Keep your lifelines clear and let blood flow freely to your heart. According to research or other evidence, the following self-care steps may help prevent artery blockage and reduce your heart attack risk:
These recommendations are not comprehensive and are not intended to replace the advice of your doctor or pharmacist. Continue reading the full heart attack article for more in-depth, fully-referenced information on medicines, vitamins, herbs, and dietary and lifestyle changes that may be helpful.
Heart attacks occur when blood flow to a portion of the heart is severely reduced or cut off. The result is death of heart muscle cells (called an infarct).
Hardening and narrowing (atherosclerosis) of the coronary arteries that feed the heart is usually the underlying problem. In some cases, a blood clot blocks blood flow; other times, the narrowing is caused by atherosclerosis alone. Spasm of the coronary arteries may also cause a heart attack.
Elevated cholesterol, triglycerides, or homocysteine; angina pectoris; and diabetes are each associated with an increased risk of heart attack. Congestive heart failure can occur in some people from severe damage to the heart resulting from a heart attack.
Product ratings for a heart attack
|Science Ratings||Nutritional Supplements||Herbs|
Vitamin C (if deficient)
Magnesium (IV immediately following an MI)
NAC (IV immediately following an MI)
Vitamin C (for those not deficient)
Reliable and relatively consistent scientific data showing a substantial health benefit.
Contradictory, insufficient, or preliminary studies suggesting a health benefit or minimal health benefit.
For an herb, supported by traditional use but minimal or no scientific evidence. For a supplement, little scientific support and/or minimal health benefit.
The first symptom of a heart attack is usually deep aching or pressure-like chest pain that may radiate to the back, jaw, or left arm. Discomfort may be mild or severe. About 20% of heart attacks are silent (i.e., they cause no symptoms and may therefore be missed). Older people may experience shortness of breath. Nausea and vomiting may also occur. Restlessness, apprehension, pallor, and sweating are common.
Dietary fat independently affects heart attack risk. The Nurses’ Health Study found that eating foods high in saturated fats (meat and dairy fat) and trans fatty acids (margarine, hydrogenated vegetable oils, and many processed foods containing hydrogenated vegetable oils) was directly associated with many nonfatal heart attacks and deaths from coronary heart disease.1 Consuming foods high in monounsaturated fat, such as olive oil, and polyunsaturated fat, as found in nuts and most vegetable oils, is linked to a decreased risk. This same study revealed that margarine increased the incidence of heart attack, particularly among women who had eaten margarine consistently for more than a decade.2 Other studies report a direct association between frequent consumption of meat and butter and heart attack occurrence.3
Research consistently shows that people who frequently eat nuts have a dramatically reduced risk of heart disease;4 5 this could be because nut consumption lowers cholesterol levels.6 7 Of nuts commonly consumed, almonds and walnuts may be most effective at lowering cholesterol, and macadamia nuts may be least beneficial.8 Hazelnuts9 and pistachio nuts10 may also help lower cholesterol.
Nuts contain many nutrients that could be responsible for protection against heart disease, including fiber, vitamin E, alpha-linolenic acid (found primarily in walnuts), oleic acid, magnesium, and arginine. Therefore, exactly how nuts lower cholesterol or lower the risk of heart disease remains somewhat unclear. Some doctors even believe that nuts may not be directly protective. Rather, people who eat nuts may not eat as much dairy, eggs, or trans fatty acids from margarine and processed food, the avoidance of which would reduce both cholesterol levels and the risk of heart disease.11 12 Nonetheless, the remarkable consistency of research outcomes strongly suggests that nuts directly protect against heart disease. Although nuts are loaded with calories, a recent preliminary study reported that adding hundreds of calories per day from nuts for six months did not increase body weight in humans13 —an outcome supported by several other reports.14 Even when increasing nut consumption has led to weight gain, the amount of added weight has been remarkably less than would be expected given the number of calories added to the diet.15
Several trials report that eating fish decreases heart attack deaths16 17 and reduces the size of the infarct,18 though some researchers have not confirmed these findings.19 The link between fish eating and heart attack prevention is supported by research showing that fish oil supplements help reverse atherosclerosis.20
Eating eggs may increase heart attack risk. People who consume eggs have been reported to be more likely to die from all types of heart disease, including heart attack, in some,21 although not all, research.22 Increased oxidation, a state associated with heart attack risk, may be the key. Cooking or exposure to air oxidizes the cholesterol in eggs.23 Eating eggs enhances LDL (“bad”) cholesterol oxidation,24 which may in turn contribute to heart attack risk.
Eating a diet high in refined carbohydrates (e.g., white flour, white rice, simple sugars) appears to increase the risk of coronary heart disease, and thus of heart attacks, especially in overweight women.25
A high-fiber diet, particularly water-soluble fiber (high in oats, psyllium seeds, fruit, vegetables, and legumes), is associated with decreased risk of both fatal and nonfatal heart attacks,26 probably because these fibers are known to lower cholesterol.27 However, large trials separately studying men and women who were followed for years, have linked the greatest protection to water-insoluble fiber (from cereals),28 29 though scientists have yet to understand why. Until the details are better understood, doctors often recommend increasing intake of fruit, vegetables, beans, oats, and whole grains. In a preliminary study,30 the total number of deaths from cardiovascular disease was found to be significantly lower among men with high fruit consumption.
Making positive dietary changes immediately following a heart attack is likely to decrease the chance of a second heart attack. In one study, individuals began eating more vegetables and fruits, and substituted fish, nuts, and legumes for meat and eggs 24–48 hours after a heart attack. Six weeks later, the diet group had significantly fewer fatal and nonfatal heart attacks than a similar group who did not make these dietary changes.31 This trend continued for an additional six weeks.32
Many doctors tell people trying to reduce their risk of heart disease to avoid all meat, margarine, and other processed foods containing hydrogenated oils and dairy fat. Fish are often suggested instead of meat; nuts instead of snack foods containing hydrogenated oils; olive oil instead of butter; nonfat yogurt, milk, and even cheese instead of full or reduced fat versions of the same foods; and oatmeal instead of eggs for breakfast.
People who eat diets high in alpha-linolenic acid (ALA), which is found in canola and flaxseed oils, have higher blood levels of omega-3 fatty acids than those consuming lower amounts,33 34 which may confer some protection against atherosclerosis. In 1994, researchers conducted a study in people with a history of heart disease, using what they called the “Mediterranean” diet.35 The diet was significantly different from what people from Mediterranean countries actually eat, in that it contained little olive oil. Instead, the diet included a special margarine high in ALA. Those people assigned to the Mediterranean diet had a remarkable 70% reduced risk of dying from heart disease compared with the control group during the first 27 months. Similar results were also confirmed after almost four years.36 The diet was high in beans and peas, fish, fruit, vegetables, bread, and cereals; and low in meat, dairy fat, and eggs. Although the authors believe that the high ALA content of the diet was partly responsible for the surprising outcome, other aspects of the diet may have been partially or even totally responsible for decreased death rates. Therefore, the success of the Mediterranean diet does not prove that ALA protects against heart disease.37
Most studies confirm that light to moderate alcohol consumption (one to three drinks per day) significantly reduces both fatal and nonfatal heart attack risk38 39 40 41 compared to heavy or no drinking,42 43 though a few reports find the link to protection both weak and statistically insignificant.44 In France, abundant red wine drinking was assumed to be responsible for the country’s remarkably low incidence of heart disease. However, a lower intake of animal fats in the French diet now appears to be the primary reason for what has been called the French paradox.45 However, as animal fat intake continues to increase in France, a trend that began in the 1970s, researchers now speculate that heart disease and heart attacks will also increase.
Although red wine has been branded best for heart disease in a few reports, all types of alcoholic beverages appear to be beneficial.46 Whether red wine has a clear advantage over other forms of alcohol remains unclear. Alcohol reduces the risk for heart attacks because it increases HDL (“good”) cholesterol47 and acts as a blood thinner.48 High levels of another risk factor for heart attacks, lipoprotein(a), have also been reported to be lowered by drinking alcohol.49
Despite this healthful effect, alcohol consumption can cause liver disease (e.g., cirrhosis), cancer, high blood pressure, alcoholism, and, at high intake, even an increased risk of heart attack. As a result, some doctors never recommend alcohol, even for people at risk for heart attack. Nevertheless, because limited intake of alcohol lowers heart attack risk, some people at high risk for heart attack who are not alcoholics, have healthy livers and normal blood pressure, and are not at an especially high risk for cancer, may benefit from light drinking. In fact, since heart disease is the leading cause of death in the United States, and alcohol reduces that risk, most studies report that light drinkers live slightly longer on average than teetotalers. In an analysis of 16 trials, men who drank less than two drinks per day and women who averaged less than one drink per day were likely to slightly outlive those who did not drink at all.50 In the same report, however, people who drank beyond these moderate levels in men and low levels in women were more likely to die sooner than were nondrinkers. In deciding whether light drinking might do more good than harm, people at high risk for heart attack should consult a doctor.
Drinking five cups of coffee or more per day has been shown to increase the risk of nonfatal heart attack in both men51 and women.52 Though many studies find such links,53 many others do not.54 Nevertheless, heavy coffee drinking should be avoided. This disparity may result in part from the fact that paper-filtered coffee does not raise cholesterol but percolated, boiled, or French press coffees do. Several recent studies have linked coffee drinking to increased blood levels of homocysteine, another risk factor for heart disease.55 56 In this regard, research has yet to absolve paper-filtered coffee, because these studies have not examined separate effects for coffee prepared by different methods.
Recent preliminary evidence has implicated salt consumption as a risk factor for heart disease and death from heart disease in overweight people.57 Among overweight persons, an increase in salt consumption of 2.3 grams per day was associated with a 44% increase in coronary heart disease mortality, a 61% increase in cardiovascular disease mortality, and a 39% increase in mortality from all causes. Blinded, intervention trials are still needed to confirm these preliminary observations.
Preliminary research conducted several decades ago suggested that high sugar consumption increased heart attack risk.58 Some researchers at that time disagreed59 and others have subsequently been unable to find a link. Nevertheless, sugar has been associated with reduced HDL (“good”) cholesterol,60 increased triglycerides,61 as well as an increase in other risk factors linked to heart attacks.62 As a result, many doctors recommend that people reduce their intake of sugar despite the fact that high sugar intake leads to only slightly higher risks of heart disease in most reports.63
Two very large studies have confirmed that smoking increases the risk of a first heart attack by more than 100% in some people.64 65 Women were found to be at greater risk than men; “inhalers” were almost twice as susceptible as non-inhalers. Quitting smoking is critical for reversing this risk. According to one study, female ex-smokers who had not smoked for three or more years were “virtually indistinguishable” from women who had never smoked in terms of heart attack risk.66 Exposure to secondhand smoke, which increases infarct size in animals67 and impairs heart function and exercise tolerance in heart attack survivors,68 should also be avoided. For people who have already had a heart attack, quitting smoking is associated with a significant decrease in mortality.69
Routine, moderate exercise is preferred over excessive exertion for people at risk for heart attacks. Research indicates that heart attack risk rises six-fold for one hour immediately following heavy physical activity (compared to moderate or no activity), particularly among people who are sedentary.70 This risk is more than five times less in people who exercise four or more times per week.71 Most studies show that regular, moderate exercise reduces overall heart attack risk. Therefore, researchers and doctors recommend that susceptible individuals engage in an exercise program.72 Exercise recommendations for people who are at risk or who have a history of heart attack need to be custom tailored to the individual. Therefore, anyone with a heart condition or anyone over the age of 40 should consult a healthcare professional before beginning an exercise plan.
Although sexual activity can trigger a heart attack, the risk is very low and73 is no greater for people with a history of angina or heart disease. Doctors recommend regular, moderate exercise to further reduce this risk.
Obesity is associated with an increased risk for heart attack, particularly among younger people.74 One study found this relationship increased in women who also had a history of diabetes or high cholesterol.75 Doctors encourage overweight people who are at risk for heart attack to lose the extra weight.
Type A behavior is typically defined by time-conscious, impatient, and aggressive feelings and the behavior that arises from those feelings. Type A behavior has been linked to increased heart attack risk in some,76 but not all, studies.77 The link between personality and heart attack remains unclear.78 In the study with the most hopeful outcome, psychological intervention aimed at modifying type A behavior was reported to successfully change not only emotional state but also to significantly lower the risk of subsequent heart attacks.79 Some healthcare professionals recommend that people at high risk for heart attacks who also have frequent feelings of impatience, lack of time, and hostility, seek counseling as a way to feel better and potentially reduce their risk of heart disease.
Researchers suggest that negative emotional states, such as hostility, distrust, anger,80 worry,81 and stress,82 promote heart attacks. Results from the National Heart, Lung, and Blood Institute (NHLBI) Family Heart Study showed that hostility was significantly associated with an increased risk of having a heart attack (in women) and increased odds of having heart surgery (in men), when a family history of heart disease was also present.83 84 According to another study, women with a history of heart disease who report stressful relationships with their husbands or partners have almost triple the risk of suffering a heart attack, dying from heart disease, or requiring bypass surgery or angioplasty, compared with women in positive relationships.85
Following a heart attack, bed rest is often recommended. However, a review of trials concluded that bed rest may actually worsen recovery from a heart attack.86
Many hospitals perform a procedure called Primary Percutaneous Transluminal Cardiac Angioplasty (PTCA) in order to clear blocked arteries. Certain individuals might benefit more from this procedure than from thrombolytic agents.
L-carnitine is an amino acid important for transporting fats that can be turned into energy in the heart. Clinical trials have reported that taking L-carnitine (4–6 grams per day) increases the chance of surviving a heart attack.87 88 89 In one double-blind trial, individuals with suspected heart attack were given 2 grams of L-carnitine per day for 28 days.90 At the completion of this study, infarct size, as well as the number of nonfatal heart attacks, was lower in the group receiving L-carnitine versus the placebo group. Double-blind research using L-carnitine intravenously also shows promise.91
Vitamin C has been reported to protect blood vessels from problems associated with heart attack risk in a variety of ways.92 93 94 However, research attempting to link vitamin C directly to protection from heart attacks has been inconsistent.95 96 The reason for this discrepancy appears related to the amount of vitamin C intake investigated in these studies. True or marginal vitamin C deficiencies do appear to increase the risk of suffering heart attacks.97 98 However, in trials comparing acceptable (i.e., non-deficient) vitamin C levels to even higher levels, additional vitamin C has not been protective.99 Therefore, though many doctors recommend that people at high risk for heart attack take vitamin C—often 1 gram per day—most evidence currently suggests that consuming as little as 100–200 mg of vitamin C per day from food or supplements may well be sufficient.
Coenzyme Q10 (CoQ10) also contributes to the energy-making mechanisms of the heart and has been reported to lower lipoprotein(a), a risk factor for heart disease.100 Animal studies confirm CoQ10’s ability to protect heart muscle against reduced blood flow.101 102 In one double-blind trial, either 120 mg of CoQ10 or placebo was given to people who had recently survived a heart attack. After 28 days, the CoQ10 group had experienced significantly fewer repeat heart attacks, fewer deaths from heart disease, and less chest pain than the placebo group.103 In another double-blind study of people suffering a heart attack, supplementation with 60 mg of coenzyme Q10 twice a day for one year significantly reduced the incidence of recurrent cardiac events (fatal or non-fatal heart attack). 104 Treatment was begun within 72 hours of the onset of the heart attack. CoQ10 used with selenium (see below) has also been reported to increase the rate of heart attack survival.105
The relation between selenium and protection from heart attacks remains uncertain. Low blood levels of selenium have been reported in people immediately following a heart attack,106 suggesting that heart attacks may increase the need for selenium. However, other researchers claim that low selenium levels are present in people before they have a heart attack, suggesting that the lack of selenium might increase heart attack risk.107 One report found that low blood levels of selenium increased the risk of heart attack only in smokers,108 and another found the link only in former smokers.109 Yet others have found no link between low blood levels of selenium and heart attack risk whatsoever.110 In a double-blind trial, individuals who already had one heart attack were given 100 mcg of selenium per day or placebo for six months.111 At the end of the trial, there were four deaths from heart disease in the placebo group but none in the selenium group (although the numbers were too small for this difference to be statistically significant). In other controlled research, a similar group was given placebo or 500 mcg of selenium six hours or less after a heart attack followed by an ongoing regimen of 100 mcg of selenium plus 100 mg of coenzyme Q10 per day.112 One year later, six people had died from a repeat heart attack in the placebo group, compared with no heart attack deaths in the supplement group. Despite the lack of consistency in published research, some doctors recommend that people at risk for a heart attack supplement with selenium—most commonly 200 mcg per day.
Several studies113 114 including two double-blind trials115 116 have reported that 400 to 800 IU of natural vitamin E reduces the risk of heart attacks. However, other recent double-blind trials have found either limited benefit,117 or no benefit at all from supplementation with synthetic vitamin E.118 One of the negative trials used 400 IU of natural vitamin E119 —a similar amount and form to previous successful trials. In attempting to make sense of these inconsistent findings the following is clear: less than 400 IU of synthetic vitamin E, even when taken for years, does not protect against heart disease. Whether 400 to 800 IU of natural vitamin E is or is not protective remains unclear.
In one study, intravenous injections of NAC (N-acetyl cysteine) decreased the amount of tissue damage in people who had suffered a heart attack.120 Whether oral NAC would have the same effect is unknown.
Fish oil contains the beneficial omega-3 fatty acids EPA and DHA, which have led to partial reversal of atherosclerosis in a double-blind trial.121 In another double-blind trial, individuals were given either fish oil (containing about 1 gram of EPA and 2/3 gram of DHA) or mustard oil (containing about 3 grams alpha linolenic acid, another omega-3 fatty acid) 18 hours after a heart attack. Both groups experienced fewer nonfatal heart attacks compared to a placebo group, while the fish oil group also experienced fewer fatal heart attacks.122 The largest published study on omega-3 fatty acids for heart attack prevention was the preliminary GISSI Prevenzione Trial,123 which reported that 850 mg of omega-3 fatty acids from fish oil per day for 3.5 years resulted in a 20% reduction in total mortality and a 45% decrease in sudden death. Other investigators suggest that fish oil reduces the amount of heart muscle damage from a heart attack and enhances the effect of blood-thinning medication.124 People wishing to supplement with fish oil should take fish oil supplements that include at least small amounts of vitamin E, which may protect this fragile oil against free radical damage.125
Blood levels of the antioxidant nutrients vitamins A, C, and E, and beta-carotene are reported to be lower in people with a history of heart attack, compared with healthy individuals.126 The number of free radical molecules is also higher, suggesting a need for antioxidants. Streptokinase, a drug therapy commonly used immediately following a heart attack, enhances the need for antioxidants.127
Taking antioxidant supplements may improve the outcome for people who have already had a heart attack. In one double-blind trial, people were given 50,000 IU of vitamin A per day, 1,000 mg of vitamin C per day, 600 IU of vitamin E per day, and approximately 41,500 IU of beta-carotene per day or placebo.128 After 28 days, the infarct size of those receiving antioxidants was significantly smaller than the infarct size of the placebo group.
Blood levels of magnesium are lower in people who have a history of heart attack.129 Most trials have successfully used intravenous magnesium right after a heart attack occurs to decrease death and complications from heart attacks.130 By far the largest trial did not find magnesium to be effective.131 However, other researchers have argued that delaying the initial infusion of magnesium and administering the magnesium for too short a period may have caused this negative result.132 People with a history of heart attack or who are at risk should consult with their cardiologist about the possible use of immediate intravenous magnesium should they ever suffer another heart attack.
Except for a link between high levels of magnesium in drinking water and a low risk of heart attacks,133 134 little evidence suggests that oral magnesium reduces heart attack risk. One trial found that magnesium pills taken for one year actually increased complications for people who had suffered a heart attack.135 While another study reported that 400–800 mg of magnesium per day for two years decreased both deaths and complications due to heart attacks, results are difficult to interpret because those taking oral magnesium had previously received intravenous magnesium as well.136 While increasing dietary magnesium has reduced the risk of heart attacks,137 foods high in magnesium may contain other protective factors that might be responsible for this positive effect. Therefore, evidence supporting supplemental oral magnesium to reduce the risk of heart attacks remains weak.
High blood levels of the amino acid homocysteine have been linked to an increased risk of heart attack in most,138 139 140 141 though not all,142 143 studies. A blood test screening for levels of homocysteine, followed by supplementation with 400 mcg of folic acid and 500 mcg of vitamin B12 per day could prevent a significant number of heart attacks, according to one analysis.144 Folic acid145 146 and vitamins B6 and B12 are known to lower homocysteine.147
There is a clear association between low blood levels of folate and increased risk of heart attacks in men.148 Based on the available research, some doctors recommend 50 mg of vitamin B6, 100–300 mcg of vitamin B12, and 500–800 mcg of folic acid per day for people at high risk of heart attack.
Low levels of beta-carotene in fatty tissue have been linked to an increased incidence of heart attacks, particularly among smokers.149 One population study found that eating a diet high in beta-carotene is associated with a lower rate of nonfatal heart attacks.150 However, beta-carotene supplementation may not offer the same protection provided by foods that contain beta-carotene. Most,151 152 but not all, trials153 have found that supplemental beta-carotene is not associated with a reduced risk of heart attacks.
Years ago, researchers reported that taking chondroitin sulfate for six years substantially reduced the risk of fatal and nonfatal heart attacks in people with heart disease.154 155 156 Chondroitin may work by inhibiting atherosclerosis and by acting as an anticoagulant. The few doctors aware of these older studies sometimes recommend that people with a history of heart disease or who are at risk for heart attack take approximately 500 mg of chondroitin sulfate three times per day.
The possibility that vitamin D supplementation may increase the risk of heart disease remains an unproven and controversial issue. A preliminary trial suggested that a high intake of vitamin D from both dietary and supplemental sources increased heart attack risk.157 However, other researchers have found that blood levels of vitamin D are no higher in people who had suffered a heart attack when compared to control groups.158 Similarly, atherosclerosis does not appear to correlate with blood levels of vitamin D.159 In fact, one trial found that higher levels of activated vitamin D correlated with less artery-clogging calcium deposits in humans.160
Relatively high blood levels of calcium—sometimes a marker for high vitamin D intake—have been associated with high risk of heart attacks in Sweden.161 However, high dietary vitamin D intake in Sweden often comes from high-fat dairy products, so the high calcium levels might simply reflect diets higher in dairy fat and have nothing to do with vitamin D.
Despite the lack of consistent evidence, some researchers continue to have concerns. Vitamin D supplementation has reversed some of the beneficial effects of estrogen use in women with risk factors for heart disease,162 an outcome confirmed by others using only 300 IU of vitamin D per day.163 Further research is required to determine whether supplemental vitamin D increases heart attack risk.
Although several reports have linked iron (both through diet and supplements) to an increased risk of heart disease, a recent analysis of 12 trials has found no link whatsoever between iron status and the risk of heart disease.164 While it remains prudent for a variety of other reasons for people not to supplement iron unless a deficiency has been diagnosed, supplemental iron now appears unlikely to substantially increase the risk of suffering a heart attack.
Preliminary clinical trials in China suggest that astragalus may be of benefit in people after they have suffered a heart attack.165 166 These studies did not attempt to show any survival or symptom reduction benefit. Therefore, further research is needed to determine whether astragalus would be of benefit to people with heart attacks or angina.
1. Hu FB, Stampfer MJ, Manson JE, et al. Dietary fat intake and the risk of coronary heart disease in women. N Engl J Med 1997;337:1491–9.
2. Willett WC, Stampfer MJ, Manson JE, et al. Intake of trans fatty acids and risk of coronary heart disease among women. Lancet 1993;341:581–5.
3. Gramenzi A, Gentile A, Fasoli M, et al. Association between certain foods and risk of acute myocardial infarction in women. BMJ 1990;300:771–3.
4. Hu FB, Stampfer MJ, Manson JE, et al. Frequent nut consumption and risk of coronary heart disease in women: prospective cohort study. BMJ 1998;317:1341–5.
5. Fraser GE, Sabaté J, Beeson WL, Strahan TM. A possible protective effect of nut consumption on risk of coronary heart disease. Arch Intern Med 1992;152:1416–24.
6. Abbey M, Noakes M, Belling GB, Nestel PJ. Partial replacement of saturated fatty acids with almonds or walnuts lowers total plasma cholesterol and low-density-lipoprotein cholesterol. Am J Clin Nutr 1994;59:995–9.
7. Sabaté J, Frasser GE, Burke K, et al. Effects of walnuts on serum lipid levels and blood pressure in normal men. N Engl J Med 1993;328:603–7.
8. Fraser GE. Nut consumption, lipids, and risk of a coronary event. Clin Cardiol 1999;22(Suppl III):III11–5 [review].
9. Durak I, Köksal I, Kaçmaz M, et al. Hazelnut supplementation enhances plasma antioxidant potential and lowers plasma cholesterol levels. Clin Chim Actia 1999;284:113–5 [letter].
10. Edwards K, Kwaw I, Matud J, Kurtz I. Effect of pistachio nuts on serum lipid levels in patients with moderate hypercholesterolemia. J Am Coll Nutr 1999;18:229–32.
11. Mirkin G. Walnuts and serum lipids. N Engl J Med 1993;329:358 [letter].
12. Mann GV. Walnuts and serum lipids. N Engl J Med 1993;329:358 [letter].
13. Fraser GE, Jaceldo K, Sabaté J, et al. Changes in body weight with a daily supplement of 340 calories from almonds for six months. FASEB J 1999;13:A539 [abstract].
14. Fraser GE. Nut consumption, lipids, and risk of a coronary event. Clin Cardiol 1999;22(Suppl III):III11–5 [review].
15. Durak I, Köksal I, Kaçmaz M, et al. Hazelnut supplementation enhances plasma antioxidant potential and lowers plasma cholesterol levels. Clin Chim Actia 1999;284:113–5 [letter].
16. Daviglus ML, Stamler J, Orencia AJ, et al. Fish consumption and the 30-year risk of fatal myocardial infarction. N Engl J Med 1997;336:1046–53.
17. Burr ML, Fehily AM, Gilbert JF, et al. Effects of changes in fat, fish, and fibre intakes on death and myocardial reinfarction: diet and reinfarction trial. Lancet 1989;2:757–61.
18. Landmark K, Abdelnoor M, Kilhovd B, Dorum HP. Eating fish may reduce infarct size and the occurrence of Q wave infarcts. Eur J Clin Nutr 1998;52:40–4.
19. Morris MC, Manson JE, Rosner B, et al. Fish consumption and cardiovascular disease in the physicians’ health study: a prospective study. Am J Epidemiol 1995;142:166–75.
20. Von Schacky C, Angerer P, Kothney W, et al. The effect of dietary omega-3 fatty acids on coronary atherosclerosis. A randomized double-blind, placebo-controlled trial. Ann Intern Med 1999;130:554–62.
21. Shekelle RB, Stamler J. Dietary cholesterol and ischaemic heart disease. Lancet 1989;1:1177–9.
22. Hu FB, Stampfer MJ, Rimm EB, et al. A prospective study of egg consumption and risk of cardiovascular disease in men and women. JAMA 1999;281:1387–94.
23. Raloff J. Oxidized lipids: a key to heart disease? Sci News 1985;127:278.
24. Levy Y, Maor I, Presser D, Aviram M. Consumption of eggs with meals increases the susceptibility of human plasma and low-density lipoprotein to lipid peroxidation. Ann Nutr Metabol 1996;40:243–51.
25. Liu S, Willett WC, Stampfer MJ, et al. A prospective study of dietary glycemic load, carbohydrate intake, and risk of coronary heart disease in US women. Am J Clin Nutr 2000;71:1455–61.
26. Pietinen P, Rimm EB, Korhonen P, et al. Intake of dietary fiber and risk of coronary heart disease in a cohort of Finnish men. The Alpha-Tocopherol, Beta-Carotene Prevention Study. Circulation 1996;94:2720–7.
27. Brown L, Rosner B, Willett WW, Sacks FM. Cholesterol-lowering effects of dietary fiber: a meta-analysis. Am J Clin Nutr 1999;69:30–42.
28. Rimm EB, Ascherio A, Giovannucci E, et al. Vegetable, fruit, and cereal fiber intake and risk of coronary heart disease among men. JAMA 1996;275:447–51.
29. Wolk A, Manson JE, Stampfer MJ, et al. Long-term intake of dietary fiber and decreased risk of coronary heart disease among women. JAMA 1999;281:1998–2004.
30. Strandhagen E, Hansson PO, Bosaeus I, et al. High fruit intake may reduce mortality among middle-aged and elderly men. The Study of Men Born in 1913. Eur J Clin Nutr 2000;54:337–41.
31. Singh RB, Rastogi SS, Verma R, et al. An Indian experiment with nutritional modulation in acute myocardial infarction. Am J Cardiol 1992;69:879–85.
32. Singh RB, Niaz MA, Ghosh S, et al. Effect on mortality and reinfarction of adding fruits and vegetables to a prudent diet in the Indian Experiment of Infarct Survival (IEIS). J Am Coll Nutr 1993;12:255–61.
33. Gramenzi A, Gentile A, Fasoli M, et al. Association between certain foods and risk of acute myocardial infarction in women. BMJ 1990;300:771–3.
34. Hu FB, Stampfer MJ, Manson JE, et al. Frequent nut consumption and risk of coronary heart disease in women: prospective cohort study. BMJ 1998;317:1341–5.
35. de Lorgeril M, Renaud S, Mamelle N, et al. Mediterranean alpha-linolenic acid-rich diet in secondary prevention of coronary heart disease. Lancet 1994;343:1454–9.
36. de Lorgeril M, Salen P, Martin JL, et al. Mediterranean diet, traditional risk factors, and the rate of cardiovascular complications after myocardial infarction: final report of the Lyon Diet Heart Study. Circulation 1999;99:779–85.
37. Rice RD. Mediterranean diet. Lancet 1994;344:893–4 [letter].
38. Rosenberg L, Slone D, Shapiro S, et al. Alcoholic beverages and myocardial infarction in young women. Am J Public Health 1981;71:82–5.
39. Kono S, Handa K, Kawano T, et al. Alcohol intake and nonfatal acute myocardial infarction in Japan. Am J Cardiol 1991;68:1011–4.
40. Jackson R, Scragg R, Beaglehole R. Does recent alcohol consumption reduce the risk of acute myocardial infarction and coronary death in regular drinkers? Am J Epidemiol 1992;136:819–24.
41. Hammar N, Romelsjo A, Alfredsson L. Alcohol consumption, drinking pattern and acute myocardial infarction. A case referent study based on the Swedish Twin Register. J Intern Med 1997;241:125–31.
42. Bianchi C, Negri E, La Vecchia C, Franceschi S. Alcohol consumption and the risk of acute myocardial infarction in women. J Epidemiol Community Health 1993;47:308–11.
43. Gaziano JM, Hennekens CH, Godfried SL, et al. Type of alcoholic beverage and risk of myocardial infarction. Am J Cardiol 1999;83:52–7.
44. Hart CL, Smith GD, Hole DJ, Hawthorne VM. Alcohol consumption and mortality from all causes, coronary heart disease, and stroke: results from a prospective cohort study of Scottish men with 21 years of follow up. BMJ 1999;318:1725–9.
45. Law M, Wald N. Why heart disease mortality is low in France: the time lag explanation. BMJ 1999;318:1471–80 [review].
46. Gaziano JM, Hennekens CH, Godfried SL, et al. Type of alcoholic beverage and risk of myocardial infarction. Am J Cardiol 1999;83:52–7.
47. Gaziano JM, Buring JE, Breslow JL, et al. Moderate alcohol intake, increased levels of high-density lipoprotein and its subfractions, and decreased risk of myocardial infarction. N Engl J Med 1993;329:1829–34.
48. Renaud S, de Lorgeril M. Wine, alcohol, platelets and the French paradox for coronary heart disease. Lancet 1992;339:1523–6.
49. Sharpe PC, McGrath LT, McClean E, et al. Effect of red wine consumption on lipoprotein (a) and other risk factors for atherosclerosis. Q J Med 1995;88:101–8.
50. Holman CDJ, English DR, Milne E, Winter MG. Meta-analysis of alcohol and all-cause mortality: a validation of NHMRC recommendations. Med J Aust 1996;64:141–5.
51. Rosenberg L, Palmer JR, Kelly JP, et al. Coffee drinking and nonfatal myocardial infarction in men under 55 years of age. Am J Epidemiol 1988;128:570–8.
52. Palmer JR, Rosenberg L, Rao RS, Shapiro S. Coffee consumption and myocardial infarction in women. Am J Epidemiol 1995;141:724–31.
53. Greenland S. A meta-analysis of coffee, myocardial infarction, and coronary death. Epidemiology 1993;4:366–74.
54. Myers MG, Basinski A. Coffee and coronary heart disease. Arch Intern Med 1992;152:1767–2.
55. Stolzenberg-Solomon RZ, Miller ER 3rd, Maquire MG, et al. Association of dietary protein intake and coffee consumption with serum homocysteine concentrations in an older population. Am J Clin Nutr 1999;69:467–75.
56. Nygård O, Refsum H, Velanb PM, et al. Coffee consumption and plasma total homocysteine: The Hordaland Homocysteine Study. Am J Clin Nutr 1997;65:136–43.
57. He J, Ogden LG, Vupputuri S, et al. Dietary sodium intake and subsequent risk of cardiovascular disease in overweight adults. JAMA 1999;282:2027–34.
58. Yudkin J, Morland J. Sugar intake and myocardial infarction. Am J Clin Nutr 1967;20:503–6.
59. Platt L, Ball KP, Brigden WW, et al. Dietary sugar intake in men with myocardial infarction. Lancet 1970 Dec 19;2:1265–71.
60. Yudkin J, Kang SS, Bruckdorfer KR. Effects of high dietary sugar. Br Med J 1980;281:1396.
61. Albrink MJ, Ullrich IH. Interaction of dietary sucrose and fiber on serum lipids in healthy young men fed high carbohydrate diets. Am J Clin Nutr 1986;43:419–28.
62. Reiser S. Effect of dietary sugars on metabolic risk factors associated with heart disease. Nutr Health 1985;3:203–16.
63. Liu K, Stamler J, Trevisan M, Moss D. Dietary lipids, sugar, fiber, and mortality from coronary heart disease. Bivariate analysis of international data. Arteriosclerosis 1982;2:221–7.
64. Prescott E, Hippe M, Schnohr P, et al. Smoking and risk of myocardial infarction in women and men: longitudinal population study. BMJ 1998;316:1043–7.
65. Nyboe J, Jensen G, Appleyard M, Schnohr P. Smoking and the risk of first acute myocardial infarction. Am Heart J 1991;122:438–47.
66. Rosenberg L, Palmer JR, Shapiro S. Decline in the risk of myocardial infarction among women who stop smoking. N Engl J Med 1990;322:213–7.
67. Zhu B, Sun Y, Sievers RE, et al. Exposure to environmental tobacco smoke increases myocardial infarct size in rats. Circulation 1994;89:1282–90.
68. Zhu B, Parmley WW. Hemodynamic and vascular effects of active and passive smoking. Am Heart J 1995;130:1270–5 [review].
69. Wilson K, Gibson N, Willan A, Cook D. Effect of smoking cessation on mortality after myocardial infarction: meta-analysis of cohort studies. Arch Intern Med 2000;160:939–44.
70. Mittleman MA, Maclure M, Tofler GH, et al. Triggering of acute myocardial infarction by heavy physical exertion. Protection against triggering by regular exertion. Determinants of Myocardial Infarction Onset Study Investigators. N Engl J Med 1993;329:1677–83.
71. Willich SN, Lewis M, Lowel H, et al. Physical exertion as a trigger of acute myocardial infarction. Triggers and Mechanisms of Myocardial Infarction Study Group. N Engl J Med 1993;329:1684–90.
72. Mittleman MA, Siscovick DS. Physical exertion as a trigger of myocardial infarction and sudden cardiac death. Cardiol Clin 1996;14:263–70 [review].
73. Muller JE, Mittleman A, Maclure M, et al. Triggering myocardial infarction by sexual activity. Low absolute risk and prevention by regular physical exertion. Determinants of Myocardial Infarction Onset Study Investigators. JAMA 1996;275:1405–9.
74. Schargrodsky H, Rozlosnik J, Ciruzzi M, et al. Body weight and nonfatal myocardial infarction in a case-control study from Argentina. Soz Praventivmed 1994;39:126–33.
75. Tavani A, Negri E, D’Avanzo B, La Vecchia C. Body weight and risk of nonfatal acute myocardial infarction among women: a case-control study from northern Italy. Prev Med 1997;26:550–5.
76. Kawachi I, Sparrow D, Kubzansky LD, et al. Prospective study of a self-report type A scale and risk of coronary heart disease: test of the MMPI-2 type A scale. Circulation 1998;98:405–12.
77. Raymond C. Distrust, rage may be ‘toxic core’ that puts ‘type A’ person at risk. JAMA 1989;261:813.
78. Dimsdale JE. A perspective on type A behavior and coronary disease. N Engl J Med 1988;318:110–2 [editorial].
79. Friedman M, Thoresen CE, Gill JJ, et al. Alteration of type A behavior and reduction in cardiac recurrences in postmyocardial infarction patients. Am Heart J 1984;108:237–48.
80. Kawachi I, Sparrow D, Spiro A 3rd, et al. A prospective study of anger and coronary heart disease. The Normative Aging Study. Circulation 1996;94:2090–5.
81. Kubzansky LD, Kawachi I, Spiro A 3rd, et al. Is worrying bad for your heart? A prospective study of worry and coronary heart disease in the Normative Aging Study. Circulation 1997;95:818–24.
82. Hammar N, Alfredsson L, Johnson JV. Job strain, social support at work, and incidence of myocardial infarction. Occup Environ Med 1998;55:548–53.
83. Knox SS, Adelman A, Ellison RC, et al. Hostility, social support, and carotid artery atherosclerosis in the National Heart, Lung, and Blood Institute Family Heart Study. Am J Cardiol 2000;86:1086–9.
84. Knox SS, Siegmund KD, Weidner G, et al. Hostility, social support, and coronary heart disease in the National Heart, Lung, and Blood Institute Family Heart Study. Am J Cardiol 1998;82:1192–6.
85. Orth-Gomer K, Wamala SP, Horsten M, et al. Marital stress worsens prognosis in women with coronary heart disease: the Stockholm female coronary risk study. JAMA 2000;284:3008–14.
86. Allen C, Glasziou P, Del Mar C. Bed rest: a potentially harmful treatment needing more careful evaluation. Lancet 1999;354:1229–33 [review].
87. Davini P, Bigalli A, Lamanna F, Boem A. Controlled study on L-carnitine therapeutic efficacy in post-infarction. Drugs Exp Clin Res 1992;18:355–65.
88. De Pasquale B, Righetti G, Menotti A. L-carnitine for the treatment of acute myocardial infarct. Cardiologia 1990;35:591–6 [in Italian].
89. Iliceto S, Scrutinio D, Bruzzi P, et al. Effects of L-carnitine administration on left ventricular remodeling after acute anterior. J Am Coll Cardiol 1995;26:380–7.
90. 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 1996;72:45–50.
91. Martina B, Zuber M, Weiss P, et al. Anti-arrhythmia treatment using L-carnitine in acute myocardial infarct. Schweiz Med Wochenschr 1992;122:1352–5 [in German].
92. Chambers JC, McGergor A, Jean-Marie J, et al. Demonstration of rapid onset vascular endothelial dysfunction after hyperhomocysteinemia. An effect reversible with vitamin C therapy. Circulation 1999;99:1156–60.
93. Fuller CJ, Grundy SM, Norkus EP, Jialal I. Effect of ascorbate supplementation on low density lipoprotein oxidation in smokers. Atherosclerosis 1996;119:139–50.
94. Rath M, Pauling L. Solution to the puzzle of human cardiovascular disease: Its primary cause is ascorbate deficiency leading to the deposition of lipoprotein (a) and fibrinogen/fibrin in the vascular wall. J Orthomol Med 1992;6:125–34.
95. Manson JE, Stampfer MJ, Willett WC, et al. A prospective study of vitamin C and incidence of coronary heart disease in women. Circulation 1992;85:865 [abstract].
96. Klipstein-Grobusch K, Geleijnse JM, den Breeijen JH, et al. Dietary antioxidants and risk of myocardial infarction in the elderly: the Rotterdam Study. Am J Clin Nutr 1999;69:261–6.
97. Nyyssönen K, Parvianinen MT, Salonen R, et al. Vitamin C deficiency and risk of myocardial infarction: prospective population study of men from eastern Finland. BMJ 1997;314:634–8.
98. Simon JA, Hudes ES, Browner WS. Serum ascorbic acid and cardiovascular disease prevalence in U.S. adults. Epidemiology 1998;9:316–21.
99. Rimm EB, Stampfer MJ, Ascherio A, et al. Vitamin E consumption and the risk of coronary heart disease in men. N Engl J Med 1993;328:1450–6.
100. Singh RB, Niaz MA. Serum concentration of lipoprotein (a) decreases on treatment with hydrosoluble coenzyme Q10 in patients with coronary artery disease: discovery of a new role. Int J Cardiol 1999;68:23–9.
101. Atar D, Mortensen SA, Flachs H, Herzog WR. Coenzyme Q10 protects ischemic myocardium in an open-chest swine model. Clin Investig 1993;71:S103–11.
102. Ishikura Y, Odagiri S, Nagata M, et al. Effects of coenzyme Q10 on ischemic myocardium during coronary artery occlusion—evaluation of the time needed to change irreversible myocardium. Sangyo Ika Daigaku Zasshi 1986;8:19–25 [in Japanese].
103. Singh RB, Wander GS, Rastogi A, et al. Randomized double-blind placebo-controlled trial of coenzyme Q10 in patients with acute myocardial infarction. Cardiovasc Drugs Ther 1998;12:347–53.
104. Singh RB, Neki NS, Kartikey K, et al. Effect of coenzyme Q10 on risk of atherosclerosis in patients with recent myocardial infarction. Mol Cell Biochem 2003;246:75–82.
105. Kuklinski B, Weissenbacher E, Fahnrich A. Coenzyme Q10 and antioxidants in acute myocardial infarction. Mol Aspects Med 1994;15 Suppl:s143–7.
106. Auzepy P, Blondeau M, Richard C, et al. Serum selenium deficiency in myocardial infarction and congestive cardiomyopathy. Acta Cardiol 1987;42:161–6.
107. Oster O, Drexler M, Schenk J, et al. The serum selenium concentration of patients with acute myocardial infarction. Ann Clin Res 1986;18:36–42.
108. Beaglehole R, Jackson R, Watkinson J, et al. Decreased blood selenium and risk of myocardial infarction. Int J Epidemiol 1990;19:918–22.
109. Kardinaal AFM, Kok FJ, Kohlmeier L, et al. Association between toenail selenium and risk of acute myocardial infarction in European men. Am J Epidemiol 1997;145:373–9.
110. Salvini S, Hennekenes CH, Morris JS, et al. Plasma levels of the antioxidant selenium and risk of myocardial infarction among U.S. physicians. Am J Cardiol 1995;76:1218–21.
111. Korpela H, Kumpulainen J, Jussila E, et al. Effect of selenium supplementation after acute myocardial infarction. Res Commun Chem Pathol Pharmacol 1989;65:249–52.
112. Kuklinski B, Weissenbacher E, Fahnrich A. Coenzyme Q10 and antioxidants in acute myocardial infarction. Mol Aspects Med 1994;15 Suppl:s143–7.
113. Rimm EB, Stampfer MJ, Ascherio A, et al. Vitamin E consumption and the risk of coronary heart disease in men. N Engl J Med 1993;328:1450–6.
114. Stampfer MJ, Hennekens CH, Manson JE, et al. Vitamin E consumption and the risk of coronary heart disease in women. N Engl J Med 1993;328:1444–9.
115. Stephens NG, Parsons A, Schofield PM, et al. Randomised controlled trial of vitamin E in patients with coronary disease: Cambridge Heart Antioxidant Study (CHAOS). Lancet 1996;347:781–6.
116. Boaz M, Smetana S, Weinstein T, et al. Secondary prevention with antioxidants of cardiovascular disease in endstage renal disease (SPACE): randomised placebo-controlled trial. Lancet 2000;356:1213–8.
117. [No authors listed]. Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzione trial. Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto miocardico. Lancet 1999;354:447–55.
118. Collaborative Group of the Primary Prevention Project (PPP). Low-dose aspirin and vitamin E in people at cardiovascular risk: a randomized trial in general practice. Lancet 2001;357:89–95.
119. Yusuf S, Dagenais G, Pogue J, et al. Vitamin E supplementation and cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators. N Engl J Med 2000;342:154–60.
120. Sochman J, Vrbska J, Musilova B, Rocek M. Infarct Size Limitation: acute N-acetylcysteine defense (ISLAND trial): preliminary analysis and report after the first 30 patients. Clin Cardiol 1996;19:94–100.
121. Von Schacky C, Angerer P, Kothney W, et al. The effect of dietary omega-3 fatty acids on coronary atherosclerosis. A randomized double-blind, placebo-controlled trial. Ann Intern Med 1999;130:554–62.
122. Singh RB, Niaz MA, Sharma JP, et al. Randomized, double-blind, placebo-controlled trial of fish oil and mustard oil in patients with suspected acute myocardial infarction: the Indian experiment of infarct survival--4. Cardiovasc Drugs 1997;11:485–91.
123. [No authors listed]. Dietary supplementation with n-3 polyunsaturated fatty acids and vitamin E after myocardial infarction: results of the GISSI-Prevenzione trial. Gruppo Italiano per lo Studio della Sopravvivenza nell’Infarto miocardico. Lancet 1999;354:447–55.
124. Landmark K, Abdelnoor M, Urdal P, et al. Use of fish oils appears to reduce infarct size as estimated from peak creatine kinase and lactate dehydrogenase activities. Cardiology 1998;89:94–102.
125. Wander RC, Du SH, Ketchum SO, Rowe KE. Alpha-tocopherol influences in vivo indices of lipid peroxidation in postmenopausal women given fish oil. J Nutr 1996;126:643–52.
126. Singh RB, Niaz MA, Sharma JP, et al. Plasma levels of antioxidant vitamins and oxidative stress in patients with acute myocardial infarction. Acta Cardiol 1994;49:441–52.
127. Levy Y, Bartha P, Ben-Amotz A, et al. Plasma antioxidants and lipid peroxidation in acute myocardial infarction and thrombolysis. J Am Coll Nutr 1998;17:337–41.
128. Singh RB, Niaz MA, Rastogi SS, Tastogi S. Usefulness of antioxidant vitamins in suspected acute myocardial infarction (the Indian experiment of infarct survival-3). Am J Cardiol 1996;77:232–6.
129. Singh RB, Rastogi SS, Ghosh S, Niaz MA. Dietary and serum magnesium levels in patients with acute myocardial infarction, coronary artery disease and noncardiac diagnoses. J Am Coll Nutr 1994;13:139–43.
130. Hampton EM, Whang DD, Whang R. Intravenous magnesium therapy in acute myocardial infarction. Ann Pharmacother 1994;28:212–9 [review].
131. [No authors listed]. ISIS-4: a randomised factorial trial assessing early oral captopril, oral mononitrate, and intravenous magnesium sulphate in 58,050 patients with suspected acute myocardial infarction. Lancet 1995;345:669–85.
132. Seelig MS, Elin RJ. Is there a place for magnesium in the treatment of acute myocardial infarction? Am Heart J 1996;132:471–7.
133. Marx A, Neutra RR. Magnesium in drinking water and ischemic heart disease. Epidemiol Rev 1997;19:258–72.
134. Rubenowitz E, Molin I, Axelsson G, Rylander R. Magnesium in drinking water in relation to morbidity and mortality from acute myocardial infarction. Epidemiology 2000;11:416–21.
135. Galloe AM, Rasmussen HS, Jorgensen LN, et al. Influence of oral magnesium supplementation on cardiac events among survivors of an acute myocardial infarction. BMJ 1993;307:585–7.
136. Singh RB, Singh NK, Niaz MA, Sharma JP. Effect of treatment with magnesium and potassium on mortality and reinfarction of patients with suspected acute myocardial infarction. Int J Clin Pharmacol Ther 1996;34:219–25.
137. Singh RB. Effect of dietary magnesium supplementation in the prevention of coronary heart disease and sudden cardiac death. Magnesium Trace Elem 1990;9:143–51.
138. Israelsson B, Brattstrom LE, Hultberg BL. Homocysteine and myocardial infarction. Atherosclerosis 1988;71:227–33.
139. Ridker PM, Manson JE, Buring JE, et al. Homocysteine and risk of cardiovascular disease among postmenopausal women. JAMA 1999;281:1817–21.
140. Bots ML, Launer LJ, Lindemans J, et al. Homocysteine and short-term risk of myocardial infarction and stroke in the elderly: the Rotterdam Study. Arch Intern Med 1999;159:38–44.
141. Stampfer MJ, Malinow MR, Willett WC, et al. A prospective study of plasma homocysteine and risk of myocardial infarction in US physicians. JAMA 1992;268:877–81.
142. Folsom AR, Nieto FJ, McGovern PG, et al. Prospective study of coronary heart disease incidence in relation to fasting total homocysteine, related genetic polymorphisms, and B vitamins: the Atherosclerosis Risk in Communities (ARIC) study. Circulation 1998;98:204–10.
143. Kuller LH, Evans RW. Homocysteine, vitamins, and cardiovascular disease. Circulation 1998;98:196–9 [editorial/review].
144. Nallamothu BK, Fendrick AM, Rubenfire M, et al. Potential clinical and economic effects of homocyst(e)ine lowering. Arch Intern Med 2000;160:3406–12.
145. Landgren F, Israelsson B, Lindgren A, et al. Plasma homocysteine in acute myocardial infarction: homocysteine-lowering effect of folic acid. J Intern Med 1995;237:381–8.
146. Ward M, McNulty H, McPartlin J, et al. Plasma homocysteine, a risk factor for cardiovascular disease, is lowered by physiological doses of folic acid. QJM 1997;90:519–24.
147. Lobo A, Naso A, Arheart K, et al. Reduction of homocysteine levels in coronary artery disease by low-dose folic acid combined with vitamins B6 and B12. Am J Cardiol 1999;83:821–5.
148. Voutilainen S, Lakka TA, Porkkala-Sarataho E, et al. Low serum folate concentrations are associated with an excess incidence of acute coronary events: the Kuopio Ischaemic Heart Disease Risk Factor Study. Eur J Clin Nutr 2000;54:424–8.
149. Kardinaal AFM, Kok FJ, Ringstad J, et al. Antioxidants in adipose tissue and risk of myocardial infarction: the EURAMIC study. Lancet 1993;342:1379–84.
150. Tavani A, Negri E, D’Avanzo B, La Vecchia C. Beta-carotene intake and risk of nonfatal acute myocardial infarction in women. Eur J Epidemiol 1997;13:631–7.
151. Rapola JM, Virtamo J, Ripatti S, et al. Randomised trial of alpha-tocopherol and beta-carotene supplements on incidence of major coronary events in men with previous myocardial infarction. Lancet 1997;349:1715–20.
152. Virtamo J, Rapola JM, Ripatti S, et al. Effect of vitamin E and beta carotene on the incidence of primary nonfatal myocardial infarction and fatal coronary heart disease. Arch Intern Med 1998;158:668–75.
153. Klipstein-Grobusch K, Geleijnse JM, den Breeijen JH, et al. Dietary antioxidants and risk of myocardial infarction in the elderly: the Rotterdam Study. Am J Clin Nutr 1999;69:261–6.
154. Morrison LM, Branwood AW, Ershoff BH, et al. The prevention of coronary arteriosclerotic heart disease with chondroitin sulfate A: Preliminary report. Exp Med Surg 1969;27:278–89.
155. Morrison LM. Reduction of ischemic coronary heart disease by chondroitin sulfate. Angiology 1971;22:165–74.
156. Morrison LM, Enrick NL. Coronary heart disease: Reduction of death rate by chondroitin sulfate A. Angiology 1973;24:269–82.
157. Linden V. Vitamin D and myocardial infarction. BMJ 1974;3:647–50.
158. Vik B, Try K, Thelle DS, Forde OH. Trømso Heart Study: vitamin D metabolism and myocardial infarction. Br Med J 1979;2:176.
159. Arad Y, Spadaro LA, Roth M, et al. Serum concentration of calcium, 1,25 vitamin D and parathyroid hormone are not correlated with coronary calcifications. An electron beam computed tomography study. Coron Artery Dis 1998;9:513–8.
160. Watson KE, Abrolat ML, Malone LL, et al. Active serum vitamin D levels are inversely correlated with coronary calcification. Circulation 1997;96:1755–60.
161. Lind L, Skarfors E, Berglund L, et al. Serum calcium: a new, independent, prospective risk factor for myocardial infarction in middle-aged men followed for 18 years. J Clin Epidemiol 1997;50:967–73.
162. Myrup B, Hensen GF, McNair P. Cardiovascular risk factors during estrogen-norethindrone and cholecalciferol treatment. Arch Intern Med 1992;152:2265–8.
163. Heikkinen AM, Tuppurainen MT, Niskanen L, et al. Long-term vitamin D3 supplementation may have adverse effects on serum lipids during postmenopausal hormone replacement therapy. Eur J Endocrinol 1997;137:495–502.
164. Danesh J, Appleby P. Coronary heart disease and iron status. Meta-analyses of prospective studies. Circulation 1999;99:852–4.
165. Chen LX, Liao JZ, Guo WQ. Effects of Astragalus membranaceus on left ventricular function and oxygen free radical in acute myocardial infarction patients and mechanism of its cardiotonic action. Chung Kuo Chung His I Chieh Ho Tsa Chih 1995;15:141–3 [in Chinese].
166. Shi HM, Dai RH, Wang SY. Primary research on the clinical significance of ventricular late potentials (VLPs), and the impact of mexiletine, lidocaine and Astragalus membranaceus on VLPs. Chung His I Chieh Ho Tsa Chih 1991;11:259, 265–7 [in Chinese].
Copyright © 2007 Healthnotes, Inc. All rights reserved. www.healthnotes.com
The information presented in Healthnotes is for informational purposes only. It is based on scientific studies (human, animal, or in vitro), clinical experience, or traditional usage as cited in each article. The results reported may not necessarily occur in all individuals. For many of the conditions discussed, treatment with prescription or over the counter medication is also available. Consult your doctor, practitioner, and/or pharmacist for any health problem and before using any supplements or before making any changes in prescribed medications. Information expires September 2008.