342 Coronary Heart Disease and Hypertension
McPherson, 2000), some studies have shown no evidence
linking occurrence of arrhythmias with psychological factors.
For example, the Cardiac Arrhythmia Pilot Study assessed
various questionnaire-assessed psychological variables for
353 patients over a year and found no relationship to rates of
increased ventricular premature contractions (Follick et al.,
1990).
Chronic Stress
In addition to the effects of acute or short-term stressors,
the possible pathophysiologic effects of chronic stressors
were studied in conjunction with CHD risk. Among the more
widely studied variables are occupational stress, low social
support, and low SES.
Occupational Stress. Work-related stress is the most
widely studied form of chronic stress. Research has sought
to elicit which occupations are most stressful and which char-
acteristics of particular occupations lead to an increased
likelihood of developing CAD (Karasek & Theorell, 1990).
Several factors were determined to contribute to the amount
of stress one experiences on the job. The psychological de-
mands of the job refer to stresses that interfere or tax a worker
and make him or her unable to perform at optimal levels.
Level of job autonomy or control refers to the ability of the
person to in”uence his or her working conditions, including
the nature, speed, and conditions of the work. Job satisfaction
includes how many of the worker•s needs are met and the
level of grati“cation attained from the overall work experi-
ence (Wells, 1985).
Karasek and colleagues (e.g., Karasek & Theorell, 1990)
proposed a job demand/control hypothesis in which occupa-
tions with high work demands combined with few opportuni-
ties to control the work or make decisions (low decision
latitudes) are associated with increased coronary disease risk.
One prospective study of 1,928 male workers followed for
6 years showed a fourfold increase in risk of cardiovascular
system-related death associated with job strain (Karasek,
Baker, Marxer, Ahlbom, & Theorell, 1981). Subsequent stud-
ies replicated these “ndings supporting a link between job
strain and CAD risk (Theorell et al., 1998) while others found
negative relationships between measured job strain and out-
comes in cardiac patients (Hlatky et al., 1995). These nega-
tive “ndings may be in part due to the population tested,
most of whom (including the controls) were symptomatic, so
job strain may have been obscured in such a population
(Pickering, 1996).
Other models linking occupational stress to CAD devel-
opment have been formulated. One such model proposes that
work stress is the result of an imbalance between high work
demand and low reward (Siegrist, Peter, Junge, Cremer, &
Seidel, 1990). This demand-reward imbalance was associ-
ated with a 2.15-fold increase in risk for the development of
new CAD. This same study, which included 6,895 working
men and 3,413 working women aged 35 to 55 years, showed
a nearly twofold increase in new CAD cases as a result of low
job control (Bosma, Peter, Siegrist, & Marmot, 1998). Peter
and Siegrist (2000) found odds-ratios ranging from 1.2 to 5.0
with respect to job strain and CAD, and odds-ratios from 1.5
to 6.1 with respect to effort-reward imbalance. These associ-
ations cannot be explained by behavioral or biomedical risk
factors, nor by physical and chemical work hazards. Rather
they de“ne new, independent occupational risk conditions.
This and other new models comparing work stress and subse-
quent CAD development have been largely positive, suggest-
ing a strong causal relationship between occupational stress
and the development of CAD.Low Levels of Social Support/Isolation/Low SES.
Certain chronic aspects of the social environment, including
isolation, low social support, and lack of economic and social
resources, can increase an individual•s risk of developing
CAD (Shumaker et al., 1994). Social support refers to the in-
strumental (i.e., tangible), informational, and emotional sup-
port obtained from a person•s social ties and community
(Cohen & Wills, 1985). In early studies, so-called •social net-
worksŽ were measured quantitatively by assessing factors
such as the extent of one•s participation in group and organi-
zational activities or the number of family members or
friends present (Rozanski et al., 1999). Some researchers
evaluated the role of living arrangements (alone, married,
marital disruption), while others focused on instrumental
support such as access to community services and activities.
It was shown that a small social network confers a two- to
threefold increase in the likelihood of developing CAD over
time. It is also imperative to look at the qualitative nature of
social support (i.e., amount of perceived emotional support).
Low levels of perceived emotional support were shown to
confer greater than a threefold increase in the risk of
future cardiac events (Blazer, 1982). Furthermore, Berkman,
Leo-Summers, and Horwitz (1992) showed a threefold in-
crease in future cardiac events in post-MI patients who re-
ported low levels of emotional support, while R. Williams et
al. (1992) observed a threefold increase in mortality over a
“ve-year period among CAD patients who were unmarried or
had no major con“dant in their life.
Other evidence also supports the positive association be-
tween social factors and the development of CAD. Cultural
and familial support are critical aspects on one•s overall