Coronary Artery Disease (CAD)

Coronary Artery Disease (CAD) is the most prevalent type of Cardiovascular Disease (CVD) which, according to the American Heart Association accounts for 35% of all deaths in the U.S. equivalent to nearly one million in the year 2004 (Corwin, 2008). It is a condition where the heart muscle (myocardium) receives insufficient oxygen because the coronary arteries fail to supply sufficient amount of blood to the heart muscle. The occlusion is usually caused by the atherosclerotic deposits of fibrous and fatty tissue; build up of cholesterol and other material, called plaque, on their inner walls (Calnan, 1991). As the buildup grows, less blood can flow through the arteries. As a result, the heart muscle can't get the blood or oxygen it needs. CAD involves various types of coronary artery conditions characterizing the disease.

Risk Factors

There are several factors associated with CAD and they are identified as nonmodifiable and modifiable risk factors which are inherent and client has no control over and those factors that client has control over respectively. Nonmodifiable factors include family history of coronary heart disease, increasing age, gender (heart disease occurs three times more often in men than in premenopausal women), race (higher incidence of heart disease in African Americans than in Caucasians) (Katzbl & Waldstbin, 2001, p. 5) while high blood cholesterol level, cigarette smoking, tobacco use, hypertension, diabetes mellitus, lack of estrogen in women, physical inactivity, and obesity are considered as modifiable factors. (Katzbl & Waldstbin, 2001, p.5)

Atherosclerosis

Also called the hardening of the arteries, atherosclerosis is a condition of the large and small arteries characterized by accumulation of fatty deposits, platelets, neutrophils, monocytes and macrophages throughout the tunica intima (endothelial cell layer) and eventually into the tunica media (smooth muscle layer). These substances create blockages or narrow the vessel in a way that reduces blood flow to the myocardium. Studies indicate that atherosclerosis involves a repetitious inflammatory response to artery wall injury and an alteration in the biophysical and biochemicalproperties of the arterial walls (Smeltzer & Bare, 2004). Arteries most often affected include the coronaries, the aorta, and the cerebral arteries. There are two reasons why arteries cannot maintain an adequate supply of blood. One of these is coronary artery spasm although this is usually a common accompaniment of coronary obstruction which is the major reason. Coronary obstruction develops when the arteries become more rigid and narrow due to the accumulation of fatty deposits (plaque) (Calnan, 1991).

Pathophysiology

Atherosclerosis begins as fatty streaks, lipids that are deposited in the intima of the arterial wall. Although they are thought to be the precursors of atherosclerosis, fatty streaks are common, even in childhood. Moreover, not all develop into more advanced lesions. The reason why some fatty streaks continue to develop is unknown, although genetic and environmental factors are involved (Smeltzer & Bare, 2004). Calnan (1991) in his book cited that the narrowing of the arteries is, in some respects, a natural product of ageing. However, there are more specific theories and two are popular at the moment. The first suggests that fats move into the arterial wall from the blood where they help produce large amounts of scar tissue. The second suggests that blood clots that form the arterial wall are integrated into the wall where they degenerate into the fat and fibrin found in the deposits. The plaques themselves become the focal point for the formation of more blood clots which can sometimes completely block off an artery. In addition, a piece of plaque may break off and move down the artery until it blocks it. However, the main effect of atherosclerosis is to cause narrowing of the arteries and the severity of the condition is dependent on the location of these deposits.

The continued development of atherosclerosis involves an inflammatory response. T lymphocytes and monocytes (that become macrophages) infiltrate the area to ingest the lipids and then die; this causes smooth muscle cells within the vessel to proliferate and form a fibrous cap over the dead fatty core. These deposits, called atheromas or plaques, protrude into the lumen of the vessel, narrowing it and obstructing blood flow. If the fibrous cap of the plaque is thick and the lipid pool remains relatively stable, it can resist the stress from blood flow and vessel movement. If the cap is thin, the lipid core may grow, causing it to rupture and hemorrhage into the plaque, allowing a thrombus to develop. The thrombus may obstruct blood flow, leading to sudden cardiac death or an acute myocardial infarction (MI), which is the death of heart tissue (Smeltzer & Bare, 2004).

Angina Pectoris

Angina pectoris is severe pain originating from the heart that occurs in response to an inadequate oxygen supply to the myocardial cells. The pain of angina may radiate down the left arm, to the back, to the jaw, or into the abdominal area (Corbin, 2008) and the cause is usually insufficient coronary blood flow. The insufficient flow results in a decreased oxygen supply to meet an increased myocardial demand for oxygen in response to physical exertion or emotional stress. In other words, the need for oxygen exceeds the supply. The severity of angina is based on the precipitating activity and its effect on the activities of daily living (Smeltzer & Bare, 2004).

There are six identified types of angina: Stable angina is the type that is predictable and consistent pain that occurs on exertion and is relieved by rest while Unstable angina (also called preinfarction angina or crescendo angina) has symptoms that occur more frequently and last longer than stable angina and the threshold for pain is lower, and pain may occur at rest. Furthermore, Intractable or refractory angina has a symptom of severe incapacitating chest pain while individuals with variant angina (also called Prinzmetal's angina) experience pain at rest with reversible ST-segment elevation and this is thought to be caused by coronary artery vasospasm. Lastly, Silent ischemia laboratory result has objective evidence of ischemia (such as electrocardiographic changes with a stress test), but patient reports no symptoms.

Pathophysiology

Angina is usually caused by atherosclerotic disease. Almost invariably, angina is associated with a significant obstruction of a major coronary artery. Several factors are associated with typical anginal pain: physical exertion, which can precipitate an attack by increasing myocardial oxygen demand; exposure to cold, which can cause vasoconstriction and an elevated blood pressure, with increased oxygen demand; eating a heavy meal, which increases the blood flow to the mesenteric area for digestion, thereby reducing the blood supply available to the heart muscle (In a severely compromised heart, shunting of blood for digestion can be sufficient to induce anginal pain.); and stress or any emotion-provoking situation, causing the release of adrenaline and increasing blood pressure, which may accelerate the heart rate and increase the myocardial workload, peripheral vascular disease, arthritis, degenerative disk disease, physical disability, foot problems) that limit the patient's ability to exercise.

Myocardial Infarction

MI refers to the process by which areas of myocardial cells in the heart are permanently destroyed. Like unstable angina, MI is usually caused by reduced blood flow in a coronary artery due to atherosclerosis and occlusion of an artery by an embolus or thrombus. Because unstable angina and acute MI are considered be the same process but different points along a continuum, the term acute coronary syndrome (ACS) may be used for these diagnoses. Other causes of an MI include vasospasm (sudden constriction or narrowing) of a coronary artery; decreased oxygen supply (eg, from acute blood loss, anemia, or low blood pressure); and increased demand for oxygen (eg, from a rapid heart rate, thyrotoxicosis, or ingestion of cocaine). In each case, a profound imbalance exists between myocardial oxygen supply and demand. Coronary occlusion, heart attack, and MI are terms used synonymously, but the preferred term is MI. The area of infarction takes time to develop. As the cells are deprived of oxygen, ischemia develops, cellular injury occurs, and over time, the lack of oxygen results in infarction, or the death of cells (Smeltzer & Bare, 2004)

Pathophysiology

Myocardial infarction (MI) is the death of myocardial cells that occurs following prolonged oxygen deprivation. It is the culminating lethal response to unrelieved myocardial ischemia. Myocardial cells begin to die after about 20 minutes of oxygen deprivation. After this period, the ability of the cells to produce ATP aerobically is exhausted, and the cells fail to meet their energy demands. Without ATP, the sodium-potassium pump quits, and the cells fill with sodium ions and water, eventually causing them to lyse (burst). With lysis, cells release intracellular potassium stores and intracellular enzymes, which injure neighboring cells. Intracellular proteins gain access to the general circulation and the interstitial space, contributing to interstitial edema and swelling around the myocardial cells. With cell death, inflammatory reactions are initiated. At the site of inflammation, platelets accumulate and release clotting factors. Mast cell degranulation occurs, resulting in the release of histamine and various prostaglandins. Some are vasoconstrictive and some stimulate clotting (thromboxane) (Corwin, 2008).

Clinical Manifestations

Meanwhile, the onset of the CAD is accompanied with a number of clinical manifestations which include chest pain (angina) which is usually constricting or squeezing pain in the pericardial or substernal area of the chest, possibly radiating to the arms, jaw, or thorax; dyspnea (shortness of breath at rest or with exertion), tachycardia develops, due to increased cardiac sympathetic stimulation and anxiety; syncope (loss of consciousness), feelings of weakness related to decreased blood flow to the skeletal muscles occur; palpitations (unpleasant awareness of forceful or rapid heartbeat); edema (swelling in lower extremities), skin color changes occur as blood flow decreases to an area. With ischemia, the area becomes pale. This is followed by local autoregulatory responses, resulting in hyperemia (increased blood flow) to the area, causing the skin to flush red; and hemoptysis (blood-streaked expectoration).

Laboratory Procedure

Cardiac catheterization

Also called cardiac cath or coronary angiogram, it is an invasive diagnostic procedure in which radiopaque arterial and venous catheters are introduced into selected blood vessels of the right and left sides of the heart. Catheter advancement is guided by fluoroscopy. Most commonly, the catheters are inserted percutaneously through the blood vessels, or via a cutdown procedure if the patient has poor vascular access. Pressures and oxygen saturations in the four heart chambers are measured. Cardiac catheterization is used to diagnose CAD, assess coronary artery patency, and determine the extent of atherosclerosis based on the percentage of coronary artery obstruction. These results determine whether revascularization procedures including PTCA or coronary artery bypass surgery may be of benefit to the patient. During cardiac catheterization, the patient has an intravenous line in place for the administration of sedatives, fluids, heparin, and other medications. Noninvasive hemodynamic monitoring that includes BP and multiple ECG tracings are necessary to continuously observe for dysrhythmias or hemodynamic instability. The myocardium can become ischemic and trigger dysrhythmias as catheters are positioned in the coronary arteries or during injection of contrast agents. Resuscitation equipment must be readily available during the procedure. Staff must be prepared to provide advanced cardiac life support measures as necessary (Smeltzer & Bare, 2004).

The procedure usually lasts for two to three hours and the client should expect that a mild sedative may be given to allow relaxation while remaining conscious and an intravenous needle will be inserted in the arm to administer medication with electrodes attached to the chest to enable the painless procedure known as an electrocardiograph. On the other hand, before the catheter is inserted into an artery or vein in the arm or leg, a local anesthesia is injected to numb the insertion site and as the catheter travels through the blood, pressure will be experienced. Moreover, after catheter is guided into the coronary-artery system, a dye or a radiocontrast material is injected to aid in the identification of any abnormalities of the heart. At this time, hot, flushing feeling or a quick passing nausea will be felt thus coughing or deep breathing may be encouraged to ease the discomfort.

It is very important that before the procedure, thorough assessment of the patient is done as to determine if client has allergies to shellfish (such as shrimp or scallops) which contain iodine wherein iodine is a common component of the dyes used in other diagnostic tests. In addition, the procedure is considered an invasive surgery thus the client is instructed that no food or drink should be ingested for at least six hours prior to the test and just before the procedure starts, the patient is encouraged to urinate and change into a hospital gown, then lie flat on a padded table that may also be tilted in order for the heart to be examined from a variety of angles.

Meanwhile, a close monitoring is done when cardiac catheterization is performed on an out-patient basis while remaining in the hospital for at least 24 hours and a bed rest is indicated for at least eight hours immediately after the test. Furthermore, if the catheter was inserted into a vein or artery in the leg or groin area, the leg will be kept extended for four to six hours while the arm will need to remain extended for a minimum of three hours if the vein or artery in the arm was used to insert the catheter. It is also expected that a hard ridge to form over the incision site that diminishes as the site heals. Bluish discoloration under the skin at the point of insertion should also be expected but fades in two weeks. It is also not uncommon for the incision site to bleed during the first 24 hours following surgery. If this should happen, the patient should apply pressure to the site with a clean tissue or cloth for 10-15 minutes.

Associated risks and complications following the procedure may include cardiac arrhythmias (an irregular heart beat); pericardial tamponade (a condition that causes excess pressure in the pericardium which affects the heart due to accumulation of excess fluid); the rare occurrence of myocardial infarction (heart attack) or stroke may also develop due to clotting or plaque rupture of one or more of the coronary or brain arteries. Before left-side catheterization is performed, the anticoagulant medication heparin may be administered. This drug helps decrease the risk of the development of a blood clot in an artery (thrombosis) and blood clots traveling throughout the body (embolization). The risks of the catheterization procedure increase in patients over the age of 60, those who have severe heart failure, or persons with serious valvular heart disease. Moreover, normal findings will reveal the absence of abnormalities of heart chamber size or configuration, wall motion or thickness, the direction of blood flow, or motion of the valves while abnormal results yield narrowing or blockage in the coronary arteries, with narrowing that is greater than 70% considered significant.

Management

Treatment for coronary artery disease (CAD) may include lifestyle changes, medicines, and medical procedures depending on the cause and severity of the condition. They are aimed at relieving symptoms, reducing risk factors in an effort to slow, stop, or reverse the buildup of plaque, lowering the risk of blood clots forming, which can cause a heart attack , widening or bypassing clogged arteries, and preventing complications of CAD.

Lifestyle changes. Adopting a healthy lifestyle is one of the best treatments for coronary artery disease. Either by itself or in combination with medical treatments, a healthy lifestyle can prevent or slow coronary artery disease. All patients with coronary artery disease can benefit from healthy lifestyles.
Cessation of smoking is essential for patients with atherosclerosis because of the damaging effects of smoke-related compounds on the endothelial cell wall (Corwin, 2008)

Diet modification can lower LDL and improve HDL levels. High-fiber foods (fruits, vegetables, whole grains), fatty fish (omega 3 fatty acids), soy products (isoflavones), and garlic have been shown to lower LDL cholesterol (Corwin, 2008).

Regular physical activity can lower many CAD risk factors, including LDL ("bad") cholesterol, high blood pressure, and excess weight. Physical activity also can lower risk for diabetes and raise levels of HDL cholesterol (the "good" cholesterol that helps prevent CAD) (National Heart Lung and Blood Institute, Diseases and Conditions Index, 2007).

Medications. Medications can help prevent the progression of coronary artery disease. If the disease is present, prescription drugs can improve blood flow to the heart. Some of the more common medications include:

- Cholesterol-lowering medications. By decreasing the amount of cholesterol in the blood, especially LDL (the "bad" form of cholesterol), these drugs decrease the primary material that deposits on the coronary arteries. Examples include statins, niacin, fibrates and bile acid sequestrants (National Heart Lung and Blood Institute, Diseases and Conditions Index, 2007).

- Aspirin. This common over-the-counter medication may be recommended as an anti-platelet, which thins the blood, and as an anti-coagulant, which reduces the tendency for blood to clot and block a coronary artery, causing a heart attack. Other anti-platelet drugs or anti-coagulants may be prescribed as well (National Heart Lung and Blood Institute, Diseases and Conditions Index, 2007).

- Nitroglycerin and other nitrates act as potent dilators of the venous system, decreasing venous return of blood to the heart. A decreased venous return decreases end diastolic volume, allowing the heart to decrease stroke volume. Nitrates dilate the arterial system as well, reducing the afterload against which the heart must pump, and increasing coronary blood flow. Dilation of a coronary artery undergoing spasm also may occur with nitrates. These effects reduce the inequalities of oxygen demand versus supply, and nitroglycerin given sublingually (under the tongue) usually reverses angina (Corwin, 2008)

- Beta-blockers. Beta-adrenergic blockers reduce angina by reducing heart rate and contractility of the heart, thereby reducing its oxygen demands. Calcium channel blockers also reduce the afterload against which the heart must pump by dilating the arteries and arterioles downstream and are particularly effective in reducing the spasm of variant angina. Calcium channel blockers should not be used in patients at risk of heart failure (Corwin, 2008)

- Calcium channel blockers. These medications help to open coronary arteries to increase blood flow to the heart muscle. They can also help reduce high blood pressure (MayoClinic Staff, 2007)

- ACE inhibitors (angiotensin converting enzyme inhibitors). Similar to beta-blockers, these help lower blood pressure and make the heart's job of pumping blood easier. In addition, ACE inhibitors have shown significant benefits for patients in recovering from a heart attack. They include ramipril, lisinopril, enalapril and captopril (MayoClinic Staff, 2007).

- Vitamins. Folic acid, B-6 and B-12 are vitamins that help to decrease homocysteine in the blood. Homocystiene has been associated with accelerated clogging of the arteries (atherosclerosis). In specific situations, some patients may be prescribed L-arginine or Omega-3 fatty acids (MayoClinic Staff, 2007).

Balloon Angioplasty. Lifestyle changes and medication might not be enough to combat the condition or lessen the effects of artery blockages, occurrence of heart attack, worsening chest pain or other symptoms, thus angioplasty might be suggested.
A procedure used to widen vessels narrowed by stenoses or occlusions is referred to as angioplasty and it is indicated to individuals with an occlusive vascular disease such as atherosclerosis wherein there is impairment of blood flow to an organ (such as the heart) or to a distal body part ( such as the lower leg) due to the narrowing of the vessel's lumen due because of fatty deposits or calcium accumulation. Furthermore, the narrowing may occur in any vessel but may occur anywhere and once there is widening of blood vessel, adequate blood flow is returned however the vessel may narrow again over time at the same location but the procedure could be repeated.

Angioplasty was originally performed by dilating the vessel with the introduction of larger and larger stiff catheters through the narrowed space. Complications of this procedure caused researchers to develop means of widening the vessel using a minimally sized device. Today, catheters contain balloons that are inflated to widen the vessel and stents to provide structural support for the vessel. Lasers may be used to assist in the break up of the fat or calcium plaque. Catheters may also be equipped with spinning wires or drill tips to clean out the plaque.

During the procedure, the patient is sedated or anesthetized, depending on the vessels involved. As such, the patient will be kept awake to report on discomfort and cough if required if a percutaneous transluminal coronary angioplasty (PTCA) is to be performed and PTCA procedures are performed in cardiac catheterization labs with sophisticated monitoring devices. On the other hand, the patient may be sedated for the procedure and a nurse will monitor the patient's vital signs during the procedure if angioplasty is performed in the radiology department's angiographic suite and if a vascular surgeon will perform the angioplasty procedure, it will be performed in an operating room or specially designed vascular procedure suite.

Meanwhile, the site of the introduction of the angioplasty equipment is prepared as a sterile surgical site. Although many procedures are performed by puncturing the vessel through skin, many procedures are also performed by surgically exposing the site of entry. And direct view of the vessel's puncture site aids in monitoring damage to the vessel or excessive bleeding at the site. Once the vessel is punctured and the guidewire is introduced, fluoroscopy is used to monitor small injections of contrast media used to visualize the path through the vessel. If the fluoroscopy system has a feature called 'roadmap', the amount of contrast media injected will be greater in order to define the full route the guidewire will take. The fluoroscopy system will then superimpose subsequent images over the roadmap while the vessel is traversed, that is, the physician moves the guidewire along the map to the destination.

Lastly, there is the risk of puncturing the vessel with the guidewire during the procedure however this is considered as a very small risk. Furthermore, it is necessary that the patients must be assessed and monitored for hematoma or hemorrhage at the puncture site and minimal risk of heart attack, emboli, and although unlikely death may also be associated with the procedure. If there is a need that the patient will be hospitalized, the length of the confinement will have a variation in length, taking into consideration the patient's overall condition, any complications, and availability of home care.

References

"h Author unknown (2007). Coronary Artery Disease. Retrieved March 30, 2008 from National Heart Lung and Blood Institute, Diseases and Conditions Index. http://www.nhlbi.nih.gov/health/dci/Diseases/Cad/CAD_WhatIs.html
"h Calnan, M. (1991). Preventing Coronary Heart Disease: Prospects, Policies, and Politics. New York: Routledge.
"h Corwin, E. (2008). Handbook of Pathophysiology, 3rd Ed. Baltimore: Lippincott Williams & Wilkins
"h MayoClinic Staff (2007).Coronary artery disease. Retrieved March 30, 2008 from http://www.mayoclinic.com/health/coronary-artery-disease
"h Katzbl, L. I., & Waldstbin, S. R. (2001). Chapter One Classification of Cardiovascular Disease. In Neuropsychology of Cardiovascular Disease, Waldstein, S. R. & Elias, M. E. (Eds.) (pp. 3-13). Mahwah, NJ: Lawrence Erlbaum Associates.
"h Smeltzer, S. & Bare, B. (2004). Brunner & Suddarth's Textbook of Medical-Surgical Nursing. New York: Lippincott Williams & Wilkins
"h Wung, S., & Drew, B. (1999). Comparison of 18-lead ECG and selected body surface potential in determining maximally deviated ST lead and efficacy in detecting acute myocardial ischemia during coronary occlusion. Journal of Electrophysiology, 32, (Suppl.) 30-37.