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.

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.

A family history of CHD puts women and men at increased risk for CHD, probably from a combination of genetic and environmental factors.¹², ¹³, ¹⁴, ¹⁵ 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.¹⁵,¹⁷ 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.

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.

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,²²,²⁴,²⁶ and it increases the risk of peripheral vascular disease, renal failure, and congestive heart failure in men and women across the life span.²⁴,³⁷ The normalization of blood pressure dramatically decreases the risk of stroke, renal failure, cardiac failure, and coronary events.³⁸, ³⁹, ⁴⁰ Even in the elderly, control of hypertension confers major benefits against stroke, coronary events, and all cardiovascular events.³⁹,⁴¹ Hypertension and the nurse’s role in its management are discussed in detail in Chapter 35.

Elevated serum total cholesterol and LDL cholesterol are associated with an increased risk of CHD in men and women of all ages.⁴², ⁴³, ⁴⁴ 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, ⁴⁹, ⁵⁰, ⁵¹ In the Framingham Heart Study, the relative risk for CHD associated with elevated Lp(a) was 1.6 in women⁴⁹ and
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

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.

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 and 32-6) 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

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, ⁶⁰, ⁶¹, ⁶² In these studies, a higher level of fitness was associated with a significantly lower rate of cardiovascular disease mortality in men and women,⁵⁹,⁶² all-cause mortality in men
and women,⁵⁹ 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.⁶³,⁶⁴ 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.