Pathophysiology Of Cad

Pathophysiology of Coronary Artery Disease

Atherosclerosis is a type of arteriosclerosis caused by a build-up of plaque in the inner lining of an artery. (Arteriosclerosis is a general term for thickening or hardening of the arteries.) (Porth 2005) Plaque is made up of deposits of fatty substances, cholesterol, cellular waste products, calcium, and fibrin, and can develop in medium or large arteries. The artery wall becomes thickened and looses its elasticity. (Fraser 2000)

The wall of an artery is composed of several layers. The lining or inner layer (endothelium) is usually smooth and unbroken. Atherosclerosis begins when the lining is injured or diseased. (Marieb 2006) Then certain white blood cells called monocytes are activated and move out of the bloodstream and through the lining of an artery into the artery's wall. Inside the lining, they are transformed into foam cells, which are cells that collect fatty materials, mainly cholesterol. (Clark 2007) In time, smooth muscle cells move from the middle layer into the lining of the artery's wall and multiply there. Connective and elastic tissue materials also accumulate there, as may cell debris, cholesterol crystals, and calcium. This accumulation of fat-laden cells, smooth muscle cells, and other materials forms a patchy deposit called an atheroma or atherosclerotic plaque. (Brown & Edwards 2005) As they grow, atheromas thicken the artery's wall and bulge into the channel of the artery. They may narrow or block an artery, reducing or stopping blood flow.

Atherosclerosis is a disease of arterial blood vessels. Atherosclerosis is commonly referred to as a "hardening of blood vessels", but this is an over-simplification. Vascular lesions known as atheromatous plaques are formed in the vessel wall, and in late stages may reduce or restrict blood flow in the lumen. When the inner covering of an unstable atheroma breaks, compromising the structural integrity of the internal artery wall, the break may allow hemorrhage into the plaque, generate stenosis, embolism, sometimes leading to severe morbidity and even death. (Osbourne 2002)

Atherosclerosis typically begins in later childhood, is usually found in most major arteries, yet it is asymptomatic and not detected by most diagnostic methods during life. It most commonly becomes seriously symptomatic when interfering with the coronary circulation supplying the heart or cerebral circulation supplying the brain, and is considered the most important underlying cause of strokes, heart attacks, various heart diseases including congestive heart failure and most cardiovascular diseases in general. (Porth 2005)

Atherosclerosis is the major cause of death and disability in the Western world. This is because atherosclerosis is the underlying medical problem in most patients with coronary artery disease. (Brown & Edwards 2005) In this chronic disease, atherosclerosis narrows the coronary arteries, the arteries supplying blood to the heart muscle. As the coronary arteries narrow, the chest pain called angina may be triggered. And the risk of a myocardial infarction, which occurs when a coronary artery is blocked completely, is increased.

The arteries provide oxygen-rich blood to the heart, brain, and other parts of the body. The inner lining of the arteries is called the endothelium. This inner lining can be injured due to high cholesterol levels, high triglycerides, high blood pressure,

smoking and/or diabetes. (Osbourne 2002) When the endothelium is damaged, substances that flow through the arteries, such as fats, cholesterol, calcium, cellular waste products and other substances (collectively known as plaque), are deposited in the artery wall, and over time begin to build up. The build up of these substances causes the arteries to harden, narrow or become blocked. Depending on where the hardening or blockage occurs, other complications then follow.

It is thought that atherosclerosis is caused by a response to damage to the endothelium from high cholesterol, high blood pressure, and cigarette smoking. Physical inactivity, diabetes, and obesity are also risk factors for atherosclerosis (Osbourne 2002). High levels of the amino acid homocysteine and abnormal levels of protein-coated fats called lipoproteins also raise the risk of coronary artery disease. The role of triglycerides, another fat that circulates in the blood, in forming atherosclerotic plaques is unclear. (Lilly 2002) High levels of triglycerides are often associated with diabetes, obesity, and low levels of high-density lipoproteins (HDL cholesterol). The more HDL ("good") cholesterol, in the blood, the less likely is coronary artery disease. (Clark 2006) These risk factors are all modifiable. Non-modifiable risk factors are heredity, sex, and age.

There are several risk factors that contribute to the development of atherosclerosis, some which can be controlled, and some that cannot.

Risk factors include documented atheroma in any artery, having diabetes or just upper normal blood glucose and insulin levels, dyslipidemia- having a high blood concentration of low density lipoprotein particles, elevated lipoprotein little a, a variant of LDL lipoproteins and very low density lipoprotein particles. having a low concentration of functioning high density lipoprotein particles, higher fibrinogen blood concentrations, homocysteine in the upper half of the normal range, and especially elevated levels, aging and being male, smoking, having close relatives who had heart disease or a stroke at a relatively young age, having high blood pressure, having trouble managing stress, especially anger, being obese and being physically less active. (George 1992)

Most humans develop atherosclerosis. Usually only "high-risk" patients are advised to change dietary choices, exercise, lose weight, take cholesterol-lowering mediation and lower blood sugar levels. Most of the proven, more effective cholesterol medications are only available by prescription, for example, Lipitor. (Clark 2006)

Atherosclerosis progresses with a gradual build-up of plaque or thickening of the inside of the walls of the artery, which causes a decrease in the amount of blood flow, and a decrease in the oxygen supply to the vital body organs and extremities. A heart attack may occur if the oxygenated blood supply is reduced to the heart. (Francis 1992)

The resident cells within the artery wall seem to signal an intrusion, "call for help", an inflammation response. Monocytes, one of the 5 main types of white blood cells circulating in the blood, enter the artery wall. Within tissues, monocytes