Coronary heart disease (CHD) is usually associated with one or more characteristics known as risk factors. A risk factor is “an aspect of personal behavior or lifestyle, an environmental exposure, or an inborn or inherited characteristic, which on the basis of epidemiologic evidence is known to be associated with” the occurrence of disease.1
Several aspects of the association between a potential risk factor and the disease are evaluated before an association is considered causal. These include the strength or magnitude of the association, the consistency or repeatability of the association, temporality (the cause precedes the disease), dose response (greater dose leads to greater likelihood of disease), the biologic and epidemiologic plausibility of the association, coherence of the potential cause with what is known about the disease, a decrease in the incidence of disease when the potential cause is eliminated, and experimental evidence.2
Although few potential risk factors meet all of these criteria, the goal of epidemiologic investigations is to establish these characteristics. The results of epidemiologic studies of disease cause are frequently presented either as disease rates or as a relative risk. The relative risk is the rate of disease in a group exposed to a potential risk factor, divided by the rate of disease in an otherwise similar group that is unexposed to the risk factor.3
For example, if the rate of fatal myocardial infarction (MI) in a group of smokers was 120 per 100,000 per year, and the rate in comparable nonsmokers was 60 per 100,000 per year, then the relative risk associated with smoking would be as follows:
The risk of MI is thus doubled in the smokers, or there is a 200% increase in risk compared with nonsmokers. A relative risk of 1.30 represents a 30% increase in risk; a relative risk of 3.0 represents a 300% increase, or a tripling of risk. United States death rates in 1998 from all cardiovascular diseases combined, acute MI, cancer, and other causes, for black and white women and men are presented in Figure 32-1
. Cardiovascular disease continues to be the leading cause of death for black and white men and women throughout their life spans. Death rates from MI increase with age in men and women. CHD incidence in women lags approximately 10 years behind that in men, and there is approximately a 20-year lag for serious clinical events such as CHD mortality4
). Data from the Behavioral Risk Factor Surveillance System (BRFSS) in 2005 showed that the prevalence of a reported history of MI was highest for the American Indian/Alaskan Native population (7.4%) and lowest among Asians (2.9%) (Table 32-1
CHD mortality rates have declined steadily since the late 1960s. From 1968 to 1984, CHD mortality declined at an average rate of 2% to 3% per year in all age groups, in both sexes, and in black and white subjects.5
Overall, cardiovascular disease death rates declined 24.7% from 1994 to 2004.4
There is ongoing speculation as to the cause of this decline in cardiovascular disease mortality, although multiple causes are likely. Decreases in case fatality rates have been documented. This indicates that changes in patient management, including more rapid access to emergency care and interventions that reduce infarct size and prevent death caused by arrhythmias, may account for some of the decline in CHD mortality.6
One recent study which examined the decrease in CHD mortality between 1980 and 2000 determined that approximately 47% of the decrease was attributed to evidence-based medical treatments such as secondary preventive therapies after MI or revascularization, treatment for acute MI, angina and heart failure, and other therapies.7
Approximately, 44% of the decrease was attributed to changes in risk factors in the population, such as decreases in total cholesterol, systolic blood pressure, physical inactivity, and smoking.
Cardiovascular disease risk factors have additive effects. The MI risk in a person with three major risk factors is higher than that of a person with two or one.8
Furthermore, for any given combination of risk factors, at a given age, the risk is lower in women than in men; however, the risk for CHD increases dramatically in women after menopause.9
In this chapter, the major known risk factors for cardiovascular disease are briefly reviewed.
CHD mortality rates increase exponentially with age for men and women (Fig. 32-2
). Until the seventh decade of life, black men
have the highest rates of CHD mortality, followed by white men, black women, and white women. The rates in men converge at approximately the seventh decade, and those in women converge in the eighth decade. Further data about CHD rates by race/ethnicity come from analysis of death rates in California from 1990 to 2000.10
The CHD death rates per 100,000 population were as follows: white women, 128; white men, 244; Hispanic women, 88; Hispanic men, 147; black women, 190; black men, 272; Chinese women, 56; Chinese men, 105; Japanese women, 55; Japanese men, 132; Asian-Indian women, 116; and Asian-Indian men, 201. Interestingly, when compared to the CHD death rates from 1985 to 1990 for the same populations, all groups showed a decrease with the exception of Asian-Indian women in which a 5% increase was noted.
▪ Figure 32-1
U.S. death rates per 100,000 population for major causes of death by gender and race/ethnicity. (From Centers for Disease Control and Prevention: CDC Wonder. (October 1998). Available from wonder.cdc.gov/WONDER/mort.oo.ex./
Table 32-1 ▪ PERCENTAGE OF RESPONDENTS AGED ≥18 YEARS WHO REPORTED A HISTORY OF MYOCARDIAL INFARCTION (MI) OR ANGINA/CORONARY HEART DISEASE (CHD), BY SELECTED CHARACTERISTICS—BEHAVIORAL RISK FACTOR SURVEILLANCE SYSTEM, UNITED STATES, 2005
No. of Respondents*
MI or Angina/CHD (%)**
American Indian/Alaska Native
Less than high school diploma
High school graduate
* Sums of the sample sizes in each category might not add up to the total number of respondents because of unknown or missing information.
† Percentage of respondents who reported a history of MI.
§ Confidence interval.
¶ Percentage of respondents who reported a history of angina/CHD.
** Percentage of respondents who reported a history of MI, angina/CHD, or both.
†† Weighted percentages are age adjusted to the 2000 U.S. standard population of adults.
Source: Morbidity and Mortality Weekly Report (MMWR) (2007). Prevalence of Heart Disease—United States 2005, 56(6), 115.
▪ Figure 32-2
U.S. coronary heart disease death rate per 100,000 population by age, gender, and race/ethnicity. (From Centers for Disease Control and Prevention: CDC Wonder. (October 1998). Available from wonder.cdc.gov/WONDER/mort.oo.ex./
Surveillance data from the BRFSS suggest that marked disparities continue to exist in the overall prevalence, morbidity, and mortality associated with CVD and major CVD risk factors.11
This report noted that the population subgroups most affected by disparity include those who are black, Hispanics/Mexican-Americans, persons with low socioeconomic status, and residents of the southeastern United States and the Appalachians. Furthermore, those with less than a high school education tend to have a higher burden of CVD and related risk factors regardless of race/ethnicity.
FAMILY HISTORY OF CARDIOVASCULAR DISEASE
A family history of CHD puts women and men at increased risk for CHD, probably from a combination of genetic and environmental factors.12
This concept is reinforced in the findings from the INTERHEART study in which the odds ratio for an acute MI in people with a family history was about 1.5.16
The population attributable risk rose from 90% with the other potentially modifiable risk factors under study (such as smoking, hypertension, etc.) to 91% with the addition of family history. Thus, a good portion of the effect of family history may be based on risk factors, which could be influenced by both environmental (lifestyle) and genetic factors. A history of MI in one first-degree relative doubles, and in two or more first-degree relatives triples MI risk.15
MI risk is strongest when MI in relatives occurs before age 55 years but is still present when MI occurs after age 55 years.15
The risk associated with a positive family history is independent of other known CHD risk factors.
▪ Figure 32-3 Prevalence of current smoking among U.S. women (A) and men (B) by age and race/ethnicity. (From National Center for Health Statistics. National Health and Nutrition Examination Survey, III, 1988-1994.)
Twin studies shed further light on the influence of family history on CHD risk. In a study of male and female Swedish monozygotic and dizygotic twins, among male twins the relative risk of CHD for monozygotic twins was 8.1, and the relative risk for dizygotic twins was 3.8 when one twin died of CHD before 55 years of age.18
Among female twins, the relative risk of CHD for monozygotic twins was 15, and the relative risk for dizygotic twins was 2.6 when one twin died of CHD before 55 years of age. In monozygotic and dizygotic twins, as the age at which one twin died increased, the risk for CHD among the remaining twin decreased.
In 2006, 45.3 million adults were current smokers, that is, 20.8% of the adult U.S. population (23.5% of men and 18.0% of women).19
Smoking prevalence varies markedly by race/ethnicity and age (Fig. 32-3
). In 2006, smoking rates for adults by race/ethnicity were as
follows: American Indian/Alaskan Native, 32.4%; black or African American, 23.0%; non-Hispanic white, 21.9%; Hispanic, 15.2%; and Asian 10.4%.19
Since 1965, rates of smoking in adults 18 years of age and older have declined by 50%.4
Data from the Youth Risk Behavior Survey show that 23% of high school students were current smokers in 2005 (23% of female students and 22.9% of male students).20
Cigarette use in this age group was stable or increased during the 1990s and then decreased significantly from the late 1990 to 2003, however, prevalence was unchanged during 2003 to 2005.
Smoking and CHD
Cigarette smoking is perhaps the most preventable known cause of CHD today, leading to more deaths from CHD than from either lung cancer or chronic obstructive pulmonary disease.21
The CHD risk increases with number of cigarettes smoked, longer duration of smoking, and younger age at initiation of smoking.22
The CHD risk of male cigarette smokers is two (aged 60 years and older) to three (aged 30 to 59 years) times that of nonsmokers,24
whereas women who are current smokers have up to four times the risk of first MI of those who have never smoked.25
This elevation in the risk of MI and CHD death is sustained from youth into advanced age for men and women.23
Smoking lowtar (<17.6 mg), low-nicotine (<1.2 mg), or filter cigarettes does not lower the risk of MI compared with high-tar, high-nicotine, or nonfiltered cigarettes29
Smoking cessation confers benefit regardless of sex, age, or presence of CHD. Men and women of all ages with documented CHD who quit smoking have half the risk of mortality compared with those who continue to smoke.30
This finding was confirmed in a systematic review of 20 prospective cohort studies of patients with CHD that reported all-cause mortality and had at least 2 years of follow-up.33
The results demonstrated that smoking cessation was associated with reduction in risk for all-cause mortality in patients with CHD; risk reduction was consistent regardless of other factors including age and gender. There are many successful approaches to smoking cessation, and these interventions are less costly than many other preventive interventions.34
Smoking cessation should be encouraged regardless of age, sex, or the presence of established disease.
Environmental Tobacco Smoke
It is estimated that 53,000 deaths annually are attributable to environmental tobacco smoke (ETS), making it the third leading preventable cause of death in the Unites States.21
Ten times as many of these deaths are caused by CHD as by lung cancer. Exposure of nonsmokers to ETS from a spouse who smokes increases the risk of CHD death by 30% in men and women. This risk increases with the amount smoked by the spouse.21
ETS causes arterial endothelial damage, may initiate or accelerate the development of atherosclerosis, and increases platelet aggregation, which may result in coronary thrombosis.21
Thus, the effects of ETS are similar to those of smoking cigarettes.
Hypertension is defined as a systolic blood pressure of 140 mm Hg or more or diastolic blood pressure of 90 mm Hg or more. Hypertension carries particular importance as a cardiovascular risk factor for several reasons: it is highly prevalent, it is relatively simple to identify, it is a major risk for devastating cardiovascular outcomes, and control of hypertension is known to decrease its risk.35
Prevalence of hypertension increases with age among white, black, and Mexican-American subjects (Fig. 32-4
). The prevalence of hypertension is highest among black persons at all ages. Results from a cross-sectional analysis of data from the National Health and Nutrition Examination Survey (NHANES) 1999 to 2002 and NHANES III 1988 to 1994 showed that the prevalence of hypertension increased from 35.8% to 41.1% among black persons, with hypertension particularly high among black women (44%).36
The prevalence of hypertension also increased among white persons from 24.3% to 28.1%. Hypertension is associated with three- to four-fold increases in the risk of CHD, stroke, and MI,22
and it increases the risk of peripheral vascular disease, renal failure, and congestive heart failure in men and women across the life span.24
The normalization of blood pressure dramatically decreases the risk of stroke, renal failure, cardiac failure, and coronary events.38
Even in the elderly, control of hypertension confers major benefits against stroke, coronary events, and all cardiovascular events.39
Hypertension and the nurse’s role in its management are discussed in detail in Chapter 35
SERUM LIPIDS AND LIPOPROTEINS
Elevated serum total cholesterol and LDL cholesterol are associated with an increased risk of CHD in men and women of all ages.42
The prevalence of hypercholesterolemia is higher in U.S. women than in men, and higher in white and black than in Mexican-American subjects (National Center, 1997) (Table 32-2
). CHD rates are lower for women than men at any given level of serum cholesterol.42
Decreasing trends in total and LDL choletesterol levels have been noted over time; the percentage of adults with a total cholesterol level of at least 240 mg/dL during 1988 to 1994 decreased from 20% to 17% during 1999 to 2002.45
The increase in the proportion of adults using lipid-lowering medication has likely contributed to the decreases that have been observed.
Serum HDL cholesterol has a protective effect against CHD. A 1-mg/dL increment in HDL is associated with a 2% (men) to 3% (women) decrement in total CHD risk, and a 3.7% (men) to 4.7% (women) decrement in CHD mortality.46
At any given level of LDL, higher levels of HDL confer protection against CHD.35
A level less than 40 mg/dL for adults is considered low HDL and increases risk for CHD. In 2005, for adults in the United States 20 years and older, the prevalence of HDL less than 40 mg/dL was 44.6 million.4
Attention has been focused on subfractions of HDL and LDL, the apolipoproteins (apoAI, apoAII, apoB), and lipoprotein(a) (Lp(a)). In a study of the predictors of premature CHD at coronary arteriography, Kwiterovich and associates47
found that apoB was more strongly associated with an increase in CHD risk in women than in men, whereas ApoAI was more strongly associated with a decrease in CHD risk in men than in women. Increasing levels of Lp(a) are also associated with an increase in CHD risk.48
In the Framingham Heart Study, the relative risk for CHD associated with elevated Lp(a) was 1.6 in women49
1.9 in men.50
LDL subclass patterns also influence CHD risk. Compared with light, buoyant LDL, small, dense LDL is associated with a three-fold increase in the risk of MI.48
▪ Figure 32-4 Prevalence of high blood pressure among U.S. women (A) and men (B) by age and race/ethnicity. (From National Center for Health Statistics. National Health and Nutrition Examinations Survey, III, 1988-1994.)
Serum cholesterol levels influence prognosis after MI. The risk for reinfarction is 3.7 times (men) to 9.2 times (women) as great when serum cholesterol levels are 275 mg/dL or greater, compared with levels of less than 200 mg/dL.52
There is evidence that normalization of serum lipids and lipoproteins reduces the CHD mortality rate.53
Hyperlipidemia and its management are discussed in more detail in Chapter 36
▪ PREVALENCE OF HYPERCHOLESTEROLEMIA*
AMONG U.S. WOMEN AND MEN BY AGE AND RACE/ETHNICITY
*On the basis of self-reported use of cholesterol-lowering medication or a total serum cholesterol value of ≥240 mg/dL.
From the National Center for Health Statistics, U.S. Department of Health and Human Services (DHHS). Third National Health and Nutrition Examination Survey, 1988-1994, NHANES III Data File (CD-ROM Series II, No. 1). Public Use Data File. Hyattsville, MD: Centers for Disease Control and Prevention, 1997.
The roles of physical activity and physical fitness in preventing cardiovascular disease and controlling cardiovascular disease risk factors are well established. In 2007, the American College of Sports Medicine and the American Heart Association recommended that “all healthy adults aged 18 to 65 years need moderate-intensity aerobic physical activity for a minimum of 30 minutes on five days each week or vigorous-intensity aerobic activity for a minimum of 20 minutes on three days each week.”54
Data analyzed using the 1996 Surgeon General’s Report on Physical Activity recommendations (at least 30 minutes of moderate-intensity physical activity on most days of the week) (Figs. 32-5
) show that only approximately half of all white women and less than 40% of black and Mexican-American women are physically active four or more times per week, and fewer than 25% of women walk at least four times per week. The proportions are only slightly higher for American men. Data from the BRFSS for the period from 1994 to 2004 demonstrate that the prevalence of leisure-time physical inactivity overall declined significantly from 29.8% in 1994 to 23.7% in 2004.55
However, based on data from the National Health Interview Survey for 1999 to 2004, only 62% of adults aged 18 years and older participated in at least some light to moderate leisure-time physical activity lasting 10 minutes or more per session.4
Thus, a large proportion of the American public could be targeted for public health interventions to increase physical activity. Studies of the effects on cardiovascular disease of both on-the-job and leisure-time activity indicate that in general, people who are more physically active or physically fit tend to have CHD less often than sedentary or less fit people. CHD tends to be less severe and occurs at a later age among those who are physically active compared with those who are sedentary.56
When data from cohort studies of occupational physical activity and CHD risk were pooled, the risk for CHD death for those with low-level occupational activity was almost twice that of those with high-level activity, and the MI risk was 40% higher in the sedentary group.57
▪ Figure 32-5 Prevalence of physical activity at least four times per week among U.S. women (A) and men (B) by age and race/ethnicity. Physical activity: walking, jogging or running, bicycling, swimming, aerobics, dancing, calisthenics, garden/yard work, and/or lifting weights. (From National Center for Health Statistics. National Health and Nutrition Examination Survey, III, 1988-1994.)
In studies that included women, the risk for angina pectoris, MI, and sudden death was two to three times higher among women with the lowest compared with the highest activity level.58
An important addition to understanding the benefits of fitness has been made by studies that measure physical fitness using standardized exercise tests and then compare fitness with later cardiovascular outcomes.59
In these studies, a higher level of fitness was associated with a significantly lower rate of cardiovascular disease mortality in men and women,59
all-cause mortality in men
and ischemic heart disease (fatal and nonfatal MI plus sudden death) in men.62
Although pooled analyses from randomized trials of comprehensive cardiac rehabilitation suggest a 19% to 25% reduction in mortality rates associated with rehabilitation, it is difficult to dissociate the benefits of the exercise component of these programs from other lifestyle changes.63
However, the potential benefits of a program of regular exercise after MI include an increase in exercise capacity, decrease in angina, improved control of other cardiovascular disease risk factors, decreased anxiety and depression, and increased self-esteem and sense of well-being.64
A large systematic review and meta-analysis of randomized controlled trials of exercise-based rehabilitation for patients with CHD confirmed the benefits of exercise-based cardiac rehabilitation.65
Exercise training is also recognized as an important adjunctive therapy, with similar benefits for those with a history of congestive heart failure.66
Activity and exercise are discussed further in Chapter 37
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