Background Numerous psychosocial factors have been hypothesized to pla
y a role in coronary heart disease. However, existing studies have yie
lded inconsistent results. Methods and Results The relations between t
ype A personality as well as suppressed versus expressed anger and ris
k of nonfatal myocardial infarction (MI) were studied in 340 patients
and 340 age-, sex-, and community-matched control subjects. Subjects w
ere interviewed at home to assess behavioral and medical cardiovascula
r risk factors, and fasting blood samples were obtained. Type A person
ality was associated with nonfatal MI in crude matched-pair analysis (
OR, 1.57; 95% CI, 1.12 to 2.20; P=.008). Adjusting for known cardiovas
cular risk factors (including treated hypertension, body mass index, t
reated diabetes, family history of premature MI, physical activity, sm
oking, alcohol, total calories per day, and saturated fat) did not sub
stantially change the magnitude of the point estimate, although the fi
nding was no longer statistically significant (OR, 1.43; 95% CI, 0.97
to 2.09; P=.069). Further adjustment for lipids, including total chole
sterol, total HDL, its subfractions (HDL(2), HDL(3)), LDL, LDL, and tr
iglycerides, markedly attenuated the association (OR, 1.12; 95% CI, 0.
66 to 1.90; P=.687), an effect due almost entirely to HDL cholesterol.
Suppressed anger was positively but not statistically significantly a
ssociated with increased risk of MI in crude matched-pair analysis (OR
, 1.33; 95% CI, 0.98 to 1.81; P=.065), in analysis adjusted for behavi
oral and medical cardiovascular risk factors (OR, 1.26; 95% CI, 0.89 t
o 1.78; P=.193), or after adjustment for lipids (OR, 1.11; 95% CI, 0.6
7 to 1.82; P=.695). Conclusions These findings suggest a possible asso
ciation of type A but not suppressed anger with risk of nonfatal MI th
at may be mediated by alterations in HDL cholesterol level. If decreas
es in HDL are not in the same causal pathway, then the apparent associ
ation between type A personality and risk of MI is due to confounding,
principally by HDL.