Abstract
Recent findings have deeply changed the current view of coronary heart disease, going beyond the simplistic model of atherosclerosis as a passive process involving cholesterol build-up in the subintimal space of the arteries until their final occlusion and/or thrombosis and instead focusing on the key roles of inflammation and the immune system in plaque formation and destabilization. Chronic inflammation is a typical hallmark of cardiac disease, worsening outcomes irrespective of serum cholesterol levels. Low-grade chronic inflammation correlates with higher incidence of several non-cardiac diseases, including depression, and chronic depression is now listed among the most important cardiovascular risk factors for poor prognosis among patients with myocardial infarction. In this review, we include recent evidence describing the immune and endocrine properties of the heart and their critical roles in acute ischaemic damage and in post-infarct myocardial remodeling. The importance of the central and autonomic regulation of cardiac functions, namely, the neuro-cardiac axis, is extensively explained, highlighting the roles of acute and chronic stress, circadian rhythms, emotions and the social environment in triggering acute cardiac events and worsening heart function and metabolism in chronic cardiovascular diseases. We have also included specific sections related to stress-induced myocardial ischaemia measurements and stress cardiomyopathy. The complex network of reciprocal interconnections between the heart and the main biological systems we have presented in this paper provides a new vision of cardiovascular science based on psychoneuroendocrineimmunology.
Highlights
Until a few years ago, atherosclerosis was considered a “lipid storage disease,” and it was expected that aggressive pharmacological treatment of hypercholesterolemia could virtually eliminate coronary artery pathologies
Results from the Whitehall II study showed that male workers with metabolic syndrome at lower job positions had higher levels of norepinephrine, cortisol and serum IL-6 and manifested a higher heart rate at rest and lower heart rate variability [89]
In an exiguous group of obese college-aged males, Caslin and colleagues showed that an acute mental stress task elicited a vigorous stress reaction, with an increase in heart rate and catecholamine release, increased immune response with inflammatory cytokine synthesis (TNF-α, IL-1 and IL-6) and hormonal changes with a significant reduction in leptin concentrations, without a significant increase in serum cortisol at an early post-task observation time point [90]
Summary
GRAPHICAL ABSTRACT | The current view of coronary heart disease has deeply changed: atherosclerosis is no longer considered a simple lipid storage disorder but a systemic inflammatory disease. Recent findings have fundamentally altered the classical vision of the heart as a “mechanical blood pump” that beats through an internal pacemaker. Chronic depression has ranked among the most important cardiovascular risk factors for poor prognosis in patients with myocardial infarction. Current understanding of the central and autonomic regulation of cardiac functions, namely, the neuro-cardiac axis, provides a physiological explanation that links psycho-emotional stressors and social adversities to acute cardiac event. Psychological distress can precipitate heart function through a dysregulated neuroendocrine and autonomic response. The complex network that links the heart, brain and the main biological systems provides a new vision of cardiovascular science based on psychoneuroendocrineimmunology, a science that studies the reciprocal interconnections between the psyche and nervous, immune and endocrine systems, integrating knowledge derived from the psychological and biological sciences of stress with molecular biology and epigenetic research. ACC, anterior cingulate cortex; HPA, hypothalamic–pituitary–adrenal axis; HRV, heart rate variability; ILs, interleukins; BP, blood pressure
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