Coronary Heart Disease 341Figure 15.1 Episodes of anger and the relative risk of MI. Reprinted with
permission from Mittleman et al. (1995). Circulation, 92, 1720...1725.include aspects of personality, acute and chronic stress, and
aspects of the social environment.
Acute Stress and Anger
Research has begun to focus on the role that acute stress and
anger may play as triggers for the development of coronary
artery disease (CAD; see Krantz, Kop, Santiago, et al., 1996).
Previous studies have observed that stressful life events, such
as the death of a spouse, often occurred within the 24 hours
preceding death among patients who died suddenly from
coronary disease (e.g., Cottington, Matthews, Talbott, & Kul-
ler, 1980; Myers & Dewar, 1975). Another study of 95,647
individuals followed up for 4 to 5 years showed the highest
relative mortality occurred immediately after bereavement,
with a twofold increase in risk for men and a threefold in-
crease in risk for women (Kaprio, Koskenvuo, & Rita, 1987).
The occurrence of natural disasters and personal traumas
has also been correlated with an increase in cardiac events.
During the Gulf War in 1991, there was a signi“cant increase
in fatal and nonfatal cardiac events among populations living
close to Tel Aviv, where missile attacks were heaviest (Meisel
et al., 1991). During a one-week period following intense
missile attacks (January 17...25, 1991), the number of cases of
acute MI treated in the intensive care unit of a Tel Aviv hos-
pital was signi“cantly greater than those treated the week
prior to the attack and to an index period corresponding to the
same week a year earlier. There was also an increase in
the sudden death rate during January 1991 as compared to the
same period one year earlier. Similarly, the number of sudden
cardiac deaths rose sharply, from a daily average of 4.6 in the
preceding week to 24 on the day a massive earthquake rocked
Los Angeles in 1994 (Leor, Poole, & Kloner, 1996).
Mittleman et al. (1995) compared patients• activities im-
mediately before the occurrence of an MI with their usual
levels of activity to assess the immediate physical and mental
triggers of onset of MI. In the study, patients were inter-
viewed a median of four days post-MI and 2.4% reported an
episode of anger prior to onset of MI. Following these anger
episodes, the risk of MI following further episodes of anger
was more than twice as high (Figure 15.1).
Researchers have studied the effects of acute stressors on
cardiac events in a laboratory setting. Using modeled forms
of stress (e.g., mental arithmetic and speaking tasks) and sen-
sitive imaging techniques, researchers were able to induce
myocardial ischemia in 30% to 60% of patients with CAD
(Krantz, Kop, Santiago, et al., 1996). This mental-stress in-
duced ischemia was observed reliably and frequently in the
laboratory in patients with CAD (e.g., Rozanski et al., 1988),
and was also studied during daily life activities (e.g., Gabbay
et al., 1996; Gullette et al., 1997), using ambulatory monitor-
ing devices in conjunction with structured diaries. Re-
searchers have observed behaviors and/or acute stressors that
trigger these ischemic episodes or other cardiac events (Kop,
1999). For example, Gabbay et al. (1996) studied 63 CAD
patients with evidence of out-of-hospital ischemia by using a
structured diary to assess physical and mental activities and
psychological states while they underwent ambulatory elec-
trocardiographic monitoring for 24 to 48 hours. Ischemia
occurred most often during times of moderately intense phys-
ical and mental activities. The emotional state of anger was
found to be an especially potent ischemic trigger, and heart
rates at onset of ischemia increased with the intensity of
anger experienced.
Several research teams studied the possible physiological
mechanisms by which acute stress may trigger coronary
events. It was found that acute psychological risk factors
may result in impaired dilation of the coronary vessels in coro-
nary patients (Howell et al., 1997), decreases in plasma vol-
ume (Patterson, Gottdiener, Hecht, Vargot, & Krantz, 1993),
and increased platelet activity and blood clotting tendency
(Patterson et al., 1995). These responses may result in an im-
balance between cardiac demand and decreased coronary
blood supply and may lead to cardiac ischemia (Kop, 1999).
Finally, acute psychological factors may also elicit electri-
cal instability of the myocardium and cause life-threatening
arrhythmias (Verrier & Mittleman, 1996). Lown (1987)
proposed that ventricular arrhythmias occur in presence of
three factors: myocardial electrical instability, an acute
triggering event (frequently related to mental stress), and a
chronic and intense psychological state. Although there is ac-
cumulating evidence that psychological factors can trigger
malignant arrhythmias (Lampert, Jain, Burg, Batsford, &[Image not available in this electronic edition.]