(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 Clot ting 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 Infarction s (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 as such exceeding 75% blockage, such as detected by
Stress Testing , were found to be responsible for only 14% of acute
Heart Attack s the rest being due to plaque rupture/ spasm. 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
Atheroma tous 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
Pain ful, 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
Atheroma tous 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 .
An increasingly growing number of other
Physiological markers and
Homeostatic mechanisms are currently under scientific investigation. Among these markers are
Low Density Lipoprotein and
Asymmetric Dimethylarginine . Patients with CHD and those trying to prevent 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 Lipoprotein s while increasing
High Density Lipoprotein s, 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.
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.
