ANGINA PECTORIS OR CORONARY ARTERY DISEASE
Angina pectoris, commonly called angina, is characterized by chest pain that results from myocardial ischemia.
Stable angina is usually predictable, occurs in situations that increase myocardial oxygen demand such as exercise or stress and is relieved by rest or sublingual nitroglycerin.
Unstable angina occurs unexpectedly and usually at rest or lasts longer than stable angina. Variant angina, also called Prinzmetal’s angina, is a form of unstable angina caused by coronary artery spasm. Unstable angina is considered an emergency and it may be a harbinger of acute myocardial infarction or sudden death.
The most common cause of angina is impaired blood flow secondary to coronary atherosclerosis.
Other CAUSES include coronary artery spasm, or constriction, of very small blood vessels in the coronary circulation, also called Cardiac Syndrome X, and factors that reduce oxygen carrying capacity to blood, such as anemia. Microvascular angina is a diagnosis of dysplasia, which is made when the angina is accompanied by an abnormal exercise test, normal coronary arteries and the absence of inducible coronary artery spasm.
The severity of angina is often graded on a 4-point scale with Functional Class IV being the most severe. This is inability to perform any physical activity without discomfort.
Medications used to treat angina include sublingual nitroglycerin for acute attacks, beta blockers and calcium channel blockers.
Surgery such as coronary artery bypass or angioplasty is recommended in some patients. Comprehensive treatment of angina also includes controlling risk factors such as obesity, hypertension, hyperlipidemia, diabetes and cigarette smoking in order to slow the progression of atherosclerosis and decrease the risk of myocardial infarction.
Dietary Factors:
1. Meal size.
In healthy volunteers who consumed 5 meals that ranged from 50-75% of a daily end requirements, there was a significant positive correlation between the meal size and myocardial oxygen consumption. This finding suggests that patients who experience postprandial angina could benefit from consuming small frequent meals as opposed to larger less frequent meals.
2. Reactive hypoglycemia
. In a number of cases reported in which attacks of angina were triggered by reactive hypoglycemia, in these cases blood sugar drops too low. In most of these patients, further episodes were prevented by dietary modifications designed to regulate blood glucose levels.
3. Alcohol.
Alcohol consumption has been shown to induce anginal attacks in a large proportion of patients with variant angina with a lag time of 1.5 to 18 hours and to decrease exercise tolerance in patients with stable exertional angina. Patients with angina should be advised to avoid alcohol or limit its intake not to provoke an attack. Alcohol-induced variant angina may also be aggravated by magnesium deficiency, which is common in heavy alcohol users.
Comprehensive dietary interventions include restriction of fat, elimination of refined sugar, and a consumption of healthy foods such as fruits, vegetables and whole grains and legumes. These studies have resulted in improving the patients. Other lifestyle changes are also recommended.
Vitamins and minerals
1. Magnesium.
In addition to preventing spasm of coronary arteries, magnesium plays a role in myocardial energy production by functioning as a cofactor for ATP syntheses. ATP is energy. Several studies have found that magnesium deficiency is common in patients with angina. In some case reports, administration of a series of magnesium injections resulted in complete resolution or marked improvement in some patients with angina. Oral magnesium supplementation was also found in a double-blind trial to be of some benefit to patients with angina.
2. Carnitine.
Carnitine plays a role in myocardial energy production by facilitating the transport of fatty acid to the mitochondria. In clinical trials, supplementation with quinitine improved exercise tolerance in patients with stable angina.
3. Co-enzyme Q10.
As a cofactor in electron transport chain, Q10 plays a role in myocardial energy production. In a double-blind trial, supplementation with Q10 decreased the frequency of anginal episodes and increased exercise tolerance compared with placebo in patients with stable angina. This study was small and was not statistically significant. Large doses of Q10 were not used and Q10 serum levels were not monitored. Further investigation is needed.
4. Arginine and beets or kale
As a precursor to nitric oxide, Arginine has a vasodilator effect and has also been shown to improve coronary small vessel endothelial function. There was an improvement of exercise capacity in patients with stable angina and decreased frequency and severity.
5. Omegas 3,7,9
Numerous studies have shown supplementation with moderate doses of fish oil, such as 1 to 3 grams, can play an important role in the prevention and treatment of cardiovascular disease and the use of such dose seems reasonable as part of a comprehensive treatment program for patients with angina.
6. Vitamin E.
Increased oxidant stress may play a role in the pathogenics of angina and coronary spasm. Antioxidants such as vitamin E might therefore be beneficial for preventing and treating angina and so administered should be in the form of mixed tocopherol as opposed to pure alpha tocopherol in order to prevent alpha tocopherol-induced depletion of gamma tocopherol, which could have deleterious effects on the cardiovascular system.
Other Treatments:
Angina can result from hypothyroidism and sometimes resolves after treatment with thyroid hormone; however, such treatments may exacerbate preexisting angina or trigger its appearance in patients with coronary heart disease. In addition, treating with thyroid hormone may trigger atrial fibrillation in susceptible individuals, especially the elderly. There are many patients with clinical evidence of hypothyroidism where the laboratory evidence appears normal. There have been reported cases of decreased angina and increased exercise tolerance. In my experience, standard laboratory tests for thyroid function are frequently normal in patients with clinical evidence of hypothyroidism. An empiric trial of thyroid hormone often relieves a wide variety of symptoms.
Summary and Recommendations for Angina:
Eat small, frequent meals.
Identify and treat hypoglycemia.
Identify and avoid allergic foods.
Restrict intake of refined sugar, alcohol and caffeine.
Consider a vegetation diet.
Take magnesium, carnitine, PQQ, Co-enzyme Q10, fish oil, vitamin E, arginine and ribose. The ribose actually will increase cardiac ATP reserve.
ARRHYTHMIAS
There are many different types of cardiac arrhythmias, which vary in severity from benign to life threatening. Some types of arrhythmias have been reported to improve with dietary modifications or nutritional supplements where others typically do not respond. Because of the potential serious nature of cardiac arrhythmias, nutritional treatment should only be undertaken by a practitioner with experience in evaluating and managing arrhythmias.
Dietary factors include allergy, caffeine intake, and alcohol intake. There have been anecdotal reports where patients after eating at Chinese restaurants with food additives or MSG have developed arrhythmias. It was assumed that the monosodium glutamate present was responsible for the adverse reaction. In addition, there are anecdotal reports of atrial fibrillation and other cardiac arrhythmias developing after ingestion of the artificial sweetener aspartame.
Nutritional Supplements for Arrhythmias:
1. Magnesium.
Magnesium deficiency can lead to various arrhythmias including ventricular premature beats, atrial fibrillation, supraventricular tachycardia, torsades de pointes, and ventricular fibrillation. Magnesium deficiency may also increase susceptibility to digitalis-induced arrhythmia. Correction of magnesium deficiency may abolish arrhythmias in some cases. Many clinical conditions are associated with magnesium deficiency. These include diuretic therapy, alcoholism, congestive heart failure, diarrhea, malabsorption, anorexia nervosa, intravenous fluid administration that is not balanced, and diabetes mellitus. Both intravenous and oral magnesium have been found to be of value in the treatment of frequent premature contractions and arrhythmias related to congestive heart failure. In addition, oral magnesium supplementation shortened prolonged QT intervals in psychiatric patients. This was a positive effect.
2. Potassium.
Potassium deficiency may cause ventricular premature beats and increased arrhythmias. Risk factors for potassium deficiency include anorexia nervosa, persistent vomiting and diarrhea, treatment with potassium-deleting diuretics, advanced age and low intake of fruits and vegetables. Deficiency of potassium and magnesium frequently occur together. Magnesium is required for the intercellular uptake of potassium, so failure to address magnesium deficiency could make it difficult to correct potassium deficiency. Potassium should only be administered by a physician.
3. Fish oil
has been reported to have an anti-arrhythmic effect in rats and monkeys. In a prospective study of 20,551 U.S. male physicians, consumption of fish oil at least once a week was associated with a reduced risk of sudden cardiac death, presumably because of a decrease in incidents of fatal arrhythmias. In a double-blind trial, supplementation with 3 grams of fish oil was beneficial for patients with various cardiac arrhythmias who did not have heart disease or heart failure. Studies have shown there is a reduction is ventricular premature beats and other arrhythmias. Double-blind trials have investigated the effect of fish oil supplementation in patients who had cardiac defibrillators implanted because of cardiac arrest or life-threatening arrhythmias have been positive. There is a reduction in the incidents of ventricular tachycardia, ventricular fibrillation and death by 31-38% compared with placebo.
4. Selenium.
There have been reported cases of cardiomyopathy caused by selenium deficiency and is also associated with various cardiac arrhythmias and heart block.
Conclusion:
In susceptible individuals, arrhythmias may be triggered by ingestion of caffeine, alcohol, allergic foods. Anecdotal evidence supports that monosodium glutamate and aspartame can trigger arrhythmias in some cases. A number of nutrients have been reported to have beneficial or possible anti-arrhythmic activity. These include magnesium, potassium, Omega-3, cooper, selenium, and even vitamin C; however, with the exception of magnesium, few clinical trials have been developed and these are ongoing at the present time. Speak to your doctor.
ATHEROSCLEROSIS AND ISCHEMIC HEART DISEASE
Atherosclerosis is a chronic, slowly progressing arterial disease that is the most common cause of death in the western society. It is characterized by endothelial dysfunction, arterial inflammation, and the formation of plaques within the blood vessels that contain cholesterol, lipids and calcium. As the plaque increases in size, they progressive obstruct the vascular lumen and restrict blood flow, potentially leading to manifestations such as angina and heart attack. In some cases, atherosclerotic plaques rupture leading to the formation of clot or thrombus, which may cause partial or complete obstruction of the involved artery. Acute obstruction may cause unstable angina, myocardial infarction, transient ischemic attack or stroke. Ischemia is defined as insufficient blood flow to a particular tissue or organ and the organ cannot meet its needs of oxygen and glucose. Ischemia is usually caused as the primary clinical manifestation of atherosclerosis.
Pathophysiology:
It is generally believed that endothelial injury is the initial stage in the process of atherogenesis. Endothelial injury leads to a cascade of events including vascular inflammation, activation of platelets, proliferation of arterial smooth muscle, and deposition of foam cells, which are macrophages with LDL cholesterol. One of the main contributors to endothelial injury is oxidized LDL. Oxidized LDL is highly atherogenic whereas native LDL appears to be relatively innocuous. Other factors that promote endothelial injury include cigarette smoke and other toxic substances, lipid peroxides, hyperglycemia or elevated blood sugar, elevated homocystine and autoimmune attacks of the blood.
Advanced glycation end products, or ameliorated blood sugar, also appear to play a role in the pathogenesis by increasing platelet aggregation, promoting inflammation, enhancing proliferation of smooth muscle and promoting lipid accumulation in arterial walls.
Risk Factors:
Risk factors for the development of atherosclerosis or its complications include hyperlipidemia, hypertension, diabetes, obesity, elevated insulin or insulin resistance. There is also an increased level of C-reactive protein, an indicator of chronic inflammation, elevated homocystine and elevated levels of fibrinogen and lipoprotein abnormalities. Other possible factors include increased blood viscosity, platelet hyperaggregability and decreased fibrinolytic activity. The effect of nutritional interventions are addressed to each of these factors. A sedentary lifestyle also increases the risks of developing cardiovascular disease.
Conventional Therapy:
The conventional approach to preventing and treating atherosclerosis and its complications include lifestyle, diet and medications. Several studies have shown that coronary disease and atherosclerosis can be reversed to some extent by pharmacologic therapy designed to lower elevated lipids or by a regimen of diet plus exercise.
The statins, which are HMG-Coa reductase inhibitors, and platelet inhibitors, such as aspirin or Plavix are among the most widely used pharmacologic treatments. Both of these classes of medications are used in every day practice.
Statin drugs appear to work both by lowering LDL cholesterol and inhibiting inflammation as demonstrated by a reduction of C-reactive protein. There is evidence that the beneficial effects of statin may be at least due to their anti-inflammatory effects, although the statins are not without side effects.
Dietary Factors:
1. Cooking and Storage of Food:
A number of atherogenic compounds are formed in food during cooking. These include oxidized cholesterol, lipid peroxides and advanced glycation end products. Oxidized cholesterol and lipid peroxides also form spontaneous during storage of form that contain cholesterol and polyunsaturated fatty acid, particularly if these foods are exposed to air and not refrigerated. The food should be stored and refrigerated in air-tight containers and consumption of food cooked at high temperatures should be kept at a minimum.
When cooking with oil, it would be preferable to use olive oil, which is high in monounsaturated fatty acids that are resistant to oxidation rather than sunflower, safflower or corn oil, which are high in polyunsaturated fatty acids that are more susceptible to becoming oxidized. Peanut oil may also be considered for cooking since its fatty acid consumption is closer to that of olive oil than that of sunflower oil.
Although canola oil is high in monounsaturated fatty acid, it also contains a moderately large amount of alpha-linolenic acid. Heating of oils that are high in alpha-linolenic acid may lead to formation of mutagenic and carcinogenic compounds. The fatty acids in butter and lard are relatively resistant to oxidation, but these foods contain cholesterol, which can be converted to atherogenic oxides during cooking.
Emphasizing boiling, poaching and stewing over frying, broiling and roasting may decrease advanced glycation end products.
2. Chlorinated water.
Chlorine is added to municipal water supplies to kill organisms. Since it is an oxidizing agent, chlorine might promote the oxidation of LDL or cause oxidant damage to the arteries. An interesting study was of American soliders who fought in Korea who were given water that was said to be heavy chlorinated such that it was virtually undrinkable. More than 75% of the soldiers that were killed in battle were found to have advanced atherosclerosis. Chlorination of water became more widespread around 1912 shortly before cardiovascular disease became common.
Chlorine can be removed from tap water by water filter or by boiling or by adding a pinch of vitamin C crystals to the water. Alternatives to chlorination include ultraviolet radiation and reverse osmosis.
3. Sucrose and fructose
. Rabbits and monkeys fed high sucrose diets developed coronary aortic atherosclerosis. In rabbits, the atherosclerosis lesions were more severe than those resulting from a high-cholesterol diet. Consumption of large amounts of sucrose by humans may cause adverse changes including increased serum levels of triglycerides, insulin and uric acid, a rising blood pressure and increasing platelet adhesiveness and decrease in HDL cholesterol. Approximately one-third of the population is susceptible to these adverse effects of sucrose and sucrose sensitivity appears to be clustered in people who are at increased risk of heart disease.
4. Dietary cholesterol and saturated fat.
The prevailing point of view is that heart disease prevention programs should include restriction of dietary cholesterol and saturated fats because consumption of these substances increases serum cholesterol levels; however, the relationship between cholesterol and saturated fat intake on cardiovascular disease is not straight forward.
Studies in animals have shown that feeding pure cholesterol does not cause atherosclerosis whereas oxidized cholesterol is highly atherogenic. The effect of cholesterol-containing foods on heart disease risks may therefore be dependent as much, or more, on how the foods are prepared or the amount of cholesterol they contain. For example, breaking the yolk of an egg, which contains all the cholesterol, during cooking exposes the cholesterol to high temperatures and oxygen in the room air, which accelerates the formation of cholesterol oxides.
Thus, boiled or poached eggs would be preferable to scrambled eggs with fried eggs probably somewhere in between. By the same reasoning, butter left exposed to room air is probably more atherogenic than butter kept covered in the refrigerator. Oxidized cholesterol is found commonly in dried egg products, powered milk, grated cheeses, french fries, processed meats, butter oil, heated butter, heated tallow and lard.
The effects of saturated fat intake on serum cholesterol is also a less amount than is commonly believed. Saturated fat, per se, may not be necessarily atherogenic as suggested by findings in a Polynesian population living near the equator. Saturated fat intake in this population is very high, approximately 47%, but vascular disease is uncomfortable.
Moreover, while some studies have found that reducing intake of saturated fat had a positive effect on heart disease, other studies have found no effect. There are certain foods that are high in saturated fats and be atherogenic for other reasons unrelated to their saturated fat content, as is likely the case with dietary cholesterol the effect of saturated fat containing foods on heart disease may depend as much or more on how the foods are prepared as on the amount of saturated fat they contain.
5. Monounsaturated fat and olive oil.
These are more resistant to oxidation than polyunsaturated fatty acids.
The consumption of these fats result in incorporation of these fatty acids into the LDL cholesterol, making them more resistant to oxidation. Olive oil is a major source of monounsaturated fats that is an important component of the Mediterranean diet, which appears to reduce the risks of cardiovascular disease.
Virgin olive oil as opposed to refined in addition to being high in monounsaturated fatty acid contains several phenolic antioxidants including caffeic acid and others. These components may be particularly useful for cardiovascular disease prevention. Phenolic components from virgin olive oils have also been shown to inhibit LDL oxidation and platelet aggregation.
6. Trans fatty acids.
The epidemic of coronary heart disease in the United States began around 1920, about 8 years after large amounts of trans fats were introduced into the diet in the form of partially hydrated vegetable oils. Consumption of trans fats increase LDL cholesterol and lipoprotein abnormalities. There is also a decrease in HDL cholesterol and impairment of endothelial function. Higher amounts of inflammation with elevated CRPs are also noted.
7. Nuts.
Consumption of nuts has been reported to lower serum cholesterol levels. In men with elevated cholesterol who substituted monounsaturated fats with walnuts in the Mediterranean diet, there was improvement of endothelial function.
8. Whole grains.
Whole grains as compared to refined grains contain heartier amounts of potentially cardioprotective substances including magnesium, trace minerals, B vitamins, essential fatty acids and fiber.
9. Soy.
Eating soy protein protects against the development and progression of osteoporosis in monkeys fed an atherogenic diet. The protection appears to be due to isoflavones present in soy protein. In humans, consumption of soy reduced lipo peroxidation and increased the resistance of LDL to oxidation. There was also improvement in protection of human endothelial cells from damage from the oxidized LDL. Due to its high mn and glutamate I do not use it personally.
10. Dietary fiber.
Fruits, vegetables, whole grains, legumes and nuts high in fiber might have a cardioprotective effect by increasing fecal infiltration of bile acids, which lowered in serum cholesterol by increasing conversion of cholesterol to bile acids in the liver. Fruits and vegetables, purple grace juice have been shown to inhibit platelet aggregation and it is noted that pomegranate juice with its polyphenols showed a reduction in mean intima-medial thickness of the right and left common coronary artery suggesting that atherosclerosis has been reversed.
11. Garlic
may reduce the risk of cardiovascular disease by lowering serum cholesterol and triglyceride levels, decreasing blood pressure, inhibit platelet aggregation, reducing fibrinogen levels, and decreasing the susceptibility of LDL to oxidation. There is also increased fibrinolytic activity. In clinical trials, treatment with certain garlic preparations slowed or halted the progression of atherosclerosis.
12. Alcohol.
The studies on alcohol are mixed. Some alcohol consumption has been reported to increase HDL cholesterol and to inhibit platelet aggregation. In addition, some of the non-alcoholic components of alcohol beverages such as trans resveratrol in red wine, silicon in beer and wine may be cardioprotective.
Nevertheless, alcohol is toxic to the heart and excessive drinking is the major cause of cardiomyopathy. Based on the available evidence, one might reasonably conclude that moderate alcohol consumption, up to two drinks per day for men and one for women, is tolerable.
13. Mediterranean diet.
The Mediterranean diet refers to the diet of olive-growing regions in the Mediterranean. In addition to olive oil, the diet emphasizes salads with greens, wheat, fruit, nuts and garlic. The virgin olive oil may have cardioprotective effect as noted above.
In patients 55-80 years old with cardiovascular disease risk factors, consumption of a Mediterranean diet supplemented with olive oil and nuts was more effective than a low-fat diet for improving cardiovascular risk factors including stabilization of glucose, systolic blood pressure, lipid levels and C-reactive protein.
In a 10-year prospective study conducted in eleven European countries adherent to Mediterranean diet was associated with reduced risks of cardiovascular disease related mortality and all-cause morbidity. In a randomized control trial, consumption of a Mediterranean diet markedly decreased the incident of death and non-fatal myocardial infarctions in men who had suffered a first myocardial infarction. Based on this data, a Mediterranean diet can be considered alternative to a traditional low-fat diet for preventing and reversing cardiovascular disease.
14. Nutritional supplement.
Nutritional supplements include magnesium, vitamin C, fish oil, a high-potency multivitamin with vitamin D, K, silicon and other nutrients such as niacin,carnitine , Q10 and ribose should be considered. Of caution with vitamin D is that vitamin D should not taken in excess and should be monitored by your doctor. Vitamin D and calcium should always be taken with vitamin K. Vitamin K has been shown to decrease aortic calcification and plays a role in the synthesis of matrix GLA protein, which is a strong inhibitor of vascular calcification.
15. Calcium.
Is there an adverse effect? In a secondary analysis of a double-blind trial designed to assess the effect of calcium supplementation and bone metal density and fractures in postmenopausal women, the incidence of composite end-point of myocardial infarction, stroke, or sudden death was 47% higher when they received a gram of calcium for 5 years than those who received placebo. Calcium supplementation might exert an adverse effect on the cardiovascular system by depleting magnesium, which is important. Calcification supplementation should therefore be accompanied by magnesium supplement, as well as vitamin K, in all cases.
Red Yeast
Red yeast rice might be indicated by your physician. Some strains of red yeast rice contain lovastatin, a statin-like compound. In clinical trials with specific red yeast preparation, there was a 31% decrease in death from heart disease and 31% decreased cause of all mortality.
In clinical trials, administration of red yeast rice specifically reduced total, as well as LDL, cholesterol. The effects were similar to those of commonly used statin drugs. Even though red yeast contains substantially lower amounts of lovastatin and other monacolin than the doses of most statins used to treat hypercholesterolemia, it is possible that the various monacolins in red yeast act additively or synergetically with other substances in the red yeast.
Red yeast also has been shown to lower C-reactive protein, which has a beneficial effect on cardiovascular disease. In one study, administration of 1200 mg of red yeast for 3 months lowered the C-reactive protein by 44%.
In addition, red yeast rice is one of the few cholesterol-lowering natural substances that has been tested with respect to clinical endpoints such as cardiovascular disease in all causes of mortality. In a double-blind trial that included 4870 patients, mean age 58, with previous myocardial infarction, treatment with red yeast for 4.5 years decreased death from coronary heart disease by 31% and all-cause mortality by 33% compared to placebo.
There were no serious side effects noted. The incidents of myopathy and hepatotoxicity is markedly lower with red yeast and is much lower than prescription statin drugs although there have been a few cases of reported myopathy, as well as liver disease, occurring in patients taking red yeast. Based on its efficacy and safety profile, red yeast rice should be considered as the preferred therapy of hyperlipidemia.
Red Yeast Rice Quality Control and Legal Issues:
In 1998, the US Food and Drug Administration (FDA) ruled that red yeast products that contain lovastatin are unapproved drugs. Although that ruling was initially overturned by the court, it was subsequently upheld in a US court of appeals. Considering that red yeast rice may be as effective as statins and is less expensive and currently much safer, one might reasonably conclude that the FDA’s position on red yeast rice adversely affects both the physical and financial health of the public.
Some products in the United States only contain a negligible amount of lovastatin and other monacolins. This is the problem.
Some products on the market also contain a small amount of citrinin, a fermentation byproduct that is nephrotoxic in animals. ConsumerLab.com analyzed 10 red yeast rice products sold in the US and found that the amount of lovastatin and total monacolin varies substantially among the different preparations.
Depending on the product used, patients would obtain anywhere from a negligible amount of monacolin to more than that was used in clinical trials of red yeast. In addition, 4 of the 10 products contain detectable amounts of citrinin. Some products were of high quality in that they had no detectable citrinin levels and also contain the amounts of lovastatin and other monacolins that were similar to the doses used in research.
Red Yeast Interactions:
Red yeast should not be combined with a statin drug because doing so may increase the increase risk of adverse side effects. In addition, red yeast rice would be expected to interact with the same drugs with which the statins interact.
Drinking grapefruit juice or eating grapefruit may increase blood levels by inhibiting their metabolism, increasing the risks.
Pomegranate also does the same.
Taking St. John’s Wart would easily decrease the levels.
As in the case of statin drugs, supplementation with red yeast rice may deplete Co-enzyme Q10, so patients taking red yeast rice should take a Q10 supplement.
See elsewhere on this site discussions on statins the pros and cons
Dr. silver also uses PEMF high-gauss magnet WHICH GROWS STEM CELLS, hyperbaric oxygen therapy, photon therapies and the far infrared sauna
IV therapy, IV ozone, IV chelation is also used.
ASK DR. SILVER IF YOU’RE A CANDIDATE FOR STEM CELLS.
Best in health,
Dean r. Silver, m.d.