiber intake and risk of coronary heart disease among men [see comments]. JAMA, 1996 Feb 14, 275:6, 447-51.
Rimm EB et al., Review of moderate alcohol consumption and reduced risk of coronary heart disease: is the effect due to beer, wine, or spirits. BMJ, 1996 Mar 23, 312:7033, 731-6.
Rimm EB & Stampfer MJ: The role of antioxidants in preventive cardiology. Curr Opin Cardiol, 1997 Mar, 12:2, 188-94.
Rocchini-AP.: Fetal and pediatric origins of adult cardiovascular disease. Curr-Opin-Pediatr. 1994 Oct; 6(5): 591-5.
Roy, L. et al: A Double-Blind, Randomized Placebo Controlled Study Comparing the Efficacy of Fish Oil and Low Dose Aspirin to Prevent Coronary Saphenous Vein Graft Obstruction After CABG. Circulation, October 1991;84(4):S2/II-285/Abstract.
Selhub, J et al., Association between plasma homocysteine concentrations and extracranial carotid-artery stenosis. NEJM. 1995, Feb. 2, 332 (5), pp. 286-291.
Sotelo MM & Johnson SR: The effects of hormone replacement therapy on coronary heart disease. Endocrinol Metab Clin North Am, 1997 Jun, 26:2, 313-28
Stampfer MJ et al., Vitamin E consumption and the risk of coronary disease in women. New Eng. J.Med. 328:1444-9, 1993.
Stary, H. C., Evolution and progression of atherosclerotic lesions in coronary arteries of children and young adults, Arteriosclerosis, 1989, 9, Suppl. I, pp. I-19 - I-32.
Stelmach, W. J.: Low-Density Lipoprotein Cholesterol and the Other Coronary Heart Disease Risk Factors in Patients With Total Cholesterol Levels Greater Than 5.17 mmol/l (200 mg/dl) in Family Practice. Journal of the American Board of Family Practice, September/October, 1991;285-294.
Stender S et al., The influence of trans fatty acids on health: a report from the Danish Nutrition Council [see comments]. Clin Sci (Colch), 1995 Apr, 88:4, 375-92.
van de Vijver LP et al., Trans unsaturated fatty acids in plasma phospholipids and coronary heart disease: a case-control study. Atherosclerosis, 1996 Sep 27, 126:1, 155-61.
Vega GL & Grundy SM: Hypoalphalipoproteinemia (low high density lipoprotein) as a risk factor for coronary heart disease. Curr Opin Lipidol, 1996 Aug, 7:4, 209-16.
Walji, Hasnain. 1994. Heart Health. A Self-help Guide to combining Orthodox & Complementary Approaches . Hodder Headline Plc.London.
William, S. B. et al. Differences in Mortality From Coronary Artery Bypass Graft Surgery at Five Teaching Hospitals (hospital variation in mortality rates). JAMA, August 14, 1991;266(6):810-815.
Zock PL & Katan MB: Trans fatty acids, lipoproteins, and coronary risk. Can J Physiol Pharmacol, 1997 Mar, 75:3, 211-6.
Zock PL & Katan MB: Butter, margarine and serum lipoproteins. Atherosclerosis, 1997 May, 131:1, 7-16.
Mitral Valve Prolapse:
Cohen, L. Et al: Idiopathic magnesium deficiency in mitral valve prolapse. Am. J. Cardiol. 1986, 57(6): 486-487.
Durlach, J. et al: Latent tetany and mitral valve prolapse due to chronic primary magnesium deficit. In: Halpern & Durlach (Eds): Magnesium Deficiency. Karger, Basel, 1985.
Fernandes, J. S. Et al: Therapeutic effect of a magnesium salt in patients suffering from mitral valvular prolapse and latent tetany. Magnesium, 1985, 4: 283.
Frances, Y. Et al: Long-term follow-up of mitral valve prolapse and latent tetany. Preliminary data. Magnesium, 1986, 5(3-4): 175-181.
Galland, L.: Magnesium deficiency in mitral valve prolapse. In: Halpern & Durlach (Eds): Magnesium Deficiency. Karger, Basel, 1985.
Gerard, R. Et al: [Mitral valve prolapse and spasmophilia in the adult.] Arch. Mal. Coeur. 1979, 72(7): 715-720.
Zeana, C. Et al: Considerations on the pathogenesis of mitral valve prolapse. Med. Interne. 1985, 23(3): 165-170.
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