The term acute coronary syndrome (ACS) is used to describe patients who have either unstable angina or an acute myocardial infarction. In ACS, it is believed that the atherosclerotic plaque in the coronary artery ruptures, resulting in platelet aggregation (“clumping”), thrombus (clot) formation, and vasoconstriction (Fig. 40-1). The amount of disruption of the atherosclerotic plaque determines the degree of coronary artery obstruction (blockage) and the specific disease process. The artery has to have at least 40% plaque accumulation before it starts to block blood flow.

Historically, an acute myocardial infarction (MI) was diagnosed by the presence of ST-segment elevation on the 12-lead electrocardiogram (ECG) (see discussion of the normal ECG in Chapter 36). However, all patients do not present with this finding. Instead, they are classified into one of three categories according to the presence or absence of ST-segment elevation on the ECG and positive troponin markers (see Chapter 35 for discussion of troponins):

Myocardial Infarction.

The most serious acute coronary syndrome is myocardial infarction (MI), often referred to as acute MI or AMI. Undiagnosed or untreated angina can lead to this very serious health problem. AMI is further divided by the American College of Cardiology (ACC)/AHA into non–ST-elevation MI (NSTEMI) and ST-elevation MI (STEMI) (Anderson, 2007). Patients presenting with NSTEMI typically have ST and T-wave changes on 12-lead ECG. This indicates myocardial ischemia. Cardiac enzymes may be initially normal but elevate over the next 6 to 12 hours. Patients presenting with STEMI typically have ST elevation in two contiguous leads on a 12-lead ECG. This indicates myocardial infarction/necrosis and requires immediate treatment.

Myocardial infarction (MI) occurs when myocardial tissue is abruptly and severely deprived of oxygen. When blood flow is quickly reduced by 80% to 90%, ischemia develops. Ischemia can lead to injury and necrosis of myocardial tissue if blood flow is not restored. Most MIs are the result of atherosclerosis of a coronary artery, rupture of the plaque, subsequent thrombosis, and occlusion (blockage) of blood flow. Other factors may be involved, however, such as coronary artery spasm, platelet aggregation, and emboli from mural thrombi (thrombi lining the walls of the cardiac chambers).

Often MIs begin with infarction of the subendocardial layer of cardiac muscle. This layer has the longest myofibrils in the heart, the greatest oxygen demand, and the poorest oxygen supply. Around the initial area of infarction (zone of necrosis) in the subendocardium are two other zones: (1) the zone of injury—tissue that is injured but not necrotic; and (2) the zone of ischemia—tissue that is oxygen deprived. This pattern is illustrated in Fig. 40-2.

Women’s Health Considerations

Many women with symptomatic ischemic heart disease or abnormal stress testing do not have normal coronary angiography (Shaw et al., 2009). Studies implicate microvascular disease or endothelial dysfunction or both as the causes for risk for CAD in women. Endothelial dysfunction is defined as the “inability of the arteries and arterioles to dilate due to inability of the endothelium to produce nitric oxide, a relaxant of vascular smooth muscle” (Bellasi et al., 2007).

Women typically have smaller coronary arteries and frequently have plaque that breaks off and travels into the small vessels to form an embolus (clot). “Positive remodeling” or outward remodeling (lesions that protrude outward) is more common in women (Bellasi et al., 2007). This outpouching may be missed on coronary angiography.

Infarction is a dynamic process that does not occur instantly. Rather, it evolves over a period of several hours. Hypoxia (decreased oxygen) from ischemia may lead to local vasodilation of blood vessels and acidosis. Potassium, calcium, and magnesium imbalances, as well as acidosis at the cellular level, may lead to changes in normal conduction and contractile functions. Catecholamines (epinephrine and norepinephrine) released in response to hypoxia and pain may increase the heart’s rate, contractility, and afterload. These factors increase oxygen requirements in tissue that is already oxygen deprived. This may lead to life-threatening ventricular dysrhythmias. The area of infarction may extend into the zones of injury and ischemia. The actual extent of the zone of infarction depends on three factors: collateral circulation, anaerobic metabolism, and workload demands on the myocardium.

The infarction may involve only the subendocardium (called a subendocardial MI) or may spread to the epicardium or to all three layers of cardiac muscle. When all three layers are involved, the MI is termed transmural. Subendocardial MIs have less effect on wall motion and cardiac output than do transmural infarctions. When fewer grams of myocardium are affected, the characteristic “Q” wave on the ECG, which may also indicate an old infarction, may not appear.

Obvious physical changes do not occur in the heart until 6 hours after the infarction, when the infarcted region appears blue and swollen. These changes explain the need for intervention within the first 4 to 6 hours of symptom onset! After 48 hours, the infarcted area turns gray with yellow streaks as neutrophils invade the tissue and begin to remove the necrotic cells. By 8 to 10 days after infarction, granulation tissue forms at the edges of the necrotic tissue. Over a 2- to 3-month period, the necrotic area eventually develops into a shrunken, thin, firm scar. Scar tissue permanently changes the size and shape of the entire left ventricle, called ventricular remodeling. Remodeling may decrease left ventricular function, cause heart failure, and increase morbidity and mortality. The scarred tissue does not contract nor does it conduct electrically. Thus this area is often the cause of chronic ventricular dysrhythmias surrounding the infarcted zone.

The patient’s response to an MI also depends on which coronary artery or arteries were obstructed and which part of the left ventricle wall was damaged: anterior, septal, lateral, inferior, or posterior. Fig. 35-3 in Chapter 35 shows the location of the major coronary arteries.

Obstruction of the left anterior descending (LAD) artery causes anterior or septal MIs because it perfuses the anterior wall and most of the septum of the left ventricle. Patients with anterior wall MIs (AWMIs) have the highest mortality rate because they are most likely to have left ventricular failure and dysrhythmias from damage to the left ventricle.

The circumflex artery supplies the lateral wall of the left ventricle and possibly portions of the posterior wall or the sinoatrial (SA) and atrioventricular (AV) nodes. Patients with obstruction of the circumflex artery may experience a posterior wall MI (PWMI) or a lateral wall MI (LWMI) and sinus dysrhythmias.

In most people, the right coronary artery (RCA) supplies most of the SA and AV nodes, as well as the right ventricle and inferior or diaphragmatic portion of the left ventricle. Patients with obstruction of the RCA often have inferior wall MIs. About half of all inferior wall MIs are associated with an occlusion of the RCA causing significant damage to the right ventricle. Thus it is important to obtain a “right-sided” ECG to assess for right ventricular involvement.

Atherosclerosis is the primary factor in the development of CAD. Numerous risk factors contribute to atherosclerosis and subsequently to CAD (also see Chapter 38).

Nonmodifiable risk factors are personal characteristics that cannot be altered or controlled. These risk factors, which interact with each other, include age, gender, family history, and ethnic background. People with a family history of CAD are at high risk for developing the disease. These factors are discussed in more detail in Chapter 35.

Modifiable risk factors are lifestyle choices that can be controlled by the patient, such as smoking and obesity. These factors are described later in the Health Promotion and Maintenance section of this chapter.

According to the American Heart Association (AHA) (2010), 64% of women and 50% of men who had a myocardial infarction (MI) (“heart attack”) were not aware that they had CAD. The average age of a person having a first MI is 64.5 years for men and 70.3 years for women (AHA, 2010). Almost 30% of patients who have an MI die within 5 years after the event (AHA, 2010).

Every 25 seconds, a person in the United States has a major coronary event and 452,000 people die each year from an MI. Many people die from coronary heart disease without being hospitalized. Most of these are sudden deaths caused by cardiac arrest (AHA, 2010).

Many patients who survive MIs are not able to return to work. CAD is the leading cause of premature, permanent disability in the United States, accounting for about 20% of disability allowances by the Social Security Administration.

The risk for CAD rises as serum cholesterol and triglyceride levels increase. In addition to measuring the total serum cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL), and triglyceride (TG) levels are important in assessing risk for CAD. LDL cholesterol is the “bad” type, and HDL cholesterol is referred to as “good” because it has protective properties. Elevated levels of LDL combined with low levels of HDL increase the risk for MI. Total serum cholesterol levels also put the patient at a higher risk for developing an MI. According to the AHA (2010), a 10% reduction in serum cholesterol may result in a 30% reduction in the incidence of CAD and MI. The fasting total cholesterol should be below 130 mg/dL. The AHA (2010) defines levels of fasting total cholesterol as:

The desired LDL level in patients who are at high risk or have existing CAD is less than 70 mg/dL. For patients at low or moderate risk, LDL should also be substantially less than 100 mg/dL (AHA, 2010). HDL cholesterol levels should be above 40 mg/dL, although this recommendation may soon be changed to a higher level. The recommended triglyceride level is less than 135 mg/dL in women and 150 mg/dL in men (Pagana & Pagana, 2010).

Approaches to decrease lipids are focused on diet, exercise, and drug therapy that lowers cholesterol and triglyceride levels. Teach patients with elevated lipid levels to:

Teach patients that adding omega-3 fatty acids from fish and plant sources has been effective for some patients in reducing lipid levels, stabilizing atherosclerotic plaques, and reducing sudden death from an MI. The preferred source of omega-3 acids is from fish three times a week or a daily fish oil nutritional supplement (1-2 g/day) containing eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) (AHA, 2010). Plant sources (flaxseed, flaxseed oil, walnuts, and canola oil) contain α-linolenic acid, and the conversion of α-linolenic acid to EPA and DHA is not as efficient in patients who consume a typical Western diet (Surette, 2008). Lovaza (omega-3 fatty acids) is a new medication approved by the Federal Drug Administration (FDA) and is used to reduce very high triglycerides (>500 mg/dL) levels. Lovaza has not been proven to prevent heart attacks or stroke.

Garlic supplements may also have a small effect on reducing lipid levels, but they have not been shown to prevent MI. Patients often take a number of other supplements, such as vitamin E, coenzyme Q10, Pantesin, and vitamin B complex to decrease the risk for heart disease. None of these substances has been found to be helpful in reducing coronary artery disease.

In the United States, an estimated 23% of men and 18% of women smoke cigarettes, putting them at increased risk for MI (AHA, 2010). About five million U.S. men and women chew tobacco, with the highest rates in the South and rural areas. Tobacco use and passive smoking from “second-hand smoke” (also called environmental smoke) substantially reduce blood flow in the coronary arteries.

Tobacco use, especially cigarette smoking, accounts for over one third of deaths from CAD. It enhances the process of atherosclerosis through mechanisms that are still poorly understood. Nicotine begins the release of catecholamines, resulting in an increased heart rate and peripheral vasoconstriction. This action causes increases in blood pressure (BP), cardiac afterload, and oxygen consumption. Cigarette smoking has also been found to cause endothelial dysfunction and increased vessel wall thickness. This process increases the risk for clot formation and vessel occlusion. The resulting hypertension may exacerbate the atherosclerotic process by increasing vessel wall permeability. Another problem with cigarette smoking is the production of carbon monoxide, which has been found to decrease the oxygen content in arterial blood. The good news is that when cigarette smoking is stopped, the risk for CAD decreases. A person who stops smoking may decrease the risk for CAD by as much as 80% in 1 year. Reducing the tar and nicotine content of the cigarettes smoked does not reduce the risk for CAD (AHA, 2010).

Ask about tobacco use, and advise the tobacco user and family members who smoke to quit using this harmful substance. Teach all patients to avoid environmental tobacco smoke at work and at home if at all possible. Additional information about tobacco use and smoking cessation is found in Chapters 32 and 35.

Physical inactivity may be the most important risk factor for the general population. Less-active, less-fit people have a 30% to 50% greater risk for developing high blood pressure (BP), which predisposes to CAD. Physical inactivity is more common among women than men, among African Americans and Hispanics than Euro-Americans, among older adults than younger adults, and among the less affluent than the more affluent (AHA, 2010). The causes for these differences are not known. Teach patients that regular physical activity helps maintain body weight and muscle mass while improving BP and lipid values.

Moderate-intensity activities like walking are associated with a major reduction in CAD risk. However, intense exercising may contribute to plaque rupture and increase the number of cardiac episodes. Teach people that participating in exercise for 30 minutes a day can reduce hypertension and increase secretions of endorphins. It also leads to decreased smoking and eating, improved metabolism, and a stronger feeling of well-being. Other benefits include decreased blood clotting and higher plasma HDL levels, increased heart volume, increased cardiac capillary blood flow, and decreased heart rate. Physical activity does not increase collateral circulation or reduce the size of existing plaques.

One in three Americans has hypertension (HTN). This disease increases the workload of the heart, which increases the risk for MI. The cause of primary HTN is not known. However, it is easily detected and usually controllable. About half of patients having a first MI have a BP greater than 160/95 mm Hg. Ways to manage hypertension and therefore reduce the risk for CAD are described in Chapter 38.

Diabetes mellitus (DM) is a major risk factor for heart disease. A woman with diabetes mellitus is twice as likely to develop CAD than a woman without DM. Heart disease is the leading cause of diabetic-related death in both men and women. Most adults with diabetes also have hypertension. Chapter 67 discusses vascular complications of diabetes in detail.

Obesity is strongly associated with the development of hypertension, diabetes, and increased serum lipid levels. Women with fat deposited around their waists are at the highest risk for CAD. Teach the importance of weight management to help prevent these chronic and potentially life-threatening diseases.

Alcohol may help prevent or contribute to the development of CAD, depending on the amount consumed. Excessive consumption, described as having more than 3 ounces (90 mL) per day, can lead to increased heart disease, hypertension, and metabolic syndrome, described in the next section. A lower amount may help prevent CAD (Suzuki et al., 2009).

A person’s response to emotional stress may also be associated with heart disease. Work stress, in particular, may be associated with left ventricular hypertrophy. During times of stress, increased heart rate increases the work of the heart, thus causing changes in the left ventricle.

Metabolic syndrome, also called syndrome X, has been recognized as a risk factor for cardiovascular (CV) disease and is being aggressively researched. Patients who have three of the factors in Table 40-1 are diagnosed with metabolic syndrome. This health problem increases the risk for developing diabetes and CAD. About 47 million people in the United States have metabolic syndrome (AHA, 2010). This increase is likely due to physical inactivity and the current obesity epidemic. Management is aimed at reducing risks, managing hypertension, and preventing complications.

Elevated levels of serum homocysteine, an amino acid, have been associated with an increased incidence of CAD. However, research findings are not consistent regarding its risk. Vitamin B supplements have been thought to decrease homocysteine. Recent studies suggest that vitamin B is not effective as secondary prevention, but few studies have been conducted on vitamin B as a primary preventive measure (Ebbing et al., 2008).

Patients with multiple modifiable risk factors have several times the risk for CAD as those without these characteristics. Although many factors place a person at risk for heart disease, there are well-documented, effective ways of promoting cardiovascular health. The most important interdisciplinary intervention is health teaching.