Coronary Heart Disease 343social support. One study of 3,809 Japanese Americans living
in California classi“ed subjects according to the degree to
which they retained their traditional Japanese values and cul-
ture (Marmot & Syme, 1976). The group with the highest
level of cultural retention were found to develop the same
amount of CAD as observed in Japan, while the most accul-
turated group had a three- to “vefold increase in CAD preva-
lence. Major CAD risk factors were not able to account for
these differences. In 1992, Egolf, Lasker, Wolf, and Potvin
published their “ndings of a 50-year comparison of CAD
mortality rates in Roseto, Pennsylvania, and a neighboring
town. Initially Roseto was a homogeneous community of
three-generation households with lower incidence levels of
CAD than the neighboring town despite shared medical re-
sources. Over time, Roseto•s homogeneous social structure
disappeared while its incidence of CAD increased.
Within industrialized societies, cardiac morbidity and
mortality are inversely related to socioeconomic status (SES)
with disease rates highest among the poorest individuals.
Initially, it was assumed that this disparity was due to differ-
ences in medical care and standard risk factors such as smok-
ing and high blood pressure, but evidence shows these
are only partly to blame (Luepker et al., 1993). This relation-
ship between cardiac outcome and socioeconomic status is
observable whether measured by education, income, or
occupation. One study (Ruberman, Weinblatt, Goldberg, &
Chaudhary, 1984) found that low-SES men were more likely
to experience isolation and life stress. These men were also
found to have a mortality rate twice as high as their more ed-
ucated counterparts. It was also found that low SES is associ-
ated with increased levels of high-risk behaviors (Winkleby,
Fortmann, & Barrett, 1990) and psychosocial risk factors
(Barefoot et al., 1991).
The reasons for the differences between SES groups in
CAD development are complex and need to be studied
more extensively. Some studies have suggested that there
may be a fetal origin to the development of CAD. These
studies have hypothesized that individuals with a low birth
weight have a tendency later in life to respond adversely to
CAD risk factors, thus putting them at higher risk for de-
veloping the disease. Since babies born into low SES fami-
lies are more prone to lower birth weights relative to their
higher SES peers, it is possible that the adverse effects of
low SES on the development of CAD begin at a very early
age and are cumulative throughout life (Eriksson et al.,
1999). Since the disparity between different SES groups is
high with regard to risk of CAD development, it remains a
major public health challenge to bring mortality rates of
lower SES groups down to the level of their higher SES
peers.
Gender and RaceCoronary artery disease remains the leading cause of death in
the United States. This relationship remains among men and
women and among both Caucasians and African Americans.
Moreover, African Americans are at an increased risk of de-
veloping premature CAD, and the proportion of African
Americans that die from CAD is at least as large as their Cau-
casian counterparts (American Heart Association, 1997).
Among women, the onset of disease is usually later (post-
menopause), but once CAD develops the case-fatality rate is
higher than for men (Douglas, 1997). While both of these
groups make up a large portion of the population suffering
from cardiovascular disease, research and treatment has
historically catered to the needs of Caucasian males. The psy-
chosocial risk factors that affect minorities and women is dis-
cussed in this section.
It was once thought that women were spared from devel-
oping CAD, atherosclerosis, and other cardiovascular disor-
ders relative to their male counterparts. Although studies have
shown that while most premenopausal women are somewhat
protected from developing CAD, postmenopausal women de-
velop the disease at a much faster rate, with the overall
incidence curve for women lagging about 10 years behind that
for males (Higgins & Thom, 1993). The majority of this pro-
tective effect has been attributed to estrogen. In fact, the
provision of estrogen replacement to initially healthy post-
menopausal women has been associated with a signi“cant
reduction in the risk of CAD development (Manson, 1994).
However, since CAD and atherosclerosis develop over
decades, it is likely that clinical events occurring in post-
menopausal women have their origins in the premenopausal
years. This hypothesis is supported by a study that found
extensive atherosclerosis in many premenopausal women
(Sutton-Tyrrell et al., 1998). Another possibility is that women
with ovarian abnormalities or failure have reduced amounts of
endogenous estrogen, leaving them more susceptible to CAD
development in later years (Rozanski et al., 1999).
In addition to possible gender differences in CAD
pathophysiology, women also are less likely to get revascu-
larization procedures and cardiac catheterizations while hos-
pitalized, and also are prescribed fewer standard cardiac
medications such as beta-blockers and nitroglycerin (Stone
et al., 1996). Historically, CAD has been less studied in
women, leaving physicians with fewer diagnostic strategies
and treatment criteria for properly treating women. Another
possibility is that there are either subtle or overt gender biases
that drive the differences in care between men and women.
For example, physicians may be in”uenced by stereotypes
of gender behavior, which could have a profound effect on