Term Paper: Coronary Artery Disease (CAD) Is a Frightening

Pages: 5 (1559 words)  ·  Style: MLA  ·  Bibliography Sources: 4  ·  Topic: Disease  ·  Buy This Paper

Coronary artery disease (CAD) is a frightening name for an all-too common illness. It is the most common type of heart disease and the leading cause of death in the United States for both men and women ("What Is Coronary Artery Disease?" NIH, 2007). More than 64 million Americans suffer from some form of cardiovascular disease, and in 2001, cardiovascular disease was responsible for more than 39% of all deaths in the United States (American Heart Association: Heart Disease and Stroke Statistics 2004, cited by "Coronary Artery Disease and Atherosclerosis, Health Concerns, 2006, p1).

The onset of coronary artery disease is not a sudden, according to the National Institute of Health's article "What Is Coronary Artery Disease?" (Nov 2007). It is a condition in which plaque slowly builds up on the lining of the coronary arteries that lead to the heart. Coronary arteries supply the heart muscle with vital, oxygen-rich blood. Plaque is made up of fat, cholesterol, calcium, and other substances found in blood. When plaque builds up in the arteries, the condition is called atherosclerosis. The reason atherosclerosis is so dangerous is because if plaque builds up on the arteries for too long, the passage through which blood can flow to the heart is reduced, leading to blood clots and a partial or complete blockage of flow of blood to the heart ("What Is Coronary Artery Disease?" NIH, Nov 2007).

The dangerous aspect of CAD is that it manifests itself "long before any symptoms are clinically evident. It is a silent killer, "a malfunction of specialized cells that line our arteries" (Coronary Artery Disease and Atherosclerosis, Health Concerns, 2006, p.1). Sometimes, people with atherosclerosis do not even have high cholesterol readings. From an epidemiological perspective, coronary artery disease is primarily characterized as an inflammation of the arteries. This is important to remember because not every patient who suffers from atherosclerosis has the same health profile, "but every single person with atherosclerosis has endothelial dysfunction," or an inflammation and immune cell activation of the endothelial cells that line the arteries, which leads to endothelial dysfunction, subsequent damage to the arteries and the build-up of arterial plaque (Coronary Artery Disease and Atherosclerosis, Health Concerns, 2006, p.1).

It is true that high cholesterol, as well as smoking, obesity, high blood pressure, and other negative behaviors can contribute to the inflammation, but they are not the only causes. "Arteries are muscular organs that change and adapt to their environment and contract and expand in response to multiple factors, helping to raise and lower blood pressure and distribute blood throughout the body" (Coronary Artery Disease and Atherosclerosis, Health Concerns, 2006, p1). The development of coronary artery disease is directly related to the health of the inner arterial wall.

Arteries are composed of three layers. The outer layer is mostly connective tissue and provides structure to the layers beneath. The middle layer is smooth muscle; it contracts and dilates to control blood flow and maintain blood pressure. The inner lining consists of a thin layer of endothelial cells (the endothelium) that provides a smooth, protective surface. Endothelial cells prevent toxic, blood-borne substances from penetrating the smooth muscle of the artery. They also respond to changes in blood pressure and release substances into the cells of the smooth muscle that help change the muscle tone of the artery. Furthermore, endothelial cells secrete chemicals that provoke a protective response in the artery after an injury. This protective response includes signaling smooth muscle cells and white blood cells to congregate at the site of an injury" ("Coronary Artery Disease and Atherosclerosis," Health Concerns, 2006, p.1). Thus, in a body exhibiting normal physiology with non-inflamed endothelial cells, the arteries are smooth and flexible and respond normally to stressors such as exercise.

But if the endothelial cells become inflamed, lipids and toxins penetrate the endothelial layer and enter the smooth muscle cells. Smooth muscle cells gather at the site of the injury, and the artery loses some flexibility. The endothelium signals white blood cells to congregate along the cell wall and produce pro-inflammatory substances, such as leukotrienes and prostaglandins, and free radicals that attack the endothelium. "Toxins soon begin to penetrate into the arterial wall, where lipids such as LDL, cholesterol, and triglycerides accumulate and become oxidized....In response to the oxidized lipids, the body mounts an intensive immune response that causes more white blood cells to attack the fats, producing more inflammation within the arterial wall. In an attempt to heal the injury, smooth muscle cells begin to produce collagen to form a cap over the injury site. The mixture of oxidized lipids, white blood cells, and smooth muscle cells forms a plaque deposit. Over time, calcium accumulates on the deposit and forms a brittle cap. If this calcified plaque ruptures, a blood clot can form, and the clot may result in a heart attack or stroke" ("Coronary Artery Disease and Atherosclerosis," Health Concerns, 2006, p.1).

This process of build-up is more likely to occur in older individuals whose endothelial cells have become 'leaky' but it can also occur with people with poor dietary or lifestyle practices that lead to cellular inflammation or even adolescents with a genetic predisposition to endothelial inflammation. "There is convincing mechanistic experimental evidence as well as descriptive clinical studies that convey that the interactions of leukocytes and vascular cells are related to the initiation, progression, and complications of atherosclerotic arterial disease. The site of inflammation may be local within the artery wall, or distant and exert effects on atherosclerotic plaques through circulating inflammatory factors" (Tellides, 2007, p.1).

Hardening of the arteries produces no physical symptoms at first. One of the first symptoms a sufferer of coronary artery disease might feel is angina, more commonly known as chest pain, although the pain might manifest itself in the shoulders, arms, neck, jaw, or back ("What Is Coronary Artery Disease?" NIH, 2007). Often, the pain tends to get worse with activity or emotional distress. ("What Are the Signs and Symptoms of Coronary Artery Disease?" NIH 2007). CAD can also affect the lungs, if the heart cannot pump enough blood throughout the body. Fluid can collect in the lungs, causing shortness of breath.

There is a strong correlation between chronic obstructive pulmonary disease (COPD) and coronary artery disease, according to American Journal of Respiratory and Critical Care Medicine (Bals & Volgelmeir, 2007, p.1). COPD is one of the most important comorbidities in patients with coronary artery disease and patients with the disease and COPD patient have a higher mortality than heart patients without lung disease. It is still uncertain if this may be due to the fact that many patients with these same ailments have similar bad habits, but there is also evidence that COPD may induce increased arterial stiffness, which in turn may promote "vascular remodeling, thickening of arterial walls, and plaque formation" (Bals & Volgelmeir, 2007, p.1).

COPD is characterized by an inflammatory state that induces premature aging of the lung and other organs, so not only may coronary artery disease contribute to breathing problems, it may also be caused by lung diseases. In other words, it "is likely that both local and distant inflammation contribute to the pathogenesis of atherosclerosis and systemic inflammatory markers" (Tellides, 2007, p.1). Coronary artery disease, chronic obstructive pulmonary disease, and other inflammatory diseases may both cause one another, and act to exacerbate the effects of both disorders in the same person.

Another disease with a strong correlation to coronary artery diseases is Type II Diabetes. Again, it was once assumed that a high-fat, high-sugar diet was higher in cholesterol, and lead to the build-up of plaque, but the real culprit may be inflammation. So-called "metabolic syndrome" or insulin resistance "has been identified as a constellation of metabolic and non-metabolic disorders related to defects in insulin sensitivity" that leads to a… [END OF PREVIEW]

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