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Review
. 2009 Mar;11(2):133-40.
doi: 10.1007/s11886-009-0020-1.

Heart-brain interactions in mental stress-induced myocardial ischemia

Affiliations
Review

Heart-brain interactions in mental stress-induced myocardial ischemia

Robert Soufer et al. Curr Cardiol Rep. 2009 Mar.

Abstract

Myocardial ischemia that results from emotional provocation occurs in as many as 30% to 50% of patients with coronary artery disease during the discourse of their lives. This emotionally provoked or mental stress ischemia is associated with poor prognosis, with emerging treatment strategies. This article outlines the conceptual constructs that support the pathophysiologic underpinnings, and biobehavioral aspects associated with this mental stress ischemia. We review a biobehavioral model in which cognitive stress is transduced in the brain. The response of the brain to psychosocial stress is a highly sophisticated and integrated process by which sensory inputs are evaluated and appraised for their importance in relation to previous experience and current goals. The biologic consequences of such stress transduced in the central nervous system has its effect on cardiovascular flow and function through changes in autonomic balance, which result in various biologic processes that culminate in the perturbation of flow and function of the heart.

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Figures

Figure 1
Figure 1
Top Panel: Brain activation of the Frontal Medial Gyrus and Limbic Hippocampal structures and associated Anterior Cingulate Gyrus. Bottom Panel: Myocardial Blood flow Image during Mental Stress with reversible ischemia of the apex (arrows).
Figure 2
Figure 2
Top panel is the brain activation during mental stress and associated myocardial ischemia. Bottom panel is the brain map of the same subject ischemic to a demand surrogate for exercise with dobutamine infusion. Grey (Green for online version) is activation and black (Red for online version) is deactivation. Brain activations during mental stress occurs in subcortical areas associated with emotion, memory and Neurohormonal sympathetic regulation. Deactivation occurs in the frontal evaluative areas, such as the dorsal lateral prefrontal cortex association with parasympathetic tone. During dobutaine the activations are associated with somatosensory areas in the periphery of the cortex
Figure 3
Figure 3
Mental Stress Provocation results in activation of visceral effectors from the CNS that promote parasympathetic withdrawal (HRV) and accentuation of sympathetic tone (Norepinephrine). This imbalance promotes inflammatory vascular factors which serve to promote vascular dysfunction and results in Mental Stress Ischemia (MSI)

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