Coronary Heart Disease
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 would have evidence of disease decades before the first symptoms 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. Current views are that an inflammatory process of the lining of the arteries, though poorly understood in specifics, promotes the disease progression.
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. As the plaques expand into the lumen of the vessel, they can affect 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.
It is interesting to note that 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 and hypertension. 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 Percutaneous Transluminal Coronary 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 blood sugar, lipoprotein transport systems, obesity, homocysteine, hypertension, sedentary lifestyle, dietary choices, smoking, uric acid, and omega 3 oils.
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 cardaic rehabiltation along with diet, smoking cessation and blood pressure and cholesterol management.
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