Dr.Proxy

Coronary artery disease is atherosclerosis of the coronary arteries that leads to a restriction of blood flow to the heart. Atherosclerosis is a chronic condition that narrows arteries by building fat-filled bulges in the arterial walls. These bulges are called atherosclerotic plaques, or simply, plaques. In some people, the plaques eventually break open, and the contents cause blood clots. If these clots are swept into the bloodstream, they can lodge in the smaller arteries downstream and completely block blood flow beyond that point.
Heart muscle is constantly active, and it requires a continuous blood supply. When a heart artery is blocked suddenly, the heart muscle it supplies stops working within a few minutes. If the blood supply remains blocked for a half-hour or more, the heart's muscle cells will begin to die.
Complete, sudden blockage of an artery is not the only problem. Even a reduced blood supply will reduce the oxygen supply to heart muscle, and oxygen-starved heart muscle responds with a characteristic feeling of pain or discomfort, called angina.
When its arteries are narrowed by atherosclerosis, a heart may still get enough oxygen to pump blood at rest. On the other hand, exercise increases the work of the heart, and narrowed arteries cannot always delivery the excess oxygen required by an exercising heart. Under these circumstances, a person with narrowed coronary arteries will get angina when exercising. One of the first symptoms of coronary artery disease is the appearance of angina when a person is working strenuously.
As atherosclerosis progresses, some of the plaques rupture and clots are formed. If a clot temporarily shuts down an artery, the patient will get sudden angina that lasts until the clot is broken or swept away. If the clot remains for an extended period of time, some heart muscle begins to die: this is a heart attack, or myocardial infarction.
In general, the sudden blockage of a coronary artery or one of its main branches is called an acute coronary syndrome, and myocardial infarctions are one form of acute coronary syndrome. Acute coronary syndrome is a medical emergency, and must be treated immediately in an emergency room.
Atherosclerosis, the cause of coronary artery disease, is a slow, long-term process. Typically, atherosclerosis begins in a person's teenage years or earlier, and the disease worsens quietly for decades. As people age, their atherosclerosis becomes more likely to involve the arteries of the heart and to become coronary artery disease.
The progression of atherosclerosis can be slowed or even stopped by a few preventive measures. These include stopping smoking, staying thin or losing weight, exercising regularly, and eating a low-fat balanced diet. To control atherosclerosis, it is also important to keep blood pressures low, to reduce high blood cholesterol levels, and to treat diabetes.
People who develop symptomatic coronary artery disease should begin or continue these anti-atherosclerotic programs. In addition, they should take aspirin daily, and they should probably take other medicines (typically, beta blockers) to reduce the workload of the heart. Nitroglycerin tablets can be used to alleviate occasional anginal pain, and surgical procedures are available to widen narrowed arteries.
Coronary artery disease is the number one killer in the developed world. In the United States, it is estimated that half of today's healthy 40-year-old men and a third of today's healthy 40-year-old women will eventually develop coronary artery disease.
The proportion of deaths in the United States that are due to coronary artery disease has been decreasing slowly but continuously over the past half-century. Nonetheless, coronary artery disease remains the single most common cause of death in the United States. One-fifth of all American deaths are attributed to coronary artery disease, and four-fifths of the deaths of people 65 years and older result from the disease.
Coronary artery disease is not just an American problem. Throughout the developed world, coronary artery disease causes more deaths and disabilities and is responsible for more economic costs than any other single illness. Moreover, it is predicted that, by the year 2020, coronary artery disease will have become the leading cause of death in the underdeveloped parts of the world.
The high death rates from coronary artery disease can be reduced by changing people's eating habits, by increasing their activity levels, and by convincing them of the dangers of cigarette smoking.

NORMAL CIRCULATION OF THE HEART

The heart is made up almost entirely of muscle. Cardiac muscle, which differs from the skeletal and smooth muscle of the rest of the body, is dependent on aerobic metabolism. This means that the heart cannot function without a constant supply of oxygen.

 

Coronary Arteries

Just beyond the aortic valve—the outflow valve of the left ventricle of the heart—the right and left coronary arteries are the first branches of the aorta. The two coronary arteries and their main branches run in grooves along the outside of the heart; these grooves separate the left and right ventricles and they also separate the atria from the ventricles. The coronary arteries and their main branches are called epicardial arteries, because they run on the outer surface of the heart.
Each major coronary artery is 2 to 4 mm wide, about half the diameter of a pencil. From the coronary arteries and their major branches, many small arteries run into the muscular walls of the heart, and these small arteries give rise to rich capillary networks that bathe the cardiac muscle cells with blood. All arteries inside the heart walls are fed by branches of either the right or left coronary arteries.
In most people, the left coronary artery supplies most of the blood used by the left ventricle and the interventricular septum, while the right coronary artery supplies most of the blood used by the walls of the right ventricle. However, people vary in the way the blood supply to the heart is divided between the right and left coronary arteries.
There is not much overlap between the territories of the major branches of the coronary arteries. Therefore, if one of the major branches suddenly becomes blocked, there is no other blood supply to the territory served by that branch, and muscle in that territory will be deprived of oxygen (Warnica, 2005).

LEFT CORONARY ARTERY

The left coronary artery splits into two main branches, the left anterior descending (LAD) coronary artery and the left circumflex coronary artery. The LAD coronary artery runs down the front of the heart along the groove between the left and right ventricles. In most people, the LAD supplies blood to the front wall of the left ventricle and to the interventricular septum. Forty to fifty percent of heart attacks are caused by an obstruction of the left anterior descending coronary artery.
The left circumflex coronary artery runs to the left (at a right angle to the LAD) along the groove between the left atrium and the left ventricle. The left circumflex coronary artery supplies blood to the side or lateral wall of the left ventricle. Fifteen to twenty percent of heart attacks are caused by an obstruction of the left circumflex coronary artery.

RIGHT CORONARY ARTERY

The right coronary artery runs to the right, along the groove between the right atrium and the right ventricle. The right coronary artery branches behind the heart and gives rise to the posterior descending coronary artery, which parallels the LAD in front. The right coronary artery supplies the bottom and backside of the heart, and, in most people, it supplies blood to the right ventricle and to the sinus and AV nodes of the heart's electrical conduction system. Thirty to forty percent of heart attacks are caused by an obstruction of the right coronary artery.

Blood Flow to the Heart

The blood flow of the heart usually keeps up with the demand. The demand is increased by exercise and strong emotions, both of which make the heart pump more quickly and more forcefully, causing the heart to use more oxygen. As a rough rule, when the heart beats twice as fast, it needs twice as much oxygen (Lanza et al., 2004). Normally, the extra oxygen needed during exercise is supplied by a faster and a more voluminous blood flow through the coronary arteries.

HEART RATE

Faster blood flow is a direct result of a faster heart rate. Blood flow to the heart automatically speeds up as the heart beats more quickly, because the coronary arteries are fed directly by the outflow of the heart.

LOCAL MUSCLE ACTIVITY

Throughout the body, the volume of blood flow is regulated by the size of the arteries. Arteries have an innate tension in their walls. This tension keeps arterial volume at a particular level, and the tension also creates a resistance to blood flow. When the arterial wall tension is reduced, the artery stretches more easily and can carry a larger volume of blood.
The natural state of coronary arteries and their main branches is relatively wide open and, in general, these arteries do not limit the volume of blood getting to the muscle cells inside the heart. Instead, it is the small arteries inside the walls of the heart that widen and narrow and that, in this way, control the volume of blood flow to the muscle cells.
The control of the arterial wall tension—the force that widens and narrows the arteries—is local. As muscle cells work harder, they change the concentration of molecules (e.g., oxygen) surrounding them. Most molecular changes resulting from hard work relax the arteries in the vicinity. In addition, during exercise or stress, sympathetic nerves reduce the tension in the walls of arteries. Together, these factors relax the walls of the arteries and increase the local blood flow.

EFFECTS OF HEART ISCHEMIA

Heart ischemia occurs when the increases in blood flow and blood volume are insufficient to supply all the oxygen needed by the heart muscle.

Muscle Cells

What happens to heart muscle cells when they become ischemic? As soon as the blood flow to an area of heart muscle is stopped, the cells begin to lose their energy stores, and within a few minutes the muscle cells are no longer able to contract. Any region of the heart that loses all its blood flow will stop working almost immediately.
Although muscle cells stop working, they do not begin to die until 20 to 40 minutes after losing their blood supply. If blood flow is restored within a half-hour, most muscle cells will eventually recover; however, the recovery can take from 10 minutes to several days. During that time, the heart acts "stunned" and may not contract well unless stimulated by ionotropic drugs (Schoen, 2005).

Another effect of sudden ischemia of the heart is electrical irregularity. Before muscle cells begin to die, they become electrically unstable. After the blockage of a major coronary artery, the electrical instability of some people's hearts leads to ventricular fibrillation and this can cause sudden death.

Symptoms

CHEST PAIN

Heart ischemia usually produces symptoms, and the classic symptom of reduced oxygen supply to the heart is a particular type of chest pain called angina pectoris, or simply angina. Angina arises many seconds or even minutes after a sudden arterial blockage.
Typically, angina pain feels like crushing or squeezing, although sometimes it is described as burning. The sensation is usually felt inside the chest, behind the sternum, and the feeling can radiate to the throat, neck, jaw, or shoulder, or down the ulnar side (the inside) of either arm. In some people, the discomfort of angina is mild, but other people get diffuse unbearable pain (Lanza et al., 2004).
Angina is a classic symptom of heart ischemia. However, angina is not a perfect indicator of heart problems. Heart ischemia can occur without angina; moreover, some people get angina although they have no detectable heart ischemia:

• 70% of temporary episodes of heart ischemia happen without chest pain or discomfort
• 20% of heart attacks (myocardial infarctions) occur with no symptoms
• >70% of heart attacks occur in people who have had few or no previous episodes of angina (AHA/ASA, 2007)

ARRHYTHMIAS

Another significant result of sudden ischemia is a change in the heart's rhythm. Such changes can be serious. The arrhythmias (notably, ventricular fibrillation) that sometimes result from heart ischemia are the cause of most sudden deaths after an acute myocardial infarction.

OVERVIEW OF CORONARY ARTERY DISEASE

Coronary artery disease (CAD) is the umbrella term for various syndromes of heart ischemia that are caused by atherosclerotic obstruction of the coronary arteries. The atherosclerotic damage ranges from gradual narrowing of the coronary arteries (due to bulging patches of plaque) to the sudden obstruction of a coronary artery by a blood clot that has been dislodged from the surface of a ruptured plaque.

Atherosclerosis

Atherosclerosis is the disorder that underlies coronary artery disease. Atherosclerosis thickens the walls of medium and large arteries. The atherosclerotic thickenings occur as bulges, called plaques, in the arterial walls. Plaques contain lipids, white cells, smooth muscle cells, and connective tissue in a poorly organized mass that lies just under the endothelial lining of the artery wall.

In the United States, atherosclerosis usually begins in childhood or adolescence and then gradually worsens over many decades. Any medium or large artery in the body can be affected. Most atherosclerosis causes no clinical problems. Many people have atherosclerosis throughout their bodies but develop no serious medical symptoms, and the disease is only discovered at autopsy (Lam 2005; Libby 2005).
On the other hand, when atherosclerosis causes the coronary arteries to become very narrow or when plaques rupture and send clots into the arteries of the heart, a person has coronary artery disease (CAD). When the effects of atherosclerosis reduce the circulation in non-heart arteries, a person can develop peripheral artery disease (PAD). In the carotid arteries, PAD can cause strokes; in the aorta, it can lead to aneurysms; in the legs, it can cause episodic pain when walking (intermittent claudication) and sometimes gangrene of the feet; in the gastrointestinal arteries, it can cause mesenteric ischemia; and in the renal arteries, it can cause stenosis leading to hypertension.

ATHEROSCLEROTIC PLAQUE

The hallmarks of atherosclerosis are atherosclerotic plaques, which develop slowly and in three stages.

Stage One: Fatty Streaks Appear

As atherosclerosis begins, the first detectable changes are the appearance of fatty streaks along artery walls. These streaks are places where excess fat is accumulating. Most of the fat (lipids) in the blood is carried by proteins in molecular complexes called lipoproteins. The surface of a lipoprotein is made of the more water-soluble lipids—cholesterol and phospholipids. The least soluble lipids—cholesteryl esters and triglycerides—are carried in the centers of the lipoproteins.
Lipoproteins come in five sizes. From the largest to the smallest, these are: chylomicrons, VLDL, IDL, LDL, and HDL. Each size of lipoprotein has its own characteristic balance of lipids. The largest lipoproteins—chylomicrons and VLDL—are especially rich in triglycerides, while 70% of all blood cholesterol is contained in the LDL lipoproteins.
When there is an excess of lipoproteins in the blood, as happens in hypercholesterolemia, more lipoproteins than normal get through the endothelial cells and into the artery walls. These excess lipoproteins stick to extracellular molecules and eventually enough excess fat becomes stuck just below the endothelial cells to form visible yellowish streaks—fatty streaks—along the arterial walls.

Stage Two: Foam Cells Develop

White blood cells are attracted to these unhealthy accumulations of lipids. Some of the white blood cells are phagocytes, scavenger cells that begin to "swallow" the lipids. These cells swell as they become filled with fat droplets; the cells look puffed up, and they are called foam cells.

Stage Three: Smooth Muscle Cells Move In

Fatty streaks containing foam cells continue to thicken. Soon smooth muscle cells from deeper in the arterial walls move into the expanding plaques. Muscle cells secrete extracellular molecules, such as collagen, and the whole fatty lesion bulges into the bloodstream and narrows the space inside the artery. As they continue to evolve, some plaques also accumulate calcium, which can sometimes be seen in x-rays.
In time, the endothelial cells covering the bulge begin to rip, letting blood come in contact with the underlying collagen and other extracellular molecules. Extracellular molecules are stimulants of blood clotting. Therefore, small blood clots and clumps of platelets form along the rips in the endothelial lining of the artery. Disrupted plaques create blood clots, and if the clots break loose, they are carried into the smaller arteries downstream. The result can be a blocked artery.

INFLAMMATION

In response to infection, the body produces inflammation—redness, tenderness, warmth, and swelling. The inflammatory response can be triggered by things other than foreign substances, and inflammation plays a key role in worsening atherosclerosis.
Inflammation is the activation of white blood cells. Just as white blood cells are activated by foreign antigens, they can also be activated by the contents of atherosclerotic plaques. As a plaque develops, white blood cells (notably, lymphocytes and macrophages) collect underneath the endothelial cells, and their reaction to the material they encounter is to begin releasing inflammatory molecules (e.g., cytokines, proteolytic enzymes). The macrophages also ingest the excess lipoproteins in the vicinity, and these macrophages become bloated foam cells.
Many of the processes in the inflammatory response weaken the structure of an atherosclerotic plaque. The foam cells do not hold together strongly. The secreted inflammatory molecules destabilize the plaque by breaking bonds between extracellular matrix molecules. In these and other ways, inflammation makes a plaque prone to rupture, leading to the formation of blood clots (Falk et al., 2004).

CAUSES AND CONTRIBUTORS

Some people have a genetic propensity for developing atherosclerosis, but it appears that the disease can occur in almost everyone. A critical causative agent is dietary fat, especially the cholesterol that is carried in the blood in low-density lipoproteins (LDL). High blood levels of LDL cholesterol can cause and worsen atherosclerosis.
Other contributors to atherosclerosis are cigarette smoking, high blood pressure, diabetes, high blood concentrations of triglycerides, and low blood levels of high-density lipoproteins (HDL) (Zevitz, 2006).

CLOTS AND VASOSPASMS

Atherosclerotic plaques bulge into arteries and narrow the space available to carry blood. Under some conditions, these plaques also generate blood clots and vasospasms. Clots (thrombi) develop when plaques along the walls of arteries rip or rupture, exposing the contents of the plaque to the bloodstream.
The rupture of a plaque can also cause the walls of the artery to constrict in that region. The resulting vasospasm narrows the artery suddenly and causes ischemia downstream. Alone and together, clots and vasospasms can cause emergency medical conditions, including heart attacks and sudden death.
The rupture of an atherosclerotic plaque can happen quickly. It can be set off by a sudden spurt of output from the sympathetic nervous system; such spurts can occur when people are waking in the morning or when people are subjected to strong emotional stress. External stresses, however, do not disrupt stable plaques. External stresses only rupture those plaques that have already become weakened and destabilized by inflammation or other internal changes (Falk et al., 2004).

ATHEROSCLEROSIS OF THE CORONARY ARTERIES

Rather than uniformly thickening arterial walls, atherosclerosis is patchy and unevenly distributed. The specific coronary arteries affected by atherosclerosis vary from person to person, but there is a common feature: within a coronary artery, plaques are found most often at branch points, places where the blood flow naturally becomes turbulent.
The narrowing of coronary arteries usually occurs slowly and, in response, new small collateral arteries have time to grow into the fields of the atherosclerotic arteries to help bolster the local oxygen supply. These collateral arteries will sometimes provide enough extra blood flow to keep the heart muscle working comfortable at a resting rate. The collateral arteries are small, however, and they do not have the capacity to keep up with the oxygen demands of heart muscle during exercise.
Even with the growth of small collateral arteries, the continual narrowing of the coronary arteries by atherosclerosis can eventually produce ischemia and anginal pain. Initially, these symptoms occur only when the patient is exercising; later, the symptoms begin to occur even when the patient is at rest.
Besides slowly narrowing the coronary arteries, atherosclerosis can cause a sudden medical crisis. The degeneration of a plaque can seed clots into the bloodstream and can also trigger local vasospasm. These lead to a marked reduction of blood flow, and the resulting damage can range from temporary to permanent and from mild to fatal (Selwyn & Braunwald, 2005).

Clinical Forms of CAD

Many people live their entire lives symptom-free even when they have atherosclerosis of the coronary arteries. Other people, however, develop symptoms and heart damage from their atherosclerosis. The ischemic heart problems of atherosclerotic coronary artery disease fall into two general classes: chronic coronary syndromes and acute coronary syndromes (Schoen, 2005).

CHRONIC CORONARY SYNDROMES

Coronary artery disease is a chronic disease that is punctuated by sudden medical emergencies—the acute coronary syndromes. The long, chronic phases of the disease have two forms, chronic stable angina and chronic ischemic heart disease (Schoen 2005; Selwyn & Braunwald 2005).

Chronic Stable Angina

When one or more coronary arteries have become narrowed and cannot meet the demands of a hard-working heart, the patient has chronic stable angina. This syndrome is characterized by ischemic heart pain that shows up when patients exercise and that goes away in a few minutes after they rest. Blood flow to the heart must be reduced by 2/3 to 3/4 before a patient develops the symptoms of chronic stable angina.
The chest pain of chronic stable angina is short-lived and occurs predictably. Particular amounts of exercise, trauma, weather changes, or strong emotions may trigger angina. In chronic stable angina, resting or nitroglycerin tablets will relieve the chest pain in a few minutes.
The occurrence of angina is influenced by the general tone of the sympathetic nervous system (which tends to be, for example, higher in the mornings) and by the demands of blood flow by the gastrointestinal tract after a meal. Therefore, although the symptoms of chronic stable angina are fairly predictable, the amount of exercise or stress that will produce these symptoms varies during the course of a day.
The chest pain of chronic stable angina can also be brought on by any medical condition that increases the work of the heart, such as hypertension, aortic stenosis, systemic infections, or thyrotoxicosis. Likewise, conditions that reduce the oxygenation of the blood, such as COPD, anemia, or high altitudes, can also cause angina.

Chronic Ischemic Heart Disease

A second chronic syndrome is chronic ischemic heart disease or ischemic cardiomyopathy, in which years of damage from ischemia have weakened the heart sufficiently that it gradually fails. Chronic ischemic heart disease is a major cause of congestive heart failure in older adults. Most of these patients have had acute myocardial infarctions in the past, although not all infarctions may have been symptomatic. In people who have had "silent" myocardial infarctions, heart failure from chronic ischemic heart disease can be the first evidence of their coronary artery disease.

ACUTE CORONARY SYNDROMES

Sudden unpredictable episodes of severe heart ischemia are called acute coronary syndromes. Acute coronary syndromes result from a disruption of plaque that then causes ischemia severe enough to injure or kill muscle cells in the heart.
Acute coronary syndromes are the leading cause of death in the United States, and an acute coronary syndrome needs immediate treatment in a prepared emergency room (Kim et al. 2004; Fenton et al. 2007). People with the highest risk of developing an acute coronary syndrome are those who already have serious cardiovascular disease or diabetes.

Sudden Cardiac Death

The most catastrophic of the acute coronary syndromes is sudden cardiac death, an unexpected death from cardiac causes that happens quickly, usually within an hour of the first symptoms. In adults, sudden cardiac death is usually (in 80–90% of patients) associated with coronary artery disease. The direct cause of these deaths is fatal arrhythmias, such as ventricular fibrillation. The arrhythmias develop in heart cells that have been made overly excitable because of sudden ischemia from a blood clot or a vasospasm.

Myocardial Infarction

Heart attacks (myocardial infarctions) are a type of acute coronary syndrome. Most myocardial infarctions are caused by clots dislodged from atherosclerotic plaque with or without vasospasms (i.e., sudden, temporary contractions of the muscles inside the walls of a heart artery).
Myocardial infarctions occur when a chunk of plaque, a blood clot, a vasospasm, or some combination of these completely obstructs a coronary artery or one of its major branches. If the obstruction persists for more than about 30 minutes, some of the cell injury will be permanent. The area of the heart damaged by a myocardial infarction is called a myocardial infarct.
A myocardial infarction produces distinctive ECG changes. In addition, the cell necrosis in the infarct allows intracellular muscle molecules to leak into the bloodstream, and these heart molecules can be detected in blood tests (Brady et al. 2006).

Unstable Angina

A third common acute coronary syndrome is unstable angina. An episode of unstable angina includes symptoms of heart ischemia that do not go away after 5 to 10 minutes of rest. These episodes are caused by sudden disruptions of plaques, although the resulting arterial blockages resolve spontaneously. In unstable angina, the level of heart damage is much less than occurs in a myocardial infarction, but unstable angina often foreshadows a subsequent myocardial infarction (Tan et al., 2005).

Who Gets Coronary Artery Disease?

Coronary artery disease creeps up quietly. In most people, atherosclerosis builds over decades. The disease progresses silently, and although it probably begins before most people are out of their teenage years, the coronary effects of atherosclerosis usually do not show up until middle age.
The most common symptom of coronary artery disease is chest pain, which can be accompanied by shortness of breath and tiredness, and these are the symptoms that often bring the patient with coronary artery disease to the doctor. However, coronary artery disease can be symptom-less and "silent" for years. Even those people who have been diagnosed with coronary artery disease because of occasional temporary chest discomfort can at the same time be suffering acute myocardial infarctions without apparent symptoms.
More than half of the people who die suddenly from coronary artery disease have had no previous symptoms. Frequently, those patients who suffer from silent myocardial infarctions also have type 2 diabetes.
In spite of the variation in the overt signs and symptoms of coronary artery disease, there are some characteristics typical of most patients with the disease (Zevitz, 2006).

AGE

In the U.S., approximately 16 million people (7% of the adult population) have coronary artery disease. Coronary artery disease is a common disease of the elderly, and the typical patient is a man >50 years old or a woman >60 years old.

GENDER

Overall, coronary artery disease is slightly more common in men: for every 9 women with coronary artery disease, there are about 10 men with the disease. Women tend to develop symptomatic coronary artery disease later than men. In the United States, men over 40 years of age have almost a 50% chance of developing the disease in their lifetime, while the chance for women over the age of 40 years is 30%. It is thought that the higher estrogen levels in premenopausal women protect them from some of the heart damage done by atherosclerosis, but this protection disappears after menopause.

RACE

African Americans have a higher prevalence of, and a higher death rate from, coronary artery disease than European Americans. In part, the difference results from the higher incidence of hypertension, obesity, metabolic syndrome, and low physical activity among African Americans. Other contributors to the racial disparity are differences in the treatments requested by the patients and also differences in the treatments received (Williams et al. 2000).
Americans of Asian Indian origin are 2 to 3 times as likely as European Americans to develop coronary artery disease. Americans of Mediterranean origin are less likely than Americans of Northern European origin to develop coronary artery disease.

PRESENTATION

Chief Complaint

When a person with coronary artery disease comes to the office, clinic, or hospital with heart symptoms, the typical chief complaint is chest discomfort. Most often, this discomfort is not called "pain" but is, instead, described as a heaviness, pressure, squeezing, smothering, or choking sensation.

ANGINA PECTORIS

Chest discomfort is a key identifying symptom of coronary artery disease. Chest discomfort or chest pain can originate from many places other than the heart, but there is a characteristic type of chest discomfort or pain, called angina pectoris (or, simply, angina), that almost always points to ischemia of heart muscles (Braunwald 2005).
Six questions will help a health screener or a frontline triage worker decide whether a patient has angina. For the symptom chest pain, ask the patient six questions:

• What is the quality of the pain? What does it feel like?
• Where is it located?
• What brings it on, and how often do you have it?
• How long does it last, and does it change over time?
• What can you do to reduce or stop the pain?
• Are there other symptoms that accompany the pain? (Braunwald, 2005)

Here is how a patient with coronary artery disease typically answers these questions.

Quality

The quality or sensation of angina has a special character. The word angina means "choking, narrowing, or tightening," and this is typically how it is described. Rather than saying pain, patients most often use words such as squeezing, tightening, constricting, pressing, or strangling to describe the feeling of heart ischemia. They may say that they feel like there is "a band across my chest," "a heavy weight in the center of my chest," or "a vise that is tightening my chest."
As patients describe the uncomfortable feeling of angina, they often clench their fist and hold it in front of their sternum. This gesture is so common that it has been given a name, Levine's sign.

Sometimes, a patient with chronic stable angina will describe angina in more painful terms, such as 'burning," but when patients give descriptions of true pain, it is often because the underlying ischemia is caused by a complete blockage of an artery, as is found in a myocardial infarction. Even then, anginal pain is described as diffuse; it is rarely described as sharp and localized.

Location

When asked, "Where do you get this uncomfortable feeling?" patients with angina usually put a hand or fist over their sternum in the middle of their chests and say "Inside here!" meaning retrosternally. When asked, "Does this discomfort extend anywhere else?" angina patients will often say that the feeling extends to the left shoulder, to the inside (the ulnar) half of either or both arms, to the neck and jaw, or sometimes to the middle of the upper back.
The pain or discomfort of angina is broad, and patients do not point to it with a finger, saying "It's right here." Also, patients rarely feel angina above the jaw, below the umbilicus, in the lower right chest, or localized below the left nipple. Moreover, the examiner usually cannot reproduce the pain by pushing gently on the skin or the chest wall.

Triggers

Anginal pain is caused when heart muscle does not get enough oxygen. Most activities have fairly predictable oxygen requirements, and in chronic stable angina, the patient gets chest discomfort at predictable levels of activity. In contrast, in unstable angina, people get chest discomfort at rest and at unpredictable times.
Any situation that increases heart rate can trigger angina in people with coronary artery disease. Exercise is a classic cause of anginal pain: hurrying, walking up an incline, walking against a strong cold wind, working with the arms extended above the shoulders, and sexual activity are all exercises that can produce ischemic heart pain. In addition, strong emotions or nightmares activate the heart through the sympathetic nervous system, and these too can cause angina.
In chronic stable angina, although the amount of exertion needed to produce chest pain is fairly predictable, the threshold for angina will vary during the day and with the weather and the temperature. After a heavy meal, for example, blood flow is diverted to the gastrointestinal organs and, under these conditions, less exertion than usual can cause angina. Lying down changes the dynamics of blood flow, and some people get angina when they get in bed at night. (Women with chronic stable angina are more likely than men to get chest discomfort when they are resting or sleeping or when they are in stressful situations.)
Other medical conditions can precipitate angina in a person with coronary artery disease. For example, anemia, systemic infections, pneumonia, or atrial fibrillation change the balance between the heart's need for oxygen and the available supply; therefore, these can bring on ischemic heart pain.
Predictable triggers are characteristic of coronary artery disease with narrowed arteries (chronic stable angina). Acute coronary syndromes are different. When coronary artery disease produces a sudden significant obstruction of blood flow, the chest pain can occur without any apparent trigger. Unstable angina, for example, is characterized by worsening and unpredictable episodes of chest pain.

Time Course

The chest discomfort of chronic stable angina typically lasts from 2 to 5 minutes; it rarely persists for as long as 10 minutes. The angina begins dully and progressively worsens for a minute or two, and then it fades away as the patient stops and rests.
In contrast, the angina of acute coronary syndromes lasts for more than 10 minutes, and with myocardial infarctions, the pain can last for hours. Quick (10–15 sec), sharp chest pains are rarely ischemic heart pains. Also, a long steady dull ache in the lower left chest is rarely an ischemic heart pain.

Relief

Chronic stable angina is a condition in which the heart receives enough blood flow when it is working quietly. Therefore, the pain of chronic stable angina usually fades away in 1 to 5 minutes if the patient stops and rests by standing or sitting quietly. (Lying down does not always relieve the pain of angina as quickly.) Nitroglycerin tablets or sprays will usually end or lessen angina in a few minutes. When rest does not relieve classic anginal pain, then it is more likely that the patient has an acute coronary syndrome.

History

In addition to a description of individual occurrences of angina, the overall history of these episodes is telling. Chronic stable angina gives fairly predictable episodes of chest discomfort over many months, although the exact pattern of the episodes differs from patient to patient. In some patients, episodes of chest pain may occur several times a day; in others, there may be symptom-free intervals of weeks, months, or years. Occasionally, anginal attacks gradually decrease or disappear if adequate collateral coronary circulation (i.e., growth of new blood vessels) develops; this does not mean, however, that the disease has gone away.
In contrast, acute coronary syndromes give unpredictable or steadily worsening episodes of ischemic symptoms. As acute coronary syndromes are developing, the symptoms may change from being occasional to happening constantly. A myocardial infarction may give prolonged severe chest discomfort and continuous fatigue.
The chest discomfort of chronic stable angina is predictable for a given patient. Therefore, any changes in the pattern or the intensity of angina should be considered serious (Braunwald 2005).

Rating

People vary in how they report angina. To compare the symptoms of different patients with coronary artery disease, the New York Heart Association and the Canadian Cardiovascular Society have developed a rating system for classifying anginal pain. In this system, patients with known coronary artery disease and angina are put in one of four categories or classes according to their physical limitations. In brief, the classes are:

• Class I. Patient can do almost any daily physical activity without getting cardiac symptoms. Angina only occurs with strenuous, rapid, or prolonged exertion.
• Class II. Patient has no symptoms either at rest or with mild physical activity, but certain normal active exercise brings on symptoms. For example, walking or climbing one flight of stairs may be symptom-free, but running or climbing many flights of stairs will bring on cardiac symptoms.
• Class III. Patient has no symptoms at rest and can perform many activities of daily living without symptoms, but mild activity can bring on symptoms. For example, dressing, showering, and walking slowly for a short distance may be symptom-free, but carrying shopping bags, climbing stairs, and walking for 1 to 2 blocks will bring on cardiac symptoms.
• Class IV. Patient sometimes has cardiac symptoms at rest, and basic activities of daily living will bring on cardiac symptoms. (Adapted from Goldman, 1981)

OTHER CAUSES OF CHEST PAIN

Chest discomfort is a classic symptom of heart ischemia. It is also a key symptom of other medical problems, the most common of which are gastroesophageal diseases (gastroesophageal reflux, other esophageal problems, ulcer disease, gallbladder disease) (Lee, 2005).

EQUIVALENT SYMPTOMS

In addition to chest pain, other symptoms are frequently caused by myocardial ischemia. These symptoms are sometimes called "anginal equivalents," and they include:

• Shortness of breath, especially when it feels localized to the middle of the chest
• Weakness and tiredness
• Faintness or dizziness

These three symptoms are especially common in older (age >75 years) patients and in diabetic patients when they have episodes of heart ischemia.
Other general anginal equivalents are:

• No chest pain, but discomfort in the shoulders, inside (ulnar side) of the left arm, neck, or lower jaw
• Indigestion or nausea

Women are more likely than men to present with dyspnea, gastrointestinal complaints, or fatigue as the primary symptom of an acute coronary syndrome. When accompanying angina, certain additional symptoms signal potential emergencies. For example, chest pain with sweating and nausea or vomiting suggests myocardial infarction.

SILENT HEART ATTACKS

Not all people with heart ischemia have symptoms. Angina is a very common indicator of heart ischemia, and the characteristics described above are frequent and typical. Nonetheless, patients with all forms of CAD can have atypical feelings of chest discomfort or anginal equivalents. Moreover, ischemia severe enough to cause myocardial infarcts can occur without any chest pain, giving what are called silent heart attacks (asymptomatic heart ischemia).

Medical History

The medical history of people with coronary artery disease will suggest that they have or are at high risk for atherosclerosis (Lam 2005). Box 4 presents some elements in a person's medical history that should alert an interviewer to the possibility of atherosclerotic coronary artery disease.

HEART ISCHEMIA

When taking a medical history, the interviewer may find that atherosclerosis of the coronary arteries has already revealed itself. A patient with CAD may already have had episodes of heart ischemia, such as myocardial infarctions.

PERIPHERAL ARTERY DISEASE

Atherosclerosis is a whole-body disease. People with coronary artery disease will often have indications of atherosclerosis in arteries outside the heart. For example, they may have a history of intermittent claudication (a result of atherosclerosis in the leg arteries), strokes or transient ischemic attacks (results of atherosclerosis in the carotid arteries), or abdominal aortic aneurysms (results of atherosclerosis in the aorta).

LIPID ABNORMALITIES

High levels of blood lipids predispose a person to atherosclerosis. Specifically, high levels of LDL cholesterol can cause atherosclerosis, and a patient with CAD may already have a diagnosis of high cholesterol.

HYPERTENSION

High blood pressure is another major risk factor for developing atherosclerosis. For example, middle-aged men with blood pressures >169/95 are 5 times more likely to have atherosclerotic heart disease than middle-aged men without high blood pressures (<140/90). A patient with coronary artery disease may already be taking antihypertensive medicines.

DIABETES MELLITUS

Diabetes puts a patient at high risk of developing coronary artery disease. Diabetes—especially type 2 diabetes—tends to increase the level of blood cholesterol and to worsen atherosclerosis. Eighty percent of the people with type 2 diabetes die from some form of cardiovascular disease, and people with diabetes are more likely to have myocardial infarctions or strokes than people without diabetes. Moreover, people with diabetes are 100 times more likely to get atherosclerosis-induced gangrene of the feet than people without diabetes.

METABOLIC SYNDROME

Metabolic syndrome is the name for a cluster of five health problems that are frequently found together. The core problems are obesity and insulin resistance, and the additional three problems are high blood pressure and two lipid problems—high levels of triglycerides and low levels of HDL cholesterol. Having metabolic syndrome quintuples a person's chances of developing type 2 diabetes and also puts a person at high risk of developing serious atherosclerotic vascular disease with coronary artery blockage (Eckel et al. 2005; Wassink et al. 2007).

Family History

People are much more likely to develop coronary artery disease if they inherit a genetic propensity for the disease. A good indicator of this propensity is the existence of close (first-degree) relatives who have had an acute coronary syndrome, such as a myocardial infarction, at an early age. For men, this would be when they were younger than 45 years, and for women, it would be when they were younger than 55 years.

Social History

Two features of people's lifestyles put them at high risk for developing coronary artery disease, smoking and high-fat diets. Smoking one or more packs of cigarettes a day for several years doubles a person's chance of dying from coronary artery disease; however, a person who stops smoking can reduce this extra risk. Likewise, eating a diet high in cholesterol, saturated fats, and trans fats increases a person's chances of developing artery problems from atherosclerosis, while low-fat diets can reduce the risk.

Physical Examination

A person with coronary artery disease who comes to the emergency department (ED) with serious cardiac symptoms can show many abnormalities on physical examination. On the other hand, a person with coronary artery disease who comes to the clinic or office for a check-up may have only a few signs of the underlying disease. During a routine physical examination, the following findings would fit with a diagnosis of coronary artery disease (Singh & Deedwania, 2005).

WEIGHT

People with excess intra-abdominal or visceral fat (an "apple-shaped build") are more likely to have atherosclerotic cardiovascular disease (Gonzalez et al. 2007; Rasouli et al. 2007). Waist circumference is a good measure of intra-abdominal fat content: a waist circumference >102 cm (>40 in) in men or >88 cm (>35 in) in women is in the high-risk range.

VITAL SIGNS

During a routine office visit, the pulse may have a normal rate and rhythm in a person with coronary artery disease. Tachycardia is common, however, when a person is suffering from an episode of heart ischemia. Bradycardia during an acute coronary syndrome can be an ominous sign.
People with coronary artery disease often have hypertension (BP ≥140/90), and the higher the blood pressure, the greater the risk of heart disease. Hypotension during a myocardial infarction is an ominous sign.
The respiration rate is usually normal in a routine office visit, but people will breathe more rapidly under the stress of heart ischemia.

SKIN

No unusual sweating is expected on a routine office visit, but acute coronary syndromes, especially myocardial infarctions, are often accompanied by profuse sweating (diaphoresis).
Smoking is a strong risk factor for atherosclerosis, and patients with coronary artery disease may have nicotine stains on their fingers or teeth.

HEAD AND NECK

The blood vessels of the retina may show the effects of hypertension or atherosclerosis (i.e., widened light reflections from the arteries, copper- or silver-colored arteries, white sheaths along the arteries, venous tapering or "nicking" at arterial-venous crossings, hemorrhages, or papilledema). Diabetes, which worsens coronary artery disease, produces a characteristic retinopathy.
Atherosclerotic plaque can produce local blood turbulence, which will sometimes give a murmur or bruit that can be heard when listening to the carotid arteries.

THORAX

The pain of heart ischemia is usually diffuse and "somewhere inside." If a person's chest pain can be reproduced by the examiner pressing on some point along the chest wall, the pain is unlikely to be angina. (In some people with myocardial infarctions, however, broad regions of the chest become tender.)
On a routine exam, the lungs of a patient with coronary artery disease can be clear and unremarkable. With myocardial infarction, on the other hand, the patient may be breathing rapidly and may complain of shortness of breath. When ischemia has brought on some degree of heart failure, valve dysfunction, or arrhythmia, patients can have fluid in their lungs and rales can be heard.
A routine physical exam of a patient with coronary artery disease may find no overt heart problems. If the patient has a history of ischemic episodes, however, there may be a number of findings. Previous heart surgeries will have left chest scars. Hypertension or heart failure may have enlarged the heart. Murmurs suggest valve or papillary muscle damage, and gallops suggest heart wall damage. In addition, an ischemic heart is more susceptible to arrhythmias.

ABDOMEN

An abdominal aortic aneurysm usually indicates atherosclerosis. Likewise, bruits from other major abdominal arteries, such as the renal arteries, can be due to atherosclerosis.

EXTREMETIES

Leg edema may be from heart failure due to chronic ischemic heart disease. Atherosclerosis can give weakened peripheral pulses. Diabetes can produce neuropathies, which show up as a decrease in the patient's ability to sense stimuli in the feet.

Laboratory Studies

A patient being evaluated for coronary artery disease should be given a number of laboratory tests. Certain tests are especially helpful in assessing a patient's risk of serious heart damage from atherosclerosis. These include blood tests of lipid levels, fasting glucose levels, creatinine levels, and the possible presence of cardiac markers, which are indicators of recent heart cell damage (Bock 2006).

BLOOD LIPIDS

High serum cholesterol levels markedly increase a person's risk for developing atherosclerosis-induced heart injury. The LDL fraction of cholesterol is the specific culprit. The table below shows both healthy and unhealthy fasting blood lipid levels.

FASTING BLOOD LIPID LEVELS

Optimal Levels
Total cholesterol	< 200 mg/dl
HDL cholesterol	≥ 60 mg/dl
LDL cholesterol	< 100 mg/dl
Triglycerides	< 150 mg/dl
Unhealthy Levels
Total cholesterol	> 240 mg/dl
HDL cholesterol	< 40 mg/dl for men < 50 mg/dl for women
LDL cholesterol	> 160 mg/dl
Triglycerides	> 200 mg/dl

Patients with coronary artery disease often have one or more lipid levels in the unhealthy range (ACC/AHA, 2003).

FASTING PLASMA GLUCOSE

A person with diabetes has a higher than normal chance of developing coronary artery disease. Diabetes will manifest as a fasting plasma glucose level of ≥126 mg/dl when measured on at least two different days.

SERUM CREATININE

Renal disease worsens atherosclerosis. The level of creatinine in a person's blood can be used to screen for a number of kidney problems.

CARDIAC MARKERS

When heart muscle is damaged, intracellular molecules leak into the bloodstream. After a myocardial infarction, specific heart proteins, cardiac markers, can be detected in a patient's blood within hours and then for many days afterward. The standard cardiac markers are the cardiac troponin molecules. Other commonly measured proteins are the creatine kinase molecules. Cardiac markers are used for diagnosing and following emergency cardiac events and are not measured at routine checkups for coronary artery disease.

Electrocardiogram (ECG)

Twelve-lead electrocardiography (ECG) is the standard method for identifying arrhythmias and conduction problems. In terms of coronary artery disease, the ECG is a quick, accurate, and noninvasive way to recognize severe heart ischemia (Zevitz, 2006).
An acute coronary syndrome changes the electrical properties of a region of heart muscle and these changes can be seen in the ECG. The location of the ischemic heart region can often be identified by the particular segments of the wave pattern that have changed. The segments of the electrical wave pattern produced during a heartbeat have been named, and it is changes in the ST segment and in the T wave that are the clearest indicators of a myocardial infarction.
About one-quarter of patients with chronic stable angina will have a normal ECG wave pattern when they are resting. To determine the degree of heart ischemia that a patient with chronic stable angina suffers when the heart is stressed, an ECG can be taken while the patient exercises—typically, walking on a treadmill or pedaling a bicycle. However, not all patients with coronary artery disease show ECG changes during stress testing.

Stress Testing

Stress testing directly assesses the ability of a patient's heart to cope with exercise. A stress test is a controlled way to increase the workload of the heart, and stress tests are used to find the threshold beyond which coronary arteries cannot supply sufficient blood to meet the heart's oxygen needs. The lower the threshold (i.e., the smaller the stress) at which symptoms appear, the worse is the patient's coronary artery disease.
Stress tests can confirm that a patient's complaint of chest discomfort is actually anginal pain. The tests can also establish the level of activity that brings on chest discomfort. Subsequent stress tests can objectively monitor both the progression of the coronary artery disease and the efficacy of treatments (Akinpelu et al., 2006).
The preferred heart stressor is graded exercise, either walking on a treadmill or pedaling a stationary bicycle. When patients cannot tolerate exercise, their heart can be stressed with a vasodilator drug, such as dipyridamole or adenosine. A physician needs to be present at all stress tests, and the tests need to be tailored to the individual patient's health.

During a stress test, symptoms of heart problems—angina, shortness of breath, severe fatigue, lightheadedness, or fainting—usually appear when patients go beyond their exercise threshold. At the same threshold, signs of heart problems—gallops, arrhythmias, hypotension, inappropriate increases or decreases in heart rate, pulmonary rales, or cyanosis—will also appear.
In addition to watching for these symptoms and signs of cardiac problems, the stress test supervisor will use more-objective monitoring. The typical objective monitor is an ECG, which shows the rate and rhythm of the heart's electrical wave pattern but echocardiography can be used to follow changes in the heart's anatomy during exercise.
ECG stress testing is most useful when physicians are:

• Trying to make a diagnosis of coronary artery disease in an unclear case
• Measuring the exercise limitations imposed by a person's coronary artery disease

Approximately one-fifth of ECG stress tests give false positives, so the test is not recommended for routine examinations of people who are not likely to have coronary artery disease. At the other end of the spectrum, a similar percent of ECG stress tests give false negatives, and an ECG stress test that appears normal cannot be used to discard an otherwise convincing diagnosis of coronary artery disease (Lee, 2005).
The American College of Cardiology and the American Heart Association have jointly published guidelines for the use of ECG (ACC/AHA, 2002, 2003) and echocardiography (ACC/AHA/ASE, 2003) in stress-testing of patients with coronary artery disease.

Imaging

Pictures of the heart and the coronary arteries can be obtained in a variety of ways. The least invasive techniques are chest x-rays and echocardiograms. Another technique, coronary arteriography, produces excellent views of the coronary arteries, but it is an invasive procedure using arterial catheters (Mettler, 2005).

CHEST X-RAYS

A chest x-ray shows the size and shape of the heart and the condition of the lungs. Patients with coronary artery disease can have normal chest x-rays, and usually chest x-rays do not help to diagnose coronary artery disease. Sometimes, however, chest films will show consequences of the disease, such as heart enlargement, aortic aneurysms, aortic dissections, or pulmonary signs of heart failure.

ECHOCARDIOGRAPHY

An echocardiogram uses ultrasound to show the size and thickness of the atria and ventricles of the heart, and it also shows the heart valves in action. Used during stress testing for coronary artery disease, echocardiography can show which heart walls or valves are most affected by ischemic episodes. Echocardiographic stress tests are not recommended as screening tools, but many doctors use these tests to confirm a clinical diagnosis of coronary artery disease in unclear cases.

CORONARY ARTERIOGRAPHY

Coronary arteriography (also called coronary angiography or cardiac catheterization) uses x-rays to follow dye injected into the heart or the coronary arteries. Coronary arteriography gives as definitive a diagnosis of arterial narrowing and blockage as is possible without major surgery. Nonetheless, its high cost and its mortality rate (about 0.1%) and morbidity rate (1–5%) limit its use as a routine diagnostic tool. Currently, coronary arteriography is most often used in coronary artery disease patients when preparing them for possible bypass grafts or other heart operations. Coronary arteriography is also used when other tests cannot determine the cause of debilitating cardiac symptoms of ischemia.

TREATMENT

Two different treatment situations arise with coronary artery disease:

• A patient presenting for a routine outpatient visit without current chest pain, dyspnea, or other worrisome cardiac symptoms can be treated over a series of well-spaced visits.
• In contrast, a patient presenting with chest pain, dyspnea, profuse sweating, extreme fatigue, or other symptoms that may be caused by a life-threatening medical crisis needs to be seen in an emergency room and evaluated immediately.

Emergency Treatment

Unless patients have already been diagnosed with chronic stable angina and recognize that they are having a typical short-lived anginal attack, they should be taken to an emergency department whenever they have an episode of chest pain or chest discomfort.

IMMEDIATE LIFE-THREATENING CONDITIONS

When a patient is experiencing ischemic heart symptoms, it is a potential emergency. Cardiologists have detailed protocols for evaluating and treating acute coronary syndromes (ACC/AHA, 2004). However, the emergency department triage always begins with the steps shown below.
Older patients (age >75 years), diabetics, and female patients are more likely to present with the sudden onset of dyspnea and fatigue as the primary symptom of an acute coronary syndrome, and new dyspnea can be the equivalent of chest pain in these individuals (Brown & Hamilton, 2006).)

CHEST PAIN NEEDS QUICK EVALUATION

Fast treatment gives the best outcome for all heart attacks. In addition, certain types of heart attacks will benefit dramatically from quick reperfusion therapies, i.e., drugs and other techniques that open the blocked arteries and that restore blood flow. These heart attacks can usually be identified on an ECG by the abnormal elevation of the ST segments of the heart beat wave forms, and they are called ST elevation myocardial infarctions (STEMIs). The chances of a patient dying from a STEMI heart attack can be decreased by about half if the blocked arteries are reopened in the first 1 1/2 hours after the symptoms begin.

Quick reperfusion therapy will reduce the amount of permanent muscle damage resulting from a STEMI. Heart damage does not happen all at once after the blockage of a coronary artery. A myocardial infarct continues to enlarge over 5 to 6 hours if the blockage is not reduced or removed.

For these reasons, the National Heart Attack Alert Program (NHAAP) of the National Heart, Lung, and Blood Institute recommends that emergency rooms aim for reperfusion of STEMI heart attacks within 30 minutes of the first symptoms, with the goal of reducing heart attack mortality by about 75% (Brady et al., 2006).

BEFORE THE HOSPITAL

Because quick treatment of a heart attack is so beneficial, professionals who transport adults to the emergency room should always assume that chest pain or a sudden onset of dyspnea is a heart attack and should begin treatment en route. This means that the responder should assess and stabilize the patient and should set up an intravenous (IV) access line and a pulse oximetry monitor. Then the patient should be given supplemental oxygen. A conscious patient should chew and swallow 160 to 325 mg of aspirin. (Aspirin can also be given as a suppository.) If chest pain continues, the patient can usually be given sublingually or aerosolized nitroglycerin (Bybee & Kopecky, 2007).

IN THE EMERGENCY DEPARTMENT

Triage

After stabilizing patients, emergency rooms should put the patients into a triage protocol for chest pain/sudden dyspnea. It is important for the first person on the triage team to remember that one-third of people with acute myocardial infarction do not offer chest pain as their chief complaint. Certain people are more likely to give non-chest pain chief complaints, even when they are suffering a myocardial infarction. Atypical presentations tend to come from people with diabetes, older adults, women, people of nonwhite ethnicities, and people with dementia. Besides dyspnea, atypical chief complaints include nausea, profuse sweating, fainting, and pain in neck, shoulder, arms, or upper abdomen (Brady et al., 2006).
To begin the evaluation, a stabilized adult patient with chest pain/sudden dyspnea or other presentations consistent with heart ischemia should get an immediate 12-lead ECG to look for STEMI. It is thought that patients with STEMIs usually have a completely blocked artery, whereas patients whose infarctions do not produce ST-elevations have an incompletely blocked artery.
When STEMI is identified, a reperfusion plan should be formulated for the patient. The two major choices for reopening a blocked artery are pharmacologic and mechanical. The pharmacologic option is administration of a fibrinolytic drug (streptokinase, alteplase, reteplase, tenecteplase) to weaken and disrupt the damaging clot. The mechanical option consists of a percutaneous coronary intervention (PCI, also known as PTCA), meaning balloon angioplasty, with or without the placement of a stent, to break up or remove the clot.
Distinguishing STEMI from non-STEMI infarctions is important. Either type of reperfusion technique will benefit STEMI patients when done quickly. In contrast, while early reperfusion by PCI will help non-STEMI patients, the use of a fibrinolytic drug can be harmful (Brady et al., 2006). Patients without the characteristic ECG changes of STEMI may have either non-STEMI infarction or unstable angina.
All chest pain/sudden dyspnea patients need a chest x-ray, and these patients should be continuously monitored: their symptoms, vital signs, and blood oxygen levels should be checked repeatedly for signs of a worsening medical condition. Electrocardiograms should also be repeated.
Stabilized patients who are unlikely to have an acute coronary syndrome still need to be analyzed for the cause of their chest discomfort. Among the causes that should be considered are pneumonia, pulmonary embolism, pneumothorax, pericarditis, rib fracture, costochondral separation, esophageal spasm, aortic dissection, renal calculus, splenic infarction, abdominal disorders, or chest injuries.

Goals

For all patients with acute coronary syndromes, the general goals are:

• Open blocked arteries
• Increase the blood flow through constricted (stenotic) arteries
• Keep the unblocked arteries open
• Increase oxygen delivery using supplemental oxygen
• Reduce the oxygen needed by the heart by easing its workload
• Make the patient comfortable

While the type of acute coronary syndrome is being identified, a basic set of treatments are instituted to begin working toward these six goals.

Oxygen

Supplemental oxygen ensures that the existing blood supply is maximally oxygenated.

Medications

Antiplatelet drugs are a key treatment. Aspirin reduces the mortality from an acute myocardial infarction, and all conscious patients with a possible acute coronary syndrome should have chewed and swallowed 160 to 325 mg of nonenteric-coated aspirin. Aspirin can also be given as a suppository.
Vasodilators can increase blood flow to heart muscle and can reduce the force need to pump blood through the arterial system. The standard vasodilator for heart arteries is nitroglycerin, which can ease ischemic pain and can also reduce mortality rates. In emergency rooms, nitroglycerin is administered either sublingually, by spray, or via IV. (Certain patients, such as those with hypotension, require graded doses of nitroglycerin and careful monitoring.)
Beta-blockers, such as atenolol, esmolol, metoprolol or propranolol, are used to lessen the oxygen requirements of the heart by slowing the heart rate and lowering the arterial tension against which the heart is working. Beta-blockers also reduce the risk of developing heart arrhythmias, which can accompany heart ischemia. The use of beta-blockers has been shown to minimize the size of infarcts and to reduce mortality rates.
Anticoagulants can keep new blood clots from forming. Heparin and the low molecular weight heparins are often used to lower the risk that unstable angina will progress to myocardial infarction. Heparin administration requires careful monitoring for bleeding, and when the drug is stopped, the patient must be watched for "rebound" ischemic episodes that sometimes occur during the subsequent 24 hours.

Analgesics

Analgesics (pain relievers), such as morphine sulfate, reduce chest pain and also reduce the sympathetic nervous system's demands on the heart muscles.
Details of the management and care of acute coronary syndromes are given in standard texts, such as Brady and colleagues (2006) and Bybee and Kopecky (2007), and in professional guidelines, such as the ACC/AHA's Guidelines for Management of Patients with ST-Elevation Myocardial Infarction (ACC/AHA, 2006).

STABLE CORONARY ARTERY DISEASE

Some people who come to the emergency department with chest discomfort will have chronic stable angina instead of an acute coronary syndrome. As with all patients with possible heart ischemia, these people should receive aspirin, nitroglycerin, and supplemental oxygen and blood should be drawn to search for cardiac marker molecules.
When a 12-lead ECG is taken, people with chronic stable angina will have a normal or only minimally abnormal wave pattern. Their ECG and vital signs will remain unremarkable for the next few hours, and repeated blood tests will find no cardiac marker molecules.
In a person with chronic stable angina, the symptoms that brought them to the ED should resolve and not return over the 2 to 3 hours that they are being monitored. If a search for noncardiac causes of their chest discomfort identifies no serious problems, these patients do not need further medical treatment in the emergency department. Instead, they should be followed as an outpatient by a coronary artery disease treatment team (Lambert, 2007).

Long-Term Treatment

A patient who has coronary artery disease that does not need immediate treatment should be enrolled in a long-term treatment plan. These patients include people with chronic stable angina and people with stable coronary artery disease after having been treated for acute coronary syndromes.
Ideally, the patient's care will be taken on by a team of doctors, nurses, dieticians, and therapists who will see the patient regularly. For patients recovering from myocardial infarctions or surgical cardiac procedures, the team should include cardiac rehabilitation specialists.
Each patient is different, and each will need an individualized treatment program. Such programs should include reassurance, medicines, therapeutic lifestyle changes, possible revascularization (reperfusion) surgery, and treatment of associated disorders (Selwyn & Braunwald, 2005).

REASSURANCE AND GUIDANCE

Many patients with coronary artery disease, and especially those who have had a myocardial infarction or heart surgery, become fearful of exercise. The first step in reassuring patients is to educate them about the disease in general and their condition in particular.
General advice should include a review of the symptoms of ischemia, rules on managing an episode of angina or dyspnea, and an explanation of what symptoms require a quick trip to an emergency room. The patient's family should be told these things too.
After a hospitalization, patients should enroll in a cardiac rehabilitation program. Comprehensive programs that include exercise, education, counseling, and help with lifestyle changes can increase exercise tolerance, decrease symptoms (such as angina and shortness of breath), improve blood lipid levels, reduce stress, make it easier to stop smoking, and improve the patient's mood. Patients with signs and symptoms of depression are less likely to complete their cardiac rehabilitation programs, and it is important to identify these patients and to get the appropriate help for them early in the program (Caulin-Glaser et al., 2007).
Health counselors should also advise patients as to how much exercise they can undertake in their daily lives. Exercise tests can be used to develop specific guidance for each patient (Davis, 2002; CFPC, 2007). Typical advice is:

• Daily walking can be encouraged immediately.
• If the hospitalization included no serious complications, patients can often resume their previous level of sexual activity in two to four weeks, depending on their tolerance for exercise. One simple test is: patients who can walk rapidly up and down two flights of stairs without heart symptoms are ready for sexual activity.
• Non-stressful driving can usually be resumed within a week (in those states that allow it).

Health workers should also help patients decide to when to return to work.
Most coronary artery disease patients have less sexual desire, and men can develop impotence. Doctors should take the initiative in discussing these problems. Sometimes, the patients or their partners feel they need explicit medical permission to resume sexual activities.
Heart patients with symptoms of depression have a higher mortality rate. At each visit, health care workers should ask about mood, appetite, sleeping, ability to concentrate, and enthusiasm for life. If symptoms of depression show up, patients should be referred to a mental health professional.

MEDICATIONS

Drug therapy is a key part of the treatment of coronary artery disease (ACC/AHA, 2003). To reduce the likelihood of developing obstructive clots, patients who have coronary artery disease or who are at high risk of developing coronary artery disease should take antiplatelet drugs daily. To lessen the work of the heart, most patients with coronary artery disease also take beta-blockers. For relief of angina, nitrates are prescribed.
Medications are essential to the care of heart patients. The approximately 10% of patients with coronary artery disease who do not take their prescribed medications regularly are twice as likely to develop acute coronary syndromes. By asking patients at each visit whether they are taking their medicines all the time, it is possible to intervene and to lower the risk of serious complications (Gehi et al., 2007).

Aspirin

Long-term antiplatelet therapy makes acute ischemic episodes less likely in all forms of coronary artery disease. Aspirin is the first-line antiplatelet drug, unless the patient has aspirin allergy or gastrointestinal bleeding. The dose is typically between 75 and 325 mg/day.
Daily aspirin should be continued indefinitely, but after a year, the dose should be lowered into the 75 to 162 mg/day range (ACC/AHA, 2006). Clopidogrel (Plavix) can be added to increase the inhibition of clot formation, and it can be given to patients when aspirin is contraindicated.

Nitroglycerin

Nitrates, such as nitroglycerin, dilate blood vessels throughout the body. By lowering the arterial resistance to blood flow, nitrates ease the work of the heart, and by dilating heart arteries, they increase the blood flow to the heart muscles.
Nitroglycerin relieves the pain of angina, and if taken approximately 5 minutes before exercise or stress, it can prevent angina. The nitroglycerin in sublingual tablets is absorbed quickly and completely, and it generally works within 2 to 3 minutes and lasts for 1/2 hour. All patients with angina should be given sublingual nitroglycerin with specific instructions about its use. Nitroglycerin is also available as an oral spray and as long-lasting tablets and patches.

Beta Blockers

Beta adrenergic blockers are antihypertensive drugs that also reduce heart rate and heart muscle tension, and in these ways, they reduce the heart's demand for oxygen. Beta blockers will lower the incidence of episodes of angina, and they will also reduce the likelihood of myocardial infarctions and death in coronary artery disease patients.
Special care must be taken when prescribing beta blockers to patients with asthma, other obstructive airway conditions (COPD), intermittent claudication, insulin-requiring diabetes, certain heart conduction problems, and clinical depression. When the side-effects of beta blockers become a problem, calcium channel blockers, such as diltiazem or verapamil, can be substituted. In patients who have had acute coronary syndromes or left ventricular weakness, beta blockers should be continued indefinitely (ACC/AHA, 2006).

ACE Inhibitors

Angiotensin-converting enzyme (ACE) inhibitors, such as ramipril (Altace), are antihypertensive drugs that can reduce the likelihood of acute ischemic episodes, strokes, and death in patients with coronary artery disease. ACE inhibitors are recommended for all coronary artery disease patients with diabetes or with a poorly functioning left ventricle (ACC/AHA 3003).

Statins

Lipid-lowering drugs are frequently prescribed for people with coronary artery disease. High levels of LDL cholesterol initiate and worsen atherosclerosis. In patients with high blood levels of cholesterol, the first medical intervention is lifestyle changes, especially a low-fat diet and increased exercise. (See Lifestyle Therapy, below.) When this does not lower a patient's cholesterol to safe levels, lipid-lowering drugs are prescribed. Statins, such as atorvastatin (Lipitor) and simvastatin (Zocor), are the preferred lipid-lowering drugs for coronary artery disease, but some lipid abnormalities should be treated with nicotinic acid or fibric acid (ACC/AHA, 2003). (Patients with liver disease should not take statins.)

LIFESTYLE CHANGES

For patients with coronary artery disease, lifestyle changes will improve their quality of life and their sense of well-being as well as slowing or even reversing their illness. Reducing dietary calories and fats (especially saturated fats) and increasing exercise can significantly reduce one's risk of developing diabetes and atherosclerotic cardiovascular disease. Therapeutic lifestyle changes are also the cornerstones of the treatment of obesity, hypertension, insulin resistance, and most dyslipidemias. Lifestyle changes are difficult to maintain, and they require that patients truly believe that the results are worth the effort (Singh & Deedwania, 2005).

Stop Smoking

Smoking injures cells throughout the body. Smoking contributes to the development of atherosclerotic cardiovascular disease, insulin resistance, type 2 diabetes, dyslipidemia, a variety of cancers, many lung diseases, gastrointestinal diseases, reproductive problems, osteoporosis, cataracts, age-related macular degeneration, and hypothyroidism.
Cigarette smoking is one of the most powerful predictors for the development of coronary artery disease in all age groups. In patients who already have coronary artery disease, smoking is associated with a higher likelihood of myocardial infarction and of sudden cardiac death.
Explain the medical consequences to patients who smoke, and strongly recommend that they stop smoking. It is difficult for smokers to quit on their own. Make an agreement with your patients that on a specific date they will begin to wean themselves from cigarettes. Then help them get into a program that includes support, counseling, and the availability of anti-smoking medications.

Exercise Regularly

Regular exercise at an appropriate level improves the body's metabolism as well as conditioning the heart muscles. Physical conditioning from a regular exercise program generally increases the amount of activity a patient can do before developing chest discomfort. Physical exercise helps in losing weight and in maintaining weight loss. It also makes smoking cessation easier, improves lipid levels, lowers blood pressure, and increases the patient's feeling of well-being. Better physical conditioning improves a person's chances of surviving a myocardial infarction.
Formal cardiac exercise programs are supervised and tailored to the abilities of the patient, and these programs increase exercise levels appropriately but gradually. In such programs, stress testing is often used as a guide when planning a safe level of exercise for a patient. Planned programs are ideal, but even the addition of light everyday exercise to a sedentary life can reduce mortality rates.

Keep Weight Low

As ideal goals, a patient's body mass should be between 18.5 and 24.9 kg/m2 and the waist circumference should be less than 102 cm (40 inches) for men and less than 88 cm (35 inches) for women. Excess weight strains the heart, and excess fat leads to continuous high levels of blood lipids. Weight loss improves blood lipid profiles and helps lower blood pressure in overweight and obese people. For coronary artery disease patients who are overweight, weight loss can reduce the severity of their angina (Bogers et al., 2007).
Exercise alone rarely leads to significant weight loss; a reduced calorie diet is necessary. Reducing patients' overall calorie intake will also improve their lipid profile. Besides eating fewer calories, scheduled meals and preplanned menus make weight loss easier. Weight loss programs include these and other techniques, and formal programs with regular advice, counseling, and supervision usually have the most success. From any starting weight, a loss of 10% should be considered a success if the patient manages to maintain the lower weight (ACC/AHA, 2006).

Eat a Low-Fat Diet

Eating nutritiously will slow the development of atherosclerosis. Simply reducing the overall calories in a patient's diet will improve their lipid profile, and reducing the amount of fat will improve lipid levels even further.
For a heart-healthy diet, it is especially important to remove foods that are high in saturated fats and trans fats. Instead, diets should be filled with fruit, vegetables, and whole grains. In addition, daily plant sterols and 10 to 25 g/day of soluble fiber (oat bran, beans, soy products, psyllium) are recommended. An ounce of alcohol taken 5 to 6 times a week as beer, wine, or hard liquor has been found to reduce the risk of mortality from coronary artery disease.

NUTRIENT COMPOSTION OF THERAPEUTIC LIFESTYLE CHANGE DIET

Nutrient	Recommended Intake
Source: NHLBI, 2004.
Saturated fat	Less than 7% of total calories
Polyunsaturated fat	Up to 10% of total calories
Monounsaturated fat	Up to 20% of total calories
Total fat	25-35% of total calories
Carbohydrate	50-60% of total calories
Fiber	20-30 grams per day
Protein	Approximately 15% of total calories
Cholesterol	Less than 200 mg/day
Total calories (energy)	Balance energy intake and expenditure to maintain desirable body weight/prevent weight gain

Oral heath problems can indirectly increase the risk of developing cardiovascular disease. People with mouth problems, such as cavities, sore gums, periodontal disease, and missing teeth prefer to eat soft foods, which are low in fiber. Dental care and tooth replacement are an often-forgotten part of improving a patient's diet.

Adapt Daily Activities

Patients can control their angina by the way they live their daily lives. Heart ischemia is brought on when heart muscle is asked to work hard. Many tasks that cause chest pain can be done without discomfort simply by doing them more slowly or in smaller chunks. Walking, climbing stairs, vacuuming, raking, and lifting can all be done in a more leisurely way. Washing, carrying, and lifting should be done with fewer items. In their jobs, heart patients may have to learn to allot more time to each task.
Patients should be taught the basics of their disease. They should learn that their sensitivity to ischemia will vary during the day (for example, angina is more likely in the early morning and just after meals) and according to the weather (cold weather is more stressful).
For some people, anger, frustration, and other strong emotions can cause ischemic episodes. These patients need help in calming their emotions, and they should be referred to therapy programs that emphasize behavioral modification and that provide practical coping techniques for stressful situations. In addition, relaxation techniques, mental focusing strategies, and yoga have all proven useful in reducing stress for patients with coronary artery disease (Littman, 2004).

Surgery

The basic treatment of stable coronary artery disease is medical therapy and lifestyle modification. In some cases, surgery to increase blood flow to ischemic areas can be added to the treatment program to improve a patient's heart functioning. The general term for these procedures is coronary revascularization surgery, and such surgeries are commonly done throughout the United States.
In general, coronary revascularization surgery should be considered for patients who still have debilitating angina after optimal medical therapy. The two types of procedures are percutaneous coronary interventions (PCI) and coronary artery bypass grafts (CABG). Percutaneous coronary intervention is usually advised for patients with significant narrowing of one, two, or—at most—three major coronary arteries when the left ventricle is functioning normally; CABG is advised for patients with more than two arterial constrictions, with weakened left ventricles, or with diabetes.
There are other therapies for patients whose medical treatment does not improve the symptoms of their coronary artery disease but who are not good candidates for either PCI or CABG. The alternatives include laser transmyocardial revascularization (an experimental surgical technique), enhanced external counterpulsation to reduce the frequency of angina, and spinal cord stimulation to relieve the pain of angina (ACC/AHA, 2003).

PERCUTANEOUS CORONARY INTERVENTION (PCI)

Percutaneous coronary interventions are used to unclog blocked coronary arteries. The procedure involves threading a catheter into the constricted region of an artery and expanding a balloon to flatten the plaque back against the walls of the artery. Usually, a wire mesh support, called a stent, is left in the region to hold the artery open. Typically, the PCI catheter is inserted through the femoral artery under local anesthesia, and the procedure takes between 30 minutes and 2 hours.
PCI gives a sufficient increase in blood flow to initially reduce angina in >95% of cases. Approximately one-fifth of treated arteries narrow again within 6 months, and angina returns within 6 months in about 1 of 10 patients (Lambert, 2007).

CORONARY ARTERY BYPASS GRAFTING (CABG)

Coronary artery bypass surgery is the most common open-heart operation performed in the United States. The procedure involves attaching an unclogged blood vessel to a blocked coronary artery beyond the obstruction. One or both internal thoracic (also called internal mammary) arteries can be rerouted, or a piece of the saphenous vein or the radial artery can be made into a conduit. The surgery is done under general anesthesia and takes between 3 and 6 hours. Usually, the procedure is done by temporarily stopping the heart and oxygenating the blood with a cardiopulmonary bypass machine. When patients have no other serious disease, there is <1% mortality from a first-time CABG surgery.

CABG reduces angina in more than 90% of cases. When a vein is used as the bypass conduit, between 1 in 10 and 1 in 5 bypasses become obstructed within a year. When arteries are used as the bypass conduits, the rate of reobstruction is less. Angina of a milder degree returns within 3 years in approximately 1 in 4 CABG patients.

Treat Associated Diseases

DIABETES

People with diabetes have a higher incidence of atherosclerotic heart and artery disease than people without diabetes, and 80% of the people with type 2 diabetes die from some form of cardiovascular disease. All coronary artery disease patients with diabetes should be enrolled in a comprehensive diabetes management program. A reasonable goal for a patient with diabetes is to reduce their glycosylated hemoglobin (A1C) level to below 7%.

HYPERLIPIDEMIA

Even a mildly elevated blood level (fasting level >100 mg/dl) of LDL cholesterol gives a person with coronary artery disease a higher risk for myocardial infarctions and sudden cardiac death. Therefore, any degree of hyperlipidemia should be treated in these people.
Besides lifestyle changes, treatment of hyperlipidemia frequently requires medication. Statins are the recommended drugs for treating high levels of  LDL cholesterol, except in people with liver disease. When needed, niacin is added, and further reductions can be achieved by adding fibrates. People with coronary artery disease should aim for LDL levels of <70 mg/dl (ACC/AHA, 2006).

HYPERTENSION

High blood pressure contributes to and worsens atherosclerosis. In a person with coronary artery disease, the goal is to reduce blood pressure to below 130/80 mm Hg. The lifestyle changes recommended for coronary artery disease—smoking cessation, regular physical exercise, weight management, improved diet, and stress reduction—will all lower blood pressure. If these do not reduce a patient's blood pressure sufficiently, then medicines should be added. Beta blockers are basic drugs for all patients with coronary artery disease, and these agents can also be used to treat hypertension; ACE inhibitors are also used to treat coronary artery disease, and these, too, can be used to treat hypertension.

DEPRESSION

People with clinical depression or with symptoms of depression have a higher incidence of myocardial infarction, poorer recovery, and a higher rate of mortality (Musselman, 2004; Ahto et al., 2007; Janszky et al., 2007). Psychotherapy, behavioral therapy, and serotonin reuptake inhibitors (SSRIs, which are safe to administer after an acute coronary syndrome) have been shown to reduce mortality and to improve recovery from myocardial infarctions (Pasternak, 2005).

INFLUENZA IMMUNIZATION

Patients with cardiovascular disease should get a yearly flu shot (ACC/AHA, 2006).

PROGNOSIS

A person with any form of coronary artery disease has a higher chance of dying when the left ventricle of the heart has been weakened. Signs of a failing left ventricle include an enlarged heart, pulmonary edema, leg and ankle edema, jugular venous distension, or a third heart sound (S₃).
Previous myocardial infarctions weaken the heart, so a history of past heart attacks also worsens a patient's prognosis (Warnica, 2005; Brady et al., 2006; Bybee & Kopecky, 2007).

Chronic Stable Angina

Patients who have chronic stable angina with

• No history of myocardial infarction
• A normal resting ECG
• Normal blood pressure

have a mortality rate of approximately 1.4% per year.
Systolic hypertension raises the mortality rate to 7.5%, an abnormal ECG raises the rate to 8.4%, and the two together raise the rate to 12%. Diabetes doubles all these rates.

Acute Coronary Syndromes

UNSTABLE ANGINA

Unstable angina is sometimes called pre-infarction. About 30% of patients who develop unstable angina have a myocardial infarction within 3 months. Unstable angina has a mortality rate of about 4% per year.

MYOCARDIAL INFARCTION

Heart attacks are the cause of most deaths from coronary artery disease. Thirty percent of myocardial infarctions are fatal, with half of those fatalities occurring before the patient reaches the hospital. Of the patients with a myocardial infarction who get to a hospital alive, about 10% die in the hospital. Patients who survive a myocardial infarction have an 8% to 10% chance of dying within a year, and most of these fatalities occur in the first 4 months after their hospitalization. Larger areas of heart injury lead to higher mortality rates (Roes, 2007).

PREVENTION

Many of the things that contribute to atherosclerosis can be eliminated from our lives. All patients should be encouraged to reduce their likelihood of developing symptomatic coronary artery disease by modifying their risk factors. There is a genetic predisposition for coronary artery disease, and those patients with a family history of early heart attacks or sudden cardiac death need to be strongly advised to work on reducing their risk factors (Maron et al., 2005; Selwyn & Braunwald, 2005; Zevitz, 2006).
Coronary artery disease is a chronic disease that becomes more likely to cause problems as a person ages. Typically, atherosclerosis has its beginnings in the childhood or teenage years and worsens gradually. There are decades during which changes in a person's life can reduce their likelihood of developing symptomatic coronary artery disease. During these years, six aspects of a person's life should be targeted to reduce the risk of coronary artery disease: smoking, weight, blood pressure, diabetes, blood lipids, and physical activity. In addition, adults who are at moderate or high risk of developing coronary artery disease should probably be taking an antiplatelet medication.
The recommendations are somewhat different for people who only have a low risk of developing coronary artery disease. Lifestyle modifications can benefit almost anyone. On the other hand, low-risk people usually do not need to take daily aspirin, and they do not necessarily need to use lipid-lowering medications if their LDL cholesterol blood level is below 160 mg/dl (NECP, 2004).

Stop Smoking

Cigarette smoking worsens coronary atherosclerosis and increases the risk of lung disease, cancer, myocardial infarction, and death. Within a year of quitting smoking, a patient's risk of acute coronary syndromes drops almost to the level of a nonsmoker. Becoming a nonsmoker also lengthens a person's life; for example, 35-year-old smokers who quit smoking increase their lifespan by 3 to 5 years. Therefore, strongly urge patients to quit smoking and help them to enroll in a smoking cessation program. In addition, advise patients to avoid spending time in places where other people smoke (ACC/AHA, 2006).

Exercise Regularly

Physical inactivity doubles a person's risk of developing symptomatic coronary artery disease. Moderate exercise is sufficient to improve blood lipid levels, reduce blood pressure, reduce obesity, lower insulin resistance, decrease the prothrombotic state, and decrease the likelihood of acute coronary syndromes. People without symptoms of coronary artery disease should aim for 30-minute exercise sessions on three or four different days each week. Moderate exercise is equivalent to a brisk walk.

Keep Weight Low

Obesity worsens coronary atherosclerosis and increases the risk of death from cardiovascular causes (Bogers et al., 2007). Obesity is also strongly linked to other problems that worsen coronary artery disease, specifically, insulin resistance, type 2 diabetes, hypertension, dyslipidemia, pro-inflammatory conditions, prothrombotic conditions, and left ventricular hypertrophy.
The body mass index (BMI) is used as a standard measure of body fat. Obesity is defined as a BMI ≥30 kg/m². To reduce the risk of coronary artery disease, a patient should aim for a BMI < 25 kg/m². People with excess intra-abdominal fat have an even greater risk of cardiovascular problems. A waist circumference of > 102 cm (40 in) for men and > 88 cm (35 in) for women indicates sufficient intra-abdominal fat to pose a high risk of coronary artery disease.
Weight-loss diets work best when part of a formal program that includes regular exercise, meal planning, behavioral counseling, and frequent meetings with an advisor or coach. Lost weight is often regained if a person leaves the weight loss program.
People who stop smoking typically gain 2 to 3 kg (4.5–7 lb). Smoking is the worse of the two problems, and stopping smoking should have the higher priority.

Eat a Low-Fat Diet

A heart-healthy diet is low in fats. Thirty percent or less of the day's total calories should come from fat, and only 7% of the day's total calories should come from saturated fat. A person's diet should include less than 200 mg of cholesterol a day and less than 2400 mg of sodium (table salt) a day. Trans fats should be eliminated entirely. People need to watch their total calories and limit them to just enough to maintain a healthy weight.

Keep Cholesterol Levels Low

High levels of LDL cholesterol appear to cause, and worsen, atherosclerosis. The National Cholesterol Education Program (NCEP, 2001, 2004) gives detailed guidelines for reducing blood levels of lipids in people with coronary artery disease. The general preventive recommendations for people who are at risk for developing coronary artery disease are: LDL cholesterol < 100 mg/dl, HDL cholesterol ≥ 35 mg/dl, and triglycerides < 200 mg/dl.
Medications (notably, statins) are frequently used to improve blood lipid levels. Equally important are increases in regular physical exercise, weight control, and a low-fat diet. Omega-3 fatty acids (in the form of fish or as capsules) are a recommended form of dietary fats (ACC/AHA, 2006).

Keep Blood Pressure Low

Hypertension worsens coronary artery disease and can cause strokes, heart failure, and kidney failure. Hypertension is also strongly linked to insulin resistance, obesity, dyslipidemia, and left ventricular hypertrophy.
Hypertension is defined as blood pressure ≥140/90 mm Hg. The treatment goal for people with the potential of developing symptomatic coronary artery disease is a blood pressure <130/80 mm Hg. Lower blood pressures appear to reduce the coronary artery disease risk even further. Besides lifestyle changes, many people need medicines (beta blockers or ACE inhibitors, adding thiazides if necessary) to lower their blood pressures to healthy levels (ACC/AHA, 2006).

Control Diabetes

Diabetes worsens atherosclerosis and increases the risk of death from cardiovascular causes. All forms of diabetes are strongly linked to dyslipidemia, and beyond this, type 2 diabetes includes insulin resistance. The presence of diabetes alone gives a person the same risk of developing an acute coronary syndrome as a diagnosis of coronary artery disease.
Diabetes is defined as a fasting plasma glucose level of ≥126 mg/dl, documented on at least two separate days. Diabetes should be managed using a comprehensive long-term plan including lifestyle changes, careful meal planning, and medications. The treatment goals are:

• Maintain fasting glucose levels below 110 mg/dl
• Maintain glycosylated hemoglobin (A1C) levels below 7.0%

Take Daily Aspirin

When taken regularly, a small amount of antiplatelet medication helps to reduce the likelihood of developing blood clots. Men with a moderate to high risk of developing coronary artery disease should take a daily antiplatelet drug prophylactically. In high-risk women, aspirin is also recommended, but for other women aspirin is prescribed more cautiously than for men (Mosca et al., 2007). Enteric-coated aspirin is the recommended form of the drug, and the preventive dose is usually 75 to 160 mg/day.

Consider Daily Alcohol

Studies have confirmed that approximately one ounce of alcohol (in any form—beer, wine, or spirits) per day reduces the risk of developing coronary artery disease (O'Keefe et al., 2007). This recommendation is always tempered by the fact that drinking more than an ounce of alcohol daily can increase the risk of dying from a variety of causes. Therefore, doctors do not recommend daily alcohol to people who have a history of heavy drinking or who may have the propensity to become a heavy drinker. Alcohol should not be recommended for people with liver disease, pancreatic disease, heart failure, unexplained heart problems, or degenerative neurologic disorders. Pregnant women should not drink alcohol.

About Hormone Replacement Therapy

Currently, hormone replacement therapy is not recommended for postmenopausal women when the only goal of the therapy is to reduce the woman's risk of developing cardiovascular disease (Mosca et al., 2007).

TELEPHONE COUNSELING

Nurses and other professionals who advise patients over the telephone should know straightforward answers to basic questions. Here are a few important questions and answers about coronary artery disease.

Advice and Triage Questions

Informational Questions

At one time, vitamin E supplements were recommended to protect people's hearts. More recently, however, it was found that vitamin E supplements should not be taken to prevent or to treat coronary artery disease