Stress has been defined as a state of threatened homeostasis that is reestablished by physiologic adaptive responses. If the adaptive responses are inadequate or excessive and prolonged, homeostasis is not attained and pathology ensues.
Among the pathologies that are related to stress and its associated emotional manifestations is coronary artery disease (CAD). It has been established by multiple laboratories that 30% to 50% of CAD patients exhibit transient, symptomless myocardial ischemia during mental stress performed in a laboratory setting. The clinical manifestations of this mental stress-induced ischemia include profound left ventricular dysfunction and the triggering of acute coronary syndrome and potentially fatal arrhythmia. Furthermore, up to 75% of ischemic episodes seen during ambulatory electrocardiographic monitoring in patients with chronic CAD occur during routine daily activities that carry a considerably lower metabolic demand than is required to provoke ischemia during exercise diagnostic testing. Furthermore, these ischemic episodes occur without symptoms. This ischemia in response to emotional provocation differs from exercise-induced ischemia with regard to several pathophysiologic determinants and clinical presentation.
Among patients with CAD, exercise has been shown to initiate various homeostatic responses and attendant changes in myocardial blood flow and ventricular function that are indices of myocardial ischemia. Emotional provocation with the attendant cognitive demand is associated in the brain with activations in regions involved in processing of cognitive stimuli. Simultaneous with these activations in regions known to be involved with cognitive and emotional function are activations of the effectors responsible for cardiovascular physiologic funtion. Accordingly, studies of the brain during emotional provocation that culminates in myocardial ischemia are cardinal to our understanding of ischemic clinical presentations.