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There are different forms of heart disease:
- Coronary heart disease, the end result of the accumulation of atheromatous plaques within the walls of the arteries that supply the myocardium
- Ischaemic heart disease, a disease characterized by reduced blood supply to the heart.
- Cardiovascular disease, a class of diseases that involve the heart and/or blood vessels (arteries and veins).
- Pulmonary heart disease, a failure of the right side of the heart.
The study of the heart (and diseases of the heart) is cardiology.
Coronary heart disease (CHD), also called coronary artery disease (CAD) and atherosclerotic heart disease, is the end result of the accumulation of atheromatous plaques within the walls of the arteries that supply the myocardium (the muscle of the heart). While the symptoms and signs of coronary heart disease are noted in the advanced state of disease, most individuals with coronary heart disease show no evidence of disease for decades as the disease progresses before the first onset of symptoms, often a "sudden" heart attack, finally arise. 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.
Atherosclerotic heart disease can be thought of as a wide spectrum of disease of the heart. At one end of the spectrum is the asymptomatic individual with atheromatous streaks within the walls of the coronary arteries (the arteries of the heart). These streaks represent the early stage of atherosclerotic heart disease and do not obstruct the flow of blood. A coronary angiogram performed during this stage of disease may not show any evidence of coronary artery disease, because the lumen of the coronary artery has not decreased in caliber. Over a period of many years, these streaks increase in thickness. While the atheromatous plaques initially expand into the walls of the arteries, eventually they will expand into the lumen of the vessel, affecting the flow of blood through the arteries. While it was originally believed that the growth of atheromatous plaques was a slow, gradual process, some recent evidence suggests that the gradual buildup of plaque may be complemented by small plaque ruptures which cause the sudden increase in the plaque burden due to accumulation of thrombus material. Atheromatous plaques that cause obstruction of less than 70 percent of the diameter of the vessel rarely cause symptoms of obstructive coronary artery disease. As the plaques grow in thickness and obstruct more than 70 percent of the diameter of the vessel, the individual develops symptoms of obstructive coronary artery disease. At this stage of the disease process, the patient can be said to have ischemic heart disease. The symptoms of ischemic heart disease are often first noted during times of increased workload of the heart. For instance, the first symptoms include exertional angina or decreased exercise tolerance. 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 heart 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 oxygen 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 heart disease. The acute rupture of a plaque may lead to an acute myocardial infarction (heart attack). It is unclear at present which plaques in an individual are more likely to rupture in the future and cause a heart attack.
Limitation of blood flow to the heart causes ischemia (cell starvation secondary to a lack of oxygen) of the myocardial cells. When myocardial cells die from lack of oxygen, this is called a myocardial infarction (commonly called a heart attack). It leads to heart muscle damage, heart muscle death and later scarring without heart muscle regrowth. Myocardial infarction usually results from the sudden occlusion of a coronary artery when a plaque ruptures, activating the clotting system and atheroma-clot interaction fills the lumen of the artery to the point of sudden closure. The typical narrowing of the lumen of the heart artery before sudden closure is typically 20%, according to clinical research completed in the late 1990s and using IVUS examinations within 6 months prior to a heart attack. High grade stenoses exceeding 75% blockage, such as detected by stress testing, were found to be responsible for only 14% of acute heart attacks. The events leading up to plaque rupture are only partially understood. Myocardial infarction is also caused, far less commonly, by spasm of the artery wall occluding the lumen, a condition also associated with atheromatous plaque and CHD. CHD is associated with smoking, obesity, hypertension and a chronic sub-clinical lack of vitamin C. A family history of CHD is one of the strongest predictors of CHD. Screening for CHD includes evaluating homocysteine levels, high-density and low-density lipoprotein (cholesterol) levels and triglyceride levels.
The pain associated with very advanced CHD is known as angina, and usually presents as a sensation of pressure in the chest, arm pain, jaw pain, and other forms of discomfort. The word discomfort is preferred over the word pain for describing the sensation of angina, because it varies considerably among individuals in character and intensity and most people do not perceive angina as painful, unless it is severe. There is evidence that angina and CHD present differently in women and men. Angina that occurs regularly with activity, upon awakening, 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 nitrate preparations such as nitroglycerin, which come in short-acting and long-acting forms, and may be administered transdermally, sublingually or orally. 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 is treated with oxygen, intravenous nitroglycerin, and morphine. Interventional procedures such as angioplasty may be done.
Coronary heart 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 uric acid and homocysteine levels may contribute. In diabetes mellitus, there is little evidence that blood sugar control actually improves cardiac risk. Some recommend a diet rich in omega-3 fatty acids and vitamin C. In terms of hypertension reduction it has been demonstrated that removing the person from a high noise environment can contribute to vasoconstriction reduction (Rosen, 1965). An increasingly growing number of other physiological markers and homeostatic mechanisms are currently under scientific investigation. Individuals with CHD 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 while increasing High density lipoproteins, keeping blood pressure normal, exercise and stop smoking. These measures limit the progression of the disease. Recent studies have shown that dramatic reduction in LDL levels can cause mild regression of coronary heart disease. Risk factor management 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.
Vegetarians have been shown to have a 24% reduced risk of dying of heart disease (source: Key TJ, Fraser GE, et al. 1999, Sep. Mortality in vegetarians and nonvegetarians: detailed findings from a collaborative analysis of 5 prospective studies. Am J Clin Nutr, 70:516S-524S). This is not surprising, as plant foods are low in saturated fat and have no cholesterol. The most powerful cholesterol-lowering agents are soluble fiber, unsaturated fats, and phytochemicals, all of which are found almost exclusively in plant foods. In the seventeen studies conducted between 1978 and 2002, the average vegan’s cholesterol level was a mere 160 mg/dl, while the average non-vegetarian’s cholesterol was 202 mg/dl. (source: Norris, J. 2003, March. Making Sense of Nutritional Research.) Physicians such as Dr. Dean Ornish and Dr. Caldwell Esselstyn have actually stopped and even reversed heart disease in patients by putting them on programs that include plant-based diets that are high in Vitamin C. Despite the strong benefits of a vegetarian diet, it is likely that with a few changes to the typical vegetarian diet, the risks of heart disease could be reduced even further. Vegetarian diets are sometimes low in Vitamin B12, which can lead to increased homocysteine levels--a risk factor for heart diease. Since vegetarians don't eat fish, some vegetarians don't have high intakes of Omega-3 fatty acids. There is strong evidence that higher intakes of Omega-3 fatty acids reduce the risk of heart disease. Both of these shortcomings can be easily overcome by taking a vitamin B12 supplement and increasing intake of omega-3 fatty acids via ground flax seeds or flax oil, walnuts, and canola oil. There is some evidence that flax may be even more beneficial than fish oil in its effectiveness in reducing C-reactive protein, an indicator of heart disease.
Cretan Mediterranean-Style diet
The Seven Country 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 a small amount of animal products. 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. The Lyon Heart Study set out to mimic the Cretan diet, but adopted a pragmatic approach. Realizing that some of the people in the study would be reluctant to move from butter to olive oil, they used a margarine based on rapeseed (canola) oil. The dietary change also included 20% increases in vitamin C rich fruit and bread and decreases in processed and red meat. On this diet, mortality from all causes was reduced by 70%. This study was so successful that the ethics committee decided to stop the study prematurely so that the results of the study could be made available to the public immediately.
Controversial research has recently suggested a link between the atherosclerosis-causing CHD and the presence of nanobacteria in the arteries. However, trials of currently available antibiotics known to inhibit or kill some of these microorganisms have not shown much benefit to patients. If an infectious role were found to be a significant factor, this could have important implications for treatment and prevention of the disease beyond the many current, proven strategies. See atheroma & atherosclerosis Ornisch has suggested that coronary heart disease is partially reversible using an intense dietary regime such as the Cretan diet coupled with regular cardio exercise. External links 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.
Ischaemic heart disease is a disease characterized by reduced blood supply to the heart. It is the most common cause of death in most western countries.
Ischaemia means a "reduced blood supply". The coronary arteries supply blood to the heart muscle and no alternative blood supply exists, so a blockage in the coronary arteries reduces the supply of blood to heart muscle. Most ischaemic heart disease is caused by atherosclerosis, usually present even when the artery lumens appear normal by angiography, see IVUS.
What is it?
Initially there is sudden severe narrowing or closure of either the large coronary arteries and/or of coronary artery end branches by debris showering downstream in the flowing blood. It is usually felt as angina, especially if a large area is affected. The narrowing or closure is predominantly caused by the covering of atheromatous plaques within the wall of the artery rupturing, in turn leading to a heart attack (Heart attacks caused by just artery narrowing are rare). A heart attack causes damage to heart muscle by cutting off its blood supply. This can cause: Temporary damage and pain (ischemia) Loss of muscle activity (acute heart failure) Permanent heart muscle damage, heart muscle does not grow back (acute myocardial infarction /infarct) Long term loss of heart muscle activity (chronic heart failure) Cardiac arrhythmias: irregular heartbeat which can be fatal. Most death is due to arrhythmias, usually tachyarrhythmias. Other structural damage to the heart including damaged heart valves, actual perforation of the heart and a thin walled fibrous floppy heart.
Prevent or delay atherosclerosis. Do not smoke. prevent/treat hypertension (high blood pressure) Exercise regularly (Exercising the heart muscle strengthens it, like any other) Avoid obesity: increasing body fat stores, especially intra-abdominal fat, increases serum cholesterol, triglycerides, insulin requirements and promotes Diabetes Mellitus plus chronically increases heart muscle workload. Avoid consumption of trans-fatty acids. These are found in any chemically modified fat product, such as margarine, in hydrogenated fats, and especially in superheated fats (such as those used for commercial deep frying). These fats are toxic and should not be consumed in any amount; however, in many western countries, limitation may be the only practical option. Some mono-unsaturated fats are beneficial in reducing the risk of heart disease when consumed in moderation. When consumed in excess, however, other health concerns arise. An increase in polyunsaturated fats is also warranted in most American diets. Dietary cholesterol intake is known to have only limited effect on serum cholesterol. Take LDLipoprotein cholesterol reducing and HDLipoprotein raising drugs and verfiy both LDLipoprotein particle counts and quantitative large HDLipoprotein response to treatment. Avoiding shift work.
Treatment of a heart attack.
The option required depends on the situation. Specialised coronary care (the sooner the better); most deaths are due to sudden onset arrhythmias - time is crucial to survival. Cardiopulmonary resuscitation (breathing support, pulse and BP monitoring & possible chest compressions). A defibrillator can stop cardiac arrhythmias. An artificial pacemaker can speed up cardiac bradyarrhythmias. Drugs such as adrenaline can increase heart rate and strength of contractions, although also promote tachyarrhythmias. Thrombolytic agents can clear away compounding blood clots. Anticoagulation can impede additional blood clots. Inotropic drugs will raise blood pressure. Unblock arteries with angioplasty ("balloon angioplasty with or without stents") or surgery.
After a heart attack
Possible angioplasty or cardiac surgery. Possibly the regular administration of anti-coagulants to prevent further blood clot complications. Possibly the administration of drugs to reduce heart arrhythmias although they many also induce arrhythmias. Lifestyle modifications are important in prevention of a second MI; increased exercise, reduction of stress, and improved dietary considerations are perhaps most important
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