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Essay Instructions: Specific subject of the paper is: "Pick any disease and describe the characteristics/symptoms of that disease, relate these alterations to the normal physiology of the diseased organ and then describe how this affects the other organs of the body."

More specifically: Coronary Artery Disease

At least two (peer reviewed) journal articles must be used as sources.

Essay Instructions: The pathophysiology of coronary artery disease. Include risk/etiology, incidence, pathology, signs and symptoms, diagnostic studies, treatment and prognosis. UTILIZE THE MOST CURRENT MEDICAL AND NURSING RESOURCES.

Essay Instructions: To editor
The topic of my paper is cardiac arrest. Since this paper is for the Anatomy and physiology class, the contents must include Anatomical, structural aspects of heart. For your convenience, I typed anatomical structure of heart and also little review for cardiac arrest. Please well organize my paper within 10 pages. I also gave you guideline for this paper.
For the anatomical part, I would like to ask you to use paragraphs which I wrote down from page (Please paraphrase my anatomical paragraphs when you use it. You don’t have to change technical words)

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Please put sources at the end of the paragraph when you cite from other sources. I will give you an idea through my paragraph.

Guideline for my research paper
the ten pages include only narrative
double spaced
there must be no less than four references.
these are to be books and journals.
the journals can be legitimate online journals.
articles must have authors-no 'anonymous' articles

utilize APA format for formatting and citations.

Do not cite after each sentence; especially if this is the same source. this indicates unacceptable paraphrasing.
the paper must be in your own words and display an understanding of your subject material.
do not summarize a number of papers or use a number of block quotes.
you need to cite information that you would not have otherwise known, but the paper is a critical evaluation of what you have read.

give your paper an appropriate title; state a definite thesis, place this at the beginning of the paper, develop the thesis and the paper with an informative summary












A&P 2 research paper
Relationship between cardiac arrest and coronary cardiac disease

Jun-Young Yang
(please paraphrase all of my paragraphs. However, you don’t have to paraphrase technical terms such as midsegittal, vascular system, etc)

Cardiac arrest is the phenomenon which caused by sudden loss of heart function. This accident can occur to person who may or may not have cardiac disease. Most common reason for patient to die from cardiac arrest is coronary disease. When cardiac vascular system stops its function by certain reason, brain cells which only use aerobic respiration to make ATP will die less than 4 to 6 minutes. In order to reduce the accident of cardiac arrest, understanding the cardio vesicular system will help to prevent coronary cardiac disease which is most common cause of heart attack. For this reason, the purpose of this paper was to understand cardiac vascular system which will includes its anatomical, functional, and pathological aspects which causing coronary cardiac diseases and find the way to effectively maintain its good condition in order to expend the life span.

In a myocardial infarction, or heat attack, part of the coronary circulation becomes blocked, and cardiac muscle cells die from lack of oxgen. The death of affected tissue creates a nonfunctional area known as an infarct. Heart attacks most commonly result from severe coronary artery disease. the consequences depend on the site and nature of the circulatory blockage. If it occurs near the start of one of the coronary arteries, the damage will be widespread and the heart may stop beating. If the blockage involves one of the smaller arterial branches, the individual may survive the immediate crisis but may have many complications, all unpleasant. As scar tissue forms in the damaged area, the heartbeat may become irregular and less effective, and other vessels can become constricted, creating additional circulatory problems.

Myocardial infarctions are generally associated with fixed, partial blockages, such as those seen in CAD. When a crisis develops as a result of thrombus formation at a plaque, the condition is called coronary thrombosis. A vessel already narrowed by plaque formation may also become blocked by a sudden spasm in the smooth muscles of the vascular wall. The individual then may experience intense pain, similar to that felt in an angina attack, but persisting even at rest. However, pain does not always accompany a heart attack, and silent heart attacks may be even more dangerous than more apparent attacks, because the condition may go undiagnosed and may not be treated before a fatal MI occurs. Roughly 25 percent of heart attacks are not recognized when they occur.
The cytoplasm of a damaged cardiac muscle cell differs from that of a normal muscle cell. As the supply of oxygen decreases, the cells become more dependent on anaerobic metabolism to meet their energy needs. Over time, the cytoplasm accumulates large quantities of enzymes involved with anaerobic energy production. As the membranes of damaged cardiac muscle cells deteriorate, these enzymes enter the surrounding intercellular fluids. The appearance of such enzymes in the circulation thus indicates that infarction has occurred. The most common enzymes that may be measured in a diagnostic blood test include cardiac troponin T, cardiac troponin I, and the MB isomer of a special form of creatine phosphokinase that occurs only in cardiac muscle, called CK-MB.
About 25 percent of MI patients die before obtaining medical assistance, and 65 percent of MI deaths among those under age 50 occur within an hour after the initial infarction. The goals of treatment are to limit the size of the infarct and to avoid additional complications by preventing irregular contractions, improving circulation with vasodilators, providing pain relief and additional oxygen, reducing the cardiac workload, and, if possible, eliminating the cause of the circulatory blockage. Anticoagulants are essential to prevent the formation of additional thrombi, and clot dissolving enzymes may reduce the extent of the damage if they are administered within six hours after the MI occurred. Current evidence suggests that tissue plasminogen activator, which is relatively expensive, is more beneficial than other fibrinolytic agents, such as urokinase or streptokinase. Follow-up treatment with Coumadin (an oral anticoagulant), aspirin, or both is recommended; without further treatment, circulatory blockages will reappear in about 20 percent of patients.
Roughly 1.3 million MIs occur in the United States each year, and half the victims die within a year of the incident. The following factors appear to increase the risk of a heart attack: smoking, high blood pressure, high blood cholesterol levels, high circulating levels of low-density lipoproteins, diabetes, male gender (below age 70), severe emotional stress, obesity, genetic predisposition, and a sedentary lifestyle. Although the heart attack rate in women under age 70 is lower than that in men, the mortality rate for women is higher-perhaps because heart disease in women is neither diagnosed as early nor treated as aggressively as that in men.
The presence of any two risk factors more than doubles the risk of heart attack, so eliminating as many risk factors as possible improvise the chances of preventing or surviving a heart attack. limiting cholesterol in the diet, exercising to reduce weight, and seeking treatment for high blood pressure are steps in the right direction. It has been estimated that a reduction in coronary risk factors could prevent 150,000 deaths each year in the United States alone. (martinin, 2009)

Heart anatomy

Knowing the heart structure and function are important to understand heart disease. Heart is the pump of the cardio vascular system. Blood leaves the heart via arteries and returns to the heart by veins. Between arteries and veins, capillary vessels which is composed of very thin layer interconnect arterioles and venous. The function of capillaries is gas exchange. Since capillaries are composed of thin layers of walls, capillaries permit the exchange of nutrients, dissolved gases, and waste products between the blood and surrounding tissues. (martinin, 2009)

The heart is located near the anterior chest wall, directly posterior to the sternum. The great veins and arteries are connected to the superior end of the heart at the attached base. The base sits posterior to the sternum at the level of the third costal cartilage, centered about 1.2 cm to the left side. The inferior, pointed tip of the heart is the apex. A typical adult heart measures approximately 12.5 cm from the base to the apex, which reaches the fifth intercostals space approximately 7.5 cm to the left of the midline. A midsagittal section through the trunk does not divide the heart into two equal halves, because the center of the base lies slightly to the left of the midline, a line drawn between the center of the base and the apex points further to the left, and the entire heart is rotated to the left around this line, so that the right atrum and right ventricle dominate an anterior view of the heart. (martinin, 2009)


(please paraphrase all of my paragraphs. However, you don’t have to paraphrase technical terms such as midsegittal, vascular system, etc)

The heart is surrounded by the pericardial which sits in the anterior portion of the mediastinum. The mediastinim, the region between the two pleural cavities, also contains the great vessels. The pericardium is the lining of the pericardial cavity. A delicate serous membrane subdivided pericardium into the visceral pericardium and the parietal pericardium. The visceral pericardium covers the outer surface of the heart and the pericardium lines the inner surface of the pericardial sac which surrounds the heart. Pericardial cavity is placed between the parietal and visceral surfaces. It normally contains 15-50 mL of pericardial fluid. The function of pericardial fluid

There are four cardiac chambers in the heart that pumps oxygen poor blood to the lungs and oxygen-rich blood to the rest of the body. The four chambers can easily be identified in a superficial view of the heart. The two right and left atria have relatively thin muscular walls and are highly expandable. When chambers are not filled with blood, the outer portion of each atrium deflates. This expandable extension of an atrium is called an auricle. The deep groove which marks the border between the atria and the ventricles is called the coronary sulcus. The anterior interventricular sulcus and the posterior interventricular sulcus mark the boundary between the left and right ventricles.

Heart wall has three distinct layers: an outer epicardium, a middle myocardium, and an inner endocardium. The epicardium is the visceral pericardium that covers the outer surface of the heart. The myocardium forms both atria and ventricles. This layer contains cardiac muscle tissue, blood vessels, and nerves. The atrial myocardium contains muscle bundles that wrap around the atria and superficial ventricular muscles wrap around bout ventricles toward the apex. Intercalated discs are used for interconnecting cardiac muscle cells. At an intercalated disc, adjacent cells are held together by desmosomes and linked by gap junctions. Intercalated discs transfer the force of contraction from cell to cell and propagate action potentials. Unlike skeletal muscle, cardiac muscle cells are small size, a single, centrally located nucleus, branching interconnections between cells, and the presence of intercalated discs.

Heart muscle consists of four chambers, right and left atira, right and left ventricle. The right atrium receives blood from the systemic circuit which transports blood to and from the rest of the body and passes it to the right ventricle. The right ventricle pumps blood into the pulmonary circuit which carries blood to and from the gas exchange surfaces of the lungs. The left atrium collects blood from the pulmonary circuit and empties it into the left ventricle which pumps blood into the systemic circuit. When the heart beats, the atria contract first, and then the ventricles contract. The two ventricles contract at the same time and eject equal volumes of blood into the pulmonary and systemic circuits.
The right atrium communicates with the right ventricle, and the left atrium communicates with the left ventricle. The right and left atrium are separated by the interatrial septum and the ventricles are separated by the interventricular septum. Atrioventricular (AV) valves extend into the openings between the atria and ventricles. These valves permit blood flow in one direction only: from the atria to the ventricles.

The right atrium receives blood from the systemic circuit through the superior vena cava and the inferior vena cava. The superior vena cava opens into the posterior and superior portion of the right atrium, delivers blood to the right atrium from the head, neck, upper limbs, and chest. The inferior vena cava, which opens into the posterior and inferior portion of the right atrium, carries blood to the right atrium from the rest of the trunk, the viscera, and the lower limbs. The cardiac venis of the heart return blood to the coronary sinus, a large, thin-walled vein that opens into the right atrium inferior to the connection with the superior vena cava.

Blood travels from the right atrium into the right ventricle through a broad opening bounded by three fibrous flaps. These flaps, called cusps or leaflets, are part of the right atrioventricular (AV) valve, also known as the tricuspid valve. The free edge of each cusp is attached to connective tissue fibers called the chordate tendineae. The fibers originate at the papillary muscles which arise from the inner surface of the right ventricle. The right AV valve closes when the right ventricle contracts, preventing the backflow of blood into the right atrium. Without the chordate tendineae to anchor their free edges, the cusps would be like swinging doors tht permitted blood flow in both directions.

The internal surface of the ventricle also contains a series of muscular ridges: the trabeculae carneae. The moderator band is a muscular ridge that extends horizontally from the inferior portion of the interventricular septum and connects to the anterior papillary muscle. This ridge contains a portion of the conducting system, an internal network that coordinates the contractions of cardiac muscle cells. The moderator band delivers the stimulus for contraction to the papillary muscles, so that they begin tensing the chordate tendineae before the rest of the ventricle contracts.

The superior end of the right ventricle has pulmonary semilunar valve which consists of three semilunar cusps of thick connective tissue. From the right ventricle, blood passes through this valve in order to enter the pulmonary trunk, the start of the pulmonary circuit. The arrangement of cusps prevents backflow as the right ventricle relaxes. Once in the pulmonary trunk, blood flows into the left pulmonary arteries and the right pulmonary arteries. These vessels branch repeatedly within the lungs before supplying the capillaries, where gas exchange occurs.

From the respiratory capillaries, blood collects into venous that forms the four pulmonary veins. The posterior wall of the left atrium receives blood from two left and two right pulmonary veins. Like the right atrium, the left atrium has the left atrioventricula (AV) valve, or bicuspid valve or mitral valve. The left AV valve permits the flow of blood from the left atrium into the left ventricle but prevents backflow during ventricular contraction.

The left ventricle is much larger than the right ventricle because it has thicker walls. Its thick, muscular walls enable the left ventricle to develop pressure sufficient to push blood through the large systemic circuit, whereas the right ventricle needs to pump blood, at lower pressure, only about 15 cm to and from the lungs. Blood leaves the left ventricle by passing through the aortic valve, or aortic semilunar valve, into the ascending aorta. Once the blood has been pumped out of the heart and into the systemic circuit the ortic valve prevents backflow into the left ventricle. From the ascending aorta, blodd flows through the aortic arch and into the descending aorta.

The heart works continuously, so cardiac muscle cells require reliable supplies of oxygen and nutrients. Although a great volume of blood flows through the chambers of the heart, the myocardium needs its own, separate blood supply. The coronary circulation supplies blood to the muscle tissue of the heart. During maximum exertion, the demand for oxygen rises considerably. The blood flow to the myocardium may then increase to nine times that of resting levels. The coronary circulation includes an extensive network of coronary blood vessels.

The left and right coronary arteries originate at the base of the ascending aorta, at the aortic sinuses. Blood pressure here is the highest in the systemic circuit. Each time the left ventricle contracts, it forces blood into the aorta. The arrival of additional blood at elevated pressures stretches the elastic walls of the aorta. When the left ventricle relaxes, blood no longer flows into the aorta, pressure declines, and the walls of the aorta recoil. This recoil, called elastic rebound, pushes blood both forward, into the systemic circuit, and backward, through the aortic sinuses and then into the coronary arteries. Thus, the combination of elevated blood pressure and elastic rebound ensures a continuous flow of blood to meet the demands of active cardiac muscle tissue. However, myocardial blood flow is not steady; it peaks while the heart muscle is relaxed, and almost ceases while it contracts.
Interconnections between arteries are called arterial anastomoses. Because the arteries are interconnected in this way, the blood supply to the cardiac muscle remains relatively constant despite pressure fluctuations in the left and right coronary arteries as the heart beats.

Two types of cardiac muscle cells are involved in a normal heartbeat: (1) specialized muscle cells of the conducting system, which control and coordinate the heartbeat, and (2) contractile cells, which produce the powerful contractions that propel blood. Each heartbeat begins with an action potential generated at a pacemaker called the SA node, which is part of the conducting system. This electrical impulse is then propagated by the conducting system and distributed so that the stimulated contractile cells will push blood in the right direction at the proper time. The electrical events under way in the conducting system can be monitored from the surface of the body through a procedure known as electrocardiography; the printed record of the result is called an electrocardiogram (EEG or EKG).

The arrival of an impulse at a cardiac muscle plasma membrane produces an action potential that is comparable to an action potential in a skeletal muscle fiber. As in a skeletal muscle fiber, this action potential triggers the contraction of the cardiac muscle cell. The atria contract first, driving blood into the ventricles through the AV valves, and the ventricles contract next, driving blood out of the heart through the semilunar valves.

The SA node generates impulses at regular intervals, and one heartbeat follows another throughout your life. After each heartbeat there is a brief pause before the next heartbeat begins. The period between the start of one heartbeat and the start of the next is called the cardiac cycle.
A heartbeat lasts only about 370 msec. although brief, it is a very busy period.

The cardiac cycle includes alternating periods of contraction and relaxation. For any one chamber in the heart, the cardiac cycle can be divided into two phases: systole and diastole. During systole, or contraction, the chamber contracts and pushes blood into an adjacent chamber or into an arterial trunk. Systole is followed by diastole, or relaxation. During diastole, the chamber fills with blood and prepares for the next cardiac cycle. The pressure within each chamber rises during systole and falls during diastole. Valves between adjacent chambers help ensure that blood flows in the required direction, but blood will flow from one chamber to another only if the pressure in the first chamber exceeds that in the second. This basic principle governs the movement of blood between atria and ventricles, between ventricles and arterial trunks, and between major veins and atria.

Work cited
Martini, F, & Nath, J. (2009). Fundamentals of anatomy & physiology. San Francisco, CA: Benjamin Cummings.


There are faxes for this order.

Essay Instructions: Write a research paper on “Renal Artery Stenosis. In writing the paper defines renal artery stenosis, the cause of the disease, the risk factors, the symptoms and manifestations of the disease and possible treatments. Then discuss in detail the relation of this pathology with Renal artery occlusion, Fibromuscular dysplasia. Then discuss the role of ultrasonography diagnosis methods in detecting the disease. Here discuses the benefits and limitations of these techniques and then use the information to analyze the role played by Color Doppler Sonographic features in excluding pathology.
In writing the paper you can use the following materials and other sources including, medical journals. But make sure that each quotations and parenthetical citations are matched with proper references. And other people’s works are given credits. You can back your writing with limited quotations in small paragraph forms with no more than one for the entire paper.
Use a case study if possible.
Here I have cut and paste you information some of the information I found from the internet. So if you decide to use them make sure you give credit to the writers.

The Paper should follow APA style and have reference list of no more that five.
********************
Alternative Names Return to top
Renal artery occlusion; Stenosis - renal artery; Occlusion - renal artery; Fibromuscular dysplasia (FMD)
Definition Return to top
Renal artery stenosis is a narrowing or blockage of the artery that supplies blood to the kidney. It is caused by atherosclerosis, fibromuscular dysplasia of the renal artery wall, or scar formation in the artery. (See also atheroembolic renal disease.)
Causes Return to top
Renal artery stenosis is caused when atheroembolic renal disease results in narrowing of the renal artery. Fibromuscular disease, a condition more common in young women in which fibrous tissue grows in the wall of the renal artery and narrows it, is a second cause. It may also be caused when scar tissue forms in the renal artery after acute arterial obstruction or traumatic injury to the kidney.
Renal artery stenosis often causes hypertension (high blood pressure) with no other signs of its presence, and it is usually discovered in investigation for the cause of hypertension that is difficult to control. Renal artery stenosis is, in fact, among the most common causes of secondary (caused by another condition) hypertension. The disorder may also be discovered when a bruit (loud whooshing sound) over the kidney is noted on examination with a stethoscope (auscultation). Auscultation is a method used to listen to the sounds of the body during a physical examination.
Information Return to top
Auscultation is usually performed by listening through a stethoscope. Health care providers routinely listen to a patient's lungs, heart, and intestines to evaluate the frequency, intensity, duration, number, and quality of sounds.
Health care providers also use auscultation to listen to the heart sounds of unborn infants. This is not performed with a stethoscope, but with sound waves. This is called a Doppler ultrasound. It can also be used to hear pulses in the hands and feet.
Related topics:


In the elderly, renal artery stenosis is most commonly associated with atherosclerotic disorders, including atherosclerotic heart disease. Atherosclerotic plaque deposits within the renal artery and causes it to become stenosed (narrowed).
Fibromuscular dysplasia is a congenital disorder involving thickening of the arterial wall and is a cause of renal artery stenosis in younger adults, particularly women 20 - 40 years old.
Renal artery stenosis may cause chronic renal failure if it affects both renal arteries or if the high blood pressure associated with this condition is prolonged or severe.
Symptoms Return to top
There are usually no symptoms.
Exams and Tests Return to top
The blood pressure may be high, and there may be a history of high blood pressure that doesn't respond to medication or is difficult to control. A bruit may be heard on examination with a stethoscope (auscultation) over the kidney.
• A radionuclide renogram may show decreased blood flow. The value of radionuclide scanning is increased if the test is done twice: once after a dose of captopril and once without the captopril.
• An MRI, kidney CT scan, or kidney ultrasound may indicate a decreased size of the kidney, and/or a decrease in blood flow through the artery because the artery has become narrow.
• Renal arteriography shows the exact location of the stenosed (blocked) area.
This disease may also alter the results of the following tests:
• Urine specific gravity
• Urine concentration test
• Renal perfusion scintiscan
Treatment Return to top
The treatment varies depending on the extent and severity of the symptoms. If the stenosis results in failure of a kidney, the second kidney may take over filtering and urine production for the body. Surgical repair of the stenosed area may be possible.
A balloon angioplasty (a radiographic procedure during which a balloon-tipped catheter is threaded through the artery) or a stent placement across the stenosis may be an alternative to surgery to open the stenosed area.
Antihypertensive medications may be needed to control high blood pressure.
Outlook (Prognosis) Return to top
Renal artery stenosis may cause eventual failure of the kidney if it progressively blocks the artery. This may result in chronic renal failure if there is only one functional kidney or if both renal arteries are affected.
Renal hypertension caused by renal artery stenosis may be difficult to treat. Surgical or balloon catheter repair often successfully opens the stenosed area. However, stenosis may recur.
Possible Complications Return to top
• Hypertension
• Malignant hypertension
• Chronic renal failure
When to Contact a Medical Professional Return to top
If your history indicates a high risk for renal artery stenosis, make an appointment to see your health care provider. However, decreased urine volume may be an emergency symptom indicating renal failure.
Prevention Return to top
Some cases of renal artery stenosis may be prevented by avoiding smoking.
Update Date: 12/9/2005

Alternative Names Return to top
Renal disease - atheroembolic; Cholesterol embolization syndrome; Atheroemboli - renal; Atherosclerotic disease - renal
Definition Return to top
Atheroembolic renal disease (AERD) is an inflammatory reaction in the small blood vessels of the kidneys.
Causes Return to top
AERD is linked to atherosclerosis. Atherosclerosis is a common disorder of the arteries. It occurs when fat, cholesterol, and other substances build up in the walls of arteries and form hard substances called plaque.
In AERD, cholesterol crystals from plaque break off and move to the kidneys and into the blood stream. Once in circulation, the crystals get stuck in tiny blood vessels called arterioles. There, they cause an intense inflammatory response. The result is organ damage due to decreased blood supply. Acute kidney failure is possible if the reaction is severe.
Atherosclerosis of the aorta is the most common cause of AERD. The cholesterol crystals may also break off during cardiac catheterization or aortic surgery.
In some cases, AERD may occur without a cause.
The risk factors for AERD are the same as risk factors for atherosclerosis.
Symptoms Return to top
AERD may not cause any symptoms. Symptoms that may occur include:
• Foot pain, ulcers on the feet, or “blue toes”
• Pain in the abdomen, nausea, or vomiting
• Pancreatitis or hepatitis (rare)
• Strokes or blindness
• Flank pain and blood in the urine (rare)
• Uncontrolled high blood pressure
Kidney failure may result in the following:
• Nausea or vomiting
• Loss of appetite
• Weight loss
• Decreased or no urine output
• Swelling
• Decrease in sensation
• Skin pigment changes
• Dry itchy skin
• Drowsiness, confusion, lethargy
Exams and Tests Return to top
The doctor will perform a physical exam. Swelling may affect the entire body. An eye exam may show particles in the small arteries of the retina.
The doctor will listen to your lungs and heart with a stethoscope. Abnormal sounds may be heard. For example, a loud whooshing sound called a bruit may be heard over the aorta or renal artery.
Blood pressure may be high. There may be multiple ulcers of the skin of the lower feet.
Tests that may be done include:
• Abdominal CT scan
• Abdominal MRI
• Abdominal x-ray
• Chem-7 or chem-20
• Complete blood count
• Kidney biopsy
• Kidney function tests including BUN and creatinine
• Kidney or abdominal ultrasound
• Renal arteriography
• Serum complement
• Serum lipids
• Urinalysis
Treatment Return to top
Medicines may be used to treat high blood pressure and lower lipid and cholesterol levels.
Other treatments for kidney failure or complications may be needed.
Your doctor may tell you to reduce fats and cholesterol in your diet. If you have kidney failure, you may need to restrict protein, salt, and fluids, or make other dietary changes.
Your doctor may also recommend other lifestyle changes such as increased exercise or weight loss. Stopping smoking is extremely important.
Outlook (Prognosis) Return to top
The outcome varies but is generally poor. The disorder slowly gets worse over time. Lifestyle changes may help slow progression of the disease.
Possible Complications Return to top
• Acute renal failure
• Chronic renal failure
• High blood pressure
• Blood clots to other location of the body -- brain, intestine, legs
When to Contact a Medical Professional Return to top
Call your doctor if you have:
• A decrease in urine output or no urine production
• Blood in the urine
• Severe abdominal pain or leg pain
• Unexplained ulcers on your legs or feet
• Toes that turn purple and occur with foot pain
Prevention Return to top
You can alter the factors that increase your risk of getting this disease. You should lose weight if you are obese, decrease or stop smoking, and follow your doctor's recommendations to control diabetes or high blood pressure. Reducing fats, especially saturated fats, in your diet may help to reduce serum lipid levels.
Update Date: 5/15/2007


Reference


Medical Encyclopedia
Atheroembolic renal diseasehttp://www.nlm.nih.gov/medlineplus/ency/article/000480.htmllustrations


Carotid stenosis, X-ray of the left artery



Carotid stenosis, X-ray of the right artery



Enlarged view of atherosclerosis



Prevention of heart disease



Developmental process of atherosclerosis



Angina




Atherosclerosis



Cholesterol producers



Coronary artery balloon angioplasty - series


Alternative Names Return to top
Arteriosclerosis; Hardening of the arteries; Plaque buildup - arteries
Definition Return to top
Atherosclerosis is a condition in which fatty material collects along the walls of arteries. This fatty material thickens, hardens, and may eventually block the arteries.
Atherosclerosis is a type of arteriosclerosis. The two terms are often used to mean the same thing.
Causes Return to top
Atherosclerosis is a common disorder of the arteries. It occurs when fat, cholesterol, and other substances build up in the walls of arteries and form hard substances called plaque.
Eventually, the plaque deposits can make the artery narrow and less flexible. This makes it harder for blood to flow. If the coronary arteries become narrow, blood flow to the heart can slow down or stop, causing chest pain (stable angina), shortness of breath, heart attack, and other symptoms.
Pieces of plaque can break apart and move through the bloodstream. This is a common cause of heart attack and stroke. Blood clots can also form around the plaque deposits. Clots block blood flow. If the clot moves into the heart, lungs, or brain, it can cause a stroke, heart attack, or pulmonary embolism.
Risk factors for atherosclerosis include:
• Diabetes
• High blood pressure
• High cholesterol
• High-fat diet
• Obesity
• Personal or family history of heart disease
• Smoking
The following conditions have also been linked to atherosclerosis:
• Cerebrovascular disease
• Kidney disease involving dialysis
• Peripheral vascular disease
Symptoms Return to top
Symptoms usually do not occur until blood flow becomes slowed or blocked. If this happens, you may have chest pain or leg pain, depending on which artery is involved. Sometimes symptoms occur only with activity.
Exams and Tests Return to top
A health care provider will perform a physical exam and listen to the heart and lungs with a stethoscope. Early atherosclerosis can create a whooshing or blowing sound ("bruit") over an artery.
Tests that may be used to diagnose atherosclerosis or complications include:
• Ankle/brachial index (ABI)
• Arteriography
• Cardiac stress testing
• CT scan
• Doppler study
• Intravascular ultrasound (IVUS)
• Magnetic resonance arteriography (MRA)
Treatment Return to top
Your doctor will probably suggest a low-fat diet, weight loss if you are overweight, and exercise.
There are many different medicines used to treat atherosclerosis. Blood thinners may be given to prevent clot formation. Medications may be also recommended to lower cholesterol and to keep your blood pressure at a healthy level.
Atherosclerosis can lead to coronary heart disease (CHD). If you have CHD that does not cause symptoms, you can be treated with either medicine or angioplasty with stenting. Recent studies show that medicine and angioplasty with stenting have equal benefits. Angioplasty with stenting does not help you live longer, but it can reduce angina or other symptoms of coronary artery disease.
Angioplasty with stenting, however, can be a life-saving procedure if you are having a heart attack
Some people may need a procedure called an endarterectomy to remove plaque build up.
See also:
• Coronary artery bypass surgery
• Minimally invasive heart surgery
Outlook (Prognosis) Return to top
Everyone starts to develop some amount of atherosclerosis as they grow older. In some people, the condition can cause complications such as a heart attack or stroke.
Possible Complications Return to top
• Coronary artery disease
• Damage to organs (such as the kidneys, brain, liver, and intestines)
• Heart attack
• Stroke
• Too little blood to the legs and feet
• Transient ischemic attack (TIA)
When to Contact a Medical Professional Return to top
Call for an appointment with your health care provider if you are at risk for atherosclerosis, especially if symptoms occur.
Talk to your doctor before starting a new exercise plan, especially if you have been diagnosed with coronary artery disease or if you have ever had a heart attack.
Prevention Return to top
The following lifestyle changes can help prevent atherosclerosis:
• Eat a low-fat, low-cholesterol, and low-salt diet.
• Eat fish. Adding fish to the diet at least twice a week has been shown to be helpful. Do not fry the fish, as this destroys the benefit.
• If you don't like to eat fish, try a fish oil supplement.
• Exercise 30 minutes every day. If you are overweight, you should get 60 to 90 minutes of exercise a day.
• Lose weight if you are overweight.
• Stop smoking.
• Mild to moderate consumption of alcohol or wine (1-2 drinks per day) may also reduce the risk of cardiovascular events. Too much alcohol, however, does more harm than good.
• If you have one or more risk factors for heart attack or stroke, ask your doctor if you should take aspirin every day. Aspirin can help some people reduce the risk of heart disease and stroke.
Work with your doctor to bring the blood pressure into the normal range. This may require medication. Follow your doctor's recommendations for treatment and control of diabetes and other diseases.
Do not take hormonal replacement therapy, folic acid supplements, vitamin C or E, or antioxidants to decrease the risk of heart disease or stroke. These methods have not been proven to prevent these conditions.
References Return to top
Boden WE, O'rourke RA, Teo KK, et al. Optimal Medical Therapy with or without PCI for Stable Coronary Disease. N Engl J Med. 2007 Mar 26; [Epub ahead of print].
Mosca L, Banka CL, Benjamin EJ, et al. Evidence-Based Guidelines for Cardiovascular Disease Prevention in Women: 2007 Update. Circulation. 2007; Published online before print February 19, 2007.
Zipes DP, Libby P, Bonow RO, Braunwald E, eds. Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 7th ed. St. Louis, Mo: WB Saunders; 2005:921-935.
Update Date: 3/30/2007

Background: Specialists have known for a long time that renal artery stenosis (RAS) is the major cause of renovascular hypertension and that it may account for 1-10% of the 50 million people in the United States who have hypertension. Apart from its role in the pathogenesis of hypertension, RAS is also being increasingly recognized as an important cause of chronic renal insufficiency and end-stage renal disease. In older individuals, atherosclerosis (ATH) is by far the most common etiology of RAS. As the renal artery lumen progressively narrows, renal blood flow decreases and eventually compromises renal function and structure.
With the increase in the elderly population and the possible increase in prevalence of RAS and ischemic nephropathy, clinicians dealing with renovascular disease (RVD) need noninvasive diagnostic tools and effective therapeutic measures to resolve the problem successfully. This review explores the natural history of this disorder, the value of a variety of invasive and noninvasive diagnostic procedures, and the consequence of allowing the artery to remain obstructed versus reversing renal artery occlusion.
Pathophysiology: In patients with ATH, the initiator of endothelial injury is not clear; however, dyslipidemia, hypertension, cigarette smoking, diabetes mellitus, viral infection, immune injury, and increased homocysteine levels may contribute to endothelial injury. In the atherosclerotic lesion site, endothelium permeability to plasma macromolecules (eg, low-density lipoprotein [LDL]) increases, turnover of endothelial cells and smooth muscle cells increases, and intimal macrophages increase. When atherogenic lipoproteins exceed certain critical levels, the mechanical forces may enhance lipoprotein insudation in these regions, leading to early atheromatous lesions.
Renal blood flow is 3- to 5-fold greater than the perfusion to other organs because it drives glomerular capillary filtration. Both glomerular capillary hydrostatic pressure and renal blood flow are important determinants of the glomerular filtration rate (GFR).
In patients with RAS, the chronic ischemia produced by the obstruction of renal blood flow produces adaptive changes in the kidney that are more pronounced in the tubular tissue. These changes include atrophy with decreased tubular cell size, patchy inflammation and fibrosis, tubulosclerosis, atrophy of the glomerular capillary tuft, thickening and duplication of the Bowman capsule, and intrarenal arterial medial thickening. In patients with RAS, the GFR is dependent on angiotensin II and other modulators that maintain the autoregulation system between the afferent and efferent arteries and can fail to maintain the GFR when renal perfusion pressure drops below 70-85 mm Hg. Significant functional impairment of autoregulation, leading to a decrease in the GFR, is not likely to be observed until arterial luminal narrowing exceeds 50%.
Frequency:
• In the US: Studies suggest that ischemic nephropathy may be responsible for 5-22% of advanced renal disease in all patients older than 50 years.
Mortality/Morbidity:
• The consequences of RAS are hypertension, which may be particularly difficult to control or may require multiple antihypertensive agents (with increased adverse effects), and progressive loss of renal function (Ischemic Nephropathy).
• In addition, the discovery of atherosclerotic RVD frequently occurs in the setting of generalized vascular disease (ie, cerebral, cardiac, peripheral), with the co-morbidity associated with disease in those vascular beds. Thus, any therapeutic intervention for RAS should logically take into account the underlying prognosis associated with these co-morbidities.
Race:
• RVD is less common in African American patients. The incidence rate in 2 studies of patients with severe hypertension was 27-45% in white persons compared to 8-19% in African American persons.
Sex:
• While the incidence of atherosclerotic RVD is independent of sex, Crowley et al showed that female sex (as well as older age, elevated serum creatinine level, coronary artery disease, peripheral vascular disease, hypertension, and cerebrovascular disease) is an independent predictor of RVD progression.
Age:
• In 1964, Holley et al reported data from 295 consecutive autopsies performed in their institution during a 10-month period. The mean age at death was 61 years. The prevalence rate of RAS was 27% of 256 cases identified as having history of hypertension, while 56% showed significant stenosis (>50% luminal narrowing), and, among normotensive patients, 17% had severe RAS (>80% luminal narrowing). Among those older than 70 years, 62% had severe RAS.
• Another similar autopsy study reported similar results, with 5% of patients older than 64 years showing severe stenosis; this figure increased to 18% for patients aged 65-74 years and 42% for patients older than 75 years.





CLINICAL Section 3 of 10

Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography


History: Patients with documented or possible renovascular hypertension may experience progressive azotemia as a consequence of the renal ischemia and/or the persistence of significant hypertension. Refractory hypertension (ie, poor control of blood pressure despite treatment with 3 or more antihypertensive agents) may occur.
Physical: The strong association of RVD with generalized ATH indicates that any typical findings associated with cerebrovascular (eg, carotid bruits, old cerebrovascular accident, transient ischemic attack), cardiovascular, or peripheral vascular disease occur frequently in patients with RVD. Abdominal bruits are highly specific for RVD when heard over the flank and are back-and-forth in nature (ie, present during both systole and diastole).
Patients with ischemic RVD present with one or more of the following clinical, historical, or diagnostic scenarios:
• Azotemia occurs in patients with peripheral vascular occlusive disease, carotid or coronary artery disease, and other signs of ATH.
• Sudden worsening of hypertension or renal function may occur.
• Acute renal failure or decreased renal function after antihypertensive therapy, especially with ACE inhibitors or angiotensin receptor blockers, may occur; an increase in serum creatinine levels of more than 15% in this setting is strongly suggestive of a high incidence of RVD.
• Unexplained renal insufficiency may develop in elderly patients.
• Congestive heart failure may occur with poor control of hypertension and renal insufficiency in the absence of a significant decrease in ejection fraction (the so-called flash pulmonary edema).
Causes: Risk factors associated with ischemic renal disease (IRD) are as follows:
• Hypertension: Of patients with IRD, 35% can be normotensive.
• Advanced age: Numerous cases occur in persons aged 60-69 years. Incidence increases in persons older than 70 years.
• Renal insufficiency
• Extrarenal ATH
• Diabetes mellitus
• Smoking
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