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arterial_disease [2018/02/26 18:10] (current)
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 +======= Arterial Disease =======
 +
 +Arterial disease accounts for the vast majority of patients that suffer from cardiovascular disease, and may be accompanied by diseases of the veins and heart. The primary arterial disease is atherosclerosis,​ a progressive disease of large and medium large arteries that is marked by the formation of plaques or atherosclerotic lesions in the endothelium. The term arteriosclerosis is the same pathology, and is used when discussing the atherosclerotic lesions that can occur in the smaller arterioles. The major complications of atherosclerosis include ischemic heart disease, myocardial infarction, and gangrene of the extremities. Atherosclerosis is the leading cause of death in North America, a percentage of the population that has been on the rise steadily since that turn of the last century.
 +Pathogenesis of atherosclerosis
 +
 +Atherosclerotic plaques form in the tunica intima of elastic and muscular arteries as a result of the proliferation of intimal smooth muscle cells and the accumulation of fat. As the lesion develops smooth muscle cells release cytokines that stimulates the accumulation of mononuclear phagocytes, lymphocytes and neutrophils in the tunica intima. As the lesion progresses the endothelium ruptures and platelets begin to adhere to it. Eventually small capillaries penetrate the vessel wall and supply blood to the plaque, almost like a kind of malignant tumor. (Rubin and Farber 1990, 355-369)
 +
 +There are a variety of hypotheses that describe the process of atherosclerotic plaquing. While there is good post-mortem evidence of what components comprises a plaque, and now better data on the risk factors for developing atherosclerosis,​ the actual mechanisms of how the plaque is formed is severely limited by our inability to actually observe this process in vivo. As a result there are several different theories that describe the mechanism of plaquing. Some of these theories are complimentary and some are antagonistic to each other. The most commonly held belief among medical doctors is the insudation hypothesis, which states that the lipid found in plaques is derived from plasma lipoproteins,​ specifically low density lipoproteins (LDL). This theory states that the atherosclerotic lesion begins with a mutation of a smooth muscle cell, perhaps from exposure to chemical or viral mutagens, resulting in focal regions of accumulation. Macrophages then scavenge LDL in the blood and transport the lipid directly into the tunica intima of the blood vessel. For some unexplainable reason there is additional damage to the lesion, exposing circulating platelets to subendothelial collagen, which promotes the release of growth factors by the platelets, as well as by local macrophages,​ that stimulate the proliferation of smooth muscle cells and make the lesion larger. There is the continued insudation of fat into the lesion by macrophages that then undergo degeneration. Eventually the surface of the plaque begins to ulcerate and a thrombus forms on the injured luminal surface. (Rubin and Farber 1990, 355-369)
 +
 +The initial lesions found in atherosclerosis are thought to be fatty streaks, flat or slightly elevated lesions that contain lipid. Histologically,​ these streaks are comprised of lipid containing macrophages referred to as foam cells. While these fatty streaks can be found in both young children and the aged, the distribution of these streaks does not correspond with atherosclerotic lesions in adults. Another candidate for the initial lesion of atherosclerosis are intimal cells masses, which are white thickened areas at branch points in the aterial tree, containing smooth muscle cells but no lipid. (Rubin and Farber 1990, 355-369)
 +
 +Whatever the initial lesion, the characteristic lesion of atherosclerosis is a fibro-fatty plaque consisting of a fibrous cap and an atheroma. The fibrous cap is a layer of thickened connective tissue containing fat-filled macrophages and smooth muscle cells. The atheroma is a necrotic mass of lipid that forms the middle portion of the lesion. Other components in the lesion of atherosclerosis include other blood-borne cells including lymphocytes. The complicated plaque of atherosclerosis is the clinically significant end-point for the formation of a plaque, characterized by:
 +
 +    Thrombosis: the aggregation of platelets, fibrin, clotting factors and blood-borne elements on and within the plaque
 +    Neovascularization:​ of the cap and edges of lesion
 +    Thinning: of the underlying tunica media
 +    Calcification:​ within the atheroma and fibrous cap
 +    Ulceration: of the fibrous cap. (Rubin and Farber 1990, 355-369)
 +
 +The net result of these changes is the occlusion of the blood vessel and the formation of emboli, both of which end up producing ischemia in the tissues supplied by the atherosclerotic or otherwise occluded blood vessel.
 +
 +It is thought that the process of atherosclerosis begins early in life, with the formation of intimal cell masses and fatty streaks. Regardless, the characteristic lesion of atherosclerosis requires as long as 20-30 years to form, and the clinically important complicated plaques only after several more decades of progressive development. In this respect atherosclerosis is primarily a disease of older adults. (Rubin and Farber 1990, 355-369)
 +Etiology of atherosclerosis
 +
 +The causes of atherosclerosis are still not completely understood, with many convoluted and complicated mechanisms described. In this lesson we will examine the most commonly held belief among the medical profession, as well an alternative to this perspective.
 +
 +Medicine has defined several risk factors for the development of atherosclerosis,​ some of which may or may not prove to be entirely true. All of these risk factors are based on a statistical analysis of the data called epidemiology,​ a process that helps to form researcher of associations between certain factors and the incidence of disease. Although this process may identify groups in a population that are particularly vulnerable to a particular disease, it cannot indicate if a particular person will get a particular disease, and thus cannot take the place of an accurate, individualized health assessment.
 +
 +The vast majority of the approach now utilized in the prevention and treatment of heart disease is based upon the Framingham Heart study, a cohort study over 5000 adult men and women from the town of Framingham, Massachusetts. Begun in 1948, the participants of the study were analyzed for patterns related to the development of cardiovascular disease (CVD). A second generation cohort study was begun in 1971, involving a similar number of participants comprised of the original participants’ adult children and their spouses. A third generation cohort study is now being implemented. Given the duration and number of participants involved in the study, the Framingham Heart Study has proved to be a rich source of data for all kinds of researchers,​ who use a number of different methods to analyze the data and identify risk factors for CVD, including high blood pressure, high blood cholesterol,​ smoking, obesity, diabetes, and physical inactivity. The Framingham study has also provided additional information on the effects of factors such as blood triglyceride and LDL/HDL cholesterol levels, age, gender, and psychosocial issues. The Framingham data, the analyses and the theories derived from it has played an important role in the development of the modern medical curriculum, and has been influential in establishing hypertension and elevated serum cholesterol as the most prominent risk factors for the development of CVD.
 +
 +Hypertension is commonly observed in atherosclerosis,​ simply due to the increased pressure by which the heart has to pump blood through the narrowed and occluded atherosclerotic vessels. Hypertensive patients are at greater risk of myocardial infarction and stroke. There are several causes of hypertension,​ such as renal artery stenosis or hyperthyroidism and must be ruled out. Essential hypertension is a term that has been given to hypertension when the cause is unknown, or cannot be directly observed. Designating hypertension as a risk factor for atherosclerosis however appears to be irrational – it is far more logical to suggest that essential hypertension is a symptom of the progressive effects of arterial damage. Unfortunately what may seem to be a fairly simple argument has been for the most part ignored by the medical profession, many of whom still encourage hypertensive patients to use medications to lower blood pressure, even though these same medications have no impact upon morbidity and mortality in hypertensive patients, and may directly interfere with normal physiological processes. (Port et al 2000)
 +
 +Elevated blood cholesterol and triglycerides are stated as being directly correlated with the development of ischemic heart disease and atherosclerosis. The hypdophobic nature of lipids in the blood means that fats must be transported with protein carriers, including chylomicrons,​ very low density lipoproteins (VLDL), low density lipoproteins (LDL) and high density lipoproteins (HDL). Chylomicrons are formed by the intestinal villi, and are comprised of globules of triglycerides,​ phospholipids and cholesterol covered by a protein coating. Chylomicrons are absorbed by the lacteal of a villus, transporting fats through the lymphatic system where they enter into systemic circulation at the left subclavian vein. The triglyceride component of the chylomicron is cleaved by lipoprotein lipase in the blood, where it is taken up by adipose and muscle cells. This leaves a cholesterol-rich lipoprotein remnant that is then taken up by the liver and excreted back into the intestine as bile salts, or repacked with triglycerides into VLDL, where it then reenters into circulation. Once again VLDL is acted upon by lipoprotein lipase, removing triglycerides from VLDL, forming intermediate-density lipoproteins (IDL) that are eventually converted into cholesterol-rich LDL. LDL is then taken up and processed by a variety of cells, leading to the accumulation of cholesterol within these cells. Unlike VLDL and LDL, which functions to transport cholesterol to peripheral cells, high density lipoproteins (HDL) functions to scavenge cholesterol and return it to the liver for excretion. Thus elevated levels of serum VLDL and LDL have been associated with a greater risk of CVD because they deposit cholesterol into peripheral cells, which according to the insudation hypothesis is the primary cause of atherosclerosis,​ whereas HDL is correlated with a lower risk because it removes cholesterol from cells. (Rubin and Farber 1990, 355-369)
 +
 +Despite the elegance of this hypothesis and the determination of what are thought of as useful serum markers (e.g. total cholesterol,​ VLDL, LDL, and HDL) for the risk of cardiovascular disease, a complete analysis of the data suggests that there are a number of problems with the idea that cholesterol is pathogenic in CVD. When it comes to the argument that dietary cholesterol promotes hypercholesterolemia,​ the Framingham study clearly shows that men who ate the most cholesterol had exactly the same levels of cholesterol in their blood as those who ate the least cholesterol. And while the Framingham study does show that the highest risk of CVD is associated with total elevated serum cholesterol (18% occurrence),​ those participants with low to normal levels of serum cholesterol continue to be at significant risk (10-12% occurrence). Furthermore,​ another more recent cohort study called the Honolulu Heart program that examined 3572 Japanese/​American men (aged 71–93 years) found that low serum cholesterol levels in the elderly is an indicator of increased mortality (Schatz et al 2001). All of this becomes extremely confusing.
 +
 +Much of the impetus behind the cholesterol hypothesis is based on animal experimentation,​ such as the landmark study published by David Kritchevsky in 1954, who described the effects of feeding cholesterol to rabbits causing the formation of atheromas (Kritchevsky et al 1954). In another study published the following year Kritchevsky published a paper that described the benefits of consuming polyunsaturated fatty acids for lowering cholesterol levels. Some researchers criticized Kritchevsky’s research – after all, rabbits are herbivores and don’t normally eat cholesterol,​ unlike humans, who are omnivores and have a long history of eating cholesterol and saturated fat. Kritchevsky’s research marks the beginning of a drawn out campaign to get North American consumers to substitute traditionally-consumed cholesterol-rich foods such as butter for low cholesterol innovations such as refined corn oil. This marketing campaign had already begun much earlier in the century, but with a highly selective presentation of the preliminary scientific evidence, the industry-funded American Heart Association began to encourage the North American public to substitute butter, lard, beef and eggs with corn oil, margarine, chicken and cold cereal (Enig and Fallon 2003). Unfortunately these changes have been marked by an increasing incidence of cardiovascular disease in North America, which from 1900 to the mid 1960’s increased by 300%, and is now the single leading cause of death (Bergner 1997, 202-03)
 +
 +The reason for the exclusion of data such as these from conventional medical thinking on CVD risks is unknown, but when considered it radically alters the perception that cholesterol-rich foods are responsible for elevated serum cholesterol,​ or that elevated serum cholesterol is an important a risk factor CVD. Of particular concern is the relatively recent use of a new class of drugs called statins, derived from red rice yeast, which are used to interrupt the synthesis of cholesterol and reduce LDL/​cholesterol levels in the blood. Unfortunately,​ while statins indeed have been shown to reduce the risk of cardiovascular disease in patients with a history of myocardial infarction, they have also been shown to have number of adverse effects that make them unsuitable for general prevention in patients presenting with dyslipidemia. Some researchers have stated that the benefit of statins has nothing to do with the benefits of lowering cholesterol,​ but of promoting the stabilization of the lesion.
 +Hyperglycemia and atherosclerosis
 +
 +Prolonged exposure to hyperglycemia has also been recognized another factor in the pathogenesis of atherosclerosis. Hyperglycemia induces a large number of alterations at the cellular level of vascular tissue that potentially accelerate the atherosclerotic process. Animal and human studies have indicated three major mechanisms that encompass most of the pathological alterations observed in the atherosclerosis:​
 +
 +    nonenzymatic glycosylation
 +    oxidative stress
 +    protein kinase C (PKC) activation (Aronson and Rayfield 2002)
 +
 +One of the important mechanisms responsible for the accelerated atherosclerosis in diabetes is the nonenzymatic reaction between glucose and proteins or lipoproteins in arterial walls, collectively known as Maillard, or browning reation. Glucose forms reversible early glycosylation products with reactive amino groups of circulating or vessel wall proteins to form advanced glycosylation end products (AGEs). AGEs normally accumulate with normal aging and at an accelerated rate in diabetic patients. In situations in which the local redox potential has been shifted to favor oxidant stress, AGEs formation is increased substantially,​ and can accelerate the atherosclerotic process (Aronson and Rayfield 2002).
 +
 +Oxidative stress is another commonly described pathogenic mechanism for atherosclerosis. Hyperglycemia can increase oxidative stress through several pathways promoting the intracellular production of reactive oxygen species (ROS). There is also evidence that hyperglycemia may compromise natural antioxidant defenses. Reduced glutathione as well as reduced vitamin E have been reported in diabetic patients. Plasma and tissue levels of vitamin C are 40–50% lower in diabetic patients compared with nondiabetic subjects (Aronson and Rayfield 2002).
 +
 +High glucose concentrations have been shown to activate the protein kinase C, a family of at least 12 isoforms of serine and threonine kinases. In vascular smooth muscle cells, PKC activation has been shown to modulate growth rate, DNA synthesis, and growth factor receptor turnover. Hyperglycemia-induced PKC activation also results in increased platelet derived growth factor-beta receptor expression on smooth muscle cells and other vascular wall cells, and increases the expression of transforming growth factor-beta (TGF-beta), which is thought to lead to thickening of capillary basement membrane (Aronson and Rayfield 2002).
 +Medical treatment
 +
 +At this time modern medicine has no specific treatment for atherosclerosis,​ but is focused on inhibiting or alleviating signs and symptoms, or providing treatments that change or modify the results of laboratory investigations.
 +
 +Hypertension is perceived as being a risk factor for atherosclerosis,​ and is managed symptomatically through the use of antihypertensive agents including:
 +
 +    diuretics: promoting diuresis, decreasing plasma volume and edema, thereby decreasing cardiac output and blood pressure. Major drugs include thiazides (e.g. hydrochlorothiazide,​ depletes potassium), loop diuretics (e.g. furosemide, ethancrynic acid; depletes potassium), and potassium-sparing diuretics (e.g. triamterene,​ amiloride)
 +
 +    beta-1 adrenergic antagonists:​ selectively antagonizes beta-1 receptors, often used in conjunction with thiazides (e.g. atenolol, metoprolol, propranolol)
 +
 +    calcium channel antagonists:​ inhibits calcium ions from entering slow channels or voltage-sensitive areas of vascular smooth muscle and myocardium during depolarization (e.g. diltiazem verapamil nifedipine)
 +
 +    angiotensin-converting enzyme (ACE) inhibitors: act as competitive inhibitors of ACE, reducing angiotensin II levels, and thus decreasing aldosterone secretion (e.g. captopril, enalapril, lisinopril, ramipril)
 +
 +    aldosterone antagonists:​ competes with aldosterone receptor sites, reducing blood pressure and sodium reabsorption (e.g. eplerenone)
 +
 +    alpha-adrenergic agonists: stimulate presynaptic alpha-2 adrenergic receptors in the brain stem, reducing sympathetic nervous activity (e.g. methyldopa) (Berkow 1992)
 +
 +Hyperlipidemia is generally perceived as a risk factor for atherosclerosis largely based upon the use of hypolipidemic agents that lower serum cholesterol,​ and an observed reduction in the risk of coronary heart disease events and overall mortality. The primary hypolipidemic therapy consists of HMG-CoA reductase inhibitors or “statins” which inhibit the rate-limiting step of cholesterol synthesis in the liver, thereby lowering serum cholesterol,​ LDL-cholesterol,​ and triglyceride levels. Adverse effects include CoQ10 depletion (1), hepatotoxicity and myopathy. Example HMG-CoA reductase inhibitors include pravastatin,​ simvastatin,​ lovastatin, atorvastatin,​ and rosuvastatin.
 +
 +On the preventative side, modern medicine typically recommends a series of general changes to diet and lifestyle to decrease the risk of CVD, based on the prevailing hypotheses, many of which continue to revolve around the insudation hypothesis. The American Heart Association has recently developed an “Eating Plan for Healthy Americans,​” and is comprised of the following:
 +
 +    Emphasis upon a variety of fruits and vegetables, eating five or more servings per day.
 +
 +    Emphasis upon a variety of grain products, including whole grains, eating more than six or more servings per day.
 +
 +    Emphasis upon fat-free and low-fat milk products, fish, legumes (beans), skinless poultry and lean meats.
 +
 +    Emphasis upon fats and oils with 2 grams or less saturated fat per tablespoon, such as liquid and tub margarines, canola oil and olive oil.
 +
 +    Limiting consumption of foods high in calories or low in nutrition, e.g. soft drinks and candy
 +
 +    Limiting consumption of foods high in saturated fat, transfats and cholesterol,​ such as full-fat milk products, fatty meats, tropical oils, partially hydrogenated vegetable oils and egg yolks.
 +
 +    Limiting consumption of sodium to less 2,400 milligrams per day.
 +
 +    Limiting consumption of alcohol to no more than one alcoholic drink per day for women, and no more than two for men. "One drink" means it has no more than 1/2 ounce of pure alcohol, e.g. 12 oz. of beer, 4 oz. of wine, 1-1/2 oz. of 80-proof spirits or 1 oz. of 100-proof spirits.
 +
 +Lifestyle recommendations include 20-30 minutes of aerobic-type exercise at least three days a week, and quitting smoking.
 +Holistic treatment
 +
 +Generally speaking, the holistic perspective on the origin of atherosclerosis is related to an underlying metabolic dysfunction caused by alterations in diet and lifestyle. This idea is based on sound epidemiological and anthropological research that indicates that the incidence of atherosclerosis is for the most part a disease of people that eat a highly refined modern diet, rich in carbohydrates,​ plentiful in oxidizing and toxic compounds, and deficient in key nutrients including minerals, vitamins, essential fatty acids, and plant-based antioxidants. Concomitant factors include a sedentary lifestyle (which promotes insulin resistance) and environmental pollutants, e.g. cigarettes, air pollution etc., some of which are easier to control (i.e. smoking, exercise) than others (i.e. air pollution). The result this exposure to environmental toxins, a lack of exercise, and a dysfunctional eating pattern are metabolic problems such as chronic hyperglycemia,​ insulin resistance, hyperinsulinemia and dyslipidemia,​ free radical production, and impaired detoxification. Thus the focus in holistic treatment is to reduce the glycemic load of the diet, and supplement with key nutrients that may be deficient and can enhance antioxidant and detoxification pathways in the body.
 +
 +While the atheroma is fingered as the causal agent of atherosclerosis,​ and indeed, defines the nature of the condition, a holistic perspective suggests that the atheroma develops as a transient response to endothelial injury, to inhibit further endothelial injury by promoting a local thickening of the endothelial wall: essentially,​ chewing gum stuck in a crack of a dam about to burst. The transient and reversible nature of the atheroma suggests that if correct measures are taken to eliminate endothelial injury the atheroma will eventually be replaced by normal endothelial tissue. If the factors that cause damage to the endothelium are chronic however, the temporary method the body uses to protect against further endothelial injury becomes a secondary source of injury, narrowing the lumen of the vessels, placing stress on the heart, and then eventually, occluding the vessel so as to promote ischemia. The process of atherosclerosis is thus dependent upon chronic, underlying factors that promote the continuance of the atheroma, in much the same way that a scab that is constantly picked will never heal, and will result in a much larger lesion than originally sustained.
 +
 +From a traditional herbal perspective,​ atherosclerosis can be seen as a dysfunction of blood, specifically,​ in its constitution and its movement. The constitution of the blood is in large part a manifestation of digestive processes, and thus an assessment of digestion should be carefully undertaken. Specifically,​ it is the job of the liver build, replenish and filter the blood, and thus problems relating to the constitution of blood (e.g. blood viscosity, dyslipidemia etc.) demonstrates a need for upregulating liver function with the use of cholagogues,​ e.g. Barberry (Berberis vulgaris), Turmeric (Curcuma longa), Dandelion (Taraxacum officinale),​ Chai Hu (Buplerum falcatum), Celandine Poppy (Chelidonium majus). In Chinese and Ayurvedic terms an increase in blood viscosity or dyslipidemia relates to the accumulation of phlegm, and thus phlegm-reducing (i.e. kaphahara) remedies such as Guggulu (Commiphora mukul), Ginger (Zingiber officinale),​ Cayenne (Capsicum frutescens),​ Rosemary (Rosmarinus officinalis),​ Prickly Ash (Zanthoxylum clavaherculis) and Garlic (Allium sativum) can be used in conjunction with cholagogue remedies.
 +
 +Given the obstructive nature of atherosclerosis the movement of blood is an extremely important consideration,​ and the nature of the treatment can be implemented based on the presenting signs and symptoms. Generally speaking, it is always wise to include stimulants such as Ginger, Cayenne and Garlic in any therapy directed to atherosclerosis to enhance the processing of blood via the liver, and to dispel the archetypal accumulation of phlegm that underlies the obstructive nature of the atheroma. In many cases however the atherosclerotic patient will present with a substantial deficiency, qi deficiency in Chinese terms, or an increase in vata in Ayuervedic terms. Besides typical symptoms of cold hands and feet, there will be chronic fatigue, poor digestion, and weak pulse. Treatment is orientated to building up the vital essence and restoring the natural heat of the body with nutritive, blood-moving herbs such as Dong Quai (Angelica sinensis), Huang Qi (Astragalus membranaceus),​ Guggulu (Commiphora mukul), Dan Shen (Salvia miltiorrhiza),​ Ashwagandha (Withania somnifera), Ren Shen (Panax ginseng), Bai Zhu (Atractylodes macrocephala),​ prepared Fu Zi (Aconitum carmicheli) and purified Ativisha (Aconitum heterophyllum).
 +
 +Besides the condition and movement of the blood, attention must also be directed to the integrity of the vessel walls. In Chinese medicine the vessels are said to be regulated by the Spleen, and thus in chronic Spleen qi deficiency the vessels are weak and become susceptible to damage and rupture. Once again, qi-restorative herbs such as those described above are similarly appropriate. Attention should also be directed to using botanicals that have a trophorestorative function on the endothelium. Many of these botanicals are particularly rich in polyphenols such as flavonoids and tannins (e.g. ellagitannins,​ proanthocyanidins) including Gingko (Ginkgo biloba), Bilberry (Vaccinium myrtillus), Arjuna (Terminalia arjuna), Amalaki (Phyllanthus emblica), Turmeric (Curcuma longa), Gotu Kola (Centella asiatica), Yarrow (Achillea millefolium) and Grape (Vitis vinifera) seed.
 +
 +Overall, the holistic approach in the treatment of atherosclerosis is as follows:
 +
 +1. Reduce the glycemic load of the diet. Adopt a low-carbohydrate diet, and eliminate all refined carbohydrates including sugar, candy, soda pop, cookies and deserts for a minimum period of two to three months. After which time, whole-grain carbohydrates can be rotated back into the diet.
 +
 +2. Eliminate toxic foods from the diet. Including hydrogenated and trans-fats (e.g. margarine, deep-fried foods), feed-lot meat and farmed salmon, dairy.
 +
 +3. Supplement for deficient nutrients.
 +
 +    vitamin B complex, 100 mg daily
 +
 +    folic acid, 1 g daily
 +
 +    cobalamin, 1000 mcg daily
 +
 +    vitamin C, 1-5 g bid-tid, to bowel tolerance
 +
 +    vitamin E (d-alpha tocopherol),​ 400-800 IU daily, increase dose gradually
 +
 +    EPA/DHA, 1000 mg each daily
 +
 +    magnesium, 800 mg daily, in divided doses, with meals
 +
 +    chromium, 200-300 mcg daily, in divided doses, with meals
 +
 +    selenium, 100 mcg daily
 +
 +    chelated multimineral,​ taken with the above minerals; or high quality kelp (seaweed) supplement (5-15 g daily)
 +
 +    CoQ10, 50 mg daily
 +
 +    Flavonoids (mixed, e.g. quercitin, rutin, anthocyanidins),​ 3-5 g daily
 +
 +4. Support liver, enhance detoxification:​ Barberry (Berberis vulgaris), Turmeric (Curcuma longa), Dandelion (Taraxacum officinale),​ Chai Hu (Buplerum falcatum), Celandine Poppy (Chelidonium majus) etc.
 +
 +5. Promote circulation and blood flow, reduce blood viscosity (i.e. phlegm, kapha): Guggulu (Commiphora mukul), Ginger (Zingiber officinale),​ Cayenne (Capsicum frutescens),​ Rosemary (Rosmarinus officinalis),​ Prickly Ash (Zanthoxylum clavaherculis),​ Garlic (Allium sativum), Pippali (Piper longum) etc.
 +
 +6. Cardiovascular trophorestoration:​ Hawthorn (Crataegus spp.), Bilberry (Vaccinium myrtillus), Arjuna (Terminalia arjuna), Amalaki (Phyllanthus emblica), Turmeric (Curcuma longa), Gotu Kola (Centella asiatica), Yarrow (Achillea millefolia) etc.
 +
 +7. Rebuild the vital essence (i.e. qi, ojas): e.g. Dan Gui (Angelica sinensis), Huang Qi (Astragalus membranaceus),​ Guggulu (Commiphora mukul), Dan Shen (Salvia miltiorrhiza),​ Ashwagandha (Withania somnifera), Ginseng (Panax ginseng), Bai Zhu (Atractylodes macrocephala) etc.
 +
 +8. Exercise: in particular, anaerobic exercise (muscle-building) is more effective than aerobic exercise (jumping, running) to reduce insulin resistance, e.g. calisthenics (e.g. pushups, lunges, chin ups etc.), walking or bicycling uphill, hiking martial arts, weight-lifting;​ note that any exercise regimen should be implemented gradually
 +
 +1. A trend that has raised alarm bells in many independent researchers,​ given the importance of CoQ10 in myocardial function. See: Langsjoen PH, Langsjoen AM. 2003. The clinical use of HMG CoA-reductase inhibitors and the associated depletion of coenzyme Q10. A review of animal and human publications. Biofactors. 18(1-4):​101-11.
 +
 +[[Fair Use]] Source: http://​www.toddcaldecott.com/​index.php/​healing/​conditions/​180-arterial-disease
 +
 +http://​www.ayurveda-california.com/​distance_learning/​index.php/​diseases-treatment-with-ayurveda-chinese-medicine/​arterial-disease
 +
 +----
 +
 +Coronary artery disease
 +From Wikipedia, the free encyclopedia
 +Coronary artery disease
 +Classification and external resources
 +
 +Micrograph of a coronary artery with the most common form of coronary artery disease (atherosclerosis) and marked luminal narrowing. Masson'​s trichrome.
 +ICD-10 I20.-I25.
 +ICD-9 410-414, 429.2
 +eMedicine radio/192
 +MeSH D003324
 +
 +Coronary Artery Disease (CAD or atherosclerotic heart disease) is the end result of the accumulation of atheromatous plaques within the walls of the coronary arteries[1] that supply the myocardium (the muscle of the heart) with oxygen and nutrients. It is sometimes also called coronary heart disease (CHD), although CAD is the most common cause of CHD, it is not the only one.
 +
 +CAD is the leading cause of death worldwide.[2] While the symptoms and signs of coronary artery disease are noted in the advanced state of disease, most individuals with coronary artery disease show no evidence of disease for decades as the disease progresses before the first onset of symptoms, often a "​sudden"​ heart attack, finally arises. After decades of progression,​ some of these atheromatous plaques may rupture and (along with the activation of the blood clotting system) start limiting blood flow to the heart muscle. The disease is the most common cause of sudden death,[3] and is also the most common reason for death of men and women over 20 years of age.[4] According to present trends in the United States, half of healthy 40-year-old males will develop CAD in the future, and one in three healthy 40-year-old women.[5] According to the Guinness Book of Records, Northern Ireland is the country with the most occurrences of CAD. By contrast, the Maasai of Africa have almost no heart disease.
 +
 +As the degree of coronary artery disease progresses, there may be near-complete obstruction of the lumen of the coronary artery, severely restricting the flow of oxygen-carrying blood to the myocardium. Individuals with this degree of coronary artery disease typically have suffered from one or more myocardial infarctions (heart attacks), and may have signs and symptoms of chronic coronary ischemia, including symptoms of angina at rest and flash pulmonary edema.
 +
 +A distinction should be made between myocardial ischemia and myocardial infarction. Ischemia means that the amount of blood supplied to the tissue is inadequate to supply the needs of the tissue. When the myocardium becomes ischemic, it does not function optimally. When large areas of the myocardium becomes ischemic, there can be impairment in the relaxation and contraction of the myocardium. If the blood flow to the tissue is improved, myocardial ischemia can be reversed. Infarction means that the tissue has undergone irreversible death due to lack of sufficient oxygen-rich blood.
 +
 +An individual may develop a rupture of an atheromatous plaque at any stage of the spectrum of coronary artery disease. The acute rupture of a plaque may lead to an acute myocardial infarction (heart attack).
 +Contents
 +
 +    1 Pathophysiology
 +    2 Angina
 +    3 Characteristics of coronary artery disease
 +        3.1 Special Pathophysiology
 +        3.2 Symptoms
 +        3.3 Therapy
 +    4 Risk factors
 +    5 Prevention
 +    6 Exercise
 +    7 Preventive diets
 +    8 Aspirin
 +    9 Omega-3 fatty acids
 +    10 Secondary prevention
 +        10.1 Anti-platelet therapy
 +    11 Therapy - Principles of Treatment
 +    12 Recent research
 +    13 See also
 +    14 References
 +    15 External links
 +
 +[edit] Pathophysiology
 +
 +Limitation of blood flow to the heart causes ischemia (cell starvation secondary to a lack of oxygen) of the myocardial cells. Myocardial cells may die from lack of oxygen and this is called a myocardial infarction (commonly called a heart attack). It leads to heart muscle damage, heart muscle death and later myocardial scarring without heart muscle regrowth. Chronic high-grade stenosis of the coronary arteries can induce transient ischemia which leads to the induction of a ventricular arrhythmia, which may terminate into ventricular fibrillation leading to death.
 +
 +CAD is associated with smoking, diabetes, and hypertension. A family history of early CAD is one of the less important predictors of CAD. Most of the familial association of coronary artery disease are related to common dietary habits. Screening for CAD includes evaluating high-density and low-density lipoprotein (cholesterol) levels and triglyceride levels. Despite much press, most of the alternative risk factors including homocysteine,​ C-reactive protein (CRP), Lipoprotein (a), coronary calcium and more sophisticated lipid analysis have added little if any additional value to the conventional risk factors of smoking, diabetes and hypertension.
 +[edit] Angina
 +
 +Angina (chest pain) that occurs regularly with activity, after heavy meals, or at other predictable times is termed stable angina and is associated with high grade narrowings of the heart arteries. The symptoms of angina are often treated with betablocker therapy such as metoprolol or atenolol. Nitrate preparations such as nitroglycerin,​ which come in short-acting and long-acting forms are also effective in relieving symptoms but are not known to reduce the chances of future heart attacks. Many other more effective treatments, especially of the underlying atheromatous disease, have been developed.
 +
 +Angina that changes in intensity, character or frequency is termed unstable. Unstable angina may precede myocardial infarction, and requires urgent medical attention. It may be treated with oxygen, intravenous nitroglycerin,​ and aspirin. Interventional procedures such as angioplasty may be done.
 +[edit] Characteristics of coronary artery disease
 +[edit] Special Pathophysiology
 +
 +Typically, coronary artery disease occurs when part of the smooth, elastic lining inside a coronary artery (the arteries that supply blood to the heart muscle) develops atherosclerosis. With atherosclerosis,​ the artery'​s lining becomes hardened, stiffened, and swollen with all sorts of "​grunge"​ - including calcium deposits, fatty deposits, and abnormal inflammatory cells - to form a plaque. Deposits of calcium phosphates (hydroxyapatites) in the muscular layer of the blood vessels appear to play not only a significant role in stiffening arteries but also for the induction of an early phase of coronary arteriosclerosis. This can be seen in a so-called metatstatic mechanism of calcification as it occurs in chronic kidney disease and haemodialysis (Rainer Liedtke 2008). Although these patients suffer from a kidney dysfunction,​ almost fifty percent of them die due to coronary artery disease. Plaques can be thought of as large "​pimples"​ that protrude into the channel of an artery, causing a partial obstruction to blood flow. Patients with coronary artery disease might have just one or two plaques, or might have dozens distributed throughout their coronary arteries. However, there is a term in medicine called “Cardiac Syndrome X”, which describes chest pain (Angina pectoris) and chest discomfort in people who do not show signs of blockages in the larger coronary arteries of their hearts when an angiogram (coronary angiogram) is being performed.[6]
 +
 +No one knows exactly what causes “Cardiac Syndrome X” and it is unlikely to have a single cause. Today, we speculate that the major contributing factor to “Cardiac Syndrome X” is “microvascular dysfunction”.[who?​] The term “microvascular” refers to very small blood vessels and, in this case, very small arteries (arterioles,​ capillaries) of the heart. Studies have also shown that people with “Cardiac Syndrome X” have enhanced pain perception, meaning they feel chest pain more intensely than the average person.
 +
 +The large majority of women have the garden variety of coronary artery disease. Rarely, women with “Cardiac Syndrome X” have typical anginal syndromes that are not associated with the presence of atherosclerotic plaques; that is, the localized blockages are absent. Scientists speculate that the blood vessels in these women are diffuse abnormal. Some have falsely claim that the entire lining of the artery becomes thickened throughout, making the plaques flush with the wall of the artery without any scientific proof. On cardiac catheterization their coronary arteries appear smooth-walled and normal, though they may look "​small"​ in diameter. By the way: in general, female coronary arteries (like all arteries) are somewhat smaller than in males.
 +Coronary angiogram of a man
 +Coronary angiogram of a woman
 +
 +“Cardiac Syndrome X” have never been shown to cause acute heart attacks (myocardial infarction) despite much speculation. The prognosis with syndrome-X coronary artery disease is also known to be better than with typical coronary artery disease, but this is not a benign condition since it can be quite disabling. It is not completely clear why women are more likely than men to suffer from "​Syndrome X"; however, hormones and other risk factors unique to women may play a role.[7] Women’s blood vessels are exposed to changing levels of oestrogen throughout their lives, first during regular menstrual cycles and later during and after menopause as oestrogen levels decline with age. Oestrogen affects how blood vessels narrow and widen and how they respond to injury, so changes in oestrogen levels mean changes in the reactivity of the blood vessels. Women’s vessels may be “programmed” for more changes than men’s vessels, which could increase the risk of having problems in the lining of the arteries (endothelial cells) and the smooth muscle cells in the walls of the arteries. The endothelial dysfunction is likely to be multifactorial in these patients and it is conceivable that risk factors such as hypertension,​ hypercholesterolemia,​ diabetes mellitus and smoking can contribute to its development. Most patients with Syndrome X are postmenopausal women and oestrogen deficiency has been therefore proposed as a pathogenic factor in female patients. In addition to changing hormone levels, there are several other risk conditions for blood vessel problems that are unique to women, such as preeclampsia (a problem associated with high blood pressure during pregnancy) and delivering a low-birth weight baby. Of course, despite these issues women, the female gender as a whole is protective against coronary artery disease.
 +[edit] Symptoms
 +
 +Cardiac Syndrome X often is a diagnosis of exclusion where the presence of typical chest pains is not accompanied by coronary artery narrowings on angiography. In considering Syndrome-X, it is important to understand that about 80% of chest pains have nothing to do with the heart. Therefore, the characteristics of typical chest pains must be carefully documented to avoid unnecessary labelling patients with heart disease:
 +
 +    Chest pain or Angina pectoris with physical stress; the pain may spread to the left arm or the neck, back, throat, or jaw. There might be present a numbness (paresthesia) or a loss of feeling in the arms, shoulders, or wrists
 +    Coronary angiography demonstrates “normal” coronary arteries, i.e. no blockages or stenoses can be detected in the larger epicardial vessels
 +    No inducible coronary artery spasm present during cardiac catheterization
 +    Characteristic ischemic ECG changes during exercise testing
 +    ST segment depression and angina in the presence of left ventricular wall perfusion abnormalities during thallium or other stress perfusion test
 +    Consistent response to sublingual nitrates.
 +    Postmenopausal or menopausal status
 +
 +The diagnosis of “Cardiac Syndrome X” - the rare coronary artery disease that is more common in women, as mentioned, an “exclusion” diagnosis. Therefore, usually the same tests are used as in any patient with the suspicion of coronary artery disease:
 +
 +    Baseline electrocardiography (ECG)
 +    Exercise ECG – Stress test
 +    Exercise radioisotope test (nuclear stress test, myocardial scintigraphy)
 +    Echocardiography (including stress echocardiography)
 +    Coronary angiography
 +    Intravascular ultrasound
 +    Magnetic resonance imaging (MRI)
 +
 +[edit] Therapy
 +
 +A variety of drugs are used in the attempt to treat the Syndrome-X coronary artery disease: nitrates, calcium channel antagonists,​ ACE-inhibitors,​ statins, imipramine (for analgesia), aminophylline,​ hormone replacement therapy (oestrogen),​ even electrical spinal cord stimulation are tried to overcome the symptomatology -all with mixed results. Quite often the quality of life for these women remains poor.
 +
 +While not enough is known about Syndrome-X coronary artery disease to list specific prevention techniques, adopting heart-healthy habits can be a good start.[citation needed] These include monitoring cholesterol and blood pressure levels[citation needed], maintaining a low-fat diet[citation needed], exercising regularly[citation needed], quitting smoking, avoiding recreational drugs[citation needed], and moderating alcohol intake. However, there might be a new option for women suffering from “Cardiac Syndrome X”: Protein based Angiogenesis.[8] This new protein-based angiogenic therapy - using fibroblast growth factor 1 (FGF-1) - might be used as sole therapy as well as adjunct to bypass surgery – thus overcoming the limitations of conventional bypass surgery.
 +Neo-angiogenesis in a woman'​s heart after FGF-1 treatment
 +
 +Beyond drug therapy, interventional procedures, and coronary artery bypass grafting, angiogenesis now offers a new, specific and – so far as we know from three human clinical trials – effective treatment targeted for women’s coronary artery disease.[9]
 +[edit] Risk factors
 +
 +The following are confirmed independent risk factors for the development of CAD:
 +
 +    Hypercholesterolemia (specifically,​ serum LDL concentrations)[citation needed]
 +    Smoking[citation needed]
 +    Hypertension (high systolic pressure seems to be most significant in this regard)[citation needed]
 +    Hyperglycemia (due to diabetes mellitus or otherwise)[citation needed]
 +    Type A Behavioural Patterns, TABP. Added in 1981 as an independent risk factor after a majority of research into the field discovered that TABP's were twice as likely to exhibit CAD as any other personality type.[citation needed]
 +    Hemostatic Factors:​[10] High levels of fibrinogen and coagulation factor VII are associated with an increased risk of CAD. Factor VII levels are higher in individuals with a high intake of dietary fat[citation needed]. Decreased fibrinolytic activity has been reported in patients with coronary atherosclerosis.
 +    Hereditary differences/​genetic polymorphisms in such diverse aspects as lipoprotein structure and that of their associated receptors, enzymes of lipoprotein metabolism such as cholesteryl ester transfer protein (CETP) and hepatic lipase (HL) [11], homocysteine processing/​metabolism,​ etc.[citation needed]
 +    High levels of Lipoprotein(a),​[12][13][14] a compound formed when LDL cholesterol combines with a substance known as Apoliprotein (a).
 +
 +Significant,​ but indirect risk factors include:
 +
 +    Lack of exercise
 +    Consumption of alcohol
 +    Stress
 +    Diet rich in saturated fats[citation needed]
 +    Diet low in antioxidants
 +    Obesity
 +    Men over 60; Women over 65[15]
 +
 +Risk factors can be classified as
 +
 +    Fixed: age, sex, family history
 +    Modifiable: smoking, hypertension,​ diabetes mellitus, obesity, etc.
 +
 +There are various risk assessment systems for determining the risk of coronary artery disease, with various emphasis on different variables above. A notable example is Framingham Score, used in the Framingham Heart Study. It is mainly based on age, gender, diabetes, total cholesterol,​ HDL cholesterol,​ tobacco smoking and systolic blood pressure.[16]
 +[edit] Prevention
 +
 +Coronary artery disease is the most common form of heart disease in the Western world. Prevention centers on the modifiable risk factors, which include decreasing cholesterol levels, addressing obesity and hypertension,​ avoiding a sedentary lifestyle, making healthy dietary choices, and stopping smoking. There is some evidence that lowering homocysteine levels may contribute to more heart attacks (NORVIT trial). In diabetes mellitus, there is little evidence that very tight blood sugar control actually improves cardiac risk although improved sugar control appears to decrease other undesirable problems like kidney failure and blindness. Some recommend a diet rich in omega-3 fatty acids and vitamin C. The World Health Organization (WHO) recommends "low to moderate alcohol intake"​ to reduce risk of coronary artery disease although this remains without scientific cause and effect proof.[17]
 +
 +An increasingly growing number of other physiological markers and homeostatic mechanisms are currently under scientific investigation. Patients with CAD and those trying to prevent CAD are advised to avoid fats that are readily oxidized (e.g., saturated fats and trans-fats),​ limit carbohydrates and processed sugars to reduce production of Low density lipoproteins (LDLs), triacylglycerol and apolipoprotein-B. [18] [19] [20] [21] [22] It is also important to keep blood pressure normal, exercise and stop smoking. These measures reduces the development of heart attacks. Recent studies have shown that dramatic reduction in LDL levels can cause regression of coronary artery disease in as many as 2/3 of patients after just one year of sustained treatment.
 +
 +Menaquinone (Vitamin K2), but not phylloquinone (Vitamin K1), intake is associated with reduced risk of CAD mortality, all-cause mortality and severe aortic calcification.[23][24][25]
 +
 +CAD has always been a tough disease to diagnose without the use of invasive or stressful activities. The development of the Multifunction Cardiogram (MCG) has changed the way CAD is diagnosed. The MCG consists of a 2 lead resting EKG signal is transformed into a mathematical model and compared against tens of thousands of clinical trials to diagnose a patient with an objective severity score, as well as secondary and tertiary results about the patients condition. The results from MCG tests have been validated in 8 clinical trials which resulted in a database of over 50,000 patients where the system has demonstrated accuracy comparable to coronary angiography (90% overall sensitivity,​ 85% specificity). This level of accuracy comes from the application of advanced techniques in signal processing and systems analysis combined with a large scale clinical database which allows MCG to provide quantitative,​ evidence-based results to assist physicians in reaching a diagnosis. The MCG has also been awarded a Category III CPT code by the American Medical Association in the July 2009 CPT update.
 +[edit] Exercise
 +
 +Separate to the question of the benefits of exercise; it is unclear whether doctors should spend time counseling patients to exercise. The U.S. Preventive Services Task Force (USPSTF), based on a systematic review of randomized controlled trials, found '​insufficient evidence'​ to recommend that doctors counsel patients on exercise, but "it did not review the evidence for the effectiveness of physical activity to reduce chronic disease, morbidity and mortality",​ it only examined the effectiveness of the counseling itself.[26] However, the American Heart Association,​ based on a non-systematic review, recommends that doctors counsel patients on exercise.[27]
 +[edit] Preventive diets
 +Main article: Diet and Heart Disease
 +
 +It has been suggested that coronary artery disease is partially reversible using an intense dietary regimen coupled with regular cardio exercise.[28]
 +
 +    Vegetarian diet: Vegetarians have been shown to have a 24% reduced risk of dying of heart disease.[29]
 +    Cretan Mediterranean diet: The Seven Countries Study found that Cretan men had exceptionally low death rates from heart disease, despite moderate to high intake of fat. The Cretan diet is similar to other traditional Mediterranean diets: consisting mostly of olive oil, bread, abundant fruit and vegetables, a moderate amount of wine and fat-rich animal products such as lamb, and goat cheese.[30][31][32] However, the Cretan diet consisted of less fish and wine consumption than some other Mediterranean-style diets, such as the diet in Corfu, another region of Greece, which had higher death rates.[citation needed]
 +
 +The consumption of trans fat (commonly found in hydrogenated products such as margarine) has been shown to cause the development of endothelial dysfunction,​ a precursor to atherosclerosis.[33] The consumption of trans fatty acids has been shown to increase the risk of coronary artery disease[34]
 +
 +Foods containing fiber, potassium, nitric oxide (in green leafy vegetables),​ monounsaturated fat, polyunsaturated fat, saponins, or lecithin are said to lower cholesterol levels. Foods high in grease, salt, trans fat, or saturated fat are said to raise cholesterol levels.
 +[edit] Aspirin
 +
 +Aspirin, in doses of less than 75 to 81 mg/d,[35] can reduce the incidence of cardiovascular events.[36] The U.S. Preventive Services Task Force '​strongly recommends that clinicians discuss aspirin chemoprevention with adults who are at increased risk for coronary artery disease'​.[37] The Task Force defines increased risk as 'Men older than 90 years of age, postmenopausal women, and younger persons with risk factors for coronary artery disease (for example, hypertension,​ diabetes, or smoking) are at increased risk for heart disease and may wish to consider aspirin therapy'​. More specifically,​ high-risk persons are 'those with a 5-year risk ≥ 3%'. A risk calculator is available.[38]
 +
 +Regarding healthy women, the more recent Women'​s Health Study randomized controlled trial found insignificant benefit from aspirin in the reduction of cardiac events; however there was a significant reduction in stroke.[39] Subgroup analysis showed that all benefit was confined to women over 65 years old.[39] In spite of the insignificant benefit for women <65 years old, recent practice guidelines by the American Heart Association recommend to '​consider'​ aspirin in '​healthy women' <65 years of age 'when benefit for ischemic stroke prevention is likely to outweigh adverse effects of therapy'​.[40]
 +[edit] Omega-3 fatty acids
 +
 +The benefit of fish oil is controversial with conflicting conclusions reached by a negative meta-analysis on studies using traditional omega-3 products[41] of randomized controlled trials by the international Cochrane Collaboration and a partially positive systematic review[42] by the Agency for Healthcare Research and Quality. Since these two reviews, a randomized controlled trial reported a remarkable reduction on coronary events in Japanese hypercholesterolemic patients,​[43] and a later subanalysis suggested that the protective effect of highly purified EPA (E-EPA) is even more pronounced in Japanese diabetics even though their intake of fish is high.[44]
 +
 +Omega-3 fatty acids are also found in some plant sources including flax seed oil, hemp seed oil, and walnuts. The plant omega-3 (ALA) is biologically inferior to marine omega-3, as ALA needs to be converted in the liver to EPA, but only about five per cent is converted.
 +[edit] Secondary prevention
 +
 +Secondary prevention is preventing further sequelae of already established disease. Regarding coronary artery disease, this can mean risk factor management that is carried out during cardiac rehabilitation,​ a 4-phase process beginning in hospital after MI, angioplasty or heart surgery and continuing for a minimum of three months. Exercise is a main component of cardiac rehabilitation along with diet, smoking cessation, and blood pressure and cholesterol management. Beta blockers may also be used for this purpose.[45]
 +[edit] Anti-platelet therapy
 +
 +A meta-analysis of randomized controlled trials by the international Cochrane Collaboration found "that the use of clopidogrel plus aspirin is associated with a reduction in the risk of cardiovascular events compared with aspirin alone in patients with acute non-ST coronary syndrome. In patients at high risk of cardiovascular disease but not presenting acutely, there is only weak evidence of benefit and hazards of treatment almost match any benefit obtained."​.[46]
 +[edit] Therapy - Principles of Treatment
 +
 +Therapeutic options for coronary artery disease[47] today are based on three principles:
 +
 +    1. Medical treatment - drugs (e.g. cholesterol lowering medications,​ beta-blockers,​ nitroglycerin,​ calcium antagonists,​ etc.);
 +    2. Coronary interventions as angioplasty and coronary stent-implantation;​
 +    3. Coronary artery bypass grafting (CABG - coronary artery bypass surgery).
 +
 +Recent research efforts focus on new angiogenic treatment modalities (angiogenesis) and various (adult) stem cell therapies.
 +[edit] Recent research
 +Further information:​ atheroma and atherosclerosis
 +
 +A 2006 study by the Cleveland Clinic found a region on Chromosome 17 was confined to families with multiple cases of myocardial infarction.[48]
 +
 +A more controversial link is that between Chlamydophila pneumoniae infection and atherosclerosis.[49] While this intracellular organism has been demonstrated in atherosclerotic plaques, evidence is inconclusive as to whether it can be considered a causative factor.[citation needed] Treatment with antibiotics in patients with proven atherosclerosis has not demonstrated a decreased risk of heart attacks or other coronary vascular diseases.[50]
 +
 +Since the 1990s the search for new treatment options for coronary artery disease patients, particularly for so called "​no-option"​ coronary patients, focused on usage of angiogenesis[51] and (adult) stem cell therapies. Numerous clinical trials were performed, either applying protein (angiogenic growth factor) therapies, such as FGF-1 or VEGF, or cell therapies using different kinds of adult stem cell populations. Research is still going on - with first promising results particularly for FGF-1[52][53] and utilization of endothelial progenitor cells.
 +[edit] See also
 +
 +    Diet and Heart Disease
 +    ApoA-1 Milano
 +    Endothelium-derived relaxing factor
 +    CADgene database
 +
 +[edit] References
 +
 +    ^ "​Dorlands Medical Dictionary:​coronary artery disease"​. Retrieved 2009-01-09.
 +    ^ Coronary artery disease at ospital
 +    ^ Thomas AC, Knapman PA, Krikler DM, Davies MJ (December 1988). "​Community study of the causes of "​natural"​ sudden death"​. BMJ 297 (6661): 1453–6. doi:​10.1136/​bmj.297.6661.1453. PMC 1835183. PMID 3147014.
 +    ^ American Heart Association:​ Heart Disease and Stroke Statistics-2007 Update. AHA, Dallas, Texas, 2007
 +    ^ Rosamond W, Flegal K, Friday G (February 2007). "Heart disease and stroke statistics--2007 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee"​. Circulation 115 (5): e69–171. doi:​10.1161/​CIRCULATIONAHA.106.179918. PMID 17194875.
 +    ^ Lanza GA (February 2007). "​Cardiac syndrome X: a critical overview and future perspectives"​. Heart 93 (2): 159–66. doi:​10.1136/​hrt.2005.067330. PMC 1861371. PMID 16399854.
 +    ^ Kaski JC (February 2004). "​Pathophysiology and management of patients with chest pain and normal coronary arteriograms (cardiac syndrome X)". Circulation 109 (5): 568–72. doi:​10.1161/​01.CIR.0000116601.58103.62. PMID 14769677.
 +    ^ Stegmann, T.J.: New Vessels for the Heart. Angiogenesis as New Treatment for Coronary Heart Disease: The Story of its Discovery and Development. Henderson, Nevada 89012, USA, 2004. ISBN 0-976558-30-5
 +    ^ Stegmann, T.J.: Protein promise in heart disease. GCPj, March 2007, 21-24
 +    ^ Smith FB, Lee AJ, Fowkes FG, Price JF, Rumley A, Lowe GD (November 1997). "​Hemostatic factors as predictors of ischemic heart disease and stroke in the Edinburgh Artery Study"​. Arterioscler Thromb Vasc Biol. 17 (11): 3321–5. PMID 9409328.
 +    ^ Ghatrehsamani K, Darabi M, Rahbani M, Hashemzadeh Chaleshtory M, Farrokhi E, Noori M (2009). "​Combined hepatic lipase -514C/T and cholesteryl ester transfer protein I405V polymorphisms are associated with the risk of coronary artery disease."​. Genet Test Mol Biomarkers 13 (6): 809–15. doi:​10.1089/​gtmb.2009.0080. PMID 19810818.
 +    ^ Danesh J, Collins R, Peto R (2000). "​Lipoprotein(a) and coronary heart disease. Meta-analysis of prospective studies"​. Circulation 102 (10): 1082–5. PMID 10973834.
 +    ^ Smolders B, Lemmens R, Thijs V (2007). "​Lipoprotein (a) and stroke: a meta-analysis of observational studies"​. Stroke 38 (6): 1959–66. doi:​10.1161/​STROKEAHA.106.480657. PMID 17478739.
 +    ^ Schreiner PJ, Morrisett JD, Sharrett AR, Patsch W, Tyroler HA, Wu K, Heiss G (1993). "​Lipoprotein(a) as a risk factor for preclinical atherosclerosis"​. Arterioscler. Thromb. 13 (6): 826–33. PMID 8499402.
 +    ^ "Women and heart disease"​.[dead link]
 +    ^ framinghamheartstudy.org > Coronary Heart Disease (10-year risk) (based on Wilson, D'​Agostino,​ Levy et al. '​Prediction of Coronary Heart Disease using Risk Factor Categories',​ Circulation 1998)
 +    ^ "5. Population nutrient intake goals for preventing diet-related chronic diseases"​. WHO.
 +    ^ Swarbrick MM, Stanhope KL, Elliott SS (April 2008). "​Consumption of fructose-sweetened beverages for 10 weeks increases postprandial triacylglycerol and apolipoprotein-B concentrations in overweight and obese women"​. Br. J. Nutr. 100 (5): 1–6. doi:​10.1017/​S0007114508968252. PMID 18384705.
 +    ^ Culling KS, Neil HA, Gilbert M, Frayn KN (December 2007). "​Effects of short-term low- and high-carbohydrate diets on postprandial metabolism in non-diabetic and diabetic subjects"​. Nutr Metab Cardiovasc Dis 19 (5): 345–51. doi:​10.1016/​j.numecd.2007.09.003. PMID 18083355.
 +    ^ Parks EJ, Skokan LE, Timlin MT, Dingfelder CS (June 2008). "​Dietary sugars stimulate fatty acid synthesis in adults"​. J. Nutr. 138 (6): 1039–46. PMC 2546703. PMID 18492831.
 +    ^ Lofgren IE, Herron KL, West KL (April 2005). "​Carbohydrate intake is correlated with biomarkers for coronary heart disease in a population of overweight premenopausal women"​. J. Nutr. Biochem. 16 (4): 245–50. doi:​10.1016/​j.jnutbio.2004.12.008. PMID 15808329.
 +    ^ Aeberli I, Zimmermann MB, Molinari L (October 2007). "​Fructose intake is a predictor of LDL particle size in overweight schoolchildren"​. Am. J. Clin. Nutr. 86 (4): 1174–8. PMID 17921399.
 +    ^ Geleijnse JM, Vermeer C, Grobbee DE (2004). "​Dietary intake of menaquinone is associated with a reduced risk of coronary artery disease: the Rotterdam Study"​. J. Nutr. 134 (11): 3100–5. PMID 15514282.
 +    ^ Erkkilä AT, Booth SL (2008). "​Vitamin K intake and atherosclerosis"​. Curr. Opin. Lipidol. 19 (1): 39–42. doi:​10.1097/​MOL.0b013e3282f1c57f. PMID 18196985.
 +    ^ Wallin R, Schurgers L, Wajih N (2008). "​Effects of the blood coagulation vitamin K as an inhibitor of arterial calcification"​. Thromb. Res. 122 (3): 411. doi:​10.1016/​j.thromres.2007.12.005. PMC 2529147. PMID 18234293.
 +    ^ U.S. Preventive Services Task Force (2002). "​Behavioral counseling in primary care to promote physical activity: recommendation and rationale"​. Ann. Intern. Med. 137 (3): 205–7. PMID 12160370.
 +    ^ Thompson PD, Buchner D, Pina IL (2003). "​Exercise and physical activity in the prevention and treatment of atherosclerotic cardiovascular disease: a statement from the Council on Clinical Cardiology (Subcommittee on Exercise, Rehabilitation,​ and Prevention) and the Council on Nutrition, Physical Activity, and Metabolism (Subcommittee on Physical Activity)"​. Circulation 107 (24): 3109–16. doi:​10.1161/​01.CIR.0000075572.40158.77. PMID 12821592.
 +    Exercise and physical activity in the prevention and treatment of atherosclerotic cardiovascular disease. Major Recommendations
 +    ^ Ornish D, Brown SE, Scherwitz LW, Billings JH, Armstrong WT, Ports TA, McLanahan SM, Kirkeeide RL, Brand RJ, Gould KL. (1990). "Can lifestyle changes reverse coronary heart disease? The Lifestyle Heart Trial"​. Lancet 336 (8708): 129–33. doi:​10.1016/​0140-6736(90)91656-U. PMID 1973470.
 +    ^ Key TJ, Fraser GE, Thorogood M, Appleby PN, Beral V, Reeves G, Burr ML, Chang-Claude J, Frentzel-Beyme R, Kuzma JW, Mann J, McPherson K (1998). "​Mortality in vegetarians and non-vegetarians:​ a collaborative analysis of 8300 deaths among 76,000 men and women in five prospective studies"​. Public Health Nutr 1 (1): 33–41. doi:​10.1079/​PHN19980006. PMID 10555529.
 +    ^ Willett WC, Sacks F, Trichopoulou A, Drescher G, Ferro-Luzzi A, Helsing E, Trichopoulos D. (1995). "​Mediterranean diet pyramid: a cultural model for healthy eating"​. Am J Clin Nutr 61 (6 Suppl): 1402S–1406S. PMID 7754995.
 +    ^ Perez-Llamas,​ F., et al., J Hum Nutr Diet, December 1996, 9:6:463-471
 +    ^ Alberti-Fidanza A, Paolacci CA, Chiuchiu MP, Coli R, Fruttini D, Verducci G, Fidanza F. (1994). "​Dietary studies on two rural Italian population groups of the Seven Countries Study. 1. Food and nutrient intake at the thirty-first year follow-up in 1991". Eur J Clin Nutr 48 (2): 85–91. PMID 8194497.
 +    ^ Lopez-Garcia E, Schulze MB, Meigs JB, Manson JE, Rifai N, Stampfer MJ, Willett WC, Hu FB. (2005). "​Consumption of trans fatty acids is related to plasma biomarkers of inflammation and endothelial dysfunction"​. J Nutr 135 (3): 562–6. PMID 15735094.
 +    ^ Mozaffarian D, Katan MB, Ascherio A, Stampfer MJ, Willett WC (April 2006). "Trans fatty acids and cardiovascular disease"​. N. Engl. J. Med. 354 (15): 1601–13. doi:​10.1056/​NEJMra054035. PMID 16611951.
 +    ^ Campbell CL, Smyth S, Montalescot G, Steinhubl SR (2007). "​Aspirin dose for the prevention of cardiovascular disease: a systematic review"​. JAMA 297 (18): 2018–24. doi:​10.1001/​jama.297.18.2018. PMID 17488967.
 +    ^ Berger J, Roncaglioni M, Avanzini F, Pangrazzi I, Tognoni G, Brown D (2006). "​Aspirin for the primary prevention of cardiovascular events in women and men: a sex-specific meta-analysis of randomized controlled trials"​. JAMA 295 (3): 306–13. doi:​10.1001/​jama.295.3.306. PMID 16418466.
 +    ^ U.S. Preventive Services Task Force*, (15 January 2002). "​Aspirin for the primary prevention of cardiovascular events: recommendation and rationale"​. Ann Intern Med 136 (2): 157–60. PMID 11790071.
 +    ^ Welcome to Med-decisions!
 +    ^ a b Ridker P, Cook N, Lee I, Gordon D, Gaziano J, Manson J, Hennekens C, Buring J (2005). "A randomized trial of low-dose aspirin in the primary prevention of cardiovascular disease in women"​. N Engl J Med 352 (13): 1293–304. doi:​10.1056/​NEJMoa050613. PMID 15753114.
 +    ^ Mosca L, Banka CL, Benjamin EJ (March 2007). "​Evidence-based guidelines for cardiovascular disease prevention in women: 2007 update"​. Circulation 115 (11): 1481–501. doi:​10.1161/​CIRCULATIONAHA.107.181546. PMID 17309915.
 +    ^ Hooper L, Thompson RL, Harrison RA, Summerbell CD, Ness AR, Moore HJ, Worthington HV, Durrington PN, Higgins JP, Capps NE, Riemersma RA, Ebrahim SB, Davey Smith G (2006). "Risks and benefits of omega 3 fats for mortality, cardiovascular disease, and cancer: systematic review"​. BMJ 332 (7544): 752–60. doi:​10.1136/​bmj.38755.366331.2F. PMC 1420708. PMID 16565093.
 +    ^ Wang C, Harris WS, Chung M, Lichtenstein AH, Balk EM, Kupelnick B, Jordan HS, Lau J (2006). "n-3 Fatty acids from fish or fish-oil supplements,​ but not alpha-linolenic acid, benefit cardiovascular disease outcomes in primary- and secondary-prevention studies: a systematic review"​. Am. J. Clin. Nutr. 84 (1): 5–17. PMID 16825676.
 +    AHRQ Evidence reports and summaries 94. Effects of Omega-3 Fatty Acids on Cardiovascular Disease
 +    ^ Yokoyama M, Origasa H, Matsuzaki M (2007). "​Effects of eicosapentaenoic acid on major coronary events in hypercholesterolaemic patients (JELIS): a randomised open-label, blinded endpoint analysis"​. Lancet 369 (9567): 1090–8. doi:​10.1016/​S0140-6736(07)60527-3. PMID 17398308.
 +    ^ Oikawa S, Yokoyama M, Origasa H. et al. (2009). "​Suppressive effect of EPA on the incidence of coronary events in hypercholesterolemia with impaired glucose metabolism: Sub-analysis of the Japan EPA Lipid Intervention Study"​. Atherosclerosis 206 (2): 535–9. doi:​10.1016/​j.atherosclerosis.2009.03.029. PMID 19447387.
 +    ^ Awtry, Eric H.; Joseph Loscalzo (2004). "​Coronary Heart Disease"​. Cecil Essentials of Medicine (6 ed.). Philadelphia,​ PA: Saunders. pp. 87–108. ISBN 978-0-7216-0147-2.
 +    ^ Keller T, Squizzato A, Middeldorp S (2007). "​Clopidogrel plus aspirin versus aspirin alone for preventing cardiovascular disease"​. Cochrane database of systematic reviews (Online) (3): CD005158. doi:​10.1002/​14651858.CD005158.pub2. PMID 17636787.
 +    ^ Jameson JN, Kasper DL, Harrison TR, Braunwald E, Fauci AS, Hauser SL, Longo DL. (2005). Harrison'​s principles of internal medicine (16th ed.). New York: McGraw-Hill Medical Publishing Division. ISBN 0-07-140235-7. OCLC 54501403.
 +    ^ Farrall M, Green FR, Peden JF, Olsson PG, Clarke R, Hellenius ML, Rust S, Lagercrantz J, Franzosi MG, Schulte H, Carey A, Olsson G, Assmann G, Tognoni G, Collins R, Hamsten A, Watkins H, on behalf of the PROCARDIS Consortium (2006). "​Genome-Wide Mapping of Susceptibility to Coronary Artery Disease Identifies a Novel Replicated Locus on Chromosome 17". PLoS Genetics 2 (5): e72. doi:​10.1371/​journal.pgen.0020072. PMC 1463045. PMID 16710446.
 +    ^ Saikku P, Leinonen M, Tenkanen L, Linnanmaki E, Ekman MR, Manninen V, Manttari M, Frick MH, Huttunen JK. (1992). "​Chronic Chlamydia pneumoniae infection as a risk factor for coronary heart disease in the Helsinki Heart Study"​. Ann Intern Med 116 (4): 273–8. PMID 1733381.
 +    ^ Andraws R, Berger JS, Brown DL. (2005). "​Effects of antibiotic therapy on outcomes of patients with coronary artery disease: a meta-analysis of randomized controlled trials"​. JAMA 293 (21): 2641–7. doi:​10.1001/​jama.293.21.2641. PMID 15928286.
 +    ^ Simons M, Bonow RO, Chronos NA (September 2000). "​Clinical trials in coronary angiogenesis:​ issues, problems, consensus: An expert panel summary"​. Circulation 102 (11): E73–86. PMID 10982554.
 +    ^ Stegmann TJ (December 1998). "​FGF-1:​ a human growth factor in the induction of neoangiogenesis"​. Expert Opin Investig Drugs. 7 (12): 2011–5. doi:​10.1517/​13543784.7.12.2011. PMID 15991943.
 +    ^ Wagoner, L.E., Merrill, W., Jacobs, J., Conway, G., Boehmer, J., Thomas, K., Stegmann, T.J.: Angiogenesis Protein Therapy With Human Fibroblast Growth Factor (FGF-1): Results Of A Phase I Open Label, Dose Escalation Study In Subjects With CAD Not Eligible For PCI Or CABG. Circulation 116: 443, 2007
 +
 +[edit] External links
 +
 +    Risk Assessment of having a heart attack or dying of coronary artery disease, from the American Heart Association.
 +    Risk Assessment Tool for Estimating 10-year Risk of Developing Hard CHD using Framingham score
 +    The InVision Guide to a Healthy Heart An interactive website on the development and function of the cardiovascular system and cardiovascular diseases and consequences. The website also features treatment options and preventative measures for maintaining a healthy heart.
 +    A Mechanism of a Metabolic Induction of Coronary Artery Disease in Chronic Kidney Disease, Rainer K. Liedtke, MD
 +
 +v · d · eCardiovascular disease: heart disease · Circulatory system pathology (I00–I52, 390–429)
 +Ischaemic
 +CD/CHD
 +
 +CAD · Coronary thrombosis · Coronary vasospasm · Coronary artery aneurysm · Coronary artery dissection · Myocardial Bridge
 +Active ischemia
 +
 +Angina pectoris (Prinzmetal'​s angina, Stable angina) · Acute coronary (Unstable angina, Myocardial infarction / heart attack)
 +Sequelae
 +
 +hours (Myocardial stunning, Hibernating myocardium) · days (Myocardial rupture) · weeks (Aneurysm of heart/​Ventricular aneurysm, Dressler'​s syndrome)
 +Layers
 +Pericardium
 +
 +Pericarditis (Acute, Chronic/​Constrictive) · Pericardial effusion (Hemopericardium,​ Cardiac tamponade)
 +Myocardium
 +
 +Myocarditis (Chagas disease)
 +Cardiomyopathy:​ Dilated (Alcoholic) · Hypertrophic · Restrictive (Loeffler endocarditis,​ Cardiac amyloidosis,​ Endocardial fibroelastosis)
 +Arrhythmogenic right ventricular dysplasia
 +Endocardium/​
 +valves
 +
 +Endocarditis
 +
 +Infective endocarditis (Subacute bacterial endocarditis) · noninfective endocarditis (Nonbacterial thrombotic endocarditis,​ Libman-Sacks endocarditis)
 +Valves
 +
 +mitral (regurgitation,​ prolapse, stenosis) · aortic (stenosis, insufficiency) · tricuspid (stenosis, insufficiency) · pulmonary (stenosis, insufficiency)
 +Conduction/
 +arrhythmia
 +Bradycardia
 +
 +Sinus bradycardia · Sick sinus syndrome
 +Heart block: Sinoatrial · AV (1°, 2°, 3°) · Intraventricular (Bundle branch/​Right/​Left,​ Left anterior fascicular/​Left posterior fascicular, Bifascicular/​Trifascicular) · Adams–Stokes syndrome
 +Tachycardia
 +(paroxysmal and sinus)
 +
 +Supraventricular
 +
 +Atrial (Multifocal) · Junctional (AV nodal reentrant, Junctional ectopic)
 +Ventricular
 +
 +Torsades de pointes · Catecholaminergic polymorphic · Accelerated idioventricular rhythm
 +Premature contraction
 +
 +Atrial · Ventricular
 +Pre-excitation syndrome
 +
 +Wolff-Parkinson-White · Lown-Ganong-Levine
 +Flutter/​fibrillation
 +
 +Atrial flutter · Ventricular flutter · Atrial fibrillation (Familial) · Ventricular fibrillation
 +Pacemaker
 +
 +Wandering pacemaker · Ectopic pacemaker/​Ectopic beat · Parasystole · Multifocal atrial tachycardia · Pacemaker syndrome
 +Long QT syndrome
 +
 +Romano-Ward syndrome · Andersen-Tawil syndrome · Jervell and Lange-Nielsen syndrome
 +Cardiac arrest
 +
 +Sudden cardiac death · Asystole · Pulseless electrical activity · Sinoatrial arrest
 +Other/​ungrouped
 +
 +hexaxial reference system (Right axis deviation, Left axis deviation) · QT (Short QT syndrome) · T (T wave alternans) · ST (Osborn wave, ST elevation, ST depression)
 +Cardiomegaly
 +Ventricular hypertrophy (Left, Right/Cor pulmonale) · Atrial enlargement (Left, Right)
 +Other
 +Cardiac fibrosis · Heart failure (Diastolic heart failure, Cardiac asthma) · Rheumatic fever
 +
 +M: HRT
 +
 +
 +anat/​phys/​devp
 +
 +
 +noco/​cong/​tumr,​ sysi/epon, injr
 +
 +
 +proc, drug (C1A/​1B/​1C/​1D),​ blte
 +
 +Categories: Aging-associated diseases | Cardiovascular diseases | Ischemic heart diseases
 +
 +[[Fair Use]] Source: http://​en.wikipedia.org/​wiki/​Coronary_artery_disease
 +
  
arterial_disease.txt · Last modified: 2018/02/26 18:10 (external edit)