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COURSE OBJECTIVE: The purpose of this course is to present an up-to-date discussion of coronary artery disease, including its prevalence, pathophysiology, medical evaluation, acute treatment and long-term management, and prevention.
Upon completion of this course, you will be able to:
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.
The 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 an 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 deliver 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 (WHO, 2007). In the United States, it is estimated that nearly 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 (Lloyd-Jones et al., 2010).
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 (Boudi, 2012; Lloyd-Jones, 2010).
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 developing world (Boutayeb & Boutayeb, 2005).
Coronary artery disease (CAD) is the result of atherosclerosis of the coronary arteries of the heart. Coronary artery disease is also called:
The main forms of coronary artery disease are:
The three main acute coronary syndromes are:
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.
A drawing of the heart, seen from the front. The coronary arteries and their main branches are large, and they run along the outer surface of the heart. The smaller arteries, which directly feed the heart muscle, dive deep into the walls of the heart. (Source: NHLBI, 2011b.)
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, 2011).
A common finding in coronary artery disease is collateral circulation, the development of additional arteries that form a natural bypass from one side of a blocked artery to the other. Research suggests that coronary collateral circulation may help to reduce ischemia, preserve ventricular function, and improve prognosis in patients with coronary artery disease (Berry et al., 2007).
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.
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.
The blood flow through the heart usually keeps up with the body’s 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 (Depre et al., 2011). Normally, the extra oxygen needed during exercise is supplied by a faster and a more voluminous blood flow through the coronary arteries.
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.
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 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.
Heart ischemia occurs when the increases in blood flow and blood volume are insufficient to supply all the oxygen needed by the heart muscle.
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, 2010).
When the blood flow is entirely stopped to a region of the heart, the muscle cells stop working almost immediately. The muscle can recover, however, if blood flow is restored in less than a half-hour. (Source: Adapted from Schoen, 2010.)
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.
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 lower part of the neck, jaw, shoulder, or back, or down the ulnar side (inside) of the left arm; in some cases the feeling can radiate to either or both arms. In some people, the discomfort of angina is mild, but other people get diffuse unbearable pain (Depre et al., 2011; Moran, 2009).
Although women tend to visit their physicians more often than men and therefore report more symptoms, including chest pain, their angina symptoms usually present in the form of upper abdominal discomfort, neck or jaw pain, or shortness of breath as opposed to crushing or squeezing chest pain. Women are also more likely than men to associate their angina with emotional or mental stress (Charney, 2011).
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:
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.
Coronary artery disease 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.
The heart damage in coronary artery disease ranges from narrowing of a coronary artery to complete blockage of a coronary artery. (Source: NHLBI, 2011c.)
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 atherosclerosis, fat and cells collect in bulges just below the surface of the lining of arteries. These bulges are called plaques. Over time, the plaques thicken and reduce the inner diameter of the arteries, allowing less blood to get to tissues beyond the plaques. (Source: NHLBI, 2011a.)
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, 2008; Libby, 2008).
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 is said to have 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.
The hallmarks of atherosclerosis are atherosclerotic plaques, which develop slowly and in three stages.
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.
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.
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.
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 & Fuster, 2011).
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, age, sex, physical inactivity, and obesity (Boudi, 2011).
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 & Fuster, 2011).
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 comfortably 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 (Antman et al., 2008b).
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, 2010).
Chronic Coronary Syndromes
Acute 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, 2010; Antman et al., 2008b).
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 two thirds to three fourths 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.
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.
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.
An acute coronary syndrome needs immediate treatment in a prepared emergency room (Kim et al., 2011). People with the highest risk of developing an acute coronary syndrome are those who already have serious cardiovascular disease or diabetes.
Similarly to other types of heart disease, risk factors for acute coronary syndromes include:
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% to 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.
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., 2009).
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, 2011).
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 symptomless 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 (Boudi, 2012).
In the United States, approximately 14 million people experience coronary artery disease and its various complications. Age is the strongest risk factor for coronary artery disease; most cases occur in patients aged 40 years or older, although mortality and morbidity are higher in the elderly. More than 80% of people who die of coronary artery disease are aged 65 years or older (Boudi, 2012; Lloyd-Jones 2010).
Percent of U.S. population with CAD, by age group. (Source: Adapted from Lloyd-Jones, 2010.)
Overall, coronary artery disease is slightly more common in men than in women: in the United States, 9.1% of men and 7.0% of women have the disease. Women tend to develop symptomatic coronary artery disease about 10 years later than men. In the United States, men over 40 years of age have a 49% chance of developing the disease in their lifetime, while the chance for women over the age of 40 years is 32% (Boudi, 2012; Lloyd-Jones et al., 2010). 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.
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. This racial disparity is also thought to result from the fact that African Americans, on average, tend to seek treatment later than European Americans and are less likely to receive invasive treatment (Boudi, 2012).
Americans of Asian Indian origin are 2 to 3 times as likely as European Americans to develop coronary artery disease (Boudi, 2012). On the other hand, coronary artery disease is less common in Hispanic and Latino Americans, as well as in Asian Americans not of Indian origin, than in European Americans (Lloyd-Jones et al., 2010).
When a man 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.
By contrast, a woman with coronary artery disease is more likely to complain of nausea or abdominal discomfort, neck or jaw pain, or shortness of breath rather than the more “classical” symptom of crushing chest pain. Coronary ischemia should therefore be considered in women who appear to be acutely ill even if they do not complain of chest pain (Charney, 2011).
Chest discomfort is a key identifying symptom of coronary artery disease, particularly in men. 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 with chest pain has angina.
Here is how a patient with coronary artery disease typically answers these questions.
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.”
Women with angina may describe the feeling as uncomfortable pressure, squeezing, fullness, or pain in the center of the chest (AHA, 2012).
Levine’s sign. Patients often clench their fists to describe the feeling of anginal pain.
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.
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. Additionally, women with angina may complain of pain or discomfort in the abdominal area.
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.
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.
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 second), 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.
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.
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).
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 similar rating systems for classifying anginal pain. In these systems, 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:
Ernest Brown is a 55-year-old African American male with diabetes that is well controlled with medication. He has had occasional, transient episodes of chest tightness over the last two weeks, and the tightness returned one day while he was pushing a wheelbarrow full of leaves up a slight incline in his yard. Since the pain didn’t seem to be going away, he decided to call his doctor.
The doctor’s receptionist had Ernest speak with the nurse, who asked Ernest about the quality and location of the chest tightness. Ernest replied that the tightness felt like a band across the center of his chest, with pain radiating through his left arm for a few seconds before subsiding. He added that this particular episode of chest tightness was triggered by exertion while doing yard work, and that he had had a couple of recent episodes while walking briskly uphill.
The nurse, suspecting that Ernest’s angina might be a sign of an imminent heart attack, told him to hang up, dial 911, and tell the dispatcher he thought he might be having a heart attack. Ernest did so, and an ambulance arrived at his home within 10 minutes. The ambulance whisked him to the emergency room, where a team of physicians and nurses was waiting to administer the emergency department protocol for a suspected myocardial infarction.
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).
In addition to chest pain, other symptoms are frequently caused by myocardial ischemia. These symptoms are sometimes called “anginal equivalents,” and they include:
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:
Importantly, health professionals should be alert to the fact that women are more likely than men to present with dyspnea, gastrointestinal complaints, back or jaw pain, or fatigue as the primary symptom of an acute coronary syndrome (AHA, 2012).
When accompanying angina, certain additional symptoms signal potential emergencies. For example, chest pain with sweating and nausea or vomiting suggests myocardial infarction.
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).
The medical history of people with coronary artery disease will suggest that they have or are at high risk for atherosclerosis (Lam, 2008). The box below presents some elements in a person’s medical history that should alert an interviewer to the possibility of atherosclerotic coronary artery disease.
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.
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).
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.
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 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. Nearly 70% of people with diabetes die from some form of cardiovascular disease, and people with diabetes are 2 to 4 times more likely to have heart disease or a stroke than people without diabetes (CDC, 2011a; AHA, 2010a).
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, 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).
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.
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.
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 (Boudi, 2012).
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.
Subcutaneous fat lies just under the skin. Visceral fat is inside the abdomen, surrounding the abdominal organs. Visceral fat is more likely to contribute to coronary artery disease than is subcutaneous fat. (Source: NHLBI.)
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.
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.
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.
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.
An abdominal aortic aneurysm usually indicates atherosclerosis. Likewise, bruits from other major abdominal arteries, such as the renal arteries, can be due to atherosclerosis.
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.
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, hemoglobin A1c, creatinine levels, and the possible presence of cardiac markers, which are indicators of recent heart cell damage (Bock, 2006; Boudi, 2012).
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 box below shows both healthy and unhealthy fasting blood lipid levels. Patients with coronary artery disease often have one or more lipid levels in the unhealthy range (Gibbons et al., 2003).
|Type||Optimal Levels||Unhealthy Levels|
|Total cholesterol||<200 mg/dl||>240 mg/dl|
|HDL cholesterol||≥60 mg/dl||<40 mg/dl for men
<50 mg/dl for women
|LDL cholesterol||<100 mg/dl||>160 mg/dl|
|Triglycerides||<150 mg/dl||>200 mg/dl|
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.
Renal disease worsens atherosclerosis. The level of creatinine in a person’s blood can be used to screen for a number of kidney problems.
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.
Twelve-lead electrocardiography (ECG or EKG) 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 detect myocardial injury, ischemia, and the presence of prior myocardial infarction (Levine, 2011).
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.
Joanne Lang is a 63-year-old woman with a history of chronic stable angina and heart valve disease. She is admitted to the emergency department (ED) complaining of new chest pain, shortness of breath, sweating, and chest tightness. The ED nurse takes her vital signs, which yield a blood pressure reading of 140/90 mmHg and a heart rate of 98. Electrocardiography is administered; Joanne’s electrocardiogram (ECG) appears below. The ED nurse suspects acute anterior myocardial infarction, and refers Joanne for further evaluation by the attending cardiologist.
(Source: Jenkins and Gerred, 2009.)
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, 2011).
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.
Stress testing uses graded exercise in a supervised session to assess the heart’s response to increases in its workload. (Source: NHLBI, 2011d.)
During a stress test, symptomsof heart problems—angina, shortness of breath, severe fatigue, lightheadedness, or fainting—usually appear when patients go beyond their exercise threshold. At the same threshold, signsof 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, and echocardiography can be used to follow changes in the heart’s anatomy during exercise.
ECG stress testing is most useful when physicians are:
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 (ACC) and the American Heart Association (AHA) have jointly published guidelines for the use of ECG (Gibbons, et al., 2002, 2003) and echocardiography (Cheitlin et al., 2003) in stress-testing of patients with coronary artery disease. More recently, the AHA issued a scientific statement on cardiopulmonary exercise testing in adults (Balady et al., 2010).
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).
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.
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 (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, 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.
Nuclear imaging involves the use of small amounts of radioactive material known as radiopharmaceuticals or radiotracers to diagnose and assess the severity of various diseases. The radiopharmaceutical is either injected into the body, swallowed, or inhaled as a gas and eventually accumulates in the part of the body being examined. A special camera or imaging device is used to detect radioactive emissions from the radiopharmaceutical, yielding pictures and detailed molecular information (RadiologyInfo.org, 2011b).
In coronary artery disease, nuclear imaging studies can be useful in assessing patients for significant stenoses (narrowing of coronary arteries). In this setting, stress and rest nuclear scintigraphic studies using the radiopharmaceuticals thallium, sestamibi, or teboroxime are occasionally helpful. A nuclear imaging examination can be administered as a treadmill nuclear stress test, a dobutamine nuclear stress test, or a dipyridamole (Persantine) or adenosine nuclear stress test (Boudi, 2012).
Radionuclide stress myocardial perfusion imaging, using thallium-201 (201 Tl) or sestamibi, can be used to quantify coronary flow reserve, which is usually assessed during exercise or with pharmacologic coronary vasodilators (Boudi, 2012).
Computed tomography, also known as CT or CAT scanning, is another common imaging tool in coronary artery disease. Coronary calcium scoring involves administration of a cardiac CT scan to collect information about the presence, location, and extent of calcified plaque in the coronary arteries. Because calcium is a marker for coronary artery disease, the coronary calcium score—a number reflecting the degree and extent of calcium deposits in the walls of the coronary arteries—can be a useful prognostic tool in coronary artery disease (RadiologyInfo.org, 2011a).
Two different treatment situations arise with coronary artery disease:
Emergency treatment for patients with coronary artery disease can be guided by the American Heart Association’s “chain of survival,” a series of actions that, when put into motion, can reduce the patient’s chance of dying from cardiac arrest. The links in the chain of survival are:
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 in an ambulance to an emergency department whenever they have an episode of chest pain or chest discomfort.
Because quick treatment of a heart attack is so beneficial, bystanders should start cardiopulmonary resuscitation (CPR) as soon as they see someone collapse, call 911, and use an automated external defibrillator (AED), if one is available (John & Ewy, 2011). 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 325 mg of aspirin. If chest pain continues, the patient can usually be given sublingually or aerosolized nitroglycerin (Reeder & Prasad, 2009).
When a patient is experiencing ischemic heart symptoms, it is a potential emergency. Cardiologists have detailed protocols for evaluating and treating acute coronary syndromes (Antman et al., 2004). However, the emergency department triage always begins with the following steps:
(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, 2009].)
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 the neck, shoulder, arms, or upper abdomen (Brady et al., 2009).
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 (see box below). 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.
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.
The number of people dying from STEMI heart attacks can be reduced by quick reperfusion treatment. (Source: NHAAP, 2002.)
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 American College of Cardiology/American Heart Association Task Force on Practice Guidelines recommends that emergency rooms aim for reperfusion within 90 minutes of the first STEMI symptoms, with an emphasis of treating at least 75% of STEMI patients within 90 minutes of presentation at the hospital (Antman et al., 2008a).
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., 2009). 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.
Nelson Martinez is a slightly overweight, 56-year-old Hispanic American with a history of hypertension and chronic stable angina. At a family gathering in a local park, he joined a pickup soccer game but started to feel chest pain and dyspnea after running around for a few minutes. Alarmed, his wife called 911, and an ambulance brought him to the closest emergency department (ED).
Nelson was admitted to the ED 30 minutes after his angina symptoms emerged. He described his symptoms to the ED nurse, who immediately recommended the attending physician order up x-rays and an ECG. The ECG revealed a STEMI, and Nelson underwent reperfusion therapy roughly 60 minutes after the first symptoms appeared.
For all patients with acute coronary syndromes, the general goals are to:
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 (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 (2009) and Reeder & Prasad (2009), and in professional guidelines, such as the AHA’s Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care (AHA, 2010b).
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, a beta blocker, and supplemental oxygen, and blood should be drawn to search for cardiac marker molecules.
When a 12-lead ECG is taken, more than 50% of 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 (Moran, 2009).
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 (Antman et al., 2008b).
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, 2008; Johns Hopkins, 2007; University of Wisconsin, 2010). Typical advice is:
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, healthcare 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.
Drug therapy is a key part of the treatment of coronary artery disease (Gibbons et al., 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.
The standard therapies for CAD include:
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).
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 starting dose is typically between 75 and 162 mg/day and should be continued indefinitely unless contraindicated. Clopidogrel (Plavix) can be added for up to 12 months to increase the inhibition of clot formation, and it can be given to patients when aspirin is contraindicated (Smith et al., 2006).
Patients may need to discontinue antiplatelet or anticoagulant therapy before undergoing elective surgery, as not stopping can lead to cancellation or postponement of the operation, or worse, cardiac events or other potentially catastrophic developments during or following surgery (Reich et al., 2011). Patients considering elective surgery should therefore coordinate their antiplatelet/anticoagulant regimens with their primary care physician, cardiologist, and surgeon.
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.
|Source: Adapted from MedlinePlus, 2010; MedicineNet, 2011.|
|When to Use||
|How to Use||
|What to Expect if It Works||Chest discomfort should get better in 1 to 5 minutes.|
|What to Do if It Doesn’t Work||If you don’t feel better after taking 1 tablet, call 911 immediately and say you are having chest pain. Alternately, if you are used to taking nitro, you can take up to 3 tablets before calling 911.|
|Typical Side Effects||
|Side Effects to Report to Doctor Immediately||
|Drugs You Can Take Before or After Nitroglycerin||
|Drugs Not to Take with Nitroglycerin||Erectile dysfunction medicines (Viagra, Cialis, Levitra)|
|Storage||Keep the tablets tightly sealed in their original container, and store them away from heat, light, and moisture.|
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 (Smith et al., 2006).
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 (Gibbons et al., 2003).
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 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 (Gibbons, 2003).
In the Heart Protection Study, a large trial of more than 20,000 high-risk patients, longer-term statin therapy was associated with greater reductions in vascular events; even after patients in the study stopped taking statins, the benefits persisted for at least 5 years without evidence of emerging hazards (Bulbulia, et al., 2011). Patients with liver disease should not take statins.
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 (Boudi, 2012).
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.
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.
As ideal goals, a patient’s body mass should be between 18.5 and 24.9 kg/m2 and the waist circumference should be <102 cm (40 inches) for men and <88 cm (35 inches) for women (Smith, et al., 2006). 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 (Smith, et al., 2006).
Eating nutritiously will slow the development of atherosclerosis. Simply reducing the overall calories in patients’ diets 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 or limit 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. Moderate alcohol intake (20 g/day or less) in men is associated with a reduced incidence of coronary artery disease events, although the mechanism behind this benefit is not well understood (Boudi, 2012).
|Source: NHLBI, 2004.|
|Saturated fat||<7% of total calories|
|Polyunsaturated fat||≤10% of total calories|
|Monounsaturated fat||≤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|
|Total calories (energy)||Balance energy intake and expenditure to maintain desirable body weight and 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.
Nutritional evaluation, counseling, and monitoring are essential to helping patients improve their diet. However, it is unrealistic to expect that a single nutritional educational session or program will result in long-term adherence to a sensible diet. Moreover, patients may find it difficult to absorb a large amount of information in a short period of time. Some patients—particularly those with comorbidities such as diabetes, obesity, or heart failure, as well as those from culturally and linguistically diverse backgrounds—may require more nutritional information and counseling than they can obtain in the context of a group program (Graham et al., 2011). These factors make it especially important for patients and their family members to consult with a dietician on a regular basis. Many hospitals offer preventive and therapeutic nutrition classes with an emphasis on cardiovascular health.
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, 2001).
Linda Ortiz, a 60-year-old Hispanic American woman with a history of type 2 diabetes and hypertension, was recently diagnosed with coronary artery disease. She has come to the doctor’s office for a follow-up appointment 2 weeks after an episode of angina that brought her to the emergency room. Linda tells the nurse that she has been compliant with her newly prescribed drug regimen of daily aspirin, an ACE inhibitor, and a statin. However, when the nurse asks her about her lifestyle, Linda admits that she has been having a hard time adhering to the recommended lifestyle changes.
The nurse counsels Linda about the importance of smoking cessation, regular exercise, and a sensible diet and gives her referrals to a dietician and an occupational therapist. She gives Linda some educational brochures about implementing these lifestyle changes, including a diary for Linda to record and track her daily activities, food intake, and medication doses. The nurse also gets Linda to agree to stop smoking within 2 months and recommends that the doctor prescribe a medication to help her quit. Additionally, the nurse helps Linda establish some exercise goals, starting with moderate walking every day and gradually progressing to more intense exercise. Finally, the nurse has Linda schedule another follow-up appointment in 2 weeks so they can track and assess her adherence to these lifestyle changes.
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 (Gibbons et al., 2003).
Percutaneous coronary intervention, also commonly known as coronary angioplasty or simply angioplasty, is 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).
In percutaneous coronary intervention (PCI), a catheter is threaded into the region of the artery that is narrowed by plaque. A balloon near the tip of the catheter is inflated, flattening the plaque against the arterial wall and widening the space inside the artery. Often a wire support (a stent) is left in place to hold the artery open. (Source: NHLBI, 2010a.)
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.
In coronary artery bypass graft (CABG) revascularization surgery, blood is routed past blockages in coronary arteries. Figure B shows how vein and artery bypass grafts are attached to the heart. (Source: NHLBI, 2010b.)
There are two main types of bypass surgery: conventional (arrested heart) and “beating heart” CABG. Conventional (or “on pump”) CABG is performed on an arrested (stopped) heart through an incision down the middle of the patient’s chest. The patient’s heart is stopped with medications, and blood is routed to a heart-lung machine, which removes CO2 and supplies oxygen, thus bypassing the processes carried out by the heart and lungs. The reoxygenated blood is returned to the body to nourish it. The patient may need blood transfusions to replenish blood volume, red blood cells, or platelets. To reduce oxygen demand, the patient is placed in therapeutic hypothermia.
In “beating heart” or “warm heart” bypass surgery, the heart is not stopped, the heart-lung machine is not used, and the patient remains at normal or only slightly lowered temperature. This type of surgery often allows patients to be discharged from the hospital more quickly than with conventional CABG, and the avoidance of the heart-lung machine has been shown to reduce the need for transfusions (Medtronic India, n.d.; St. Mary Medical Center, 2012).
CABG reduces angina in more than 90% of cases. When a vein is used as the bypass conduit, 10% to 20% of 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.
Early and frequent physical therapy (PT), starting as soon as one day after surgery, can help restore a normal pattern of daily functioning in a patient with coronary artery disease. A customized PT program may include exercises for range of motion, muscle strengthening, and coordination. Whole body movement may progress from walking in brief bursts, to walking the length of the corridor, to climbing stairs.
Approximately 6 weeks after surgery, many patients proceed to cardiac rehabilitation, a more intense form of PT that is usually conducted on an outpatient basis and supervised by a trained medical professional and exercise physiologist. The goals of cardiac rehab are to maximize strength, prevent regression of coronary artery disease, and reduce the likelihood of future heart problems (Liberati, 2011).
The exercise component of cardiac rehab is generally divided into four phases (Morris et al., 2011):
Phase I (inpatient): The first phase of cardiac rehab takes place before the patient is discharged from the hospital. This phase generally consists of evaluation and assessment of the patient’s condition, motivation, and risk factors, accompanied by education and discharge planning. The patient is gradually introduced to exercise on day 2 of cardiac rehab, with an intensity of exercise up to 4 metabolic equivalents (METS, i.e., 4 times the resting metabolic rate, or 4 times the amount of oxygen consumed at rest [Jetté et al., 1990]). Ideally, by day 4, the patient will be walking in the corridor for 5–10 minutes three or four times a day.
Phase II (after discharge): The patient is given clear instructions on his or her individualized exercise plan, and the rehabilitation team maintains regular contact via telephone and perhaps the occasional home visit. The initial mode of exercise is usually walking on level ground, with an intensity goal of between 2 and 4 METS or a score of 11 to 12 on the Rating of Perceived Exertion Scale (i.e., moderate intensity) (CDC, 2011b). Patients are generally advised to stay indoors for the first day or two because they may expect to feel fatigued and/or anxious, though patients with uncomplicated coronary artery disease may be advised to increase their walking distance progressively to 3 to 5 kilometers (km) a day after 4 to 6 weeks.
Phase III (outpatient exercise program): The goal of this phase is to enable the patient to exercise safely in a structured environment and to understand the benefits of exercise. Before starting an exercise program, it is common for a patient to undergo an exercise stress test until symptoms become apparent. The exercise test can be used as either a diagnostic or prognostic tool or as a test of functional capacity.
Cardiac patients should exercise in the low to moderate range of exercise intensity, corresponding to 60%–75% of maximum heart rate or 60%–70% of maximum heart rate reserve, which is equivalent to a score of 12 to 14 on the Rating of Perceived Exertion Scale. (The maximum heart rate is usually calculated by subtracting the patient’s age from 220. The heart rate reserve is calculated by subtracting the resting heart rate from the maximum heart rate.) The outpatient exercise program may last from 8 to 12 weeks, and patients generally attend 2 to 3 times a week.
Exercises during this phase should promote total physical conditioning, using treadmills, cycle and arm ergometers, stair climbers, and rowing machines. While such exercises are largely aerobic in nature, resistance training can be used in patients at low to moderate risk. However, patients are advised to spend some time on aerobic-type exercises before they initiate resistance exercise. The exercise session should be preceded by a warm-up period lasting approximately 15 minutes, and the session itself lasts for 30-35 minutes, followed by a 10-minute cool-down period.
Phase IV: The patient exercises independently and maintains the recommended lifestyle modifications. Increased physical activity and enhanced physical fitness can promote cardiovascular health, provided that the patient keeps up with the exercise program. Indeed, the change in exercise behavior that the patient achieves during phase III must be lifelong in order to have any lasting benefit.
John Townsend, age 65, is recovering in the hospital from CABG surgery to reopen a blocked coronary artery. The day after his surgery he is visited by a nurse and a physical therapist, who brief him on the cardiac rehabilitation regimen he is about to undergo. John expresses anxiety about having to undergo cardiac rehab so soon, but the nurse and physical therapist reassure him that the regimen will be helpful and manageable and that it will start slowly.
John starts his cardiac rehab program the next day. The nurse and physical therapist help him get out of bed and walk him to the door of his room and back again. That exercise is repeated twice more that day. The next day, the nurse helps John venture out to the corridor, and he is able to walk slowly to the nurses’ station, which is 20 yards from his room. John takes two more corridor walks that day, and takes four such walks each of the next two days.
By the time he is discharged on day 5 post-surgery, John is able to walk in the corridor for 10 minutes at a time. The nurse and physical therapist give John detailed instructions on continuing with and ramping up his exercise plan while at home, and promise to check in with him periodically over the next 2 weeks, after which he is to see his doctor for a follow-up visit.
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 patients with diabetes is to reduce their glycosylated hemoglobin (A1C) level to below 7%.
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 (Smith et al., 2006).
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 (Mayo Clinic, 2012). 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.
People with clinical depression or with symptoms of depression have a higher incidence of myocardial infarction, poorer recovery, and a higher rate of mortality (Cowles, 2011; 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).
Patients with cardiovascular disease should get a yearly flu shot (Smith et al., 2006).
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, 2011; Brady et al., 2006).
Patients who have chronic stable angina with
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.
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.
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).
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 (Blaha et al., 2011; Antman et al, 2008b; Boudi, 2011).
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 one’s 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 (NCEP, 2004).
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, healthcare providers should strongly urge patients to quit smoking and help them to enroll in a smoking cessation program. In addition, they should advise patients to avoid spending time in places where other people smoke (Smith et al., 2006).
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 3 or 4 different days each week. Moderate exercise is equivalent to a brisk walk.
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 to 7 lbs). Smoking is the worse of the two problems, and stopping smoking should have the higher priority.
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.
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 (Smith et al., 2006).
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 (Smith, et al., 2006).
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:
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.
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.
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).
Healthcare 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.
Q:I think I’m having a heart attack, but I’m not sure. Should I call my doctor? Should I drive to the hospital?
A:Don’t waste time calling your doctor, and don’t take any chances. Hang up now and call 911 immediately. Don’t drive yourself to the hospital. Hang up and call 911 now. Emergency medical technicians can start to treat you on the way to the hospital. While you wait for the ambulance, if you can take aspirin, chew 1/2 of a regular 325 mg aspirin or 2 baby aspirins (81 mg each), then sit down and try to relax.
Q:I’m afraid of taking too many medicines. What natural remedies can I use for my coronary artery disease?
A:Your fears are understandable. All medicines have side effects, and all medicines can be dangerous in higher-than-recommended doses. If you are having side effects that make your life difficult or if you are worried about something, then talk directly to your doctor. Don’t be shy about telling your physician what is bothering you. A good doctor wants to make your life better, not worse.
Coronary artery disease is a serious medical problem, and the best advice you can get is from someone who has devoted their professional life to studying the disease. Your doctor is the best source of information on alternatives to your current medicines. We don’t recommend listening exclusively to friends or relatives. Also, it is not safe to follow advertisers’ suggestions or to rely solely on advice from labels of over-the-counter products.
Natural remedies, such as herbs and plant or animal extracts, are chemicals just like the medicines that you are taking. “Natural” often means that the chemical is not as pure or as precisely measured as a prescription drug. When the natural remedy is not purified, you are taking all the impurities as well as the chemical—in fact, you don’t know exactly what things you are taking, which can be dangerous. When the natural remedy is not as well measured as a prescription drug, you don’t know exactly how much you are taking, which can also be dangerous.
There are a couple of herbs and other natural products that are especially dangerous for patients with coronary artery disease:
Often, there are safe alternatives to the standard therapy for a disease. Talk with your doctor and ask for an alternative that is safe.
Q:What does a heart attack feel like?
A:Most people get a very uncomfortable pressure, squeezing, or pain in the center of their chest. This chest pain lasts for more than a few minutes; sometimes it goes away briefly, but it soon comes back. Some people feel the pain in their arms, shoulders, back, jaw, or stomach. There can also be a feeling of breathlessness, lightheadedness, cold sweat, or nausea.
Q:How can I tell whether I am a person likely to have a heart attack?
A:One good way is to ask your doctor. You can also get an idea by counting how many of the following things apply to you:
These are nine things that increase your risk of having a heart attack. The more of them that apply to you, the greater your chances of heart trouble. Most things in the list can be fixed or controlled. Each thing that you fix will reduce your risk of a heart attack.
Q:Will I die if I have a heart attack?
A:Most people who have heart attacks survive, and the survival rates have been improving as new medicines and new medical procedures are developed. If you have a heart attack, your chances of doing well go way up if you get to an emergency department quickly. If you think you are having a heart attack, don’t take chances. Call 911 if your symptoms don’t go away in a few minutes.
Q:But I would be embarrassed having an ambulance zooming up to my house with lights flashing and sirens blaring. It would be even worse if I weren’t really having a heart attack.
A:Of course, those are normal feelings. The paramedics in the ambulance and the doctors in the emergency department know that it isn’t easy for a person to figure out if they are really having a heart attack. They also know that when people wait too long to get help, they are more likely to die. No one will give you a hard time if you are not actually having a medical crisis.
If there is even a small chance that you could have a heart attack, your doctor should have already warned you. Your life is worth more than a little embarrassment, so call 911 if there is any possibility that you might be having a heart problem.
Q:What is a stress test?
A:In a stress test, you exercise in a safe place to see how well your heart handles increased activity. Usually, you walk on a treadmill or pedal a bicycle while a doctor watches your pulse rate, your blood pressure, and your ECG.
You will probably be asked to come to the hospital in comfortable clothes and soft shoes. When you arrive in the exercise room, electrode pads will be stuck to the skin of your chest, and the wires will be attached to an ECG machine, which records the electrical activity of your heart.
Then you will exercise—slowly at first, and gradually harder. Your heart rate will get faster, your blood pressure will go up, and you will breathe harder. Meanwhile, the doctor will keep an eye on the electrical activity of the heart. If you get any heart symptoms, the test will be stopped. The goal is to measure exactly how much work (stress) your heart can cope with, and if your heart has difficulty, what specific heart problem is occurring.
Q:I’ve heard that women get different heart disease than men. Is this true?
A:As far as we know, women and men get the same disease, called coronary artery disease or coronary heart disease. This disease is caused by the same atherosclerosis in both men and women, and it affects the heart arteries (coronary arteries) the same way in everyone.
Just as with men, coronary artery disease is the number one killer of women in the United States. For both men and women, the likelihood of getting heart disease increases as a person gets older. The same things also increase the chances of getting the disease for both men and women: cigarette smoking, a fat-filled diet, being overweight, having high cholesterol, doing little or no physical exercise, having diabetes, having high blood pressure, and coming from a family that tends to have heart disease.
Nonetheless, there are some differences in how the disease affects men and women. Before menopause, women are less likely to get heart disease than men of the same age. After menopause, a woman’s risk increases to levels similar to men, but this risk can be reduced earlier, in a woman’s premenopausal years, by improving her lifestyle (stopping smoking, maintaining a moderate weight, eating nutritiously, exercising regularly, keeping her blood pressure low, treating diabetes).
Another difference between the sexes is that, while many women get the same kind of chest tightening (called angina) as men, women with heart attacks get other symptoms more often than men. When having a heart attack, women are more likely than men to feel sharp chest pains, excess tiredness, dizziness, difficulty breathing, nausea, or indigestion.
Q:I am taking birth control pills. Are they bad for my heart?
A:The older variety of birth control pills had a higher dose of hormones, and this increased a woman’s risk of getting a heart attack or a stroke. Today’s birth control pills and birth control patches contain lower doses of hormones and do not make women more likely to have a heart attack. The evidence is not entirely clear for strokes, but if there is any increase in the risk of strokes, the increased risk is small.
The safety of modern, low-dose birth control pills is clear for women who don’t have any other problems that might put them at risk for heart attacks or strokes. A woman who already has a higher chance than usual of getting heart or artery disease needs to talk with her doctor about the best birth control choices for her particular situation.
Q:My doctor says my medicine is a beta blocker. What’s that, and what is it blocking?
A:A beta blocker is a drug that slows your heart rate and lowers your blood pressure. This kind of drug blocks the stress caused by the particular nerves that make you tense when you are frightened.
Q:I’ve heard that trans fats are bad for your heart, but what are trans fats?
A:Yes, trans fats are the worst kind of fats for your heart and arteries. Trans fats are also called hydrogenated fats, and most trans fats are man-made and added to processed foods to make the food last longer. On ingredients labels, trans fats are usually called “partially hydrogenated” oils or fats, and on nutrition labels, they are listed as trans fats (usually a subclass of saturated fats). Trans fats are often found in vegetable shortenings, margarines, cakes, crackers, cookies, snack foods (potato chips, corn chips, popcorn), and in foods like fried potatoes that have been cooked in partially hydrogenated oils.
When choosing foods, look at the nutrition labels. The U.S. Food and Drug Administration (FDA) offers these practical suggestions about managing the fats in your diet:
Q:Is vitamin E good for my heart?
A: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.
Online calculator of a person’s 10-year risk for heart attack (National Cholesterol Education Program)
Ahto M, Isoaho R, Puolijoki H, Vahlberg T, Kivela S-L. (2007). Stronger symptoms of depression predict high coronary heart disease mortality in older men and women. International Journal of Geriatric Psychiatry, 22, 757–63.
Akinpelu D. (2011). Treadmill stress testing. eMedicine. Retrieved January 2012 from http://emedicine.medscape.com
Alaeddini J. (2011). Angina pectoris. eMedicine. Retrieved January 2012 from http://emedicine.medscape.com
American Heart Association (AHA). (2012). Go red for women: about heart disease and stroke. Retrieved February 2012 from http://www.goredforwomen.org
American Heart Association (AHA). (2010a). Cardiovascular disease & diabetes. Retrieved January 2012 from http://www.heart.org
American Heart Association (AHA). (2010b). Guidelines for CPR and ECC. Circulation, 122, S639–S933.
Antman EM, Hand M, Armstrong PW, et al. (2008a). 2007 Focused update of the ACC/AHA 2004 guidelines for the management of patients with ST-elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation, 117, 296–329.
Antman E, Selwyn AP, Braunwald E, Loscalzo J. (2008b). Ischemic heart disease. In DL Kasper, et al. (Eds.), Harrison’s principles of internal medicine (ch. 237) (17th ed.) New York: McGraw-Hill.
Antman EM, Anbe DT, Armstrong PW, et al. (2004). ACC/AHA guidelines for management of patients with ST-elevation myocardial infarction—executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the 1999 Guidelines for the Management of Patients With Acute Myocardial Infarction). Circulation, 110, 588–636.
Balady GJ, Arena R, Sietsema K, et al. (2010). Clinician’s guide to cardiopulmonary exercise testing in adults: a scientific statement from the American Heart Association. Circulation, 122, 191–225.
Berry C, Balachandran KP, L’Allier P, Lesperance J, Bonan R, Oldroyd KG. (2007). Importance of collateral circulation in coronary heart disease. European Heart Journal, 28, 278–291.
Blaha MJ, Ketlogetswe KS, Ndumele CE, Gluckman TJ, Blumenthal RS. (2011). Preventive strategies for coronary heart disease. In V Fuster, RA Walsh, and RA Harrington (Eds.), Hurst’s the heart (ch. 51) (13th ed.). New York: McGraw-Hill.
Bock JL. (2011). Cardiac injury, atherosclerosis, and thrombotic disease. In RA McPherson and MR Pincus (eds.), McPherson & Pincus: Henry’s clinical diagnosis and management by laboratory methods (ch. 18) (22nd ed.). Philadelphia: Saunders.
Bogers RP, et al. (2007). Association of overweight with increased risk of coronary heart disease partly independent of blood pressure and cholesterol levels. Archives of Internal Medicine, 167(16), 1720–28.
Boudi FB. (2012). Coronary artery atherosclerosis. eMedicine. Retrieved February 2012 from http://emedicine.medscape.com
Boudi FB. (2011). Overview of atherosclerosis. eMedicine. Retrieved January 2012 from http://emedicine.medscape.com
Boutayeb A & Boutayeb S. (2005). The burden of non-communicable diseases in developing countries. International Journal for Equity in Health, 4, 2. Retrieved January 2012 from http://www.equityhealthj.com
Brady WJ, Harrigan RA, Chan T. (2009). Acute coronary syndrome. In JA Marx et al. (Eds.), Rosen’s emergency medicine: concepts and clinical practice (ch. 76) (7th ed.). Philadelphia: Mosby.
Braunwald E. (2005). The history. In DP Zipes, et al. (Eds.), Braunwald’s heart disease: a textbook of cardiovascular medicine (ch. 7) (7th ed.). Philadelphia: Saunders.
Brown JE & Hamilton GC. (2009). Chest pain. In JA Marx et al. (Eds.), Rosen’s emergency medicine: concepts and clinical practice (ch. 18) (7th ed.). Philadelphia: Mosby.
Bulbulia R, Bowman L, Wallendszus K, et al. (2011). Effects on 11-year mortality and morbidity of lowering LDL cholesterol with simvastatin for about 5 years in 20,536 high-risk individuals: a randomised controlled trial. Lancet, 378, 2013–2020.
Caulin-Glaser T, Maciejewski PK, Snow R, et al. (2007). Depressive symptoms and sex affect completion rates and clinical outcomes in cardiac rehabilitation. Preventive Cardiology, 10(1), 15–21.
Centers for Disease Control and Prevention (CDC). (2011a). National diabetes fact sheet: national estimates and general information on diabetes and prediabetes in the United States, 2011. Retrieved January 2012 from http://www.cdc.gov
Centers for Disease Control and Prevention (CDC). (2011b). Physical activity for everyone: perceived exertion (Borg Rating of Perceived Exertion Scale). Retrieved February 2012 from http://www.cdc.gov
Charney P. (2011). Women and coronary artery disease. In V Fuster, RA Walsh, and RA Harrington (Eds.), Hurst’s the heart (ch. 103) (13th ed.). New York: McGraw-Hill.
Cheitlin MD, Armstrong MF, Aurigemma GP, et al. (2003). ACC/AHA/ASE 2003 guideline update for the clinical application of echocardiography: summary article. Circulation, 103, 1146–1162. Retrieved February 2012 from http://circ.ahajournals.org
Coven DL. (2012). Acute coronary syndrome. eMedicine. Retrieved January 2012 from http://emedicine.medscape.com
Cowles MK, Musselman DL, McDonald WM, Nemeroff CB. (2011). Effects of mood and anxiety disorders on the cardiovascular system. In V Fuster, RA Walsh, and RA Harrington (Eds.), Hurst’s the heart (ch. 96) (13th ed.). New York: McGraw-Hill.
Davis AM. (2008). Cardiac rehabilitation. In WR Frontera et al. (Eds.), Essentials of physical medicine and rehabilitation (ch. 112) (2nd ed.). Philadelphia: Hanley & Belfus.
Depre C, Vatner SF, Gross GJ. (2011). Coronary blood flow and myocardial ischemia. In V Fuster, RA Walsh, and RA Harrington (Eds.), Hurst’s the heart (ch. 54) (13th ed.). New York: McGraw-Hill.
Eckel RH, Grundy SM, Zimmet PZ. (2005). The metabolic syndrome. Lancet, 365(9468), 1415–28.
Falk E & Fuster V. (2011). Atherothrombosis and thrombosis-prone plaques. In V Fuster, RA Walsh, and RA Harrington (Eds.), Hurst’s the heart (ch. 52) (13th ed.). New York: McGraw-Hill.
Gehi AK, Ali S, Na B, Whooley MA. (2007). Self-reported medication adherence and cardiovascular events in patients with stable coronary heart disease. Archives of Internal Medicine, 167(16), 1798–1803.
Gibbons RJ, Abrams J, Chatterjee K, et al. (2003). ACC/AHA 2002 guideline update for the management of patients with chronic stable angina. Circulation, 107, 149–58. Available online at http://circ.ahajournals.org
Gibbons RJ, Balady GJ, Bricker T, et al. (2002). ACC/AHA 2002 guideline update for exercise testing: summary article. Circulation, 106, 1883–1892. Retrieved February 2012 from http://circ.ahajournals.org
Goldman L, Hashimoto B, Cook EF, Loscalzo A. (1981). Comparative reproducibility and validity of systems for assessing cardiovascular functional class: advantages of a new specific activity scale. Circulation, 64, 1227.
Gonzalez AS, et al. (2007). Predictors of the metabolic syndrome and correlation with computed axial tomography. Nutrition, 23(1), 36–45.
Graham IM, Fallon N, Ingram S, et al. (2011). Rehabilitation of the patient with coronary heart disease. In V Fuster, RA Walsh, and RA Harrington (Eds.), Hurst’s the heart (ch. 67) (13th ed.). New York: McGraw-Hill.
Janszky I, Ahlbom A, Hallqvist J, Ahnve S. (2007). Hospitalization for depression is associated with an increased risk for myocardial infarction not explained by lifestyle, lipids, coagulation, and inflammation: The SHEEP Study. Biological Psychiatry, 62(1), 25–32.
Jenkins D & Gerred S. (2009). ECG Library: acute anterior myocardial infarction.Retrieved February 2012 from http://www.ecglibrary.com
Jetté M, Sidney K, Blümchen G. (1990). Metabolic equivalents (METS) in exercise testing, exercise prescription, and evaluation of functional capacity. Clinical Cardiology, 13, 555–565.
John J & Ewy GA. (2011). Cardiopulmonary and cardiocerebral resuscitation. In V Fuster, RA Walsh, and RA Harrington (Eds.), Hurst’s the heart (ch. 50) (13th ed.). New York: McGraw-Hill.
Johns Hopkins Medicine. (2007). Heart health special report: exercising safely after a heart attack. Retrieved January 2012 from http://www.johnshopkinshealthalerts.com
Kim MC, Kini AS, Fuster V. (2011). Definitions of acute coronary syndromes. In V Fuster, RA Walsh, and RA Harrington (Eds.), Hurst’s the heart (ch. 56) (13th ed.). New York: McGraw-Hill.
Lam JYT. (2008). Atherosclerosis. In RS Porter and JL Kaplan (Eds.), The Merck manual of diagnosis and therapy, online (19th ed.). Retrieved January 2012 from http://www.merckmanuals.com
Lambert CR. (2007). Angina pectoris. In RE Rakel and ET Bope (Eds.), Conn’s current therapy 2007 (59th ed.). Philadelphia: Saunders.
Lee TH. (2005). Guidelines: chronic stable angina. In DP Zipes, et al. (Eds.), Braunwald’s heart disease: a textbook of cardiovascular medicine (ch. 50) (7th ed.). Philadelphia: Saunders.
Levine E. (2011). Electrocardiography. eMedicine. Retrieved January 2012 from http://emedicine.medscape.com
Libby P. (2008). The pathogenesis, prevention, and treatment of atherosclerosis. In AS Fauci, et al. (Eds.), Harrison’s principles of internal medicine (ch. 235) (17th ed.) New York: McGraw-Hill.
Liberati L. (2011). Physical therapies for coronary artery bypass grafts. LiveStrong.com. Retrieved January 2012 from http://www.livestrong.com
Littman B. (2001). Psychiatric consultation in patients with cardiovascular disease. In JL Jacobson & AM Jacobson (Eds.), Psychiatric secrets (ch. 72) (2nd ed.). Philadelphia: Hanley & Belfus.
Lloyd-Jones D, Adams RJ, Brown TM, et al. (2010). Heart disease and stroke statistics—2010 update. Circulation, 121 e46–e215.
Mayo Clinic. (2012). High blood pressure (hypertension). Retrieved January 2012 from http://www.mayoclinic.com
Mayo Clinic. (2010). Acute coronary syndrome: risk factors. Retrieved January 2012 from http://www.mayoclinic.com
MedicineNet. (2011). Nitroglycerin—sublingual, Nitrostat. Retrieved January 2012 from http://www.medicinenet.com
MedlinePlus. (2010). Nitroglycerin. Retrieved January 2012 from http://www.nlm.nih.gov
Medtronic India Pvt. Ltd. (n.d.). Fact sheet: coronary bypass (CABG) surgery: conventional vs. beating heart. Retrieved February 2012 from http://wwwp.medtronic.com
Mettler FA Jr. (2005) Essentials of radiology (2nd ed.). Philadelphia: Elsevier.
Moran JF. (2009). Angina pectoris. In RE Rakel and ET Bope (eds.), Conn’s current therapy 2009 (61st ed.). Philadelphia: Saunders.
Morris DC, Clements SD Jr, Pepper J. (2011). Management of the patient after cardiac surgery. In V Fuster, RA Walsh, and RA Harrington (Eds.), Hurst’s the heart (ch. 66) (13th ed.). New York: McGraw-Hill.
Mosca L, et al. (2007). Evidence-based guidelines for cardiovascular disease prevention in women: 2007 update. Circulation, 115, 1–21. Retrieved February 2012 from http://circ.ahajournals.org
National Cholesterol Education Program (NCEP). (2004). ATP III update 2004: implications of recent clinical trials for the ATP III guidelines. Retrieved September 2007 from http://www.nhlbi.nih.gov
National Cholesterol Education Program (NCEP). (2001). Third report of the expert panel on detection, evaluation, and treatment of high blood cholesterol in adults (Adult Treatment Panel III). Retrieved September 2007 from http://www.nhlbi.nih.gov
National Heart Attack Alert Program (NHAAP). (2002). Slide Show. Access to timely and optimal care of patients with acute coronary syndromes: community planning considerations. Retrieved September 2007 from http://hp2010.nhlbihin.net
National Heart, Lung, and Blood Institute (NHLBI). (2011a). What is coronary heart disease? Retrieved January 2012 from http://www.nhlbi.nih.gov
National Heart, Lung, and Blood Institute (NHLBI). (2011b). Anatomy of the heart. Retrieved January 2012 from http://www.nhlbi.nih.gov
National Heart, Lung, and Blood Institute (NHLBI). (2011c). What is a heart attack? Retrieved January 2012 from http://www.nhlbi.nih.gov
National Heart, Lung, and Blood Institute (NHLBI). (2011d). What to expect during stress testing. Retrieved January 2012 from http://www.nhlbi.nih.gov
National Heart, Lung, and Blood Institute (NHLBI). (2010a). How is coronary angioplasty done? Retrieved January 2012 from http://www.nhlbi.nih.gov
National Heart, Lung, and Blood Institute (NHLBI). (2010b). What is coronary artery bypass grafting? Retrieved January 2012 from http://www.nhlbi.nih.gov
National Heart, Lung, and Blood Institute (NHLBI). (2004). Adult Treatment Panel III (ATP III) guidelines: therapeutic lifestyle changes—nutrient composition of TLC diet. Retrieved January 2012 from http://hp2010.nhlbihin.net
O’Keefe JH, Bybee KA, Lavie CJ. (2007). Alcohol and cardiovascular health: the razor-sharp double-edged sword. Journal of the American College of Cardiology, 50(11), 1009–14.
Pasternak RC. (2005). Comprehensive rehabilitation of patients with cardiovascular disease. In DP Zipes, et al. (Eds.), Braunwald’s heart disease: a textbook of cardiovascular medicine (ch. 43) (7th ed.). Philadelphia: Saunders.
RadiologyInfo.org. (2011a). Cardiac CT for calcium scoring. Retrieved February 2012 from http://www.radiologyinfo.org
RadiologyInfo.org. (2011b). General nuclear medicine. Retrieved January 2012 from http://www.radiologyinfo.org
Rasouli N, Molavi B, Elbein SC, Kern PA. (2007). Ectopic fat accumulation and metabolic syndrome. Diabetes, Obesity and Metabolism, 9(1), 1–10.
Reeder GS & Prasad A. (2009). Acute myocardial infarction. In RE Rakel and ET Bope (Eds.), Conn’s current therapy 2009 (61st ed.). Philadelphia: Saunders.
Reich DL, Mittnacht AJC, Kaplan JA. (2011). Anesthesia and the patient with cardiovascular disease. In V Fuster, RA Walsh, and RA Harrington (Eds.), Hurst’s the heart (ch. 88) (13th ed.). New York: McGraw-Hill.
Roes SD, et al. (2007). Comparison of myocardial infarct size assessed with contrast-enhanced magnetic resonance imaging and left ventricular function and volumes to predict mortality in patients with healed myocardial infarction. American Journal of Cardiology, 100(6), 930–36.
St. Mary Medical Center. (2012). Coronary artery bypass graft (CABG). Retrieved February 2012 from http://www.stmaryhealthcare.org
Schoen FJ. (2010). Blood vessels and the heart. In V Kumar, et al. (Eds.), Robbins and Cotran: pathologic basis of disease (chs. 11 & 12) (8th ed.). Philadelphia: Elsevier.
Smith SC Jr, Allen J, Blair SN, et al. (2006). ACC/AHA guideline for secondary prevention for patients with coronary and other atherosclerotic vascular disease: 2006 update. Circulation, 113, 2363–72. Retrieved January 2012 from http://circ.ahajournals.org
Tan WA. (2011). Unstable angina. eMedicine. Retrieved January 2012 from http://emedicine.medscape.com
United States Food and Drug Administration (U.S. FDA). (2005). Revealing trans fats. Retrieved February 2012 from http://publications.usa.gov
University of Wisconsin-Madison School of Medicine and Public Health. (2010). Exercise and activity after a heart attack. Retrieved January 2012 from http://www.uwhealth.org
Vogel JHK, et al. (2005). Integrating complementary medicine into cardiovascular medicine. Journal of the American College of Cardiology, 46(1), 184–221.
Warnica JW. (2011). Coronary artery disease. In RS Porter and JL Kaplan (Eds.), The Merck manual of diagnosis and therapy, online (19th ed.). Whitehouse Station, NJ: Merck. Retrieved January 2012 from http://www.merckmanuals.com
Wassink AMJ, Olijhoek JK, Visseren FLJ. (2007). The metabolic syndrome: metabolic changes with vascular consequences. European Journal of Clinical Investigation, 37(1), 8–17.
World Health Organization (WHO). (2007). The top 10 causes of death, fact sheet #310. Retrieved January 2012 from http://www.who.int