Stress and Silent Ischemia
Willem J. Kop
Uniformed Services University of the Health Sciences
John S. Gottdiener
St. Francis Hospital, Roslyn, NY
David S. Krantz
Unijbmed Services University of the Health Sciences
Evidence indicates that both chronic (Appels, 1990; Friedman & Rosenman, 1959; Kop, 1997; Williams et al., 1980) and acute (Krantz, Kop, Santiago, & Gottdiener, 1996) psychologically stressful circumstances can promote coronary artery disease (CAD) progression and its clinical manifestations such as chest pain, myocardial infarction, and sudden cardiac death. Current models of the effects of mental and physical stress on the heart suggest that behaviorally induced autonomic nervous system activation can produce clinical cardiovascular events at several levels: by promoting atherosclerosis and subsequent plaque formation in the coronary artery wall; by directly triggering disturbances in cardiac rhythm (arrhythmias) through alterations of the neural activation of the heart; and by producing intermediate pathologic or pathophysiologic processes causing ischemia in patients with CAD (Krantz et al., 1996b). This chapter addresses the third level, that is, mental and physical triggers of cardiac ischemia.
The characteristic symptom of coronary artery disease is stress-induced angina1 pain. Angina is a consequence of myocardial ischemia, which may develop when the oxygen supply to the heart does not meet cardiac oxygen demand (Krantz et al., 1996b). Myocardial ischemia is commonly manifest in patients with CAD. However, many cardiac ischemic episodes are asymptomatic, or “silent” (Deanfield et al., 1983; Krantz et al., 1994; Nabel, Rocco, Barry, Campbell, & Selwyn, 1987). The absence of symptoms may interfere with patients' recognition of impending cardiac events as well as the accuracy with which symptoms are described to medical professionals (Kenyon, Ketterer, Gheorghiade, & Goldstein, 1992; Theisen et al., 1995). Moreover, the incidence of painless and undetected acute myocardial infarction is estimated to be approximately 10% (Kannel & Abbott, 1984). This chapter focuses on silent ischemia during episodes of mental stress in laboratory settings and activities of daily life and addresses possible biobehavioral mechanisms that may explain stress-induced silent ischemia. Specifically, it describes: the prevalence of mental stress-induced myocardial ischemia in the laboratory; the characteristics of (silent) ischemia in field studies; possible mechanisms for the onset of ischemia with mental stress and its characteristic absence of cardiac symptoms; and the predictive value of silent ischemia for adverse prognosis in patients with CAD.
Myocardial ischemia is a consequence of an imbalance between cardiac demand (the workload of the heart) and coronary blood supply (the delivery of oxygenated blood to the heart via the coronary arteries). As is discussed later, mental and physical stress may increase cardiac demand by increasing heart rate and blood pressure; and, in addition, other evidence indicates that mental stress may also reduce coronary blood supply to the heart. Thus, mental stress may cause cardisc