International Data

What Say You?

How can we serve you better?

More content please... - 33.7%
A bit more pictures would be better - 19.4%
More up to date content - 12.3%
Nothing! your site is superb! - 34.6%

Angina

Introduction

What should I know about angina?

Discomfort in the chest is likely the most frequent complaint for which people seek medical attention. Chest discomfort can result from numerous things including cramping and soreness in the muscles of the rib cage, "heartburn" or other concerns associated with the upper region of the digestive tract, conditions involving the lungs such as a collapsed lung or even potentially life-threatening conditions involving the heart such as a heart-attack.

Angina, also known as angina pectoris, is a condition that can cause chest pain, ranging from mild to quite severe. Angina occurs when not enough oxygen is able to reach the heart muscle, usually due to a decrease in blood flow. Numerous conditions can affect the blood flow to the heart and thus the amount of oxygen reaching the heart muscle. These conditions include coronary artery disease, coronary artery spasm, irregular rhythms of the heart, infections, anemia and even a heart attack can cause angina to occur.

Generally, angina occurs when extra stress is placed on the heart such as during physical exercise or even at times of stress, anxiety and depression. (1) This is known as stable angina and is generally due to the presence of coronary artery disease. Unstable angina can occur at rest and at other unpredictable times such as in the middle of the night. Unstable angina can also be described as frequent and severe chest discomfort in patients that have not experienced chest discomfort previously or increased frequency, severity and worsening of angina in people diagnosed with stable angina. A rare third type of angina is referred to as variant angina, which can occur during exertion or while at rest generally resulting from a spasm in a coronary artery. (2)

Statistic

American Heart Association, Biostatistical Fact Sheet, 2001.

    12,400,000 victims of angina (chest pain due to coronary heart disease), heart attack and other forms of coronary heart disease are still living (6,000,000 males and 6,300,000 females). Estimates are that 6,400,000 people in the United States suffer from angina. An estimated 400,000 new cases of angina occur each year. (Framingham Heart Study, National Heart, Lung, and Blood Institute) The estimated age-adjusted (2000 standard) prevalence of angina is greater in women than in men. Angina rates in women age 20 and older were 3.9 percent for non-Hispanic white women, 6.2 percent for non-Hispanic black women and 5.5 percent for Mexican-American women. Rates for men in these three groups were 2.6, 3.1 and 4.1 percent, respectively. In 1998, 85,000 Americans were discharged from short-stay hospitals with a first listed diagnosis of angina pectoris. About 51 percent were age 65 and older. About 36,000 males diagnosed with angina pectoris were discharged from short-stay hospitals in 1998. 49,000 females diagnosed with angina were discharged from short-stay hospitals in 1998.

Signs and Symptoms

The following list does not insure the presence of this health condition. Please see the text and your healthcare professional for more information.

The chest discomfort associated with angina is generally described as a dull pressure, heaviness, squeezing or smothering but can also include sharp pain. The discomfort is usually in the chest and can spread up into the throat, the upper back and into the left shoulder and arm. Sweating, shortness of breath and nausea can also be experienced. As noted, angina can occur at any time but generally is associated with increased physical activity or at times of high emotional stress. The symptoms usually build in intensity and then fade away, lasting 1 to 5 minutes, but can last considerably longer. When the symptoms seemed to be associated with physical activity, immediate rest can help relieve the discomfort as can nitroglycerin tablets, a prescription medication. (3)

Occasional chest pain should be evaluated by a health care provider. Medical history and physical exam involving extensive evaluation of pulse, blood pressure, the heart and lungs among other things should be performed. An electrocardiogram (ECG or EKG) evaluating the rhythms of your heart and possibly an exercise stress test for your heart may be ordered. Other tests and procedures are available for use in the cases of more severe coronary artery disease. (4) Significant and severe chest pain needs to be immediately evaluated in an emergency room so that you can be properly evaluated for the possibility of a heart attack. All of these tests are used to help the physicians determine the cause for the angina pain and to help determine the course of treatment. (5)

General

  • Chest discomfort described as dull pressure, heaviness, squeezing or smothering, can include sharp pain
  • Sweating
  • Shortness of breath
  • Nausea

Treatment Options

Conventional

One of the first recommendations that will be made by a health care provider will the necessary addition or elimination of certain dietary and lifestyle habits. These are discussed in Diet and Lifestyle.

Nitrates are widely used throughout coronary artery disease, not only in angina but also in heart attacks and heart failure. These drugs work by dilating blood vessels, thus decreasing oxygen requirements. One of the most useful nitrates for angina is sublingual nitroglycerin. This small tablet is placed under the tongue at the first sign of an angina attack. It is quickly absorbed and generally provides relief of the chest discomfort. Occasionally, a second or third dose may be necessary. One problem with nitrates is that patients can easily develop a tolerance to the medication, thus causing it to not work as well. Longer acting nitrates, such as topical creams and patches as well as capsules that can be swallowed are also available for use. (6)

Beta-blockers are another class of medications that have been shown to be effective in patients with stable angina. These medications decrease oxygen demand of the heart by decreasing the heart rate and the force of contraction. Another class of drugs known as calcium channel blockers are beneficial for patients with stable angina. They relax blood vessels decreasing the oxygen demand of the heart. Some calcium channel blockers may help slow the heart rate as well. There are three groups of calcium channel blockers and some are not appropriate for people with other types of heart disease. (7) Talk to your healthcare provider about which medications are right for you.

Patients with unstable angina pectoris, in addition to the medications listed above, may require additional therapy due to other complications of their disease state. Antiplatelet therapy, including aspirin, ticlopidine, clopidogrel and glycoprotein IIb/IIIa receptor antagonists, may be warranted. Antithrombin therapy could also be necessary. This type of therapy includes heparin, low-molecular weight heparins and warfarin. Thrombolytic therapy is another possibility in people with unstable angina. (8) Depending on the disease state causing angina and the severity of it, other treatments including surgical procedures may also be necessary.

Nutritional Suplementation


Selenium

Low plasma selenium has been considered a significant risk factor for cardiovascular disease. (9) Selenium has a cardioprotective effect against drugs and other xenobiotics that are cardiotoxic (e.g. Adriamycin). Selenium has a known antiviral capability, which may protect the heart from agents such as the coxsackie B4 viruses. (10)


Potassium

People consuming diets containing foods that are high in potassium have a lower incidence of hypertension. (11) Epidemiological evidence reveals that increasing potassium intake can lower blood pressure in individuals who have essential hypertension and increasing dietary potassium can also result in a reduction of antihypertensive medications. (12)


Omega-3 Fatty Acids

The authors of a paper in the June 2000 issue of the Mayo Clinic Proceedings provide a nice summary of the history of omega-3 fatty acids as they have gradually been recognized to play a key role in the prevention and treatment of cardiovascular-related diseases. Their review states the following. "During the past 25 years, the cardiovascular effects of marine omega-3 (omega-3) fatty acids have been the subject of increasing investigation. In the late 1970s, epidemiological studies revealed that Greenland Inuits had substantially reduced rates of acute myocardial infarction compared with Western control subjects. These observations generated more than 4,500 studies to explore this and other effects of omega-3 fatty acids on human metabolism and health. From epidemiology to cell culture and animal studies to randomized controlled trials, the cardioprotective effects of omega-3 fatty acids are becoming recognized. These fatty acids, when incorporated into the diet at levels of about 1 g/d, seem to be able to stabilize myocardial membranes electrically, resulting in reduced susceptibility to ventricular dysrhythmias, thereby reducing the risk of sudden death. The recent GISSI (Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto miocardico)-Prevention study of 11,324 patients showed a 45% decrease in risk of sudden cardiac death and a 20% reduction in all-cause mortality in the group taking 850 mg/d of omega-3 fatty acids. These fatty acids have potent anti-inflammatory effects and may also be antiatherogenic. Higher doses of omega-3 fatty acids can lower elevated serum triglyceride levels; 3 to 5 g/ d can reduce triglyceride levels by 30% to 50%, minimizing the risk of both coronary heart disease and acute pancreatitis." (13)


Magnesium

Magnesium is a key mineral for cardiovascular health. It performs functions similar to numerous cardiovascular drugs. It inhibits platelet aggregation (like aspirin), thins the blood (like warfarin), blocks calcium uptake (like nifedipine), and relaxes blood vessels (like ACE inhibitors such as enaparil). Magnesium also increases oxygenation of the heart muscle by improving cardiac contractibility. (14)

Adequate magnesium may be associated with reduced incidence of specific types of angina. (15) Research indicates that magnesium may not be successful as a treatment for variant angina. (16) Adequate levels of magnesium are also associated with a reduction in cardiac spasms, and arrhythmias, and magnesium has relaxing and antispasmodic effect on the blood vessels. On the other hand, magnesium deficiency is associated with increased incidence of atherosclerosis, hypertension, strokes, and heart attacks. It is now recognized that many heart attacks happen to individuals with relatively healthy hearts but who are deficient in magnesium. (17)


Coenzyme Q10 (CO-Q10)

Coenzyme-Q10 (CoQ10) is a nutrient recently being recognized as playing a role in cardiovascular health. It functions as an antioxidant and is also a cofactor in several enzymatic steps in the generation of energy in the mitochondria of all cells. The heart is the most active muscle in the human body, a decline in energy due to a deficiency of CoQ10 can first affect heart function.

CoQ10 has been recognized as an effective part of a treatment plan for angina. CoQ10 has been studied extensively in regard to treatment, efficacy, dosage and areas of prevention. (18) In one double-blind study, patients with severe congestive heart failure who were given 150 mg/day of CoQ10 had a 38% decrease in hospitalizations due to worsening of heart failure compared to the control group. At the same time, episodes of pulmonary edema decreased by 60% and angina episodes decreased by 53%. (19) In another study it was shown that the symptoms of cardiovascular disease got progressively worse as CoQ10 levels declined. Treatment with 100 mg of coenzyme Q10 daily resulted in both subjective and objective improvement in 69% of patients with cardiomyopathy and 43% of patients with ischemic heart disease. (20)


Vitamin B6, Vitamin B12

Over the past several years, elevated homocysteine has become recognized as one of the primary risk factors to cardiovascular disease. In one metabolic pathway, vitamin B6 is necessary to convert homocysteine to cystathionine. In another metabolic pathway, folic acid and vitamin B12 are required to remethylate homocysteine back to methionine. A deficiency of any one of these three B-vitamins can lead to elevated homocysteine. (21)

Several studies have documented the fact that supplementation with folic acid, vitamin B6, and vitamin B12 can effectively lower homocysteine levels. There are wide variations in the dosages of these B-vitamins used in different studies. It is now recognized that even moderate elevations of homocysteine represent a strong independent risk to cardiovascular disease.


L-Carnitine

Carnitine is an important nutrient for cardiovascular health. Carnitine’s primary function is to facilitate the transport of fatty acids across cellular membranes into the mitochondria where they are utilized in the production of energy. This is extremely important for the heart, which is the most energy-demanding muscle in the body. Studies report that carnitine can be therapeutically useful in the treatment of various forms of cardiovascular disease such as angina, (22) , (23) acute myocardial infarction, (24) peripheral vascular disease, (25) arrhythmias, (26) and abnormal blood lipids. (27)


Soy Isoflavones

It has been proposed that isoflavones play a beneficial role in the prevention of atherosclerosis via several mechanisms. A study involving monkeys suggested that improvements in cholesterol levels were partially responsible for lower rates of atherosclerosis in the groups fed soy protein diets. (28) Genistein reportedly inhibits platelet aggregation or the clumping together of platelets to form a clot or thrombus. Also, genistein reportedly decreases the replication and division of smooth muscle cells which is one of the primary cell types that can adversely affect plaques. (29) , (30) Antioxidant properties and effects on the flexibility of arterial walls may also have a positive impact on the prevention of atherosclerosis. (31)


Arginine

L-arginine is a precursor to endothelium-derived nitric oxide. Arginine’s primary function involves the metabolism of protein and nitrogen, as well as the production of a number of important compounds. It also plays a role in maintaining health of the circulatory system. Due to its affect on platelet aggregation, L-arginine has been reviewed as a potential component of treatment plans for patients with stable angina pectoris. (32) One study reviewed arginine for its effects in intractable angina pectoris. The authors concluded that arginine may be beneficial as a treatment for this type of angina and that it also has antiinflammatory properties. (33) An additional small study noted improvement in the symptoms of 8 patients with microvascular angina pectoris after treatment with arginine. (34)


Vitamin E

The consumption of vitamin E has been shown to play a role in the prevention of atherosclerosis, lower the rates of ischemic heart disease and decrease the number of non-fatal heart attacks in people with these diseases. (35) Vitamin E has also demonstrated some benefit in people with angina due to a coronary spasm. A study involving 60 people with coronary spastic angina received either 300mg of vitamin E per day or placebo. The vitamin E group showed improvements in the measurements in the study and demonstrated a decrease in angina attacks. (36) Another study evaluated four groups of patients; active variant angina from coronary artery spasm, inactive variant angina (no angina attacks for the past 6 months), a group with a significant coronary artery narrowing and stable angina and a group without any coronary artery disease. The vitamin E blood levels in the group with active variant angina were lower than the other groups. As the levels of vitamin E in this group increased the incidence of angina attacks decreased. The study investigators feel that these findings suggest a relationship between a vitamin E deficiency and coronary artery spasm. (37)

Not all vitamin E studies support the benefits to the cardiovascular system. A study followed over 9,000 people for 4.5 years who took vitamin E or placebo and ramipril, a prescription medication, or placebo. This study tracked many different types of cardiovascular conditions. One of these conditions was unstable angina. Though this angina is different than the angina mentioned in the previous studies, vitamin E had no apparent effect on any of these cardiovascular conditions. (38)

Herbal Suplementation


Garlic

Garlic has been reported to lower total cholesterol, LDL cholesterol and triglycerides, and increase HDL cholesterol. (39) , (40) , (41) Garlic may be of benefit in the prevention of heart disease and atherosclerosis. (42) , (43) Garlic may inhibit platelet aggregation and influence blood viscosity through its fibrinolytic activity. (44) , (45) , (46) This leads to the use of garlic in the prevention of strokes, heart attacks and various thrombus events. (47) , (48) , (49) Also, the antioxidant effect in aged garlic has been reported to be beneficial in preventing stroke and arteriosclerosis. (50)

A recent study reported no effect of garlic oil on serum lipids. (51) However, the product used was garlic oil, which is processed and heated garlic. The impact of processing is an important fact to keep in mind when using garlic supplements. Changes can occur in the active constituents when exposed to cooking or other processing which can render the garlic product virtually ineffective. Cooking is known to denature proteins and therefore may inactivate the enzyme (allinase) that is necessary in converting alliin into allicin, the major bio-active constituent in garlic.


Hawthorn

Hawthorn is used as a vasodilator and circulatory stimulant. (52) It has been used extensively by doctors in Europe in its standardized form in various cardiovascular and peripheral circulatory conditions. Its combination of effects on the heart leads to its use as a tonic, especially for the elderly where mitral stenosis and minor heart failure may be present. Studies have reported a reduction in blood pressure due to arteriosclerosis and chronic nephritis with the use of hawthorn. (53) It is also used for peripheral vascular diseases, such as Raynaud’s disease. Hawthorn is used in Europe by physicians to help maintain digoxin levels while decreasing the need for the pharmaceutical medication. Hawthorn is reported to have the ability to regulate both low and high blood pressure. Its bioflavonoids reportedly dilate both peripheral and coronary blood vessels. (54) This leads to its use in decreasing angina attacks.

Diet & Lifestyle

As noted, significant diet and lifestyle changes greatly improve the frequency and severity of angina. Eating a healthy diet is always important. People at high risk for cardiovascular disease can benefit from reducing high cholesterol levels, (55) high blood sugars, high blood pressure and maintaining a healthy body weight. Exercise has been shown to increase blood flow to and around the heart (56) , (57) though these studies did not evaluate just stable angina patients.

One of the most important things a person can do is to stop smoking. Though stopping may not improve your angina symptoms, studies have shown lower death rates in people with ischemic heart disease. (58) , (59) , (60) Most importantly, before making any changes to your diet and lifestyle, talk to your healthcare provider first to determine what is right for you.

References

  1. View Abstract: Spertus JA, McDonell M, Woodman CL, Fihn SD. Association between depression and worse disease-specific functional status in outpatients with coronary artery disease. Am Heart J. Jul2000;140(1):105-10.
  2. Selwyn AP, Braunwald E. Ischemic Heart Disease. In: Fauci AS, Brunwald E, Isselbacher KJ, et al, eds. Harrison’s Principles of Internal Medicine 14th ed. New York: McGraw-Hill; 1998:1365-75.
  3. Selwyn AP, Braunwald E. Ischemic Heart Disease. In: Fauci AS, Brunwald E, Isselbacher KJ, et al, eds. Harrison’s Principles of Internal Medicine 14th ed. New York: McGraw-Hill; 1998:1365-75.
  4. Williams SV, Fihn SD, Gibbons RJ. American College of Cardiology.; American Heart Association.; American College of Physicians-American Society of Internal Medicine. Guidelines for the management of patients with chronic stable angina: diagnosis and risk stratification. 1999;2092-197.
  5. View Abstract: Zanger DR, Solomon AJ, Gersh BJ. Contemporary Management of Angina: Part I. Risk Assessment. Am Fam Physician. 1999;60:2543-52.
  6. Parker JD, Parker JO. Nitrate therapy for stable angina pectoris. NEJM. Feb1998;338(8):520-31.
  7. View Abstract: Zanger DR, Solomon AJ, Gersh BJ. Contemporary Management of Angina: Part II. Medical Management of Chronic Stable Angina. Am Fam Physician. 2000;61:129-38.
  8. Yeghiazarians Y, Braunstein JB, Askari A, Stone PH. Unstable angina pectoris. NEJM. Jan2000;342(2):101-114.
  9. View Abstract: Neve J. Physiologic and Nutritional Importance of Selenium. Experientia. 1991;47:187-193.
  10. View Abstract: Oster O, Prellwitz W. Selenium and Cardiovascular Disease. Biological Trace Elements. 1990;24:91-103.
  11. View Abstract: Langford HG. Dietary potassium and hypertension: Epidemiologic data. Am Intern Med. 1983;98(2):770-772.
  12. Krishna G. Potassium and blood pressure regulation. Drug Therapy. 1993;88-92.
  13. View Abstract: O’Keefe JH, Harris WS. From Inuit to implementation: omega-3 fatty acids come of age. Mayo Clin Proc. Jun2000;75(6):607-14.
  14. Gaby AR. Magnesium: An Inexpensive, Safe, and Effective Treatment for Cardiovascular Disease. J Advancement Med. 1986;1:179-81.
  15. View Abstract: Redwood SR, Bashir Y, Huang J, Leatham EW. Effect of magnesium sulphate in patients with unstable angina. A double blind, randomized, placebo-controlled study. Eur Heart J. Aug1997;18(8):1269-77.
  16. View Abstract: Sueda S, Saeki H, Otani T, Mineoi K. Limited efficacy of magnesium for the treatment of variant angina. J Cardiol. Sep1999;34(3):139-47.
  17. View Abstract: Eisenberg MJ. Magnesium deficiency and sudden death. Am Heart J. Aug1992;124(2):544-9.
  18. View Abstract: Kogan AK, Syrkin AL, Drinitsina SV, Kokanova IV. The antioxidant protection of the heart by coenzyme Q10 in stable stenocardia of effort. Patol Fiziol Eksp Ter. Oct1999;(4):16-9.
  19. View Abstract: Morisco C, et al. Effect of coenzyme Q10 in patients with congestive heart failure: a long-term multicenter randomized trial. Clin Invest. 1993;71:S134-S136.
  20. View Abstract: Mortensen SA, et al. Coenzyme Q10: clinical benefits with biochemical correlates suggesting a scientific breakthrough in the management of chronic heart failure. Int J Tissue React. 1990;12(3):155-62.
  21. View Abstract: Wilcken DE, et al. B vitamins and homocysteine in cardiovascular disease and aging. Ann N Y Acad Sci. Nov1998;854:361-70.
  22. View Abstract: Cacciatore L, Cerio R, Ciarimboli M, et al. The therapeutic effect of L-carnitine in patients with exercise-induced stable angina: a controlled study. Drugs Exp Clin Res. 1991;17(4):225-35.
  23. View Abstract: Cherchi A, Lai C, Angelino F, et al. Effects of L-carnitine on exercise tolerance in chronic stable angina: a multicenter, double-blind, randomized, placebo controlled crossover study. Int J Clin Pharmacol Ther Toxicol. Oct1985;23(10):569-72.
  24. View Abstract: Singh RB, Niaz MA, Agarwal P, et al. A randomised, double-blind, placebo-controlled trial of L-carnitine in suspected acute myocardial infarction. Postgrad Med J. Jan1996;72(843):45-50.
  25. View Abstract: Hiatt WR, Nawaz D, Brass EP. Carnitine metabolism during exercise in patients with peripheral vascular disease. J Appl Physiol. Jun1987;62(6):2383-7.
  26. View Abstract: Rizzon P, Biasco G, Di Biase M, et al. High doses of L-carnitine in acute myocardial infarction: metabolic and antiarrhythmic effects. Eur Heart J. Jun1989;10(6):502-8.
  27. View Abstract: Arsenian MA. Carnitine and its derivatives in cardiovascular disease. Prog Cardiovasc Dis. Nov1997;40(3):265-86.
  28. View Abstract: Anthony MS, Clarkson TB, Williams JK. Effects of Soy Isoflavones on Atherosclerosis: Potential Mechanisms. Am J Clin Nutr. Dec1998;68(Suppl6):1390S-93S.
  29. View Abstract: Messina MJ, Persky V, Setchell KDR. Soy Intake and Cancer Risk: A Review of the in Vitro and in Vivo Data. Nutr Cancer. 1994;21:113.
  30. View Abstract: Kellie S, Murphy CT, Westwick J. Tyrosine-kinase Activity in Rabbit Platelets Stimulated with Platelet-activating Factor. The Effect of Inhibiting Tyrosine Kinase with Genistein on Platelet-signal-molecule Elevation and Functional Responses. Euro J Biochem. 1993;216:639.
  31. View Abstract: Lichtenstein AH. Soy Protein, Isoflavones and Cardiovascular Disease Risk. J Nutr. Oct1998;128(10): 1589-92.
  32. View Abstract: Sozykin AV, Noeva EA, Balakhonova TV. Effect of L-arginine on platelet aggregation, endothelial function adn exercise tolerance in patients with stable angina pectoris. Ter Arkh. 2000;72(8):24-7.
  33. View Abstract: Blum A, Porat R, Rosenschein U, Keren G. Clinical and inflammatory effects of dietary L-arginine in patients with intractable angina pectoris. Am J Cardiol. May1999;83(10):1488-90.
  34. View Abstract: Egashira K, Hirooka Y, Kuga T. Effects of L-arginine supplementation on endothelium-dependent coronary vasodilation in patients with angina pectoris and normal coronary arteriograms. Circulation. Jul1996;94(2):130-4.
  35. View Abstract: Stephens NG, et al. Randomised Controlled Trial of Vitamin E in Patients with Coronary Disease: Cambridge Heart Antioxidant Study. Lancet. Mar1996;347(9004):781-86.
  36. View Abstract: Motoyama T, Kawano H, Kugiyama K, Hirashima O, Ohgushi M, Tsunoda R, et al. Vitamin E administration improves impairment of endothelium-dependent vasodilation in patients with coronary spastic angina. J Am Coll Cardiol. Nov1998;32(6):1672-9.
  37. View Abstract: Miwa K, Miyagi Y, Igawa A, Nakagawa K, Inoue H. Vitamin E deficiency in variant angina. Circulation. Jul1996;94(1):14-8.
  38. View Abstract: Yusuf S, Dagenais G, Pogue J, Bosch J, Sleight P. Vitamin E supplementation and cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators. N Engl J Med. Jan2000;342(3):154-60.
  39. Ernst E. Cardioprotection and Garlic. Lancet. 1997;349(9045):131.
  40. View Abstract: Steiner M, et al. A Double-blind Crossover Study in Moderately Hypercholesterolemic Men that Compared the Effect of Aged Garlic Extract and Placebo Administration on Blood Lipids. Am J Clin Nutr. 1996;64(6):866-70.
  41. View Abstract: Agarwal KC. Therapeutic Actions of Garlic Constituents. Med Res Rev. 1996;16(1):111-24.
  42. Fogarty M. Garlic's Potential Role in Reducing Heart Disease. Br J Clin Pract. 1993;47(2):64-65.
  43. View Abstract: Orekhov AN, et al. Direct Anti-atherosclerosis-related Effects of Garlic. Ann Med. 1995;27(1):63-65.
  44. View Abstract: Kiesewetter H, et al. Effect of Garlic on Platelet Aggregation in Patients with Increased Risk of Juvenile Ischaemic Attack. Eur J Clin Pharmacol. 1993;45(4):333-36.
  45. View Abstract: Bordia A. Effect of Garlic on Blood Lipids in Patients with Coronary Heart Disease. Am J Clin Nutr. 1981;34(10):2100-03.
  46. Bordia A, et al. Protective Effect of Garlic Oil on the Changes Produced by 3 Weeks of Fatty Diet on Serum Cholesterol, Serum Triglycerides, Fibrinolytic Activity and Platelet Adhesiveness in Man. Indian Heart J. 1982;34(2):86-88.
  47. View Abstract: Kendler BS. Garlic (Allium sativum) and Onion (Allium cepa): A Review of Their Relationship to Cardiovascular Disease. Prev Med. 1987;16(5):670-85.
  48. View Abstract: Arora RC, et al. The Long-term Use of Garlic in Ischemic Heart Disease--An Appraisal. Atherosclerosis. 1981;40(2):175-79.
  49. View Abstract: Koscielny J, et al. The Antiatherosclerotic Effect of Allium sativum. Atherosclerosis. May1999;144(1):237-49.
  50. View Abstract: Ide N, et al. Aged Garlic Extract Attenuates Intracellular Oxidative Stress. Phytomedicine. May1999;6(2):125-31.
  51. Garlic Oil: No Impact on Lipids. Harv Heart Lett. Sep1998;9(1):6.
  52. View Abstract: Morelli V. Alternative therapies: Part II. Congestive heart failure and hypercholesterolemia. Am Fam Physician. Sep2000;62(6): 325-30.
  53. Racz-Kotilla E, et al. Salidiuretic and Hypotensive Action of Ribes-Leaves. Planta Medica. 1980;29:110-14.
  54. Wagner H, et al. Cardioactive Drugs IV. Cardiotonic Amines from Crataegus oxyacantha. Planta Medica. 1982;45:99-101.
  55. View Abstract: Davey Smith G, Song F, Sheldon TA. Cholesterol lowering and mortality: the importance of considering initial level of risk. BMJ. 1993;306:1367-73.
  56. View Abstract: Sebrechts CP, Klein JL, Ahnve S, Froelicher VF, Ashburn WL. Myocardial perfusion changes following 1 year of exercise training assessed by thallium-201 circumferential count profiles. Am Heart J. 1986;112:1217-26.
  57. View Abstract: Todd IC, Bradnam MS, Cooke MBD, Ballantyne D. Effects of daily high intensity exercise on myocardial perfusion in angina pectoris. Am J Cardiol. 1991;68:1593-9.
  58. View Abstract: Vlietstra RE, Kronmal RA, Oberman A, Frye RL, Killip T. Effect of cigarette smoking on survival of patients with angiographically documented coronary artery disease. Report from the CASS registry. JAMA. 1986;255:1023-7.
  59. View Abstract: Hermanson B, Omenn GS, Kronmal RA, Gersh BJ. Beneficial six-year outcome of smoking cessation in older men and women with coronary artery disease. Results from the CASS registry. N Engl J Med. 1988;319:1365-9.
  60. View Abstract: Neaton JD, Wentworth D, on behalf of the Multiple Risk Factor Intervention Trial Research Group. Serum cholesterol, blood pressure, cigarette smoking, and death from coronary heart disease. Overall findings and differences by age for 316,099 white men. Arch Intern Med. 1992;152:56-64.