There are three logical ways in which a behavior pattern might be associated with
CHD or sudden cardiac death risk status. First, the behavior pattern might be
a marker of some underlying inborn structural weakness that makes CHD or sud-
den cardiac death more likely. The second mechanism, which has been widely
discussed and researched, is the behavior pattern's possible association with ex-
aggerated psychophysiological reactivity to certain situational circumstances, the
hyperresponsitivity hypothesis, and this reactivity may in turn increase the
atherosclerotic process. The third possibility, the dangerous situations hypothe-
sis, is that Type A's are exposed or expose themselves to inherently more risky
circumstances dangerous to cardiovascular health. For example, they may delay
in seeking medical attention after experiencing angina symptoms. Of course, these
three possibilities are not mutually exclusive; all may plausibly contribute to the
higher risk status of certain individuals. In the following sections, we present
a review of the literature regarding each of these explanations. Because our pur-
pose is to point out problems, provide a taxonomy, and suggest new research
directions, the review is selective.

The first possibility we examine is one of an overt behavior pattern, which may
be an indicator of some inborn physical weakness or abnormality of the cardio-
vascular or related systems that increases the development of atherosclerosis or
sudden death. For example, perhaps Type A's possess arterial walls that are phys-
iologically more conducive to the occurrence of lesions; or perhaps Type A's
have a genetically acquired tendency toward ECG abnormality. This hypothesis
suggests that the so-called risky behavior is itself harmless, merely serving to
indicate the presence of some preexisting abnormality.

An inborn structural explanation for the link between Type A and CHD has
generally been given little credence. In fact, it is rarely mentioned as a potential
causal mechanism. Lack of interest in this avenue of explanation is a result in
part of early study of Type A's prospective role as a predictor of premature CHD
mortality and morbidity. Rosenman et al. ( 1975) found that Type A was related
to a twofold risk for CHD even when controlling for traditional risk factors, such
as basal level blood pressure, diabetes, parental CHD history, and serum levels
of cholesterol, triglyceride, and lipoproteins. These data suggested that Type A
is an independent risk factor that exerts its pathogenic influence via mechanisms
other than the standard risk factors.

In particular, the finding that Type A remains a significant risk factor after
controlling for parental CHD history appears to be a strong argument against
the role of genetic-structural differences. Also, recent evidence suggests that fam-
ily history of CHD does not account for the association between hostility and
degree of arterial occlusion ( MacDougall, Dembroski, Dimsdale, & Hackett,
1985). However, it is possible that there were some false negatives (i.e., parents
with angina or even MIs that went undetected) in these data sets. Also, the fact

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