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A lot of people still aren't getting the message that heart disease is the leading cause of death and disability among American women today. All too often, patients and health care providers alike seem unaware of this fact. Heart disease will become an increasingly significant public health concern for society as the huge baby boomer generation continues to age. Because women typically live longer than men, it's an especially important issue for them.
Heart disease is not an inevitable consequence of normal aging. The risk factors for heart disease have been clearly identified, and many of them can be modified to such an extent that development of heart disease can be delayed or even halted. While new medications and procedures have revolutionized the treatment of heart disease over the past decade, basic measures such as a healthful diet, weight control, exercise, and smoking cessation remain the cornerstones of prevention.
Nurses are vital in the management and treatment of heart disease in every setting. They can serve as role models to their own families and communities through their lifestyle choices. Nurses have the opportunity to educate patients and families about heart disease, whether in an acute care facility or a health care provider's office. Through education comes the knowledge to help prevent heart disease - information that can improve the quality of life for millions of women.
Chapter One: Women and Heart Disease: An Equal Opportunity Killer
A generation ago, heart disease was considered a man’s problem. Today, we know better, and the statistics are stunning. It is the leading cause of death for all American women regardless of ethnicity. In 2004, the latest year for which complete figures exist, cardiovascular disease killed over 461,150 American women while combined cancer deaths ran a distant second at 272,810.1,2 The cardiovascular death rate of 150/100,000 for American women exceeds that of most European countries, Canada, Japan, Israel, Australia, and New Zealand.1,3 Overall, about 7.2 million American women are living with heart disease today.3
In the United States, about half of all female deaths are due to cardiovascular disease, and one in three adult females has some form of it.1 While more women today than in the past are aware that heart disease is the leading killer of women (46% knew it in 2003 compared to 30% in 1997), only 13% of women in one study felt it was their greatest personal health risk.4 Instead, the majority of women continue to identify cancer, especially breast cancer, as the biggest risk to their own health.4 This makes the prevention, identification, and treatment of heart disease an important public health concern for nurses, and a pressing personal concern for all women.
While the term cardiovascular disease includes stroke, coronary heart disease, valvular disease, rheumatic heart disease, and congenital heart defects, this home study course will focus on coronary heart disease (CHD) and the conditions most closely associated with it. It will discuss normal cardiac function and the development of CHD. The differences in how CHD affects females and males will be explored. Current diagnostic procedures as well as medical and surgical treatments for heart disease will be reviewed.
The course will review the risk factors for heart disease, concentrating on those that can be modified to prevent or mitigate its development and progression. A chapter on case studies will provide nurses the opportunity to practice critical thinking skills using the new information provided in the course. Among topics included in the appendices are heart-healthy food selections, a sample exercise program, and a list of resources for additional information.
Gender bias?
Evidence is mounting that the differences in how heart disease affects women and men are very real. Even some of the risk factors described in the next chapter that are common to both sexes are stronger predictors of CHD in women than men. Because many women don’t perceive heart disease as a substantial risk to themselves, they often delay seeking treatment longer than men do, possibly because their symptoms don’t follow the well-publicized pattern of heart disease in men. Instead, symptoms may be attributed to the flu, indigestion, or fatigue.5 Other reasons for the delay in seeking treatment for possible cardiac problems include older age, social isolation, lower socioeconomic status, insurance reasons, lack of access to health care, and caregiver responsibilities.5
Many women may feel their physician won’t take them seriously or that their symptoms are not bad enough to warrant attention.5 However, even when women experience symptoms and report them to their providers, the symptoms may go unrecognized as indicative of heart disease or may be misdiagnosed. Often, women’s complaints are wrongly attributed to mental rather than physical problems.6 Even when a physician correctly recognizes the signs of cardiac problems in a woman, she probably won’t receive the aggressive diagnosis and treatment that a man would receive. For example, she is less likely to receive thrombolytic therapy and to be referred for coronary angiography or percutaneous coronary interventions.5,6
Signs of heart disease are more subtle in women than in men, less obvious than the hallmark symptom of severe left-sided chest pain. The leading early warning symptom of myocardial infarction for women is unusual fatigue, followed by sleep disturbances, shortness of breath, indigestion, and anxiety during the previous month.7 Symptoms indicating the onset of acute MI in women include shortness of breath, weakness, fatigue, cold sweat, and dizziness.7 While clinicians continue to consider chest pain the most important symptom for both sexes, 43% of the women in one study experienced no chest pain.7 In fact, approximately 64% of women who died suddenly of CHD experienced no symptoms.1
Healthcare providers need to recognize and treat cardiac risk factors and heart disease in women just as aggressively as in men. While the death rate from cardiovascular disease has decreased for both sexes in recent years, it has decreased less in women than in men.6 The less-frequent recognition of heart disease in women can have deadly consequences. Approximately 38% of American women die within the first year of a heart attack compared to 25% of men.5 About 35% of women will suffer another MI within a year compared to 18% of men.5 And women are twice as likely as men to die after having bypass surgery.5
Not only does heart disease affect women differently than men, it affects women among various ethnic groups differently. Because an increasingly large number of American women are members of minority ethnic groups, it’s vital to recognize how heart disease affects these groups. For example, 6% of white women aged 20 and older have CHD while 7.8% of African American women have CHD, largely because African American women experience a higher rate of diabetes, hypertension, and obesity.8,9 African American women aged 55 to 64 are twice as likely to have an MI as white women.5
For years, research into heart disease focused primarily on men. Now that we know heart disease is the biggest killer of women, females as well as males are being included in studies of heart disease and its risk factors. A number of major research projects are under way that focus exclusively on heart disease in women. These include research into the best method to evaluate cardiac ischemia in women, the use of stress echocardiography as a diagnostic tool in women, the reduction of triglycerides in women, and the effects of healthy lifestyles for women. While additional research is needed about CHD in female minority populations, these studies will go a long way toward better understanding and treatment of heart disease in women.
What is heart disease?
During the course of a 70-year lifespan, the average human heart beats more than 2.5 billion times. Not only must the heart energetically pump 2,000 gallons of oxygenated blood to every part of the body during its 100,000 daily beats, it must also oxygenate itself while doing so. Blood flow to the heart is supplied by the left and right coronary arteries, which branch off the aorta right after it leaves the left ventricle. The coronary arteries fill when the left ventricle contracts, forcing blood out of the heart through the aortic valve and into the aorta. The outflow of blood from the left ventricle fills the coronary arteries via the coronary sinus valves, which lie just beyond the aortic valve.
The left coronary artery then branches into the left anterior descending and circumflex arteries. Together, these important arteries supply blood to the anterior portion of the septum, the anterior muscle mass of the left ventricle, and the lateral wall of the left ventricle. The right coronary artery supplies blood to the posterior portions of the heart and to the vital electrical generation sites of the heart—the atrioventricular and sinoatrial nodes. (See Figure 1.) The left ventricle receives the most blood because it’s the largest chamber and it works the hardest. In the healthy heart, blood flow to the coronary arteries increases with demand, as with exercise or excitement.
Science continues to gain insight into arteriosclerosis, the primary cause of CHD. Atherosclerosis is a complex process characterized by patchy thickenings within the intima (the endothelial or innermost layer) of the coronary arteries. Atherosclerosis occurs in medium and large arteries, especially in regions of turbulent blood flow where smaller arteries branch off from larger ones. Such areas may promote endothelial injury and inhibit production of nitric oxide, a substance that has both vasodilator and antiinflammatory properties.10
Atherosclerosis is believed to be essentially an inflammatory response causing endothelial injury. Atherosclerotic plaque gradually forms at the sites of injury. Plaque contains lipids; inflammatory cells (i.e., macrophages, T-cells); smooth muscle cells; connective tissue (i.e., collagen); thrombi; and calcium deposits. The earliest detectable lesions of atherosclerosis are fatty streaks inside the artery formed when low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) bind to endothelial cells and are oxidized in the
Figure 1

subendothelium. Macrophages transform these cells into lipid-laden foam cells, resulting in the characteristic white streaks.10
Macrophages also stimulate proinflammatory cytokines that recruit smooth muscle cells from the media (the middle arterial layer) to the intima, resulting in more macrophages and more inflammation. Calcification occurs within the plaque via a process similar to bone formation.10 Over time, the plaque develops a fibrous cap made of smooth muscle cells surrounded by connective tissue, as well as intra- and extracellular lipids.
The strength of the fibrous cap over the lesion determines whether the plaque is stable or unstable. Some atherosclerotic plaques are stable and may regress, remain static, or grow gradually over several decades until they cause stenosis or occlusion of the artery. (See figure 2.) It is not uncommon for such stable plaques to occlude an artery by more than 50%; they may result in predictable, exercise-induced stable angina.10 This is the scenario previously believed to be responsible for CHD. Stable plaques are the less common outcome of atherosclerosis; much more common are the unstable plaques.10
Figure 2

In unstable plaques, the fibrous cap’s resistance to rupture depends on its strength and composition. Unstable plaques with weak caps are vulnerable to erosion and rupture, leading to acute thrombosis, arterial occlusion, and myocardial infarction long before they are large enough to cause stenosis. In many cases, these plaques did not appear to be significant during angiography. Events at the cellular level result in T-cells secreting cytokines, which inhibit smooth muscle cells from synthesizing and depositing collagen, a process that tends to reinforce and strengthen the cap.10
Ultimately, the cap ruptures, exposing its contents to circulating blood. This triggers thrombosis, the formation of a blood clot at the injured site. Five possible outcomes occur:10
Plaque stability depends on many factors, such as the proportion of lipids, inflammatory cells, smooth muscle cells, connective tissue, and location in relation to blood flow. Intraplaque hemorrhage may have an important role in transforming a once-stable lesion into an unstable one. Unstable plaques have a higher macrophage content and a thick lipid core. They may narrow the vessel by less than 50% and tend to rupture unpredictably.10 A stable plaque has a thicker cap and fewer lipids.
A new view of CHD in women is emerging ? the concept of microvascular dysfunction. Discoveries from the federally funded Women’s Ischemia Syndrome Evaluation (the WISE study) show that many women have a form of heart disease that may explain their atypical symptoms. Rather than showing large plaques partially occluding major coronary arteries (as occurs with men who have CHD), new tests reveal that the coronary arteries and the smaller arteries feeding the myocardium become stiff and fail to dilate properly and so cannot accommodate the increased blood flow needed during activity or stress.11 This helps to explain why many women don’t experience the classic crushing chest pain signaling a major coronary event. Instead, they suffer diffuse discomfort, exhaustion, shortness of breath, and other symptoms at rest and during daily routines. As vessels continue over time to lose their elasticity, blood flow is reduced, and many small areas of the myocardium gradually die rather than dying suddenly as often happens with men.11
At present, this microvascular disease is difficult or impossible to detect with standard diagnostic procedures. For example, a woman with a positive stress test is 4.5 times more likely than a man with a positive stress test to have a normal-appearing angiogram. Also, it may explain why women who have angioplasty and coronary artery bypass surgery don’t do as well as men. Opening the large coronary arteries in the presence of microvascular disease is not
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Table 1 |
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2007 Evidence-based Guidelines The American Heart Association has released new evidence-based guidelines for the prevention of cardiovascular disease in women that it developed along with organizations including the Centers for Disease Control and Prevention; the National Heart, Lung, and Blood Institute; the · Recommended lifestyle changes to help manage blood pressure include weight control, increased physical activity, alcohol moderation, sodium restriction, and an emphasis on eating fresh fruit and vegetables and low-fat dairy products. · Women who smoke should stop. If necessary, they should use counseling, nicotine replacement, or other forms of smoking cessation therapy. · Physical activity recommendations for women who need to lose weight or sustain weight loss include a minimum of 60 to 90 minutes of moderate-intensity activity (e.g., brisk walking) on most, and preferably all, days of the week. · All women should try to reduce their saturated fat intake to less than 7% of calories. · Hormone replacement therapy and selective estrogen receptor modulators are not recommended to prevent heart disease. · Antioxidant supplements (such as vitamins E and C and beta-carotene) should not be used for primary or secondary prevention of CVD. Folic acid should not be used to prevent CVD. · Routine low-dose aspirin therapy may be considered in women 65 or older regardless of CVD risk status if benefits are likely to outweigh risks. The upper dosage of aspirin for high-risk women increases to 325 mg per day from 162 mg. |
enough. Scientists postulate that inflammation is at the heart of this process, and women have many more inflammatory and autoimmune diseases than
do men.11
The human body is very adaptable, and it may take decades for symptoms of CHD to appear. However, when blood flow reaches critically low levels due to narrowing or constriction or is completely shut off due to obstruction, cells beyond the blockage are damaged because they don’t receive enough oxygen. The decreased levels of oxygen kick anaerobic metabolism into action, and the resulting lactic acid causes the chest pain of cardiac ischemia (angina).
Heart function is an incredibly complex process involving the interaction of electrical, neurogenic, mechanical, and chemical functions. All of these activities require a continuing supply of oxygen. If blood flow through a coronary artery is blocked for longer than a couple of hours, myocardial heart cells beyond the blockage suffer irreparable damage and die. Acute coronary syndrome or myocardial infarction, with its myriad of consequences, results. The next chapter will discuss the major risk factors leading to the development of CHD in women.
Chapter Two - Recognize the Risk Factors for CHD
What does risk mean? Used in a health context, it represents the likelihood of developing a particular disease, disability, or cause of death. However, risk is about vulnerability, not inevitability. Everyone will have at least one uncontrollable risk factor for developing coronary heart disease, such as aging, gender, genetics and family history, or past behavior. Some risk factors common to both women and men affect women differently than men. Having several risk factors multiplies the chance of developing CHD. The amplification of these combined risk factors makes it critical to modify those that can be controlled. You can’t change your age or your genes; however, some of the most serious risk factors are within a woman’s ability to completely or at least partially control. Every woman should be aware of her risk factors. The first step is, of course, assessment. Yet physicians and other healthcare professionals are not doing enough to assess their female patients and counsel them about ways to reduce the risk factors for heart disease, such as regular exercise, good nutrition, and weight reduction. In fact, only one-third of women recall discussing heart disease risk with their healthcare providers.1 Women also receive fewer lifestyle advice, lipid-lowering therapy, and optimal control of hypertension.1 Documentation in the medical record of cardiac risk factors may well increase the likelihood that discussions between patient and healthcare provider will routinely occur during future visits.
The next section discusses the risk factors for CHD that cannot be changed (age, gender, genetics, and family history); the six major risk factors that can be changed or at least partially controlled (smoking, hypertension, hyperlipidemia, diabetes, physical inactivity, and obesity); and some of the lesser or newly emerging contributing risk factors (alcohol, homocysteine, stress, C-reactive protein, periodontal disease, hypothyroidism, and air pollution).
Risk factors you can’t change
Heredity
Children of parents with heart disease are more likely to develop it regardless of ethnicity, probably because of a combination of genetic and environmental conditions, such as poor eating habits and a pattern of inactivity. A woman whose father or brother developed CHD before age 55 or whose mother or sister developed it before age 65 is at a higher risk of developing CHD herself than is a woman whose family has little or no heart disease.2 Certain ethnic groups are also at increased risk, again, partly because of genetics and partly because of cultural factors. For example, African Americans have more frequent and more severe hypertension than Caucasians, giving them a higher rate of CHD.3 Heart disease is also higher among Mexican Americans and American Indians, partially because of the higher rates of obesity and diabetes.3 Women with a known family history of heart disease should be especially vigilant in controlling risk factors that can be mitigated by lifestyle changes.
Age and gender
Increasing age is a constant risk factor for both men and women. Over 83% of people who die of CHD are 65 or older.3 Both sexes have more heart-related problems associated with aging, such as hypertension, high cholesterol levels, obesity, diabetes, and inactivity. While it must be remembered that CHD is the biggest killer of American women, women remain at lower risk for the disease than do men at all ages. For example, the lifetime risk of developing CHD after age 40 is 49% for men and 32 % for women.4 The incidence of CHD in women lags behind men by 10 years and by 20 years for more serious clinical events, such as MI and sudden death.4 The cardioprotective effect of endogenous estrogen is readily apparent; CHD rates in women after menopause are two to three times higher than those of women the same age before menopause.4 The average age of first MI in men is 65.8 years and for women, 70.4 years.4 Because women on average are older than men when they have an MI, they are more likely to die of the MI within a few weeks.3
In 2007, researchers announced a surprising new finding relating to the significance of inflammation in women. In a large study, a previously unknown gene was discovered that makes women, but not men, more susceptible to developing CHD.5 Both sexes participated in the study, which followed the group from their teens into their 40s. While some people of both sexes carried the gene (Leukotriene C4 synthase, or LTC4S), it was linked to premature heart disease only in women. The gene leads to an excessive inflammatory response at the site of blood vessel injury in women; these women cannot repair damage to their blood vessels as well as women without the gene. Previously, the gene has also been linked with an increased risk of asthma, another inflammatory disease.5
Risk factors you can change
Smoking
There’s no two ways about it: Smoking is a woman’s single biggest risk factor for heart attack.6 Approximately 18.5% of American women smoke, compared to 23.4% of men.7 While fewer women than men traditionally smoke, that difference is decreasing, largely because the number of adolescent females who smoke is going up.7 While smoking is the biggest preventable risk factor for CHD for both sexes, it is more strongly associated with increased risk in women. For example, a smoking man has a 45% greater risk of developing congestive heart failure than does a nonsmoking man; for a smoking woman, the risk of developing CHF is 88% higher than for a nonsmoking woman.8 Male smokers die 13.2 years earlier than do male nonsmokers while female smokers die 14.5 years earlier than their nonsmoking sisters.4 Women who smoke and use oral contraceptives also greatly increase their risk of CHD compared to women who don’t smoke, especially if they are over 35 years old.6 Heavy smokers ¾ those who smoke two or more packs per day ¾ are up to 20 times more likely to develop CHD than are nonsmokers.2
Overall, smokers’ risk of developing CHD is two to four times that of nonsmokers.3 There are no safe cigarettes, and there is no safe level of smoking. Not only does smoking lead to more severe atherosclerosis, it increases blood pressure, decreases exercise tolerance, increases the tendency for blood to clot, and decreases the amount of cardioprotective high-density lipoprotein (HDL), all risk factors for CHD.6 And, of course, smoking increases the risk for several kinds of cancer (especially lung cancer), as well as decreased bone density.6,7 Nonsmokers are not necessarily safe either: Between 37,000 and 40,000 people die of cardiovascular disease each year as a result of secondhand smoke.6
Women should not smoke and should avoid environmental tobacco smoke.9
Hypertension
Not only is hypertension one of the major risk factors for CHD, it’s also the biggest one for stroke and a major cause of CHF and renal failure, as well. When hypertension exists with other risk factors such as smoking or diabetes, the risk of heart attack greatly increases. An estimated 75 million Americans have hypertension, making it a widespread concern for all healthcare workers.4 In 95% of people with hypertension, no individual cause can be ascertained (essential or primary hypertension).10 Development of hypertension is believed to have multiple causes, including genetic and environmental factors. Hypertension is a complex process and may include the following pathologies:10,11
The incidence of hypertension varies by age, sex, and ethnicity. Before age 45, more men than women have hypertension; between ages 45 and 54, the numbers are approximately equal; after that, the rate of hypertension among women greatly exceeds that of men.4 Hypertension is an especially severe problem among African American women, with 46.6% of them having hypertension compared with 31.9% of whites and 31.4% of Mexican Americans.4 High blood pressure is also two to three times more common among women taking oral contraceptives than in women not taking them, especially if they are obese, smoke, or are over 35.4
The traditional definition of hypertension is a blood pressure reading at or above 140/90. (See Table 8, “Classification of Blood Pressure for Adults,” on page 67 for descriptions of hypertension and prehypertension.) Although screening for hypertension is widely available, many women don’t know that they have it. Even after hypertension is identified, it often goes untreated or is inadequately treated. It’s extremely important to control hypertension. The risk of developing cardiovascular disease starting at 115/75 mmHg doubles with each increment of 20/10 mmHg.12 Nearly 69% of people who have a first heart attack, 77% of people who have a first stroke, and 74% of people with heart failure have blood pressure readings over 140/90.4 The number of deaths due to hypertension are increasing, rising by 54.6% between 1994 and 2004.4 Data from the Framingham Heart Study show that Americans who are normotensive at age 55 will still have an estimated 90% risk of eventually developing hypertension.12
Encourage an optimal blood pressure of less than 120/80 through lifestyle approaches.9
Hyperlipidemia
Cholesterol is a fatty substance that is carried in the blood in “packages” called lipoproteins. Three commonly measured components of cholesterol are total cholesterol; low-density lipoproteins (LDL), also called “bad cholesterol”; and high-density lipoproteins (HDL), or “good cholesterol.” LDL carries fat from the liver to the rest of the body, unloads fat in the cells, and circulates it in the blood. An elevated LDL means that more fat will be deposited in the coronary arteries as LDL circulates through the blood stream. LDL first binds to the endothelial cells lining the coronary arteries, then oxidizes, becoming a major component of harmful plaque and a significant contributor to the development of CHD.11 In general, the higher the LDL, the greater the risk of CHD although an elevated level of LDL is less predictive of CHD in women than in men.8
On the other hand, HDL protects against the development of atherosclerosis and CHD by picking up LDL deposits in the blood, thereby preventing them from building up in the arteries. HDL carries LDL back to the liver to be destroyed. Low levels of HDL reduce the body’s ability to fight LDL. The higher the HDL level, the lower the risk of CHD. Throughout the lifespan, HDL in women is five to 10 points higher than in men, and a low level of HDL is a stronger predictor of heart disease for women than for men.8
Triglycerides are another type of fat carried in the blood that is produced in the liver and ingested in food. In women, triglycerides rise after menopause and by age 65 exceed those of men .8 Elevated triglycerides are considered more of a risk factor for CHD in women than in men.8 Obesity, diabetes, alcohol consumption, and a high intake of saturated fat all contribute to elevated triglycerides. Some forms of genetic high triglycerides are an independent risk factor for CHD, producing an increase in CHD mortality, even in the presence of normal cholesterol. This makes it important that every woman know all her lipid levels. (See Table 3, “Looking at Lipids,” on page 34.)
Even with everything that’s known about the dangers of hyperlipidemia, many people are not taking the message to heart. Over 55 million women are estimated to have a total cholesterol at or above 200 mg.4 Reducing total cholesterol by just 10% may result in a 30 % reduction in CHD!4
Optimal levels of lipids and lipoproteins in women are LDL less than 100, HDL over 50, triglycerides under 150, and non-HDL (total cholesterol minus HDL) under 130. These should be achieved/maintained through lifestyle approaches.9
Diabetes
Diabetes adversely affects every organ and tissue in the body, including the cardiovascular system. It is closely associated with hypertension, dyslipidemia, obesity, and inactivity, all of which are additional compounding factors in the development of CHD. The chronic systemic inflammation caused by frequent hyperglycemia irritates blood vessel walls and contributes to atherosclerosis. In fact, diabetes is so damaging to the heart that a woman with diabetes is considered to be at the same risk from CHD as someone who already has the diagnosis of CHD.13
An estimated 9.7 million American women – about 8.8% – are known to have diabetes.14 However, an additional 2 million to 3 million more women may have diabetes but have not yet been diagnosed.14 Diabetes does not strike all ethnic groups equally. African American, Mexican American, and American Indian women all have greater rates of diabetes than do white women while Asian women experience the lowest rate.4 Only about 10% of people with diabetes have Type 1 diabetes (characterized by insulin deficiency), which is largely genetic; 90% have Type 2 diabetes (characterized by defects in insulin secretion and sensitivity), which is closely linked to poor diet, overweight and obesity, and a low level of physical activity.15
Approximately two-thirds of people with diabetes will die of CHD; all too often, people with diabetes are unaware that CHD is the biggest threat to their health.4 Overall, the risk of CHD death among women with diabetes is more than three-fold greater than among women without it.8 Regardless of the presence of other cardiac risk factors, CHD and heart-related death are higher for women with diabetes than for men with diabetes. For example, the past few years have seen a decline in CHD mortality of 13% in men with diabetes, but an increase in CHD mortality of 23% among women with diabetes.15 Additionally, post-MI outcomes are worse for women with diabetes than men with diabetes at 28 days and two years.14
Lifestyle and pharmacotherapy should be used to achieve an HbA1c under 7% in women with diabetes.9
Obesity
Overweight and obesity are generally measured with government tables for body mass index. (See Chapter 4.) A woman is overweight if her BMI is between 25 and 29.9, obese between 30 and 39.9, and extremely obese at 40.0 or higher.4 Obesity is less often calculated by DEXA scan (dual energy X-ray absorptiometry), measuring the thickness of body fat with calipers, sending a small amount of electricity through the body, or putting a person in an underwater chamber that uses air displacement to measure body volume.16
Obesity is at epidemic levels in the
More men than women are overweight, but more women than men are obese. Obesity a major risk factor for CHD, as well as Type 2 diabetes, hypertension, and hyperlipidemia, all separate risk factors for CHD.16 Women who are obese are more likely than nonobese women to develop cancer of the gallbladder, uterus, cervix, and ovaries.16 Obesity is also linked to stroke, fatty liver disease, osteoarthritis, gout, reproductive problems, and gastroesophageal reflux (the primary cause of esophageal cancer.)16
Obesity increases CHD risk via several mechanisms: It increases cardiac preload, increases cardiac output, and expands plasma volume.16 There is an increase in stroke volume and left ventricular filling pressures as demands on cardiac output rise. Obesity increases hypertension substantially; a 10% increase in body weight increases systolic blood pressure an average of 6.5 mmHg.8
Metabolic syndrome is a group of five risk factors that when considered individually may not be significant, but when occurring in a group greatly increase the risk for CHD. If three out of five of the following factors are present, a woman is considered to have metabolic syndrome:17
Nearly one-fourth of
Women should maintain or lose weight through an appropriate balance of physical activity, caloric intake, and formal behavioral programs when indicated in order to maintain or achieve a BMI between 18.5 and 24.9 with a waist circumference of under 35 inches.9
Sedentary lifestyle
The heart is just like any other muscle?regular exercise is required to keep it working effectively and efficiently. Obesity and physical inactivity are closely related. In general, people who are more physically fit have a better lipid profile, less hypertension, less diabetes, and overall less heart disease than do sedentary people.
The increased risk of CHD associated with inactivity ranges from 1.5 to 2.4, a risk increase comparable to that of high cholesterol, hypertension, and smoking.4 Yet a woman doesn’t have to run a weekly marathon to benefit her cardiovascular health. For example, exercising at moderate intensity (for example, rapid walking) for 30 minutes, five days a week, coupled with a 5% to 7% weight loss can prevent or delay the onset of Type 2 diabetes, which is a major risk factor for CHD.16 The risk for angina, MI, and sudden death is two to three times higher among women with the lowest level of physical activity compared to those with the highest level.18
Despite the proven benefits of exercise, most women are not getting enough; up to 25% of women admit they do not get any regular physical exercise at all.6 In 1996, only 28% of women got the recommended amount of physical activity each week; by 2004, that number had grown to only 29%.4,13 Traits associated with higher levels of exercise include being male, young, white, college-educated, and in higher income brackets.4 People with lower levels of physical activity include women, older people, people from minority groups, and those with less education.4 Physical inactivity is higher in African American, Mexican American, and American Indian women.4
Women should accumulate a minimum of 30 minutes of moderate-intensity physical activity on most, and preferably all, days of the week.9
Other risk factors
There are a few other risk factors that may contribute to CHD that are newly identified or of relatively lesser significance than the major factors described above. These include:
Alcohol: Drinking too much alcohol can raise blood pressure, lead to high triglycerides, and contribute to obesity.3 However, the risk of heart disease for moderate drinkers (defined as one drink per day for women) is lower than for nondrinkers.3
Psychosocial factors: Stress can increase blood pressure, heart rate, and the demand for myocardial oxygen and can sometimes lead to myocardial ischemia and angina. While it is difficult to study the impact of human behavior on cardiovascular disease in the laboratory, personality traits such as anger and hostility, as well as psychological states like anxiety and depression, may very well contribute to CHD or trigger cardiovascular events.19,20
Hypothyroidism: Hypothyroidism, with its many systemic symptoms, has come to be recognized as a common disease of older women that is all too frequently misdiagnosed. Left untreated, it may result in hyperlipidemia and increased disease of the coronary arteries.2
C-reactive protein: C-reactive protein is part of the body's normal response to infection and inflammation. Chronically elevated levels indicate a chronic inflammation of the coronary arteries and are associated with an increased risk for angina, heart attack, and death.21 Studies are showing that C-reactive protein appears to be an independent predictor of cardiovascular disease in women, but not in men.21,22 One source found it to be a better indicator of CHD in women than are elevated total cholesterol and LDL.21
Homocysteine is an amino acid formed by the breakdown of a dietary protein that is highly toxic to vascular endothelium. It is present in increased amounts in women after menopause. Even a mild elevation appears to increase the risk for CHD. In one study of MI among women younger than 45, those with the highest levels of homocysteine had 2.3 times the risk of MI compared to those in the lowest quartile.18 Adequate levels of dietary folate help to break homocysteine down into harmless substances.18
Periodontal disease: Emerging studies suggest that periodontal disease may be associated with CHD and acute MI. Diseased gums have been shown to release large amounts of bacterial endotoxins into the bloodstream. Endotoxins promote the inflammatory response and trigger the liver to produce more C-reactive protein, a known predictor for cardiovascular disease. DNA of known oral pathogens has been identified in atherosclerotic plaques, as well.23 However, it remains uncertain if the etiology of increased risk for CHD in the presence of periodontal disease is primarily due to the oral bacteria themselves or to the systemic inflammation they induce.24
Oral contraceptives: The older, higher-dose of oral contraceptives increased the risk for both fatal and nonfatal MI among women. Today's lower-dose pills have little or no risk associated with them, except for women who are heavy smokers, especially those over age 35. One study suggested a five-fold increase in the risk of MI among women who both smoke and use oral contraceptives while another study found no increased risk among women 18 to 44 who take oral contraceptives and smoke.18
Sleep deprivation: A newly recognized risk factor for cardiovascular disease is chronic sleep deprivation. One study showed that people who napped at least three times a week for 30 minutes had a 37% lower coronary mortality than those who did not nap.25 Another study, based on results of the Nurses Health Study, showed that people who slept five hours or less per night had a 45% increase in risk for CHD after adjusting for confounding factors.26 Busy women should think about allowing themselves to nap during the day when they have time or if they can make time.
Air pollution: Another risk factor newly identified in 2007 is the effect of long-term air pollution, especially that known as fine particulate matter (less than 2.5 microns in diameter).27 A study showed that postmenopausal women living in areas with high levels of air pollution had a greater risk of developing cardiovascular disease and dying of it than those living in areas of lower pollution.27 Researchers found that each 10-unit increase in fine particulate matter was linked to a 24% increase in the risk of a cardiovascular event and a 76% increase in the risk of cardiovascular death for the women after correcting for other risk factors, such as hypertension, high cholesterol, and smoking.27
There is hope!
With all these risks for heart disease, it seems inevitable that every woman will die of a heart attack sooner or later, but it’s not necessarily so. As we’ll see in later chapters, many of the risk factors for CHD are under a woman’s direct control, and even a small reduction in some of them can significantly increase the chance for a healthy and productive life. In fact, a woman can reduce her risk of CHD by an astonishing 82%, simply by living a healthy lifestyle.28 As more and more studies now include women, better ways will be developed to control or modify heart disease in females.
Chapter Three: Modify Risk Factors: Lipids and Estrogen Update
Think you can’t live without pepperoni pizza, bacon and egg breakfasts, and dishes of Chunky Monkey ice cream piled high? Think again. Those foods are loaded with cholesterol and saturated fat, major contributors to hyperlipidemia. Whether it’s called high cholesterol, dyslipidemia, or hyperlipidemia, a high level of fat in the blood is one of the primary causes of heart disease. Many of the risk factors discussed in the previous chapter can be modified. This chapter and the following three will discuss how to make changes that can greatly benefit a woman’s heart and health, starting with changes to improve hyperlipidemia.
Remember that combined risk factors multiply rather than add to the chance of developing CHD. The presence of multiple risk factors creates a pattern of morbidity that spirals downward toward heart disease, disability, and death. Hyperlipidemia, obesity, and inactivity are closely related. Breaking one link in this risky triad can bring about healthful changes in the other risk factors, as well. While there are genetic causes for several kinds of hyperlipidemia, this chapter will concentrate on hyperlipidemia caused primarily by dietary excesses that can be voluntarily modified.
What‘s it all about?
The two main lipids (fatty substances that are insoluble in water) carried in the blood are cholesterol and triglycerides. Cholesterol is a waxy, fat-like material
that occurs naturally in all parts of the body. It's an essential element in the formation of many tissues, cell membranes, nerve cells, hormones, and bile acids. The liver makes about 1,000 mg of cholesterol daily (all that people need) from dietary fats and stored carbohydrates.1 Excess cholesterol comes from dietary intake, especially meat, poultry, egg yolks, and regular dairy products; somewhat less cholesterol is found in seafood and fish. Plant foods do not contain cholesterol although some contain fat. Triglycerides are also produced in the liver using dietary fats and calories (especially those due to excessive alcohol intake).
Before menopause, women’s cholesterol is usually lower than men’s, but it begins to climb at age 40 and exceeds that of men after menopause.2 The higher the level of total cholesterol and LDL, the greater the risk of CHD; conversely, the higher the level of HDL, the lower the risk of heart disease. Research has shown that high levels of triglycerides and low levels of HDL appeared to be stronger risk factors for heart disease in women than in men, and that elevated LDL is less predictive in women than men.2
There are no symptoms of high cholesterol. The rate of high cholesterol and abnormal lipids varies somewhat by ethnicity although not as much as some of the other cardiac risk factors. (See Table 3.)
Table 3
Lipid Levels in American Women
Cholesterol above LDL at or above HDL less
Ethnicity 200 mg/dL 240 mg/dL 130 mg/dL than 40 mg/dL
White 49.7% 18.2% 33.8% 8.8%
African American 42.1% 12.5% 29.8% 6.9%
Mexican American 50.0% 14.2% 30.7% 13.0%
Source: See Reference 3.
More than 55 million American women have a total blood cholesterol above the recommended level of 200 mg/dL, putting them at increased risk for heart disease.3 The importance of controlling lipids cannot be overemphasized. For example, a 10-point decrease in total cholesterol may reduce the risk of CHD by as much as 30% while each 5 mg/dL increase in HDL reduces the risk by 10%.2,4 This makes it imperative for every woman to know her lipid levels and keep them in line with recommendations.
In patients without known CHD, lowering lipids has been shown to reduce first cardiac events up to 37%.5 In people with existing CHD, a reduction in lipids can decrease coronary deaths by 24% to 42% and can reduce mortality from all causes by 30%.5 Improvement in lipids is also associated with a decreased risk of stroke and a lesser need for angioplasty and coronary bypass surgery.5
Conditions that can adversely affect lipid levels include:4
Screening
While each woman should check with her healthcare provider to ascertain a lipid screening schedule appropriate for her particular needs, the United States Preventive Services Task Force lipid screening guidelines recommend:6
The National Cholesterol Education Program (part of the National Heart, Lung, and Blood Institute) recommends everyone be tested for total cholesterol, LDL, HDL, and triglycerides beginning at age 20 and every five years thereafter if results are normal.7 More frequent testing in the presence of elevated lipids or multiple risk factors should be determined by the care provider.
People undergoing treatment for hyperlipidemia by therapeutic lifestyle changes (described below in the treatment section) or medications are likely to require testing at more frequent intervals. Nurses should strongly encourage patients to follow the lipid screening schedule set by their healthcare providers and should do so themselves. See Table 4 for normal and abnormal values.
Table 4
|
Looking at Lipids |
|
Total cholesterol HDL < 200 Desirable < 40 Low; at risk 200-239 Borderline high ³ 60 High; optimal ³ 240 High |
|
LDL Triglycerides < 100 Optimal < 150 100-129 Near optimal 150-199 Borderline 130-159 Borderline high 200-499 High 160-189 High ³ 500 Very high ³ 190 Very high |
|
Notes: 1. Lipids are measured in milligrams per deciliter. 2. The above numbers are for people without known CHD; optimal |
|
Source: See reference 7. |
sectionheader >Assess for treatment
Managing cholesterol is a good place to begin a risk modification program for the primary prevention of CHD because fat intake is largely controllable. In the absence of genetic abnormalities, many people can achieve a significant reduction in their total cholesterol by changing their diet.
In 2004, the National Cholesterol Education Program published an update to the 2001 Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (referred to as Adult Treatment Panel III or ATP III). The guidelines are periodically reviewed and are the newest available as of this writing. ATP III provides an evidence-based structure for healthcare providers to move the population toward better health. ATP III focuses on primary prevention of CHD in people with multiple risk factors. An elevated level of LDL is the main target for therapy, and the aggressiveness of treatment is stratified according to concurrent risk factors. Recommended steps for developing a treatment plan for hyperlipidemia include:7
Therapeutic lifestyle changes
Few people would disagree that reducing cholesterol by diet and exercise, when possible, is preferable to taking medications that have the potential for serious adverse effects. Patients are more likely to accept and follow recommendations if healthcare providers, such as nurses, physicians, and nutritionists provide support and guidance. When a TLC plan is developed and implemented in partnership between healthcare provider and patient, it has a far better chance of success. The challenge is to engage more patients before heart disease is present. Long-term reinforcement and support from healthcare professionals is invaluable for people contemplating such lifestyle changes because it can be so difficult to make and adhere to these changes.
ATP III recommends a multifaceted approach to reducing the risk for CHD. The essential features of TLC are:7
The ATP III practice model suggests six weeks of TLC, followed by a recheck of LDL. If the goal LDL is not achieved, more stringent adherence to dietary goals should be instituted, including an increase in fiber and plant stanols and sterols, as well as possible referral to a dietitian. If in another six weeks the LDL goal is not achieved, prescription medications to lower cholesterol may be considered, along with treatment for metabolic syndrome (if present) and intensification of weight management and physical activity.7 (See Table 5, “The TLC Diet,” for the nutritional component of TLC.)
Other components of TLC include weight management and physical activity. Weight loss is important because it helps lower LDL and triglycerides, and can decrease the risk for metabolic syndrome. Women with a waist measurement of more than 35 inches should discuss weight loss with their healthcare provider. Unless contraindicated by physical limitations, regular physical activity — 30 minutes a day on most, if not all, days of the week — is highly recommended to improve health.7 Exercise may increase HDL while at the same time lowering LDL.
Table 5
|
The TLC Diet | |
| Nutrient | Recommended intake |
| Saturated fat | Less than 7% of total calories |
| Polyunsaturated fat | Up to 10% of total calories |
| Monounsaturated fat | Up to 20% of total calories |
| Total fat | 25 to 35% of total calories |
| Carbohydrates | 50 to 60% of total calories |
| Fiber | 20-30 grams daily |
| Protein | Approximately 15% of total calories |
| Cholesterol | Less than 200 mg daily |
| Total calorie expenditure | A balance of caloric intake & expenditure to maintain desirable body weight |
Know your fats
Not all fats are created equal, and it’s important to understand the differences. Most people are aware that animal foods are high in the saturated fat known as cholesterol and that cholesterol intake should be minimized. But some vegetable oils are also saturated fats, but they do not contain cholesterol. To make things more confusing, shrimp are high in cholesterol, but have little saturated fat! Saturated and trans fats (described below) are the ones to avoid.
Saturated fats: Saturation is a term used to describe the chemistry of a fat, i.e., a saturated fat has all the hydrogen that an atom of carbon can hold. Saturated fats are usually firm and stable at room temperature (think of the streaks of white fat on a steak or the yellow globs of fat on a chicken). Cholesterol is one kind of saturated fat. Cholesterol is found in animal products, such as meats, egg yolks, whole dairy products, poultry, and to a lesser extent, fish. Some vegetable oils, such as palm oil, coconut oil, and cocoa butter, are also saturated, but they do not include cholesterol because they are not from animal products. Read food labels; saturated fat should not exceed 7% of daily caloric intake.8
Trans fats: Trans fats are vegetable oils — which don’t contain cholesterol — that have had hydrogen added to them. Depending on the amount of hydrogen added, the term hydrogenated or partially hydrogenated will be seen on package labels. These fats are found in commercial baked goods and are used for cooking in many restaurants and fast-food chains to prolong shelf life and to add flavor.8 Even though trans fats do not have cholesterol, they can increase total cholesterol and LDL and can decrease HDL.8 Trans fat should not exceed 1% of daily caloric intake.8 In 2006, New York passed the nation’s first ban on use of trans fats in restaurants, giving eateries until July 2008 to comply. Other cities and states may soon follow. The FDA estimates the average American eats 4.7 pounds of artery-clogging
Polyunsaturated and monounsaturated fats don’t increase blood cholesterol; in fact, they may lower it by helping the body get rid of newly formed cholesterol. They keep total cholesterol down and may help reduce arterial plaque. These fats have at least one available hydrogen bonding site. Polyunsaturated fats easily combine with oxygen (oxidize) and become rancid. They are liquid at room temperature and in the refrigerator, and include oils from safflower, sesame, soy, corn, and sunflower seeds, as well as nuts. Monounsaturated fats are liquid at room temperature, but they begin to solidify in the refrigerator. They include olive, canola, and peanut oils. Avocados are also monounsaturated.
While polyunsaturated and monounsaturated fats may be helpful as a way to control chole