Handbook of Health Psychology

By Andrew Baum; Tracey A. Revenson et al. | Go to book overview

An important and unresolved issue is the dissociation between chest pain and cardiac ischemia. Possible mechanisms of asymptomatic ischemia have been discussed, including cardiovascular factors such as lower cardiac demand and lesser severity of ischemia, the autonomous nervous system function, elevated endogenous opioids, and psychological factors such as lower depression scores and denial of symptoms. In addition, possible differences in cerebral processing may account for altered perception of pain in cardiac ischemia. Large studies will be needed to determine the individual and interactive contributions of biologic and psychological factors in silent ischemia.

Finally, a series of studies are now available in support of the predictive value of mental stress-induced ischemia for future cardiac events in patients with established coronary artery disease. Most studies were restricted to patients with a prior positive exercise test for ischemia. This limits the possibility to disentangle the predictive value of ischemia induced by mental versus physical stress. In addition, further research is needed to clarify the biobehavioral mechanisms accounting for the higher incidence of adverse events in patients with ischemia during mental stress in the laboratory. It could be that patients with mental stress-induced ischemia have a worse cardiac condition to start with, but it is also conceivable that increased cardiovascular reactivity and a higher prevalence of ischemic episodes during the activities of daily life account for the predictive value of mental stress ischemia. Given the specific hemodynamic characteristics of mental stress-induced ischemia, pharmacological treatments targeted to counteract coronary vasoconstriction combined with psychological interventions directed at reducing anger, hostility, and depressive symptoms may ultimately prove beneficial in the treatment of patients with coronary artery disease.


ACKNOWLEDGMENTS

The research presented in this chapter was made possible by grants from the National Institutes of Health (HL47337, HL58638), the USUHS (R07233), and the Dutch Heart Foundation (94–098).

The opinions and assertations expressed herein are those of the author and should not be construed as reflecting those of the USUHS or of the U.S. Department of Defense.


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